Dr. F. Lings Otolaryngology Notes

Arranged by:
Dr. Fouad Shamsan
The contents is according to:
Bailey's Head and Neck Surgery - Otolaryngology (2001)
Cumming's Otolaryngology - Head and Neck Surgery (1999)
The arrangement is according to :
Bailey's Head and Neck Surgery - Otolaryngology (2006)

Table of Contents
I Basic Science & General Medicine:
1- Antimicrobial Therapy …………………………………………………………………………………………..1
2- Microbiology, Infections, & Antibiotic Therapy……………………………………………………..4
3- Degenerative & Idiopathic Diseases………………………………………………………………………7
4- Connective Tissue Diseases…………………………………………………………………………………14
5- Granulomatous Diseases of Head & Neck…………………………………………………………..17
6- Geriatric Otolaryngology…………………………………………………………………………………..…25
7- Headache & Facial Pain……………………………………………………………………………………….28
8- Manifestation of AIDS…………………………………………………………………………………………31
9- Principle Of Surgery (POS) 69 Notes………………………………………………………………..…35
10- Pathology Review ……………………………………………………………………………………………….40
11- Selected Pharmacopia………………………………………………………………………………………..49
12- POS Systemic Response to Injury………………………………………………………………………..56
13- POS Fluid & Electrolyte Management of Surgical patient……………………………………73
14- POS Hemostasis, Surgical Bleeding & Transfusion……………………….74
15- POS Shock…………………………………………………………………………………………………………...92
16- POS Surgical Infections……………………………………………………………………………………….99
17- POS Burns………………………………………………………………………………………………………….108
18- POS Wound Care & Wound Healing…………………………………………………………………125
19- POS Transplantation…………………………………………………………………………………………134
20- POS Surgical complications………………………………………………………………………………163
21- Physiologic Monitoring of Surgical Patient………………………………………………………183
22- POS Notes & Points from Previous Exams……………………………………………………….190
23- Radiotherapy……………………………………………………………………………………………………208
II Rhinology & Allergy:

24- Antimicrobial Guidelines for Acute bacterial Rhinosinusitis………………………….209
25- Olfactory Function & Dysfunction………………………………………………………………….211
26- Nasal Function & Evaluation……………………………………………………………………….….214
27- Sinus Anatomy & Function…………………………………………………………………………….218
28- Nose & Paranasal Sinuses………………………………………………………………………………225
29- Secrets- Nasal Septal Abnormalities………………………………………………………………232
30- Nonallergic Rhinitis………………………………………………………………………………………..233
31- Allergic Rhinosinusitis……………………………………………………………………………………239
32- Nasal Obstruction………………………………………………………………………………………….243
33- Sinus Surgery – External Approach………………………………………………………………..248
34- Midline Nasal Masses……………………………………………………………………………………251
35- Sinus Imaging………………………………………………………………………………………………….258
36- Rhinosinusitis- Current Concept & Management………………………………………….262
37- Endoscopic Sinus Surgery……………………………………………………………………………..272
38- Approaches to Sphenoid Sinuses…………………………………………………………………276
39- Sphenoid Sinus Diseases……………………………………………….…………………………….281
40- Complications of Sinus Surgery……………………………………………………………………284
41- Epistaxis………………………………………………………………………………………………………..289
42- Cumming's- Manifestation of Systemic Diseases of Nose…………………………..295
43- Cumming's- CSF Leaks…………………………………………………………………………………300
44- Pediatric Rhinosinusitis……………………………………………………………………………….306
45- Congenital Malformation of the Nose…………………………………………………………310
46- Juvenile Nasopharyngeal Angiofibroama…………………………………………………….314
47- Limmiere Syndrome……………………………………………………………………………………317
48- Medical Management of Acute Bacterial Sinusits……………………………………..318
49- Mucoceles of the Paransal Sinuses……………………………………………………………..321
50- Radiation induced Sarcoma…………………………………………………………………………336
51- Secrets-Anatomy & Physiology of the Nose………………………………………………..338
52- Secrets- Rhinitis …………………………………………………………………………………………..339
III General Otolaryngology:

53- Cervical Fascia & Spaces……………………………………………………………………………….340
54- Anatomy & Physiology of Salivary Glands…………………………………………………….346
55- Salivary Glands Imaging………………………………………………………………………………….350
56- Nonneoplastic Diseases of the Salivary Glands……………………………………………..355
57- Controversies of Salivary Gland Diseases ……………………………………………………..359
58- Taste……………………………………………………………………………………………………………….361
59- Stomatitis……………………………………………………………………………………………………….364
60- Pharyngitsis…………………………………………………………………………………………….........373
61- Odontogenic Infections…………………………………………………………………………………377
62- TMJ Disorders……………………………………………………………………………………………….382
63- Snoring & OSA………………………………………………………………………………………………..386
64- Deep Neck Infection……………………………………………………………………………………..393
65- Neck………………………………………………………………………………………………………………400
66- Salivary Glands……………………………………………………………………………………………...406
67- Secrets- ENT Manifestation of AIDS……………………………………………………………..408
IV Airway & Swallowing:

68- Bronchosopy & Esophagoscopy…………………………………………………………………..409
69- Upper Digestive Tract Anatomy & Physiology…………………………………………….410
70- Upper Airway Anatomy & Function…………………………………………………………….413
71- Upper Digestive Tract Evaluation & Imaging……………………………………………….417
72- Airway Evaluation & Imaging………………………………………………………………………..419
73- Esophageal Disorders…………………………………………………………………………………421
74- Tracheotomy & Intubation…………………………………………………………………………429
75- Controversies in Upper Airway Obstruction ………………………………………………433
76- Management of Intractable Aspiration………………………………………………………435
77- Evaluation of Dysphonic Patient………………………………………………………………….439
78- Oral Cavity & Pharynx…………………………………………………………………………………..441
V Voice:
79- Alaryngeal Speech…………………………………………………………………………………………….443
80- Laryngitis……………………………………………………………………………………………………………446
81- Hoarseness & VC Paralysis………………………………………………………………………………..451
82- Benign Lesion of the Larynx……………………………………………………………………………...458
83- Controversies in Laryngology……………………………………………………………………………462
84- Cumming's- Larynx Anatomy……………………………………………………………………………..465
85- Cumming's- Electromyogaraphy of Latyngeal & Pharyngeal Muscles……………….470
86- Cumming's- Laryngeal & Pharyngeal Function…………………………………………………..472
87- Cumming's- Neurological Evaluation of Larynx & Pharynx………………………………..478
88- Cumming's- Phonosurgical Procedures……………………………………………………………..483
89- Cumming's- Benign Vocal Fold Disorders…………………………………………………………..488
90- Cumming's- Laser Surgery in Larynx……………………………………………………………………496
91- Voice Rehabilitation after Laryngectomy………………………………………………………….…499
92- Glottic & Subglottic Stenosis……………………………………………………………………………….502
93- Laryngeal Development………………………………………………………………………………………504
94- Larynx…………………………………………………………………………………………………………………..509
VI Trauma:
95- Auricular Trauma Salvage……………………………………………………………………………………512
96- Facial Trauma………………………………………………………………………………………………………514
97- Auricular Trauma…………………………………………………………………………………………………519
98- Laryngeal Trauma…………………………………………………………………………………………………521
99- Management of Soft Tissue Trauma……………………………………………………………………525
100- Mandibular Fractures……………………………………………………………………………..528
101- Maxillary & Periorbital Fractures……………………………………………………………534
102- Fractures of Nasal & Frontal Sinuses………………………………………………………541
103- Penetrating Face & Neck Trauma…………………………………………………………….548
104- Complex Facial Trauma with Plating…………………………………………………………552
105- POS- Trauma……………………………………………………………………………………………..554
VII Pediatric Otolaryngology:

106- Airway Imaging in Children……………………………………………………………………….569
107- Pediatric Sleep Disordered Breathing………………………………………………………571
108- Laryngeal Stenosis……………………………………………………………………………………573
109- Stridor, Aspiration & Cough……………………………………………………………………..578
110- Causatic Ingestion & FB in the Aerodigestive Tract…………………………………584
111- Congenital Neck Masses & Cysts……………………………………………………………..588
112- Congenital Anomalies of the Nose……………………………………………………………593
113- Cleft Lip & Palate………………………………………………………………………………………597
114- Tonsillitis, Tonsillectomy & Adenoidectomy…………………………………………….601
115- Contarvorsies in Tonsillectomy, Adenoidectom & T-tubes………………………606
116- RCTsin Tonsillectomy, Ad, & T-tubes………………………………………………………..608
117- Congenital Anomalies of Aerodigestive Tract………………………………………….609
118- Neonatal Respiratory Disorders……………………………………………………………….613
119- Recurrent Respiratory Papillomatosis………………………………………………………614
120- The Syndromal Child…………………………………………………………………………………618
121- Pediatric Malignancies……………………………………………………………………………..621
122- Otitis Media with Effusion ……………………………………………………………………….627
123- Genetic Hearing Loss…………………………………………………………………………………631
124- Pediatric Audiology…………………………………………………………………………………...636
125- Pediatric Facial Fractures………………………………………………………………………….639
126- Congenital Vascular Lesion………………………………………………………………………643
127- Embryology of Face Lip & Palate………………………………………………………………646
128- ENT Problems in Syndromic Child…………………………………………………………….650
129- Eustachian Tube………………………………………………………………………………………..663
130- Cleft Palate Repaire…………………………………………………………………………………..669
131- Non Genetic HL………………………………………………………………………………………….672
132- Pediatric Taracheotomy Decanulation………………………………………………………675
133- SNHL Evaluation…………………………………………………………………………………………676
134- Tonsils & Adenoid……………………………………………………………………………………..678
VIII Head & Neck Surgery:

135- Carotid Body Tumors………………………………………………………………………………. 737
136- Cumming's- Hemangioma & Vascular Anomalies of H & N ……………….......743
137- Cumming's- Malignant Lesion of Oral Cavity……………………………………………749
138- Principle of Chemotherapy………………………………………………………………………753
139- Principle of Radiation Oncology……………………………………………………………….758
140- Cutaneous Malignancies………………………………………………………………………….764
141- Malignant Melanoma……………………………………………………………………………….772
142- Neoplasm of Nose & PNS………………………………………………………………………….778
143- Orbital Tumors……………………………………………………………………………………………788
144- Salivary Glands Neoplasm………………………………………………………………………….795
145- Lip Cancers………………………………………………………………………………………………….805
146- Neoplasm of Oral Cavity…………………………………………………………………………..…811
147- Odontogenic Cysts, Tumors, & Related Jaw Lesions…………………………………..818
148- Head & Neck Dissection…………………………………………………………………………...…825
149- Controversies in Management of N0 Neck………………………………………………….834
150- Cumming's- Malignant Tumors of Larynx & Hypopharynx…………………………..838
151- Lymphoma of the Head & Neck…………………………………………………………………..842
152- Thyroid Diseases & Surgery………………………………………………………………………….847
153- Parathyroid Diseases & Surgery……………………………………………………………………859
154- Nasophryngeal Carcinoma……………………………………………………………………………864
155- Oropharyngeal Cancers…………………………………………………………………………………870
156- Hypopharyngeal Cancers………………………………………………………………………………875
157- Cervical Esophageal Cancers………………………………………………………………………880
158- Early Glottic Carcinoma………………………………………………………………………….……884
159- Early Supraglottic Carcinoma………………………………………………………………………888
160- Early Glottic & Supraglottic Carcinoma……………………………………………………….891
161- Advance Cancer of Larynx………………………………………………………………………….893
162- Tracheal Tumors…………………………………………………………………………………………900
163- Vascular Tumors………………………………………………………………………………………….903
164- Cranial Base Surgery…………………………………………………………………………………...911
165- Surgical Techniqu to Enhance Prosthetic Rehabilitation…………………………….926
166- Cut. Malig. Merk Cell Carcinoma………………………………………………………………...929
167- Neck Cancers – Unknown Primary………………………………………………………………931
168- Osteoradionecrosis & Hyperbaric Oxygen Therapy…………………………………….933
169- TNM Staging of Head & Neck Tumors…………………………………………………………935
170- Tracheal Resection……………………………………………………………………………………..948
171- Treatments Outcomes………………………………………………………………………………..949
172- Velopharyngeal Insufficiency………………………………………………………………………954
IX Otology:
173- Audiological Tests………………………………………………………………………………………958
174- Cumming's – Tympanostomy Tubes…………………………………………………………..962
175- Development of Ear …………………………………………………………………………………..965
176- Anatomy & Physiology of Hearing………………………………………………………………971
177- Vestibular Function & Anatomy…………………………………………………………………977
178- Balance Function Tests……………………………………………………………………………….981
179- Audiotary Assesment………………………………………………………………………………….986
180- Cumming's – Temporal Bone Anatomy………………………………………………………994
181- Neurophysiologic Intraoperative Monitoring……………………………………………1006
182- Imaging Studies of Temporal Bone1…………………………………………………………1009
183- Imaging Studies of Temporal Bone2…………………………………………………………1015
184- Imaging Studies of Temporal Bone.…………………………………………………………..1020
185- Infections of the External Ear…………………………………………………………………….1031
186- Neoplasm of the Ear & Lateral Skull Base………………………………………………….1037
187- Congenital Aural Atresia…………………………………………………………………………….1045
188- Intracranial & Intratemporal Complications of OM……………………………………1050
189- Middle Ear & Temporal Bone Trauma………………………………………………………..1056
190- Cholesteatoma……………………………………………………………………………………………1061
191- Surgery of Mastoid & Petrosa…………………………………………………………………….1066
192- Reconstruction of TM & Ossicular Chain…………………………………………………….1074
193- Otosclerosis………..………………………………………………………………………………………1078
194- Acute Paralysis of Facial nerve…………………………………………………………………...1083
195- Otologic Manifestation of Systemic Diseases……………………………………………..1095
196- Infections of the Labyrinth…………………………………………………………………………..1101
197- Noise Induced HL……………………………………………………………………………………….1107
198- Ototoxicity……….…………………………………………………………………………………………1110
199- CPA Tumors………………………………………………………………………………………………..1112
200- Sudden Sensory Hearing Loss…………………………………………………………………….1120
201- Tinnitus………………………………………………………………………………………………………1123
202- Autoimmune Inner Ear Diseases……………………………………………………………....1127
203- Aging in the Auditory & Vestibular System……………………………………………....1129
204- Cochlear Implant & Other Implantable Prosthesis………….…………………………1132
205- Hearing Aid & Assistive Listening Devices………………………………………………….1138
206- PERIPHERAL VESTIBULAR DISORDERS……………………………….……………………….1143
207- CENTRAL VESTIBULOPATHY………………………………..........................................1147
208- MED. MANAGEMENT OF VEST. DISORDERS AND VEST. REHABILITATION….1151
209- SURGICAL MANAGEMENT OF VESTIBULAR DISORDERS…………………………….1153
210- Cumming's- TEMPORAL BONE NEOPLASMS AND LATERAL CRANIAL BASE
SURGERY…………………………………………………………………………………………………………………1156
211- Cumming's- AGING AND AUDITORY SYSTEMS – PRESBYCUSIS….……………….1160
212- CONGENITAL AURAL ATRESIA…………………………………………………..………………..1162
213- Ear & Temporal Bone………………………………………………………………….……………….1165
214- ELECTRONYSTAGMOGRAPHY……………………………………………………………………..1171
215- MENIERE’S DISEASE………………………………………………………………….……………..…1175
216- ELECTRONYSTAGMOGRAPH.,……………………………………………………………………..1177
217- FACIAL NERVE ANATOMY…………………………………………………………………………..1189
218- The Halmagyi (Head Impulse)Test ……………………………………………………………..1192
219- Head-Shaking Nystagmus (HSN) ……………………………………………………………....1193
220- Malignant Otitis Externa ………………………………………………………………………..….1194
221- NEOPLASMS OF THE EAR AND LATERAL SKULL BASE PATHOLOGY…………….1195
222- Otoplasty………………………………………………………………………………………………….…1197
223- PERIPHERAL VESTIBULAR DISORDERS……………………………………………….……...1198
224- TBD – Lateral Approach…………………………………………………………………….…..…..1208
225- TBD – Middle Fossa Approach……………………………………………………………………1213
226- Temporal Bone Anatomy……………………………………………………………………………1215
227- Vestibulo-Ocular Reflex (VOR)…………………………………………………………………..1230
X Facial Plastic & Reconstructive Surgery:

228- Local Skin Flaps……………………………………………………………………………………………1231
229- MICROVASCULAR FREE FLAPS…………………………………………………………………..1238
230- MANDIBULAR RECONSTRUCTION………………………………………………………..……1247
231- SURGICAL RECONSTRUCTION AFTER MOHS SURGERY……………………………..1253
232- SCAR CAMOUFLAGE……………………………………………………………………………….…1256
233- NASAL RESTORATION WITH FLAPS AND GRAFTS- Large defect ……………….1259
234- NASAL RESTORATION WITH FLAPS AND GRAFTS- Small defect…………………1263
235- SURGERY FOR EXOPHTHALMOS………………………………………………………………..1265
236- FACIAL REANIMATION……………………………………………………………………………….1268
237- FACIAL ANALYSIS………………………………………………………………………………………..1273
238- PREOPERATIVE EVALUATION OF THE AESTHETIC SURGERY PATIENT……….1278
239- SURGICAL ANATOMY OF THE NOSE………………………………………………………….1280
240- INTRODUCTION TO RHINOPLASTY…………………………………………………………….1284
241- EXTERNAL RHINOPLASTY APPROACH……………………………………………………..…1288
242- REFINEMENT OF THE NASAL TIP………………………………………………………………..1290
243- SPECIAL CONSIDERATIONS IN RHINOPLASTY…………………………………………..…1294
244- REVISION RHINOPLASTY………………………………………………………………………….…1298
245- BLEPHAROPLASTY………..…………………………………………………………………………….1302
246- THE AGING FACE (RHYTIDECTOMY)………………………………………………………..…1306
247- THE AGING NECK………………………………………………………………………………………..1311
248- THE AGING FOREHEAD………………………………………………………………………………1312
249- CONGENITAL AURICULAR MALFORMATION………………………………………………1318
250- CHIN AND MALAR AUGMENTATION……………………......................................1322
251- CHEMICAL PEELING…………………………………………………………………………………….1325
252- CERVICOFACIAL LIPOSURGERY……………………………………………………………………1328
253- MANAGEMENT OF BENIGN FACIAL LESIONS……………………………………………..1331
254- MANAGEMENT OF ALOPECIA………………………………......................................1336
255- LASER SKIN RESURFACING…………………………………………………………………………1338
256- TISSUE EXPANDERS…………………………………………………………………………………...1343
IX OTOLARYNGOLOGY FACTS AND POINTS……………………………………….………………1345
IIX Review Questions:

- IN FACIAL PLASTICS AND RECONSTRUCTIVE SURGERY…………………………………………..1355
- IN GENERAL OTOLARYNGOLOGY…………………………………………………………………………...1361
- IN HEAD AND NECK ONCOLOGY………………………………………………………………………………1367
- IN LARYNGOLOGY…………………………………………………………………………………………………..1378
- IN OTOLOGY AND NEUROTOLOGY……………………………………………………………………….…1381
- IN PEDIATRIC OTOLARYNGOLOGY…………………………………………………………………………..1394
- IN RHINOLOGY…………………………………………………………………………………………………………1402
- IN TRAUMA………………………………………………………………………………………………………………1407
MICROBIOLOGY AND DRUG SELECTIONS
FOR TREATMENT OF INFECTIONS
IN THE EAR, NOSE, THROAT, HEAD AND NECK
ACUTE OTITIS MEDIA
Microbiology Primary Alternatives
-Streptococcus pneumoniae (25%) -amoxicillin or clavulin -cefpodoxime, cefdinir

-Hemophilus influenzae (20-25%) -high-dose amoxicillin or -cefuroxime, cefditoren
-Moraxella catarrhalis (10-20%) clavulin if pneumococcal -cetriaxone IM (one injection
-Streptococcus pyogenes (group A - resistance every other day x 3)
2%) -levo-gati-moxifloxacin (adults)
-Staphylococcus aureus (1%) -azithromycin
-others (20%)
-mixed infections (5%)
-children < 2ya, pts with frequent OM, previous Abx within 3 months, seriously ill high dose
amoxcillin/clavulanate or ceftriaxone IM
-for high-penicillin-resistant pneumococcal strains:
-ceftriaxone IM or IV
-levo-gati-moxifloxacin (adults)
-vancomycin IV
-treatment course: 5 days usually
ACUTE BULLOUS MYRINGITIS and ACUTE SUPPURATIVE OTITIS MEDIA

-in absence of prior tympanic membrane perforation or cholesteatoma are variants of acute otitis media
-caused by the same organisms and treated with the same agents
PERSISTENT OTITIS MEDIA WITH EFFUSION

-if asymptomatic, antibiotics not required
ACUTE MASTOIDITIS
-Streptococcus pneumoniae -vancomycin IV plus ceftriaxone -levofloxacin IV

-Streptococcus pyogenes (group A) IV -gatifloxacin IV
-coag-negative Staphylococcus -moxifloxacin IV
-others: -clindamycin IV plus ceftriaxone
-S. aureus IV
-hemophilus -ampicillin/sulbactam IV
-proteus
-bacteroides
F.Ling - Antimicrobial Therapy (1)
1
CHRONIC SUPPURATIVE OTITIS MEDIA
-with TM perforation, with or without cholesteatoma
-Pseudomonas aeruginosa -ototopicals: -adjunctive therapy

-Staph. aureus and epidermidis -ofloxacin -oral ciprofloxacin +/-
-Proteus sp. -ciprofloxacin clindamycin
-Klebsiella sp. -IV pip/tazo
-E. coli
-anaerobes with cholesteatoma -IV ceftazidime +/- clindamycin
ACUTE (DIFFUSE) OTITIS EXTERNA
-Pseudomonas aeruginosa -alcohol/acid mixtures -neomycin/polymyxin/

-S. aureus -ciprofloxacin hydrocortisone
ACUTE LOCALIZED OTITIS EXTERNA (FURNUCULOSIS)
-S. aureus -cephalexin -clindamycin

-cloxacillin
OTOMYCOSIS
-Aspergillus niger -clotrimazole solution -acetic/citric acids in alcohol

-Aspergillus flavus -non prescription: (VoSol)
-Aspergillus fumigatus -3% boric or 2% acetic acid in -aqueous merthiolate
-Candida albicans 70% isopropyl alcohol -betadine
-Gentian violet
-M-cresol acetate (Cresylate)
-boric acid/iodine powder
2
NECROTIZING (“MALIGNANT”) OTITIS EXTERNA
-Pseudomonas aeruginosa -topical ciprofloxacin
PLUS
-oral antipseudomonas quinolone
(Cipro)
PLUS added intravenous

antipseudomonals:
-ceftazidime or cefepime
-ciprofloxacin or levofloxacin
-piperacillin/tazobactam plus:
-gentamicin or tobramycin
or amikacin
-imipenem or meropenem
ACUTE RHINOSINUSITIS
-Hemophilus influenzae (38%) -for mild, no prior treatment -for moderate-severe or prior treated
-Streptococcus pneumoniae -amoxicillin +/- clavulanate -clavulin
(37%) -erythromycin plus TMP/SMX or -double dose amoxicillin (90
-other hemophilus sp (8%) doxycycline mg/kg/day children, 3-4 g/day
-Streptococcus pyogenes (group adults, in divided doses)
A - 6%) -respiratory quinolones
-Moraxella catarrhalis (5%) -levofloxacin
-alpha streptococci (3%) -gatifloxacin
-gram negative bacilli/mixed -moxifloxacin
anaerobes (3%) -cefpodoxim, cefdinir, cefuroxime,
cefditoren
-length of treatment: courses of 3, 4, 5 and 8 days yield similar cure rates as do 10 day courses
-nonresponders (in 5 days) will need to be switched to one or the alternative agents to treat virulent or resistant
bacteria for 10-14 days or more with even a third agent
3
MICROBIOLOGY, INFECTIONS AND ANTIBIOTIC THERAPY
ANTIMICROBIAL AGENTS
Penicillins
-pen G and V:
-highly active against:
-Strep pyogenes (B-hemolytic group A)
-Strep pneumoniae
-actinomycosis
-inactivated by penicillinase (B-lactamase):
-S. aureus
-H. influenzae
-M. catarrhalis
-S. pneumoniae: becoming increasingly resistant to penicillins and cephalosporins due to protein
binding
-antistaphylococcal penicillins
-methicillin, oxacillin, cloxacillin, dicloxacillin, nafcillin
-resist penicillinase
-aminopenicillins:
-ampicillin, amoxicillin
-extend activity spectrum to gram-negative organisms:
-Proteus, E. coli, H. influenzae
-resistance in B-lactamase producing organism
-augmented penicillins:
-clavulanate (amoxil) and sulbactam (ampicillin)
-for management of staphylococci, H. influenzae, M. catarrhalis, anaerobic organisms
Cephalosporins
-commonly and safely used by pts with history of penicillin rashes
-first generation:
-Keflex and Ancef:
highly effective against gram-positive organisms such as streptococci, pneumococci
except for penicillin-resistant strains, and staphylococci except MRSA
-mostly used for S. aureus
-second-generation:
-cefuroxime:
-highly active against gram-positive cocci
-H. influenzae and M. catarrhalis including pen-resistant strains
-penetrates blood-brain barrier fairly well
-third-generation:
-cefixime:
-oral agent highly effective against H. influenzae and M. catarrhalis
-ceftriaxone:
-parenteral agent effective against H. influenzae, M. catarrhalis, S. pneumoniae, N.
meningitidis, N. gonorrheae
-first choice for treating patients with intracranial and orbital complications of acute
sinusitis and otitis media
-usually less active against gram-positive bacteria
-anaerobic bacteria are also relatively resistant
F.Ling - Antibiotics (1)
4
Other B-Lactam Antibiotics
-imipenem and meropenem
-active against S. pyogenes, most S. pneumoniae organisms, S. aureus, H. influenzae, B. fragilis
and most anaerobic organisms and the coliforms including P. aeruginosa
-used as single agent against infection by unidentified organisms but CSF penetration is not assured
Macrolides
-has anti-inflammatory effect
-elevate theophylline levels
-erythromycin
-effective for respiratory infections d/t streptococci, most pneumococci, mycoplasmata and
chlamydiae, legionellosis, diptheria, and pertussis
-azithromycin and clarithromycin
-extend antimicrobial activity to include H. influenzae and M. catarrhalis
Clindamycin
-highly active against gram-positive cocci, including many but not all strains of penicillin-resistant
pneumococci
-effective against S. aureus and anaerobic infections of the aerodigestive tract (B. fragilis)
-risk of pseudomembranous colitis
Tetracyclines
-effective against Mycoplasma, Chlamydia, and Legionella
-stain enamel in forming teeth: avoided in children younger than 10 and pregnant women
Quinolones, Fluoroquinolones
-broad spectrum
-elevate theophylline levels
-potential for cartilage damage and arthropathy in children
-ciprofloxacin and ofloxacin:
-antipseudomonas quinolones
-levofloxacin, gatifloxacin, gemifloxacin:
-respiratory quinolones
-for respiratory and pharyngeal infections
-effective against B-hemolytic S. pyogenes, S. pneumoniae, S. aureus, H. influenzae, M.
catarrhalis , Mycoplasma, Chlamydia, Legionella, Bordetella pertussis
Vancomycin
-highly active against gram-positive cocci including MRSA, penicillin-resistant strains of pneumococci,
enterococci, and gonococci
-high concentrations in patients with renal impairment can cause ototoxicity
Metronidazole
-highly active against anaerobic bacteria
-B. fragilis
-all aerobic bacteria are resistant to this agent
-penetrates BBB well
Aminoglycosides
-used against P. aeruginosa and other hospital-acquired infections
-ineffective in anaerobic infections
-risk of ototoxicity (~10%)
5
Sulfonamides
-older agents effective in the management of H. influenzae but not of pneumococcal, streptococcal, and
staphylococcal infections
TREATMENT STRATEGIES
Otitis Media
-S. pneumoniae, H. influenzae, M. catarrhalis
-first line:
-amoxil:
-most strains of S. pneumoniae
-H. influenzae (20% resistant) and M. catarrhalis (80% resistant)
-second line:
-clavulin, 2nd generation cephalosporin
-macrolides
-high dose penicillin for penicillin resistant organisms
-for high-level resistance:
-vancomycin, levofloxacin, gatifloxacin, moxifloxacin, gemifloxacin
Sinusitis
-acute:
-same bacteria as in OM
-same drug choices
-intracranial or orbital complications:
-pneumococcal infection suspected Rx ceftriaxone, cefuroxime or trovafloxacin
-chronic:
-anaerobes and S. aureus
-clindamycin or clavulin
Pharyngitis
-caused by S. pyogenes in 30%
-also N. gonorrhoeae, Mycoplasma, Chlamydia and H. influenzae
Tonsillitis
-frequently caused by S. pyogenes
-clindamycin, cephalexin effective
Mastoiditis
-same treatment as AOM
-pneumococci and H. influenzae tend to intracranial extension Rx ceftriaxone
-chronic suppurative otomastoiditis including cholesteatoma: S. aureus, Proteus, B. fragilis and other
anaerobic organisms
-Pseudomonas
Suppurative Otitis
-necessitates combination drug therapy:
-polymyxin for pseudomonal infection and neomycin for S. aureus, Proteus organisms and others
6
DEGENERATIVE AND IDIOPATHIC DISEASES
BONY LESIONS OF THE SKULL
Fibrous Dysplasia
-medullary bone replaced by fibroosseous tissue
-three clinical forms:
-monostotic FD (75-80%)
-polyostotic FD (20-25%)
-Albright syndrome:
-polyosotic fibrous dysplasia associated with abnormal skin pigmentation, precocious
puberty and other non-skeletal diseases
-20-25% of polyostotic pts
-onset usually <30 ya
-90% asymptomatic
-symptoms: local swelling, pain, displaced teeth or nerve-compression symptoms
-most commonly affected bones: ribs, femur for MFD; femur, tibia for PFD
-head and neck (25%): maxilla and mandible
-radiographic sign: expanded “ground glass” lesion
-histology: marrow replaced by whorled spindle cells with lack of “osteoblastic rimming”
-1/200 cases undergoes malignant degeneration osteosarcoma
-treatment: complete excision
Ossyfying Fibroma
-similar to fibrous dysplasia, but onset is 10 years later
-usually more discrete
-osteoblastic rimming present
-treatment: excision
Paget Disease
-most often occurs between 55-70 ya
-90% have polyostotic disease
-classic symptoms: enlarging skull, dorsal kyphosis, bowing of legs
-other symptoms:
-bone pain (most common)
-spinal root compression
-normal pressure hydrocephalus
-repeated fracture with nonunion
-disease process:
-lytic phase: increased osteoclastic activity with replacement with vascular stroma
-mixed phase: increased osteoblastic activity with osteoclastic activity “cotton wool” appearance
on X-rays
-osteoblastic phase sclerosis on X-rays
-elevated ALP levels and increased urine hydroxyproline levels; hypercalcemia
-occurs more commonly in skull than in face
-can undergo malignant transformation to osteosarcoma ~1-5%
-treatment: calcitonins, disodium etidronate or mithramycin
F.Ling - Degenerative and Idiopathic Diseases (1)
7
Fibrous Dysplasia Compared with Paget’s Disease
Characteristic Fibrous Dysplasia Paget’s Disease
age <30 yr >40 yr
presentation monostotic polyostotic
most commonly affected bones ribs, femur lumbar sacrum
most commonly affected head and neck region maxilla skull
treatment curettage calcitonin
RECURRENT PAROTID SWELLING DIFFERENTIAL

DIAGNOSES FOR
-Mikulicz disease: RECURRENT PAROTID
-autoimmune “pseudosialectasis” localized to parotid gland SWELLING
-primary Sjogren: Autoimmune diseases
-sicca syndrome: autoimmune parotitis associated with -Mikulicz’s disease
xerophthalmia or xerostomia -Primary Sjogren’s
-secondary Sjogren: -Secondary Sjogren’s
Mikulicz’s syndrome
-primary Sjogren associated with connective tissue disorder -recurrent sialadenitis
-Mikulicz syndrome: all cases of recurrent parotid swelling that are not -sialosis
autoimmune conditions -multinodular gland
-sialographic appearance of recurrent parotid swelling:

-autoimmune diseases -normal main ductal system, diffuse spherical collection of contrast
material
-chronic sialadenitis -dilation and stricture of main ductal system, rare sialectasis
-sialosis -enlarged gland, sparse peripheral ducts
-multinodular gland -displacement of ductal system around multiple masses
Autoimmune Parotid Swelling

-on x-ray, globular collections are d/t weakened acini allowing extravasation of contrast material
-usually presents as unilateral recurrent swelling that is painless, of unpredictable duration and rarely
associated with edema
-Sjogren syndrome
-second most common connective tissue disorder
-ages 40-60
-F:M = 9:1
-xerostomia, xerophthalmia, parotid swelling
-other symptoms: dry skin, vaginal pruritus, arthralgia, myalgia
-autoantibodies:
-SS-A and SS-B (primary Sjogren)
-HLA-B8 and HLA-DW3 (primary Sjogren)
-HLA-DW4 (secondary Sjogren)
-other: RF, ANA may be present; ESR elevated; polyclonal hypergammaglobulinemia
-5% develop lymphoproliferative neoplasm
-lip biopsy:
-focus is 50 or more lymphocytes, histiocytes or plasma cells
-score determined by counting # foci in 4 mm2
-focus score > 1 characteristic of Sjogren syndrome
-treatment: supportive; XRT and parotidectomy an option
8
Mikulicz Syndrome
-recurrent sialadenitis:
-unilateral, swollen, red, tender gland with purulent discharge
-sialography: dilation and focal narrowing of Stensen duct
-treatment:
-demonstration and removal of any stones
-antibiotics, warm compresses and sialogogues
-excision of gland in severe cases
-sialosis:
-recurrent bilateral nontender parotid swelling
-secondary to various conditions:
-cirrhosis, diabetes, alcoholism, malnutrition, ovarian insufficiency, thyroid
insufficiency, pancreatic insufficiency
-drugs: sulfisoxazole, phenalbutazone, catecholamines, iodide-containing compounds
-multinodular gland:
-autoimmune diseases
-granulomatous diseases: tuberculosis, sarcoidosis
-lymphoproliferative neoplasms
-Warthin’s tumour
-other tumours
MIDLINE DESTRUCTIVE DISEASES
“Lethal midline granuloma”

-Wegener’s granulomatosis
-polymorphic reticulosis
-idiopathic midline destructive disease
-non-Hodgkin lymphoma
Wegener Granulomatosis
-vasculitis, multinucleated giant cells and palisading histiocytes
-granuloma and typical polymorphonuclear cells
-tx: azathioprine, cyclophosphamide and steroids
Lymphomatoid Granulomatosis (T-Cell Lymphoma)

-aka: angiocentric T-cell lymphoma, polymorphic reticulosis, midline lethal granuloma
-composed of a polymorphic rather than a monomorphic infiltrate
-occurs in all age groups; peak 40-50 ya
-M:F = 1.7:1
-usually present with pulmonary symptoms: cough, SOB, hemoptysis
-H+N symptoms:
-ulcerating lesions of upper respiratory tract usually confined to nose and paranasal sinuses
-similar to Wegener granulomatosis
-histology:
-sheets of atypical polymorphonuclear cells
-no granuloma or palisading histiocytes
-treatment: XRT for localized disease; cyclophosphamide and prednisone for multiregional disease
-mortality rate: 50-70%
Malignant Lymphoma
9
Idiopathic Midline Destructive Disease
-differentiated histologically from Wegener granulomatosis and lymphomatoid granulomatosis
-composed of sheets of typical polymorphs; no granuloma and no vasculitis
Polyarteritis Nodosa
-affects only small to medium-sized arteries
-rarely affects lungs
Allergic Granulomatosis and Vasculitis

-Churg-Straus syndrome:
-asthma, systemic vasculitis and tissue and peripheral eosinophilia
-polyps, rhinorrhea, obstruction, crusting and septal perforation
-palisading histiocytes, granuloma, vasculitis, typical polymorphs
Foreign-Body Granulomas
-cocaine use; intranasal steroid injections for allergies
-multinucleated giant cells and presence of foreign material
-absence of vasculitis
NONNEOPLASTIC NONTRAUMATIC SUBGLOTTIC STENOSIS
-Wegener’s, amyloidosis, sarcoidosis, relapsing polychondritis
Amyloidosis
-deposition of extracellular fibrillar proteins in various tissues
-rare in pediatric age group
-types:
-primary systemic form (56%):
-heart, tongue, GI tract
-secondary systemic form (8%):
-associated with chronic destructive diseases: tuberculosis, rheumatoid arthritis and
osteomyelitis
-kidney, adrenals, liver, spleen
-localized form (9%):
-any of above
-myeloma associated (26%):
-heart, tongue, GI tract
-histochemical studies: amyloid composed of light-chain immunoglobulins
-extracellular proteins that are green and birefringent under polarized light after staining with Congo red
-orbit most common site of deposition for localized amyloid in H+N
Sarcoidosis
-idiopathic disease characterized by noncaseating granuloma
-usually occurs in 3rd and 4th decade
-may be associated with impaired T-cell function, delayed hypersensitivity and energy
-H+N symptoms:
-cervical adenopathy (most common)
-deposits in supraglottic larynx dysphonia, dyspnea, dysphagia
-nasopharyngeal lesions
-parotid gland enlargement
-neurologic impairment
10
-orbital mass or lacrimal gland enlargement
-uveitis
-diagnosis:
-CXR - mediastinal lymphadenopathy
-hypercalcemia
-ACE (angiotensin converting enzyme) levels used to follow course of disease
-Kveim reaction: granulomatous reaction appearing 4 weeks after intradermal injection of sarcoid
spleen or lymph node extracts (experimental)
-treatment: oral steroids
Relapsing Polychondritis
-inflammation of cartilage and other tissues with a high concentration of glycosaminoglycans
-manifestations:
-auricular chondritis (50%)
-nonerosive polyarthritis (50%)
-nasal chondritis (15%)
-inflammation of ocular structures (15%)
-chondritis of respiratory tract (15%)
-cochlear and vestibular damage
-chondritis rapidly develops and resolves in 5-10 days
-involved cartilage becomes deformed: saddle-nose deformity; cauliflower ear
-mortality related to respiratory involvement (ie laryngeal collapse) or cardiovascular disease (eg. aneurysm
or valvular insufficiency)
-treatment: symptomatic; steroids for life threatening conditions
THYROIDITIS
Hashimoto Thyroiditis
-most common form of thyroiditis
-goitrous thyroiditis associated with elevated levels of antithyroid antibodies
-slowly progressive painless enlargement
-histology: lymphocytic infiltration with fibrosis and Hurthle cell change of follicular cells
-disease progresses to hypothyroidism
-most specific test: antimicrosomal antibody; positive in 90% of pts
-treatment: thyroid hormone replacement; FNA for solid lesions to r/o associated lymphoma or neoplasms
Subacute Thyroiditis
-two types:
-granulomatous
-thought to be caused by viral infection
-painful
-infiltration of giant cells
-transient hyperthyroidism transient hypothyroidism
-complete recovery in most cases; 10% have persistent goiter
-lymphocytic
-painless
-lymphocytic infiltrate
-permanent goiter and hypothyroidism more commonly seen than in granulomatous
thyroiditis
11
Acute Suppurative Thyroiditis
-mostly seen in immunocompromised
-typical pathogen: S. aureus
-treatment: antibiotics and surgical drainage
Reidel Thyroiditis
-rare fibrosing thyroiditis
-seen predominantly in women
-treatment: thyroid hormone replacement or surgical release of obstruction if required
12
CONNECTIVE TISSUE DISEASES
Autoantibody Relationships
-SLE -anti-native DNA, Anti-Sm

-RA -RF, Anti-RA33
-Sjogren -Anti-Ro (SS-A), Anti-La (SS-B)
-Systemic sclerosis -Anti-Scl-70, Anti-centromere
-Polymyositis/dermatomyositis -Anti-Jo-1
-Mixed connective tissue disease -Anti-U1-RNP
-WG -c-ANCA
-prevailing histopathologic feature is varying amount of connective tissue and blood vessel inflammation
with abundant fibrinoid deposits
SYSTEMIC LUPUS ERYTHEMATOSUS
Head and Neck Manifestations

-skin and mucosal lesions
-malar rash in 50% of pts
-oral ulcerations; secondary moniliasis and xerostomia
-orthokeratosis and parakeratosis
-keratotic plugging, acanthosis and pseudoepitheliomatous hyperplasia
-ulceration or perforation of nasal septum: 3-5%
-laryngeal and tracheal manifestations
-true vocal fold thickening or paralysis
-cricoarytenoid arthritis
-subglottic stenosis
-acute enlargement of parotid glands: up to 10%
-neuropathy: cranial nerve dysfunction
Treatment
-rheumatologic assessment
-NSAIDS, topical and low-dose systemic steroids, antimalarial
-low-dose methotrexate
-high-dose steroids and azathioprine and cyclophosphamide reserved for visceral involvement
-oral ulcers:
-Klack’s solution: tetracycline, cortisone, diphenydramine, nystatin
RHEUMATOID ARTHRITIS
-inflammation of synovial tissue with symmetric involvement of peripheral joints

-TMJ dysfunction
-cricoarytenoid joint involvement
-~30% pts with RA are hoarse
-may present with dyspnea on exertion, anterior neck or ear pain, fullness in throat, dysphagia and
aspiration
-ossicular joint involvement rare conductive hearing loss during RA flare
F.Ling - Connective Tissue Diseases (1)
13
Treatment
-salicylates, NSAIDs, gold salts, penicillamine, hydroxychloroquine, immunosuppressive agents
SJOGREN SYNDROME
-see Ch 13 - Degenerative and Idiopathic Diseases
-increased (33-44 times) risk of lymphoma
-salivary gland biopsy best single criterion (spec 83%, sens 81%)
SYSTEMIC SCLEROSIS

-typical facies: tight skin, thin lips, vertical perioral furrows
-dysphagia most common initial complaint
-decreased or absent peristalsis with mild to moderate dilatation
-decreased ability to open mouth secondary to skin changes
-skin manifestations: telangiectasia, calcinosis, linear scleroderma
-laryngeal involvement: voice change
Treatment
-symptomatic
-PPIs for reflux esophagitis
POLYMYOSITIS AND DERMATOMYOSITIS
-characterized by proximal muscle weakness and nonsuppurative inflammation of skeletal muscle

-weakness of neck muscles
-difficulties in phonation and deglutition d/t weak tongue muscles
-nasal regurgitation
-dysphagia
Treatment
-steroids for symptomatic patients
-methotrexate and other immunosuppressives
RELAPSING POLYCHONDRITIS
-see Ch 13 - Degenerative and Idiopathic Diseases
VASCULITIDES
-rare: 1/100000 per year
-M=F; 5th or 6th decade
-involves small and medium-sized arteries
-ENT manifestations few:
-thromboembolic occlusion of end arteries of inner ear
14
-sudden bilateral SNHL
-vestibular disturbance
-cranial nerve palsies
Churg-Straus Syndrome
-allergic angiitis granulomatosis
-systemic small-vessel vasculitis, extravascular granulomas, hypereosinophilia
Hypersensitivity Vasculitides
-include hypersensitivity angiitis, Henoch-Schonlein purpura, cryoglobulinemia vasculitis
-1/100000 per year
-triad: respiratory tract granuloma, vasculitis, glomerulonephritis
-white; 5th decade
-typical clinical features: bilateral pneumonitis (95%), chronic sinusitis (90%), mucosal ulceration of
nasopharynx (75%) and evidence of renal disease (80%)
-most common oral cavity findings: hyperplasia of gingiva and gingivitis
-subglottic stenosis in 8.5%: poor prognostic sign
-otologic problems in 20-25%: serous otitis media, suppurative otitis media, SNHL, pinna changes
Giant Cell Arteritis

-headache (47%)
-tender temporal artery (50%)
-jaw claudication (50%)
-ESR > 50 mm/h
-dx: temporal artery biopsy
-tx: corticosteroids
Behçet Disease
-vasculitis affecting Japanese and Mediterranean population
-3rd decade
-oral and genital ulcers and uveitis or iritis
-aphthous-like ulcers; punched out and covered with a pale pseudomembrane
-heal in a few days with scarring
-morbidity secondary to CNS involvement, arthritis, and large-vessel arthritis
-tx of ulcers: corticosteroid creams
Cogan Syndrome
-Meniere-like audiovestibular dysfunction, interstitial keratitis, and nonreactive tests for syphilis
-bilateral deafness results in 65% of cases
-accompanied by large- or medium-vessel systemic vasculitis
Kawasaki Disease
-mucocutaneous lymph node syndrome
-pediatric age group
-most common cause of acquired heart disease in children
-symptoms:
-fever (spiking despite Abx treatment)
-conjunctivitis
-red and dry lips
-erythema of oral mucosa
15
-polymorphous truncal rash
-desquamation of fingers and toes
-cervical lymphadenopathy
-“strawberry tongue”
-20-25% untreated children develop coronary artery dilatation or aneurysm
-death from rupture or thrombosis of coronary aneurysm from 2-12 weeks after onset of disease
-treatment with IV gammaglobulin and aspirin in first 10 days reduce incidence of coronary abnormalities
10-fold
16
GRANULOMATOUS DISEASES
OF THE HEAD AND NECK
NEOPLASTIC DISORDERS
Histiocytosis X
-sheets of polygonal histiocytes (Langerhans’ cells) with variable eosinophil, plasma cells, and
lymphocytes
-Langerhans’ cells = histiocytes containing cytoplasmic inclusions known as X bodies
-otitis media most frequent otologic finding
Eosinophilic Granuloma
-localized form of histiocytosis X
-affects children and young adults
-osteolytic lesions with predilection for frontal and temporal bones
-other symptoms:
-proptosis (sphenoid involvement)
-acute mastoiditis
-middle ear granulation tissue
-tympanic membrane perforations
-facial paralysis
-tx: surgical excision; XRT for inaccessible lesions
-excellent prognosis
Hand-Schuller-Christian Disease
-chronic disseminated form of histiocytosis X
-presents in children and young adults (rare in elderly)
-classic triad in 10%:
-skull lesions (polyostotic), exophthalmos and diabetes insipidus
-other symptoms:
-facial paralysis
-external auditory canal polypoid lesions
-tx: XRT, surgery, chemotx or combination
-mortality 30%
Letterer-Siwe Disease
-acute disseminated form of histiocytosis X
-children < 3ya
-uniformly fatal
-clinical:
-fever, proptosis, splenomegaly, hepatomegaly, exfoliative dermatitis, thrombocytopenia
-tx: radiation therapy and chemotherapy
Fibrous Histiocytoma
-painless mass lesion occurring in sun-exposed skin and orbital tissues
-histology:
-biphasic cell population of fibroblasts and histiocytes with spindle-shaped cells with elongated
nuclei arranged in cartwheel pattern
-tx: local excision with clear margins
F.Ling - Granulomatous Diseases (1)
17
Lobular Capillary Hemangioma
-risks: young males, postpubescent females, pregnancy
-circumscribed aggregates of capillaries arranged in lobules
-clinical:
-painless, friable, ulcerated or polypoid lesion on lips (40%), nasal cavity (30%, epistaxis), tongue
(20%), or oral mucosa (15%)
-mainly arise on septum
-female predominance in pts 18-39; based on hormonal factors
-in pregnant women, regresses after delivery
-tx: surgical excision
Necrotizing Sialometaplasia
-pathophysiology:
-infarct of mucosal salivary gland tissue resulting in a self-healing inflammatory process
-histology:
-metaplastic epithelial cells lining small salivary gland ducts with preservation of lobular
architecture
-lobular necrosis
-pseudoepitheliomatous hyperplasia
-most often occurs at junction of hard and soft palate
-lesion is sharply demarcated ulcer may be mistaken for SCCa
-spontaneous resolution over course of weeks to months
INFLAMMATORY DISEASES OF UNKNOWN ETIOLOGY
Sarcoidosis
-multisystem granulomatosis
-cause unknown
-clinical course variable
-most often in 3rd-5th decade
-histology:
-non-caseating epithelioid granuloma
-accumulation of T-cells
-mononuclear phagocytes
-derangement of normal tissue architecture
-symptoms:
-40% asymptomatic
-pulmonary involvement (88%, cough, hilar adenopathy, dyspnea)
-cervical adenopathy (25-50%, most common H+N presentation)
-salivary glands parotid mass, uveoparotid fever (Heerfordt’s disease)
-larynx supraglottic region most commonly affected in larynx (epiglottis most common);
submucosal infiltration
-other:
-uveitis, nasal mass, orbital mass, nasal perforations
-cutaneous lesions (erythema nodosum, rashes)
-“Darrier Rousey” nodule (subcutaneous lesion)
-hepatic and renal involvement
-splenomegaly
-cardiac (arrhythmia)
-bone lesions
-neuropathies
18
AUTOIMMUNE OR VASCULITIC DISEASE
-systemic disorder: ELK (ENT, Lungs,
HEAD AND NECK MANIFESTATIONS OF WG
Kidney)
-4th to 5th decade; M:F ~2:1 Nasal (60-80%) -chronic sinusitis, nasal crusting, bloody
-necrotizing granuloma with vasculitis in one rhinorrhea, PND, septal perforation
Otologic (20-25%) -SOM +/- SNHL 2o cochlear vasculitis
or more major organ systems
Ocular (40%) -granulomatous keratitis, uveitic, retinal
-granuloma, necrotizing vasculitis, artery involvement
and arthritis involving small arteries Tracheal -stridor from subglottic narrowing
must be demonstrated
-C-ANCA:
-cytoplasmic staining anti-neutrophil cytoplasmic antibodies
-used for diagnosis; high specificity (> 90%)
-used to monitor disease activity as levels parallel this
Goodpasture Syndrome
-antiglomerular basement membrane nephritis
-lacks sinus involvement
-intermittent inflammation of cartilage
-pinna, nose, trachea and larynx most commonly involved
-tx: NSAIDs, steroids or dapsone
Systemic Lupus Erythematosus

-laryngeal involvement:
-thickening of true vocal cords
-limited excursion of arytenoids
-perichondritis and chondritis of laryngeal and tracheal cartilages
-cricoarytenoid and cricothyroid arthritis
-nasal:
-septal perforation
Sjogren Syndrome
-autoimmune disorder of exocrine glands
-xerostomia, keratoconjunctivitis sicca and connective tissue disease
Periarteritis Nodosa
-fibrinoid necrosis of medium sized arteries with frequent involvement of kidneys
-non-specific nasal mucosal lesions
Churg-Strauss Syndrome
-triad: hyper-eosinophilia, allergic rhinitis, asthma and systemic vasculitis of medium and small muscular
arteries
-three phases:
-prodromal phase: atopy and allergic rhinitis
-hypereosinophilia
-systemic necrotizing vasculitis
-tx: high dose systemic steroids
19
Behcet Disease
-recurrent aphthous ulceration of upper aerodigestive tract and genitalia
-ocular inflammation
-cutaneous vasculitis
-no treatment known
FOREIGN BODY REACTIONS
Cocaine-induced Midline Granuloma

-secondary to infection with S. aureus
Cholesterol Granuloma
-arise as consequence of inadequate ventilation with impaired drainage and haemorrhage of middle ear or
paranasal sinuses
-cholesterol precipitates from erythrocyte breakdown causes FB reaction with neovascularization and
formation of granulation tissue
Gout
-rare
-involvement of cricoarytenoid joint: pain, dysphagia, hoarseness, aspiration, stridor and possible airway
compromise
INFECTIOUS DISEASES
Bacterial Infections
Cat-Scratch Disease
-Rochalimae (Bartonella) henselae
-intracellular, pleomorphic, gram-negative, non-AFB
-seen with Warthin-Starry silver stain
-hx of cat exposure, primary inoculation site, regional adenopathy
-histology:
-suppurative and necrotizing granulomatous lymphadenitis with stellate abscesses
-tx: supportive with I+D for abscesses
Bacillary Angiomatosis
-young adults
-cutaneous papules and subcutaneous nodules
Brucellosis
-aerobic, gram-negative bacilli
-exposure from infected cattle (butter)
-tx: tetracycline
Rhinoscleroma
-Klebsiella rhinoscleromatis
-tx: tetracyline or streptomycin
20
Leprosy
-Mycobacterium leprae
-laryngeal ulcerations, lymphadenopathy, hyposmia, nasal collapse, fish-mouth deformity, facial nerve
paralysis, eyebrow and eyelash loss
-tx: dapsone
Nontuberculous Mycobacteria
HEAD AND NECK MANIFESTATIONS OF
-children aged 1-6 years more frequently TUBERCULOSIS
affected
-more commonly causes (1) corneal ulceration Lymph nodes -lymphadenopathy
and/or (2) cervical lymphadenopathy Larynx -granulomas or ulcerations, edema, polyploid
changes; most common site of involvement is
-transmission from soil to mouth or eye the arytenoids
-Dx: biopsy for C+S; AFB staining Eyes -conjunctivitis, keratitis, uveitic
Salivary glands -diffuse glandular involvement, usually of the
Tuberculosis parotid
Oral cavity -painful or painless ulcers, most frequently
-scrofula involving tongue
-rare in head and neck Ear -granulomas, tympanic membrane
-Dx: positive PPD, CXR, biopsy perforations, watery otorrhea, mastoiditis
-tx: isoniazid and rifampin daily for 9-12
months
Actinomycosis
-anaerobic or micro-aerophilic Actinomyces species
-from dental manipulation or trauma
-visible sinus tracts and lymphadenopathy
-purplish discolouration of overlying skin
-histology: sulfur granules
-tx: surgical debridement and Pen G IV x2-6 weeks
Syphilis
-Treponema pallidum
-dx:
-VDRL for screening
-dark-field examination
-fluorescent treponemal antibody-absorption test (ft-Abs)
-Warthin-Starry tissue staining
-histopathology:
-mononuclear infiltrate
-obliterative arteritis
-hydrops
-gummas and osteolytic lesions in otic capsule
-stages:
-primary:
-chancre at inoculation site, lymphadenopathy
-secondary: “Great Imitator”
-highly contagious, general malaise and fever, arthralgia, hepatosplenomagaly, genital
condyloma lata, nephrotic syndrome, “mucous patches”
-latent: asymptomatic phase
-tertiary:
-noninfectious stage
-may occur years after initial infection
-slow progressive
21
-neurosyphilis
-aortic involvement
-gummas
-H+N symptoms:
-lymphadenopathy
-laryngeal: laryngitis with mild edema of the larynx, vocal fold paralysis, dysphagia
-oral cavity: chancre, granulomatous infiltration of tongue, palate
-otologic: abrupt profound SNHL, Meniere’s symptoms, interstitial keratitis, TM perforation,
gummas of temporal bone
-nasal: saddle nose deformity, rhinitis, osseous and cartilaginous destruction, septal perforation
-tx: penicillin, ampicillin, tetracycline, erythromycin, steroids for otologic involvement
Anthrax
-Bacillus anthracis
-painless necrotic ulcer with surrounding edema +/- regional lymphadenopathy
Tularemia
-ticks, rabbits, deer
-photophobia, decreased visual acuity and cervical and preauricular lymphadenopathy
-exudative pharyngitis
-tx: streptomycin
Granuloma Inguinale
-Calymmatobacterium granulomatis
-tx: tetracycline, ampicillin or SMX-TMP
Fungal Infections
Histoplasmosis
-Histoplasma capsulatum
-airborne transmission
-endemic to Missouri and Ohio River Valley causes chronic pulmonary infection
-most infections are subclinical
-immunocompromised: granulomatous lesions of lips, gingiva, tongue, pharynx and larynx
-may mimic carcinoma
-dx: culture on Sabouraud’s medium, skin test, complement fixation test, latex agglutination
-tx: amphotericin B
Blastomycosis
-Blastomyces dermatitidis
-airborne transmission
-endemic to Central America and the Midwest USA)
-cutaneous disease, pulmonary involvement and constitutional symptoms
-oropharyngeal and verrucous laryngeal lesions
-histopathology:
-intraepithelial microabscess
-single bifringent broad based bud (yeast form)
-tx: amphotericin B; itraconazole
22
Coccidioidomycosis
-Coccidioides immitis
-rare: skin, mucous membranes, thyroid, eyes, trachea, salivary glands, epiglottis
Candidiasis
-Candida albicans
-tx: nystatin or ketoconazaole
Rhinosporidiosis
-Rhinosporidium seeberi
-indolent, painless, warty excrescences on nasal, palatal and conjunctival mucous membranes
-tx: excision
Phycomycosis
-Mucor, Rhizopus or Absidia
-facial pain, fever, bloody rhinorrhea, facial swelling and sinus tenderness
-proptosis, visual loss, cranial nerve palsies and obtundation
-tx: amphotericin B and aggressive surgical debridement
Cryptococcosis
-Cryptococcus neoformans
-d/t immunosuppression
-rare: membranous nasopharyngitis, meningitis, hearing loss
Aspergillosis
-Aspergillus fumigatus
-allergic, noninvasive or invasive
Parasitic Infections
Leishmaniasis
-Leishmania from sandfly bites
-cutaneous or mucocutaneous lesions
-bloodborne spread to oral cavity and oropharynx
-progressive inflammation and destruction of soft tissues of mouth and nose may occur
Myiasis
-infestation of body by maggots and transmitted by screwworm fly
Toxoplasmosis
-Toxoplasma gondii
-from cat feces or infected poorly cooked lamb or pork
TRAUMA-INDUCED DISORDERS
Intubation Granuloma
-involve vocal process of arytenoids
-contact ulcer granuloma pedunculate polyp
23
Teflon Granuloma
-from vocal cord injections
Reparative Granuloma
-secondary to local trauma in oral cavity
Pyogenic Granuloma
-granulation tissue formed in response to minor trauma with secondary infection
24
GERIATRIC OTOLARYNGOLOGY
HEARING, PRESBYCUSIS, HEARING AIDS, AND ASSISTIVE DEVICES
TYPES OF PRESBYCUSIS
Audiometric Profile
Location in Cochlea Pure Tones Discrimination
Sensory Basal end High-tone abrupt slope Related to frequency range
Neural All turns All frequencies Severe loss
Metabolic Apical region All frequencies Minimal loss
Cochlear Conductive All turns: basal > apical High-tone gradual slope Related to steepness of slope
-increasing number and decreasing cost of assistive listening devices are factors in improving quality of life
for pts with mild presbycusis
TINNITUS
-incidence increases with age

-present in 20% of people over age 50
-severe tinnitus in 4% of people over 50
-may be factor contributing to depression
-nortriptyline seems to effectively reduce the severity of tinnitus in depressed pts
DISEQUILIBRIUM AND ATAXIA OF THE ELDERLY
-presbyastasis:
-disequilibrium
-degenerative changes such as vacuolization of sensory epithelium of SCC ampullae plus
fragmentation of otoconia
-morphologic changes in vestibular nerves, Scarpa ganglion, and cerebellum
-decreased sensory input, decreased integrating ability and weakened muscular function balance
problems
VOICE DISORDERS IN THE ELDERLY VOICE EFFECTS OF AGING
-atrophic changes
-voice quality deteriorates with aging -mostly in males
-anatomic and functional causes known: -increased pitch
-ossification of laryngeal cartilages -thin reedy voice
-limitation of arytenoid cartilage excursion -edema and polyploid change
-females
-incomplete glottic closure -lower pitched voice
-decreased number of collagen and elastin fibers -pharyngeal formants also lower
-atrophy of laryngeal muscles -smoking relationship
-fundamental vocal frequency increases but may decrease if -voice stability
-wobbling and tremolo (standard
there is edema or polyploid degeneration of vocal folds deviation from fundamental
-some changes in vocal quality may result from unsuccessful frequency and jitter)
efforts to compensate for effects of aging
F.Ling - Geriatric Otolaryngology (1)
25
-males:
-attempts to drop pitch
-gravelly, breathy, glottal fry
-easy fatigue
-apparently bowed vocal cords
-females:
-attempts to raise pitch
-squeezed, strained
-effortful voice
-variable ventricular band adduction
OLFACTION AND GUSTATION IN THE ELDERLY
-aging is associated with specific morphologic changes:

-loss of zonal distribution of receptor sustentacular, and basal cells
-dilatation of Bowman glands and invagination of respiratory epithelium into lamina propria
-area of olfactory neuroepithelium may be reduced with replacement by respiratory epithelium
-degenerative diseases, drugs that decrease cell turnover, radiation therapy, viral infections, endocrine
disorders, neoplasms, and trauma may account for decrements in taste smell in the elderly
GERIATRIC SINUSITIS AND NASAL SYMPTOMS
-older pts more likely to consult physicians for nasal drainage, postnasal drip, gustatory rhinitis, and
decreased olfactory ability
-diminished capacity of immune system is believed to be a factor in increased frequency and severity of
sinusitis in geriatric age group
PRESBYPHAGIA
-predisposing factors: stroke, epilepsy, drugs, tumours, and infection

-progressive decrease in pharyngeal sensation with increased age may lead to increased aspiration
-cricopharyngeal achalasia:
-dysphagia secondary to cricopharyngeal muscle dysfunction
-may be helped by cricopharyngeal myotomy
PERIPHERAL NERVES
-general tendency to lose myelinated nerve fibers with increasing age, pathologic changes in Schwann
cells, an increase in cross-sectional area of nerves, and vascular changes (such as endothelial proliferation
and media fibrosis)
GERIATRIC IMMUNOLOGY
-with increasing age, immune system becomes less effective in protecting against infections and neoplastic
disease
-lymphocytes are not as effective in older people for the following reasons:
-function of helper and cytotoxic T-cell activity declines
26
-general response to antigens and immunogen decreases
-thymus gland involutes
-older T and B cells seem to produce a weaker response intrinsically
-quality of overall response is decreased (less IgG and fewer antibodies are produced)
BENIGN AND NONSQUAMOUS NEOPLASMS
-anaplastic or undifferentiated thyroid cancer is much more common in pts over 65

-medullary carcinoma and thyroid lymphomas seen more often
-well-differentiated thyroid carcinoma behaves much more aggressively
-recurrence rate for papillary carcinoma higher
-salivary gland malignancies seen more frequently
SKIN CHANGES OF AGING
-level of mitotic activity decreases, leading to evidence of atrophy

-age related skin changes:
-decreased moisture content and cellular cohesion in stratum corneum
-effacement of rete ridges of epidermis
-heterogeneity of keratinocyte nuclei
-decreased population of melanocytes and Langerhans’ cells
-thinning of dermis
-decreased elastic tissue
-loss of oxytalan fibers
-haphazard collagen deposition
-fewer small vessels, fibroblasts, macrophages, mast cells, Pacini’s corpuscles, Meissner’s
corpuscles, and sweat glands
-smaller sebaceous glands
27
HEADACHE AND FACIAL PAIN
PATTERNS OF REFERRAL FOR JAWS AND TEETH
-TMJ and muscles of mastication

-source of pain that radiates to head and ear
-TMJ innervated by auriculotemporal nerve
-muscle pain more intense and more common
-tooth pain
-poorly localized
-pulpal death results in localization of pain to offending tooth
CLINICAL SYNDROMES
Tension-type Headache
-bilateral
-stress related
-continuous nonpulsatile headache
-usually responsive to NSAIDs
-persists days or weeks, not disabling
Migraine
-premonitory symptom
-aura
-disabling unilateral headache
-often reported as a sick headache or sinus headache
-nausea and vomiting common
-photo- and phonophobia common
-precipitated by red wine and some foods
-preventive therapy initiated in pts suffering two or more attacks per month
-treatment strategies:
-aborting further development of pain by starting drugs shortly after first warning symptoms or at
earliest onset of pain
-treating pain if abortive therapy fails
-preventing headache by limiting predisposing events; promote healthy lifestyle
Cluster
-provoked by EtOH
-seasonal
-may be associated with allergy
-stereotypic attacks
-autonomic symptoms can cause confusion with sinusitis
OTHER CAUSES OF FACIAL PAIN
Trigeminal Neuralgia
-lancinating pain along distribution of CN V
-brief but may result in significant functional impairment
-occurs in 5th, 6th and 7th decades
-triggers are small areas on face that precipitate an attack when touched
F.Ling - Headache and Facial Pain (1)
28
-not associated with any neurological impairment
-must rule out other neurological causes
-treatment:
-trials of carbamazepine, gabapentin, baclofen, phenytoin, sodium valproate, chlorphenesin
-2 week trial for a drug
-adjunctive therapy: TCA and NSAIDs
Glossopharyngeal Neuralgia
-unilateral lancinating pain located in posterior pharynx, soft palate, base of tongue, ear, mastoid or side of
head
-workup and treatment same as for trigeminal neuralgia
Post-traumatic Neuralgia
-most often include lateral parietal and occipital regions
-treatment includes same medications used for trigeminal neuralgia
-local infiltration of trigger points with bupivicaine can be effective
Postherpetic Neuralgia
-VSV infection of trigeminal nerve in childhood as chickenpox
-reactivation later in life by trauma or stress
-immunocompromised pts treated with acyclovir, NSAIDs or opioids for pain during acute phase
-other patients treated with 10d course of oral prednisone 40 mg/day, tapering after 5 days
-pain persisting > 2 months = postherpetic neuralgia
-opioid and NSAIDs often are of little use at this stage
-anticonvulsants most useful; combined with TCA or baclofen
Atypical Facial Pain

-diagnosis of exclusion
-bilateral and changes locations frequently over weeks to months
-daily, constant, psychological factors common (60-70%): depression, somatization, and adjustment
disorders most common
Brain Tumour
-30% of pts with brain tumour have headache at time of diagnosis
-characteristic feature is crescendo quality of headache with greater intensity and frequency of pain along
with less response to analgesics over time
Pseudotumour Cerebri (Benign Intracranial Hypertension)

-papilledema, normal neurologic examination, normal CT, CSF pressure above 200 mmH2O, normal CSF
chemistries
-treatment: weight reduction, low-salt diet, medications directed at reducing CSF production (eg.
acetazolamide), lumbar drain
Subdural Hematoma
Subarachnoid Hemorrhage
Temporal Arteritis
-95% pts are > 60 ya
-daily moderate to severe headache, scalp sensitivity, generalized fatigue
-carotid artery pain, jaw claudication
-enlarged, thickened or tender scalp arteries
29
-treatment: prednisone (60 mg od)
Hypertension
-poor correlation between headache and chronic elevations in blood pressure
-acute headache associated with rapid rises in BP may be indication of pheochromocytoma, renal artery
stenosis, or hyperadrenalism
Post-traumatic Headache
-typically frontal and occipital, often present at some level day and night, poorly responsive to medications
-treatment: reassurance and a course of antidepressants (eg. TCA, SSRI)
Low Intracranial Pressure Headache

-most often as complication of lumbar puncture
-worse in sitting position
-nausea is common, and episodes of transient CN IV or III paresis are reported
-spontaneous recovery within days
Infection of the Nervous System

-meningitis, encephalitis etc..
Chronic Daily Headache

-use of pain relievers >3x/wk often associated with refractory headache
30
MANIFESTATIONS OF AIDS
Head and Neck Manifestations of HIV by Anatomical Location
Oral and Pharynx Neck Otologic

-oral candidiasis -deep-space neck abscess -acute and chronic otitis media
-oral hairy leukoplakia -infectious lymphadenopathy -otitis externa
-herpes stomatitis (mycobacterium, pneumocystis, CMV, -mastoiditis (invasive aspergillosis,
-thrombocytopenic purpura EBV, totxoplasmosis, cat-scratch pneumocystis, mycobacterium)
-recurrent apththous ulcers disease, bacterial) -malignant otitis
-bone loss (bacillary angiomatosis) -neoplastic lymphadenopathy -SNHL
-gingivitis (acute necrotizing ulcerative (Hodgkin’s and NHL, metastatic disease, (cryptococcal or mycobacterial
gingivitis, necrotizing stomatitis) thyroid tumours) meningitis, otosyphilis, toxoplasmosis,
-Kaposi’s sarcoma, NHL, SCCa -persistent generalized adenopathy autoimmune demyelisation of the
cochlear nerve, CPA tumours)
Larynx Salivary Glands -TM perforations
-epiglottitis -lymphoepithelial cysts of parotid gland -aural polypa
-Kaposi’s Sarcoma -parotitis -facial nerve paralysis
-NHL -salivary gland neoplasms (Herpes Zoster, CMV, EBV, HIV,
-laryngitis (mycobacterium, fungal, autoimmune demyelisation, malignant
CMV, EBV, bacterial) Paranasal Sinus otitis externa, meningitis and
-rhinosinusitis encephalitis)
(mucor, aspergillosis, pseudomonas) -temporal bone neoplasms
-nasal tumours (Hodgkin’s and NHL, Kaposi’s
(Kaposi’s sarcoma, nasal lymphomas) sarcoma)
-HIV is a retrovirus that attaches to CD4+ cells marker of T-helper cells, macrophages, and other
immunological cells
-results in a decrease in T-helper lymphocytes and impaired function of macrophages, neutrophils, B-
lymphocytes and complement activation
-AIDS defining illness:
-candidiasis, CMV disease, Kaposi’s sarcoma, Pneumocystis carinii, etc..
-CD4+ count < 200 cells/ul
DERMATOLOGIC
-molluscum contagiosum
-pearly umbilicate papules; usually 2-5 mm, occasionally giant; predilection for eyelids
-tx: surgical excision, curettage or cryotherapy
-complics: frequent recurrence following treatment; can cause functional problems if extensively
involving and treated in eyelid areas
-bacillary angiomatosis
-subcutaneous nodules or friable papules; multiple organ involvement; negative cultures; classic
histopathologic appearance
-tx: erythromycin, 500 mg qid or rifampin 600 mg qd
-if unrecognized and untreated, can have multisystem involvement and possibly death
-cutaneous Cryptococcus
-most common dermatologic condition associated with HIV
-pustular or granulomatous lesions; histopathologic or culture identification
-tx: search for systemic infection, and treat systematically with amphotericin B and/or flucytosine
-complics: cryptococcal meningitis associated with 30% mortality rate even when treated
F.Ling - Manifestations of AIDS (1)
31
-seborrheic dermatitis
-white scaly plaques or patches with or without erythema and inflammation
-tx: hydrocortisone cream; ketoconazole cream
-complics: can become secondarily infected with S. aureus
-herpes zoster/Ramsay Hunt

-typical dermatomal distribution
-tx: oral acyclovir, 800 mg 5 times/day; analgesic
-complics: often produces permanent cranial nerve palsy; systemic disease associated with high
morbidity
-Kaposi sarcoma
-violaceous papular or ulcerated skin lesions, often multiple; can be associated with regional
adenopathy and mucosal lesions
-tx: low-dose XRT, systemic (vincristine or vinblastine), or intralesional (vinblastine)
chemotherapy
-complics: secondary infection produces severe symptoms; occasionally causes airway obstruction
or other functional problems
OTOLOGIC
-primary dermatologic conditions affecting EAC: KS and seborrheic dermatitis
-serous and acute otitis media most common otologic conditions
-ETD 2o to nasopharyngeal lymphoid hypertrophy
-Staphylococcus and Pseudomonas in acute or chronic OM is more common
-P. carinii and Candida have been cultured in middle ear aspirates of AIDS patients
-mild to moderate SNHL often reported: viral infection suspected
NOSE AND PARANASAL SINUSES
-can be sites of herpetic lesions, KS and NHL

-recurrent and chronic sinusitis
-persistent low-grade viral or bacterial infection of OMC
-usual pathogens: Staphylococcus species, S. pneumoniae, H. influenzae and anaerobic bacteria
-Pseudomonas aeruginosa implicated in 20% tx /w clindamycin and ciprofloxacin
-invasive fungal sinusitis must be suspected in individuals with pain out of proportion to findings on
examination despite being on empiric antibiotics
ORAL CAVITY AND PHARYNX
-Oral candidiasis:
-most common oral lesion in AIDS
-pseudomembranous plaques with underlying red inflamed mucosal surface
-tx: topical antifungal: nystatin tid or clotrimazole;
systemic antifungal: ketoconazole 200 mg qd or fluconazole
-can produce severe local symptoms; candida esophagitis must be considered
-Herpetic stomatitis:
-ulcerative, punched-out lesions occurring on any mucosal surface
-tx: oral acyclovir, 200 mg 5 times/day; topical analgesics
32
-frequent recurrence; may develop drug resistance
-Aphthous ulcers:
-usually single, but may be multiple; usually on mobile mucosal surface; may become extremely
large “giant apththous ulcers”
-tx: topical analgesics; topical steroids in Orabase; occasionally intralesional or systemic steroids
-can produce severe debilitating symptoms resulting in nutritional imbalance
-Hairy leukoplakia:
-whitish thickening of mucosa on lateral tongue; often has corrugated appearance
-usually asymptomatic
-EBV present in epithelium
-tx: none necessary; treat candidal superinfection when present; acyclovir may be beneficial
-Kaposi’s sarcoma:
-violaceus lesions; predilection for hard palate
-may be flat or nodular; may become ulcerated and secondarily infected
-tx: intralesional or systemic chemotherapy; palliative surgical or laser excision, radiation therapy
-can produce local symptoms when ulcerated or infected; occasionally causes airway obstruction
or severe dysphagia
-Non-Hodgkin’s lymphoma:
-second most common neoplasm associated with AIDS
-nodular, ulcerative; Waldeyer’s ring area often involved; biopsy diagnostic
-tx: chemo or XRT
-often causes local symptoms of obstruction or pain; frequent dissemination including
lymphomatous meningitis
-Gingival and periodontal disease:

-ulcerative and necrotizing gingivitis; poorly responsive to aggressive therapy
-tx: aggressive local hygiene, debridement of severely involved tissue followed by Betadine and
Peridex mouth rinses; oral metronidazole is often an effective adjunct
LARYNX
-must consider fungal, viral and mycobacterial infections

-KS and NHL can also occur in the larynx
NECK
-salivary gland disease:

-xerostomia common complaint
-generalized parotid enlargement caused by lymphocytic infiltration
-parotid masses: usual parotid neoplasms, KS, NHL or lymphoepithelial cysts
-indications for cervical lymph node biopsy:
-marked constitutional symptoms
-localized lymphadenopathy
-single disproportionately large node in a patient with persistent generalized lymphadenopathy
-cytopenia or elevated ESR or both and a patient with otherwise negative evaluation
-patient reassurance of an ambiguous tissue diagnosis
33
-ddx lymphadenopathy:
-malignancy
-tuberculous, atypical mycobacterial infections
-histoplasmosis
-toxoplasmosis
-cat-scratch disease
34
F.Ling - POS notes and points (1)
Principles of Surgery
“69" other notes and points from previous exams ;)
Last minute facts to cram into your already saturated brain.

The following sources have been used:
-Harrison’s 14th ed.
-Schwartz 7th ed
-Ganong - Review of Physiology
-Merck Manual 17th ed
-Katzung - Review of Pharmacology
-Robbin - Pathology of Disease
-Rush Review
-Sanford Antimicrobial Manual (1997)
-Way - Current Management in Surgical Disease
1. Internal maxillary does pass through the deep lobe of the parotid
2. Aldosterone mechanism of action: resorption of sodium at cortical collecting duct (Ganong 345)
3. Non-caseating granulomas
-TB (can be caseating also) and sarcoid (Robbin 81)
4. Actinomycosis:
-draining sinuses
-involves skin sinus tracts with pus
-sulfur granules on histo
-tx: surgical drainage, penicillin for at least 8 weeks can be up to 1yr until drainage stops
-(Merck 1181)
5. Horner’s Syndrome: miosis, ptosis, anhydrosis, enophthalmos (Merck 652)
6. Early endoscopy is OK for caustic ingestion (Harrison 1585, Schwartz 1159)
7. Nasal fractures most common facial fracture in trauma; mandibular fracture second
8. Azathioprine causes cholestasis (Schwartz 430)
9. Renin (Ganong 421):
-factors that increase secretion: sympathetic activity, circulating catecholamines, prostaglandins
-factors that decrease secretion: hyperaldosteronism, angiotensin II, vasopressin, reabsorption across
macula densa, afferent arteriolar pressure
10. Melanoma treatment (Schwartz 525):
-Clark level I - < 0.75mm: 2cm margin, no lymph node dissection if not affected
-Clark levels II, III, IV - 0.76-4mm: excise with 2-3cm margin, lymph node dissection controversial
-Clark level V - > 4.0 mm: metastasis likely, no lymph node dissection
11. Most common type of melanoma: superficial spreading (70-80%)
12. Bites (Sanford 1997, Harrison 836)
-dogs:
- responsible for 80% domestic animal bites
-only 15-20% get infected
-bugs: strep viridans, staph, pasturella, anaerobes etc...
-cats:
-80% of bites get infected
-P. multocida most responsible
-humans:
-more frequently infected than other animal bites
-bugs: strep viridans (100%), staph epi (53%), staph aureus (29%), eikenella (15%), anaerobes
etc..
13. Presentation of CMV post transplantation:
-leukopenia with fever, pneumonia, gastroenteritis, hepatitis, retinitis, sepsis
35
14. Highest risk for surgery: CHF (Goldman index 11) > MI less than 6 months (Goldman index 10)
15. Indications for thrombolytics in PE (Way 800)
-shock, RV failure, severe pulmonary hypertension and may die with additional emboli
16. Pancreatic alpha cells rich in beta-adrenergic receptors (stimulation) glucagon
Pancreatic beta cells rich in alpha-adrenergic receptors insulin
17. Growth Hormone secretion:
-stimulated by: ACTH, thyroxine, alpha-adrenergic stimulation, glucagon
-inhibited by: hyperglycemia, FFA, cortisol, somatostatin
18. Effects of PTH:
- sCa: renal and intestinal resorption
- sPO4 via renal excretion
-1 hydroxylation of 25-OH vitamin D
-stimulates osteoclasts
19. ATN: hemegranular casts; SG < 1.015
Prerenal: hyaline casts; SG > 1.018
20. Amikacin for treatment of pseudomonas that is resistant to tobramycin or gentamicin (Merck 1174)
21. Oral Abx for pseudomonas: cipro (or other quinolones), oral indanyl carbenicillin
22. Persantine = dipyrimadole: decreases platelet aggregation, dilates coronary arteries
23. OCP and DVT (Merck 1998, Schwartz Ch 11):
-related to increases in blood clotting factors
-possibly increased platelet adhesion
-increased levels of globulins, particularly factors VII and X hypercoagulable state
-decreased antithrombin III
24. TTP (Merck 945)
-syndrome of: platelets, fragmented RBC, renal failure, fever, manifestations of ischemic damage (eg.
confusion, seizure, jaundice etc.)
-tx: plasmapheresis, steroids; if refractory, splenectomy, vincristine or cyclophosphamide have been used
25. Cytochrome P450 inducers: barbiturates, phenytoin, rifampin, carbamazepine
26. Cytochrome P450 inhibitors: cimetidine, INH, ketoconazole, allopurinol, erythromycin, MAOI, disulfiram,
verapamil
27. Thromboxanes synthesized in platelets; prostacyclines synthesized in endothelial cells
28. Serotonin found in enterochromaffin cells of the gut, CNS, and platelets
29. Arginine (Schwartz 246, Rush 48):
-helps to decreases protein catabolism
-reduces urinary nitrogen excretion
-improve immune function (T-cell proliferation)
-improve wound healing (?accelerates it)
-secretagogue activity on pituitary and pancreatic hormones: GH, PRL, glucagon, insulin, IGF,
catecholamines
30. Cryptococcus (Merck 1218)
-cannot be contracted via blood transfusion
-acquired by inhalation of soil contaminated with encapsulated yeast
-tx: Ampho B (with flucytosine)
31. Ionized calcium required for neuromuscular stability (Rush 15)
32. Preoperative TPN (Schwartz 444)
-increases wound healing
-increases risk of nosocomial and catheter related sepsis in non-severely malnourished individuals
-increases immune function pre-op and lowers mortality and decreases septic complications
33. Arthus reaction (Merck 1010)
-aka. Type III hypersensitivity
-due to presence of Ab that binds to injected Ag immune complex formation, complement activation and
neutrophil chemotaxis
36
34. Ramsay-Hunt Syndrome:

-facial palsy, vesicular eruption over distribution of cranial nerve or cervical plexus, severe ear pain
-associated SNHL and vestibular dysfunction
-tx: acyclovir
35. 75-80% of IgG is intravascular
36. Three classic landmarks to identify main trunk of facial nerve for parotidectomy:
-mastoid tip
-posterior belly of digastric
-“cartilagenous pointer” of the tragus
37. Renal Tubular Acidosis (Merck 1900)
I: unable secrete H+ at distal nephron
-metabolic acidosis, volume contraction, hypokalemia
-hypercalciuria, increased mobilization of bone Ca
II: unable to reabsorb bicarbonate in proximal tubule
-metabolic acidosis, volume contraction, hypokalemia
III: rare, combination of I and II
IV: unresponsiveness of distal tubule/CCD to aldosterone hyperkalemia
38. Daily fluid requirements in children (Rush 436):
-premature infants: 150 ml/kg/d
-newborn: 80-90 ml/kg/d
-infants > 30d to adulthood: use 100:50:20 rule
39. Cord injury syndromes (Way 824):
-anterior cord syndrome: damage to spinothalamic (P+T) tracts and corticospinal (motor) tracts
-central cord syndrome: preservation for distal leg and sacral motor and sensory fibers
-Brown-Sequard syndrome: ipsilateral loss of motor, proprioception, LT; contralateral P+T loss
40. Renal graft rejection:
-oliguria, weight gain, hypertension, increased BUN/Cr, increased graft size, graft tenderness, fever and
leukocytosis
41. Jaundice of Pregnancy (Harrison 1675):
-2nd-3rd trimester
- ALP, bilirubin
-AST/ALT normal
-benign, self-limited
42. Glucose requiring tissues: neurons, RBC, renal medulla, bone marrow (Rush 42)
43. Paget’s Disease of Bone (Merck 473):
- bone turnover
-Pelvis > femur > skull > tibia > vertebrae > clavicle
-X-ray: bone density, cortical thickening, bowing, overgrowth
-Labs: ALP, hydroxyproline in urine, Ca normal or , phosphate normal
-osteosarcoma
44. High Output renal failure (Rush 103):
-may occur with no antecedent oliguric phase
-clinical and lab findings may be similar to oliguric RF
-damage to distal nephron with patchy necrosis
-usually spontaneously resolves
45. Autosomal dominant conditions:
-vWD, MEN, familial adenomatous polyposis, Marfan’s syndrome
46. Esophageal perforations:
-most common cause: instrumentation
-most common non-iatrogenic cause: Boerhaeve’s syndrome
47. Maximum dose of lidocaine: 300-(?500) mg; bupivicaine 2mg/kg, 175mg/dose or 400mg/24h (Epocrates)
48. Hepatitis B: 10-15% will have chronic hepatitis
37
49. Hepatitis C: 75-80% will develop chronic hepatitis

50. Drugs that do not need adjusting in renal failure (Schwartz 150)
-chloramphenicol
-ampicillin (minor)
-erythromycin
-clindamycin
-ceftriaxone
51. NO released from endothelium and causes vasodilation and capillary permeability
52. Renal failure blood values: H, K, PO4, Mg; Ca, Na
53. Magnesium: clinical effects similar to calcium; blood levels parallel potassium levels
54. Paraneoplastic syndromes:
-ACTH/Cushing: small cell lung ca
-SIADH: small cell lung ca
-Horner’s syndrome (not really paraneoplastic): SCC/Pancoast tumour
-Hypercalcemia/PTH-like hormone: SCC lung, breast ca, RCC
-Erythrocytosis/erythropoietin: RCC
-Acanthosis nigricans: gastric/uterine/lung ca
55. Gompertzian curve: sigmoid curve describing growth of tumours early exponential growth that slows as
tumour size increases
56. Radiation to thyroid: 40% risk of developing thyroid carcinoma
57. Contraindications for thrombolytics:
-absolute:
-prior hemorrhagic stroke, any stroke w/n past 6-12 months, brain neoplasm, suspected aortic
dissection
-relative:
-major surgery or trauma prior 2-3weeks, bleeding diathesis, coumadin, prolonged CPR > 10 min,
pregnancy, uncontroled HTN > 180/110
-streptokinase contraindicated if given in prior year
58. Tissue ischemia times (Schwartz 2037):
-skin 12h
-nerve 8h
-muscle 6h
-(brain 4min)
59. Most common non-bacterial infection in late burns: candida
60. Nerve most likely injued in 4 compartement fasciotomy following tibial fracture: peroneal (superficial)
61. Contraindications to flex/ex views of C-spine:
-altered sensorium, subluxation on lateral C-spine film, any neurological deficit (eg. Brown Sequard)
62. Prostate cancer:
-does not metastasize to brain
-can metastasize to colon
-can cause DIC
63. Sensory innervation of ear:
-middle ear: CN XI
-tympanic membrane and EAC: CN V3 (auriculotemporal branch), VII, X
-pinna:
-CN V3
-cervical plexus:
-lesser occipital nerve (C2): skin posterior to auricle
-great auricular nerve (C2,3): lower ½ of auricle
64. Methyldopa hemolytic anemia Coomb’s test
65. HIV most often presents as generalized lymphadenopathy
66. CEA elevated in: heavy cigarette smokers, cirrhosis, ulcerative colitis, maligancies
38
67. Radiological signs of hyperparathyroidism aka osteitis fibrosa cystica (Harrison 2229):
-reabsorption of phalangeal tufts and subperiosteal absorption
-thinning of dura lamina of teeth
-salt and pepper appearance of skull
68. Tissue expansion (Schwarz 2105):
-epidermal thikening in first week goes back to normal
-decreased dermal thickness
-increases vascularity of skin
69. Hydrogen secretion in kidneys (Ganong 660-661):
-three major reactions to remove tubular fluid hydrogen:
a. HCO3 CO2+H2O
b. HPO4 H2PO4
c. NH3 NH4
39
Staging criteria: primary tumor (T)
Tx Minimum requirements to assess primary tumor cannot be
met
T0 No evidence of primary tumor
TIS Carcinoma in situ
T1 Tumor confined to antral mucosa of infrastructure with no
bone erosion or
destruction
T2 Tumor confined to suprastructure mucosa without bone
destruction, or to infrastructure with destruction of medial or
inferior bony walls only
Osama Marglani
T3 More extensive tumor invading skin of cheek, orbit, anterior
ethmoid sinus, or pterygoid muscle
T4 Massive tumor with invasion of cribriform plate, posterior
ethmoid sinus,
sphenoid sinus, nasopharynx, pterygoid plate, or base of skull
Inflammatory polyp.
Inverted papillomas and The medium-power microscopic
exophytic squamous papillomas appearance of this lesion is
are both characterized by characteristic of a nasal
proliferations of the same type inflammatory polyp. Note the
of epithelium. In inverted edematous connective tissue
papillomas, this epithelium filled with numerous eosinophils
characteristically grows down (bright pink granules) and
into preexisting mucosal plasma cells (blue cells with
glands, displacing and eccentric round nuclei and
replacing the normal epithelium perinuclear pink zone in the
as it proliferates. As the cytoplasm). The overlying
abnormal epithelium continues respiratory-type epithelium
to expand below the surface, it shows some reactive expansion
causes a broad-based mucosal (hyperplasia) of the basal cell
elevation. layer but the overlying ciliated
epithelial cells are still present.
Rhinosporidium
seeberi .
Rhinosporidiosis
occurs in the
Americas, Europe,
Africa, and Asia but is
most common in the
tropics, with the
highest prevalence in
southern India and Sri
Lanka.
R. seeberi is
visualized with fungal
stains such as
methenamine silver
and Periodic acid-
40
1
clival chordoma, "Large cells with
multiple vacuoles
depicting tumor and are called
cranial nerve 'physaliferous
relationships prior to cells' because of
a resemblance to
resection of the jellyfish.
petrous apex and These
removal of the tumor. neoplasms
arise from
remnants of
primitive
notochord .
Carcinomas may arise within a Squamous papilloma

preexisting papilloma or directly
from non-papillomatous epithelium. These are finger-like
All of the epithelial cells here have structures that project into
malignant cytologic features
(nuclear enlargement, variability in the air passages above the
size and shape) and they are surrounding mucosa. They
arranged in a disorganized growth
pattern. are surfaced by abnormally
A most important feature is that thick, non-keratinizing
these abnormal cells have invaded stratified squamous
the connective tissue where they
infiltrate as small irregular nests epithelium. The epithelial
and even as individual cells. cells are arranged in an
Contrast this growth pattern with orderly pattern and they do
the smooth, expansile epithelial
proliferations in the inverted not have the cytologic
papilloma. features of malignancy.
Contrast the normal surface

3 types. squamous epithelium with that
of the adjacent invasive
WHO. carcinoma. This tumor is
classified as a squamous cell
I keratinizing, carcinoma because some of the
tumor cells exhibit recognizable
II nonkeratinizing, squamous differentiation (note
the glassy pink nests of
keratinized malignant cells
III undifferentiated within the tumor). Keratinizing
and non-keratinizing squamous
subtypes cell carcinomas may arise
anywhere from the nasal
vestibule to the lung as well as
inside the oral cavity.
41
2
! !
Cystic lesions The ameloblasts are
the palisaded cells
with the nuclei pulled
away from the
basement membrane
around a stellate
reticulum like tissue
and in a fibrous stroma
.
REVERSED
POLARIZATION.
Normal thyroid tissue with

follicles filled with colloid .
Thyroid cells form follicles,
spheres of epithelial cells
(always single-layered in
health, usually more-or-less
cuboidal, variably tall or
short).
The C-cells (parafollicular
cells) of the thyroid are
visible between the follicles
" "
Psammoma body within a
papillary cancer . calcified sphere, or
large clear areas within the psammoma body
nuclei which look like "Little
Orphan Annie" eyes are
circled in blue .
Although these nuclear
features are
characteristic of
papillary carcinoma, Papillary thyroid
they are not carcinoma accounts
pathognomonic for about 80% of all
Papillary cancer (low thyroid carcinomas
resolution). Notice the
frond-like projections.
42
3
$ % & ' #
Medullary (C-cell) Follicular
carcinoma of the adenoma H/E
thyroid with amyloid preparation
stroma . x 100
Immunohistochemica
l anti-calcitonin Follicular
antibody stain of a carcinoma
medullary carcinoma accounts
showing strong red for less than
positivity 10%
Lymphocytic Anaplastic
infiltrate in the carcinoma
thyroid, with histology H/E
lymphoid follicle preparation
formation and x 200
fibrosis.
) " (
Schwannoma
(neurilemoma) is a
benign neoplasm of
the Schwann cells of
the neural sheath .
43
4
% ' )
(HE x100). Antoni type A tissue shows
fascicles of spindle-shaped
Typical cellular Schwann cells streaming
around numerous acellular,
groups ("Zellballen") eosinophilic areas
surrounded by a surrounded by paralleled or
palisaded spindled cells
capillary network. with blunt, elongated nuclei
Round, fairly regular The cells of these Verocay
bodies all orient their long
nuclei. Variable, axes toward the acellular
often granular area, and the areas
themselves are oval, linear
cytoplasm. or serpiginous in shape.
Tx Primary tumor cannot be assessed

T1 Tumor < 2cm in greatest dimension
T2 Tumor 2-4 cm in greatest dimension
T4 Tumor > 6 cm in greatest dimension
All categories are subdivided: (a) no local extension; (b) local

extension.
Local extension is clinical or macroscopic invasion of skin, soft
tissue, bone, or nerve.
Microscopic evidence alone is not a local extension for
classification purposes.
pleomorphic adenomas
originate from the
intercalated duct cells
and myoepithelial cells
oncocytic tumors
originate from the
striated duct cells
acinous cell tumors
originate from the acinar
cells,
Mucoepidermoid
tumors and squamous
cell carcinomas develop
in the excretory duct
cells.
44
5
The diverse microscopic pattern
of this lesion is one of its most pleomorphic
characteristic features.
Islands of cuboidal cells
adenoma showing
arranged in ductlike structures the epithelial (E) and
is a common finding.
the stromal (S)
Loose chondromyxoid stroma,
hyalinized connective tissue, components.
cartilage(,arrows) and even
osseous tissue are observed.
This neoplasm is typically
encapsulated, although tumor
islands may be found within the
fibrous capsule.
Nerve (N) invaded by Adenoid cystic

carcinoma with Swiss
adenoid cystic cheese pattern.
carcinoma It is the second-most
(the blue area common malignant
surrounding the tumor of the salivary
glands.
nerve). ACC is the most
Spread may occur common malignant
by emboli along the tumor found in the
submandibular,
nerve lymphatics sublingual, and minor
salivary glands.
, + ( +
Warthin's tumor (benign Hodgkin's disease
papillary cystadenoma
lymphomatosum) is the involving the
second most common parotid
benign tumor of the parotid
gland. gland. Note the
It accounts for 2-10% of all Reed-Sternberg
parotid gland tumors. cell. (Fine needle
Bilateral in 10% of the aspiration, Pap,
cases.
630x)
may contain mucoid brown
fluid inFNA
45
6
High Power Mid Power
Lymphocytc
infilterates.
The acinic cell adenocarcinoma

occurs mainly in the parotid Electron microscopy shows
gland, a tremendous number of
This lesion is characterized by a mitochondria in the epithelial
benign histomorphologic picture cells, which are responsible
but by occasional malignant for its granular eosinophilic
behavior.
appearance.
These lesions are treated by
surgical excision with a Mitochondria-rich oncocytes
generous margin of normal are found in Warthin’s
tissue on the periphery. tumors .
They do not tend to metastasize
to lymph nodes but favor bone Oncocytes selectively
and lung as metastatic sites. incorporate technetium Tc
Bilateral involvement occurs 99m and appear as hot
in 3% of patients, making spots on a radionucleotide
acinic cell carcinoma the scan.
second-most common
neoplasm, after Warthin’s
tumor, to exhibit bilateral
presentation.
$
$
Mucoepidermoid carcinoma (MEC) is the MECs contain two
most common malignant tumor of the parotid major elements:
gland and the mucin-producing cells
and epithelial cells of
second-most common malignancy the epidermoid variety.
(adenoidcystic carcinoma is more common) MEC is divided into
of the submandibular and minor salivary low-grade (well
glands. differentiated), high-
MECs constitute approximately 35% of grade (poorly
salivary gland malignancy, and 80% to 90% differentiated)
of MECs occur in the parotid gland.
46
7
-
It is composed of uniform
basaloid epithelial cells with
a monomorphous pattern.
The arrangement of tumor

cells may be trabecular ,
tubular or solid.
Histologically, these tumors

are distinguished from
pleomorphic adenomas
by their absence of
chondromyxoid stroma and
the presence of a uniform
epithelial pattern.
Tx Primary tumor cannot be assessed

T1 Tumor < 2cm in greatest dimension
T4 Tumor > 6 cm in greatest dimension
All categories are subdivided: (a) no local extension; (b) local

extension.
Local extension is clinical or macroscopic invasion of skin, soft
tissue, bone, or nerve.
Microscopic evidence alone is not a local extension for
classification purposes.
& &
A very high power Spider web.
view of the The buccal
dermoepidermal
mucosa
junction
involved most
Civatte bodies often
(arrows),
reticular form
keratinocyte
enlargement, and
most common
coarse collagen
bundles are illustrated.
47
8
ominous
characteristic of
squamous
carcinoma is its
ability to surround
nerves and to
infiltrate for long
distances in a
perineural fashion
Many nuclei show marked

clumping of hyperchromatism
chromatin. There is and extremely
an abnormal mitotic atypical mitoses
figure in the center of
the photomicrograph.
Most cells are easily

identifiable as
squamous cells. At
one end there is a
mass of parakeratin
("keratin pearl").
48
9
Otolaryngology - Head and Neck Surgery Page 1 of 7
Dr. F. Ling's
Otolaryngology - Head and Neck

Surgery Notes
Selected Pharmacopoeia
ANALGESI CS
Nonsteroidal Anti-Inflammatories - COX-2 Inhibitors
 celecoxib (Celebrex): 200 mg PO qd or 100 mg PO bid

 rofecoxib (Vioxx): 50 mg PO qd < 5 days
 valdecoxib (Bextra): 10 mg PO qd
Nonsteroidal Anti-Inflammatories - Other
 ibuprofen (Motrin, Advil, Nuprin, Rufen): 200-800 mg PO tid-qid.

Peds > 6 mo: 5-10 mg/kg PO q6-8h
 ketorolac (Toradol): 15-30 mg IV/IM q6h or 10 mg PO q4-6h prn
 naproxen (Naprosyn): 250-500 mg PO bid
Opioids
Approximate Recommended Starting Dose

Opioid equianalgesic Adults > 50 kg Children/Adults 8-50 kg
Agonists
IV/SC/IM PO IV/SC/IM PO IV/SC/IM PO
10 mg 30-60 mg 10 mg 30 mg 0.1 mg/kg 0.3 mg/kg

morphine
q3-4h q3-4h q3-4h q3-4h q3-4h q3-4h
75 mg 130 mg 60 mg 60 mg 1 mg/k q3-
codeine n/r
q3-4h q3-4h q2h q3-4h 4h
0.1 mg 0.1 mg
fentanyl n/a n/a n/a n/a
q1h q1h
0.015 0.06
1.5 mg 7.5 mg 1.5 mg 6 mg q3-
hydromorphone mg/kg q3- mg/kg q3-
q3-4h q3-4h q3-4h 4h
4h 4h
0.75
100 mg 300 mg 100 mg
meperidine n/r mg/kg q2- n/r
q3h q2-3h q3h
3h
30 mg 10 mg 0.2 mg/kg
oxycodone n/a n/a n/a
q3-4h q3-4h q3-4h
49
file:///C:/Users/user/Desktop/Dr%20flings%20Notes/Contents/Pharmacopoeia.htm 3/22/2013
Equianalgesic Table
Drug SC PO
Morphine 10 mg 20 mg
Hydromorphone 2 mg 4 mg
Oxycodone N/A 7.5-10 mg
Codeine 60 mg 120 mg
Fentanyl 100-150 ug TD
Meperidine 75 mg 300 mg
Methadone N/A 2 mg
Breakthrough Doses with TD Fentanyl

Hydromorphone
Fentanyl TD Morphine PO
PO
25 mcg/h 10 mg q2h prn 2 mg q2h prn
50 mcg/h 20 mg q2h prn 4mg q2h prn

75 mcg/hr 30 mg q2h 6 mg q2h prn
100 mcg/h 40 mg q2h prn 8 mg q2h prn
 codeine: 0.5-1 mg/kg up to 15-69 mg PO/IM/IV/SC q4-6h
 fentanyl: 1 patch q72h [25, 50, 75, 100 mcg/h]
 hydromorphone (Dilaudid): Adults: 2-4 mg PO q4-6h. 0.5-2 mg

IM/SC or slow IV q4-6h. 3 mg PR q6-8h
Opioid Antagonists
 naloxone (Narcan): Opioid overdose: 0.4-2.0 mg q2-3 min prn
ANAESTHESI A
 midazolam (Versed): adult sedation/anxiolysis: 5 mg or 0.07 mg/kg

IM; or 1 mg IV slowly q2-3 min up to 5 mg
 propofol: 20-40 mg IV q10sec until induction (2-2.5 mg/kg)
Local Anaesthetics
 Maximum recommended doses:
50
 Lidocaine 5 mg/kg. Max 300 mg
 Lidocaine with epinephrine 7 mg/kg. Max 500 mg
 Cocaine 3 mg/kg. Max 200 mg
ANTI M I CROBI ALS
Antifungal Agents
 fluconazole (Diflucan): 200 mg first day, then 100 mg IV/PO qd. Peds:
6 mg/kg first day, then 3 mg/kg qd
 itraconazole: 100-200 mg PPO qd
 ketoconazole (Nizoral): 200-400 mg PO qd . Contraindicated iwth

midazolam, pimozide, triazolam
 nystatin: Thrush: 4-6 ml PO swish and swallow qid. [Susp 100,000

units/ml]
Antiviral Agents
 acyclovir: Zoster: 800 mg PO qid x 7-10 days
Cephalosporins
 cefazolin (Ancef): 0.5-1.5 g IM/IV q6-8h. Peds: 25-50 mg/kg/day

divided q6-8h
 cephalexin (Keflex): 250-500 mg PO qid. Peds: 25-50 mg/kg/day
 cefprozil (Cefzil): 250-500 mg PO bid. Peds otitis media: 15

mg/kg/dose PO bid
 cefuroxime (Cefin, Kefurox): 750-1500 mg IM/IV q8h. Peds: 50-100

mg/kg/day IV divided q6-8h. 250-500 mg PO bid. Peds: 20-30
mg/kg/day susp PO divided bid
 cefotaxime: 1-2 g/day IM/IV q12h. Peds: 50-180 mg/kg/day IM/IV

divided q4-6h
 ceftazidime: 1 g IM/IV or 2 g IV q8-12h. Peds: 30-50 mg/kg IV q8h
 ceftriaxone: 1-2 g IM/IV q24h. Peds: 50-75 mg/kg/day up to 2 g

divided q12-24h
Macrolides
51
 azithromycin (Zithromax): 500 mg IV qd. PO: 10 mg/kg upt to 500

mg on day 1, then 5 mg/kg up to 250 mg qd to complete 5 days. GAS
pharyngitis: 12 mg/kg up to 500 mg qd x 5d. Short regimens for peds
OM: 30 mg/kg PO single dose or 10 mg/kg PO qd x 3 days
 clarithromycin (Biaxin): 250-500 mg PO bid. Peds: 7.5 mg/kg PO bid
 erythromycin base: 250-500 mg PO qid, 333 mg PO tid, or 500 mg PO

bid
Penicillins
 penicillin G: Pneumococcal pneumonia and severe infections: 250,000-

400,000 units/kg/day (8-12 MU in adult) IV divided q4-6h
 penicillin V: Adults: 250-500 mg PO gid. Peds 25-50 mg/kg/day

divided bid-qid
 amoxicillin: 250-500 mg PO tid, or 500-875 mg PO bid. Acute sinusitis

with antibiotic use in past month and/or drug-resistant S penumoniae rate
> 30%: 3-3.5 g/day PO. Peds: 40 mg/kg/day PO divided tid or 45
mg/kg/day divided bid. OM/sinusitis in children at high risk for
penicillin-restant S pneumoniae (age <2 yo, antibiotics within <3 mo,
day care): 90 mg/kg/day PO divided bid-tid x 10 days for < 2yo, x5-7
dyas for > 2yo [Caps 250, 500 mg, tabs 500, 875 mg, susp 125, 250
mg/5ml, 200& 400 mg/5ml]
 amoxicillin-clavulanate (Clavulin): 500-875 mg PO bid or 250-500 mg

tid. Peds: 45 mg/kg/day PO divided bid or 40 mg/kg/day divided tid for
otitis, sinusitis, pneumonia
Prophylaxis for Bacterial Endocarditis (for dental, oral, respiratory tract,

or esophageal procedures)
 amoxicillin 2 g PO 1h before procedure
 ampicillin 2 g IM/IV within 30 minutes before procedure
 clindamycin 600 mg PO/IV; cephalexin 2 g PO or cefazolin 1 g IM/IV

within 30 minutes before procedure
Quinolones
 ciprofloxacin: 200-400 mg IV q8-12h. 250-750 mg PO bid
 levofloxacin (Levaquin): 250-500 mg PO/IV qd
 gatifloxacin (Tequin): 400 mg IV/PO qd
Sulfonamides
52
 trimethoprim-sulfamethoxazole (Bactrim, Septra): One tab PO bid,

double strength (DS, 160 mg/800 mg) or single strenth (SS, 80 mg/400
mg). Peds: 5 ml susp/10 kg (up to 20 ml)/dose PO bid
Other
 clindamycin: 600-900 mg IV q8h. 150-450 mg PO qid. Peds: 20-40

mg/kg/day IV divided q6-8h or 8-25 mg/kg/day susp PO divided tid-qid
 metronidazole (Flagyl): 500 mg PO bid. Anaerobic infections: 1 g or

15 mg/kg IV, then 500 mg or 7.5 mg/kg IV/PO q6h. Peds: 7.5 mg/kg
IV q6h. C difficile diarrhea: 500 mg (10-15 mg/kg/dose for peds) PO
tid
 vancomycin: 1 g IV q12h. Peds: 10-15 mg/kg IV q6h. C difficile: 40-

50 mg/kg/day up to 500 mg/day PO divided qid x7-10 days
CARDI OVASCULAR
ACE Inhibitors
 captopril (Capoten): 25 mg PO bid-tid. Max 450 mg/day
 enalapril (Vasotec): 5 mg PO qd. Max 40 mg/day
 fosinapril (Monopril): 10 mg PO qd. Max 80 mg/day
 ramipril (Altace): 2.5 mg PO qd. Max 20 mg/day
Beta-blockers
 metoprolol: 100 mg PO qd or 50 mg PO bid. Max 450 mg/day
Diuretics
 furosemide (Lasix): 20-80 mg IV/IM/PO, increase dose by 20-40 mg

q6-8h until desired response, max 600 mg/day
 hydrochlorothiazide: 12.5-25 mg PO qd. Max 50 mg/day
 triamterene + HCTZ (Dyazide): 37.5/25 mg and 50/25 mg
DERM ATOLOGY
 fucidic acid (Fucidin): apply tid-qid [cream 2% fusidic acid 5,15,30 g,

ointment 2% sodium fusidate 5,15,30 g]
53
 mupirocin (Bactroban): apply tid [cream/ointment 2% 15,30 g]
ENDOCRI NE
 calcium supplementation
 normal range: 2.2-2.6 mmol/L
 mild depletion: 1.9-2.2 mmol/L
 moderate depletion: 1.5-1.9 mmol/L
 severe depletion: < 1.5 mmol/L
I V replacement
 Hypocalcemia (severe or symptomatic)
 100 to 200 mg of elemental calcium (approx. 4.5 to 9 mEq
or 10 to 20 mL of a 10% solution) injected slowly IV over
10 minutes
 will usually raise serum total calcium by 0.25 mmol/L
(1 mg/dL) with levels returning to baseline in about
30 minutes
 To maintain levels above baseline, intermittent boluses a
continuous infusion of 1-2 mg/kg/hour of elemental calcium
may be necessary
 eg. 10 g calcium gluconate to 1L NS or D5W and run
at 50-100 cc/h (500-1000 mg/h ~ 45-90 mg elemental
Ca/h)
 serum calcium will usually normalize with this
infusion regimen in 6-12 hours
 infusion rate may need to be decreased to 0.3 to 0.5
mg/kg/hour of elemental calcium as the serum
calcium begins to approach normal levels
Name Type Strengthper tab (mg) Elemental Calcium(mg)

Alka-Mints calciumcarbonate 850mg 340mg
Caltrate calciumcarbonate 1500mg 600mg
OsCal calciumcarbonate 625or 1250mg 250or 500mg
Rolaids calciumcarbonate 550mg 220mg
TitralacTablets calciumcarbonate 420mg 168mg
TitralacLiquid calciumcarbonate 1000mg 400mg
TumsandTumsE-X calciumcarbonate 500or 750mg 200or 300mg
TumsUltraandTums
calciumcarbonate 1000or 1250mg 400or 500mg
500
Calcium Strength of each Amount of elemental Number of tablets to

supplement tablet (mg) calcium per tablet (mg) provide 1000 mg calcium
Calcium carbonate 625 250 4
650 260 4
750 300 4
835 334 3
54
1250 500 2
1500 600 2
Calcium citrate 950 200 5
Calcium gluconate 500 45 22
650 58 17
1000 90 11
Calcium lactate 325 42 24
650 84 12
Calcium 500 115 9
phosphate, dibasic
Calcium 800 304 4
phosphate, tribasic 1600 608 2
PULM ONARY
 racemic epinephrine: Severe croup: 0.05 ml/kg/dose diluted to 3 ml

with NS. Max dose 0.5 ml [2.25% racepinephrine in 15 & 30 ml]
 dexamethasone (Decadron): Croup: 0.15-0.6 mg/kg PO or IM x1.

Acute asthma: >2 yo: 0.6 mg/kg to max 16 mg PO qd x 2 days
55
!
" #
$ !$ % & ! ' () (
-hormone response pathways activated by:
-mediators released by injured tissue
-neural and nociceptive input originating from site of injury
-baroreceptor stimulation form intravascular volume depletion
Hormones Regulated by the Hypothalamus, Pituitary, and Autonomic System

Hypothalamus Pituitary Autonomic System
Corticotropin-releasing hormone Anterior pituitary: Norepinephrine

(CRH) ACTH: Cortisol IGF Epinephrine
Thyrotropin-releasing hormone TSH: Thyroxine, Aldosterone
(TRH) Triiodothyronine Renin-angiotensin
Growth hormone-releasing hormone Growth hormone Insulin
(GRH) FSH, LH: sex hormones Glucagon
Luteinizing hormone-releasing Somatostatin Enkephalins
hormone (LHRH) Prolactin
(endorphin)
Posterior pituitary:
Vasopressin
Oxytocin
Hormone-Mediated Receptor Activity:

-three major types of signal transduction mechanisms:
-receptor kinases (eg. insulin and IGF)
-G protein-coupled receptors (activated by peptide hormones, neurotransmitters, prostaglandins)
-ligand-gated ion channels
Hormone-Mediated Intracellular Pathways:

-cAMP:
-one of most common intracellular second messengers
-activation of adenylate cyclase converts ATP to cAMP activation of intracellular protein kinases
- cAMP associated with functional lymphocyte responses that generally are immunosuppressive:
- T-cell proliferation, lymphokine production, and cytotoxic function
- plasma cell production of Ab
- PMN chemotaxis and production of superoxides, H2O2 and lysosomal enzymes
- histamine release by basophil and mast cells
-intracellular receptors:
-eg. cytosolic glucocorticoid receptor
! ( ! ! ! )! * +)
Corticotropin-Releasing Hormone:
-synthesis:
-stress (pain, fear, anxiety) paraventricular nucleus of hypothalamus CRH synthesis
-proinflammatory cytokines and ADH
-negative feedback: circulating glucocorticoid decrease CRH mRNA transcription
56
-secretion:
-stimulated by angiotensin II, neuropeptide Y, serotonin, ACh, IL-1, IL-6
-inhibited by GABA, substance P, ANP, endogenous opioids, l-arginine
-stimulates ACTH production and release
-mechanism:
-via cAMP production in ACTH producing corticotrophs
Adrenocorticotropic Hormone (ACTH):

-synthesized, stored and released by anterior pituitary upon CRH stimulation
-precursor: proopiomelanocortin (POMC)
-cleaved to: alpha-melanocyte stimulating hormone, beta-lipotropic, beta-endorphin, and ACTH
-diurnal variation:
-highest late at night and lasts until just before sunrise
-most injury is characterized by elevations in CRH and ACTH; proportional to severity of injury
-pain and anxiety are prominent mediators
-other mediators include ADH, AT II, cholecystokinin, VIP, catecholamines, oxytocin, proinflammatory
cytokines
-ACTH acts in zona fasciculata of adrenal increased glucocorticoid production
-desmolase-catalysed side-chain cleavage of cholesterol pregnenolone
Cortisol/Glucocorticoids:
-cortisol essential for survival after significant physiological stress
-functions:
-potentiates actions of glucagon and epinephrine hyperglycemia
-promotes gluconeogenesis in liver (eg. inducing PEP-carboxykinase and transaminase)
-decreases insulin-binding to insulin receptors in muscles and adipose tissue
-induces proteolysis and augments release of lactate in skeletal muscle shifts substrate for hepatic
gluconeogenesis
-stimulates lipolysis and inhibits glucose uptake by adipose tissues
-adrenal insufficiency (Addison’s Crisis):
-from adrenal suppression secondary to exogenous glucocorticoid
-weakness, nausea, vomiting, fever, hypotension
-hypoglycemia (from gluconeogenesis), hyponatremia ( renal Na absorption), hyperkalemia
Macrophage Inhibitory Factor:

-glucocorticoid antagonist produced by anterior pituitary
-can potentially reverse immunosuppressive effects of glucocorticoid systemically via anterior pituitary secretion
and at local sites of inflammation where MIF is produced by T-lymphocytes
Thyrotropin-Releasing Hormone and Thyroid Stimulating Hormone:

-TRH synthesis, storage, and release of TSH
-TSH thyroxine (T4) production
- TSH release by TRH and estrogen
- TSH release by T3, T4, corticosteroids, growth hormones, somatostatin, and fasting
-T4 converted to T3 by peripheral tissues
-T4 and T3 involved in negative feedback to inhibit TRH and TSH release
-function of thyronines:
-enhance membrane transport of glucose and increase glucose oxidation
-increase formation and storage of fat when CHO intake is excessive
-increase in cellular metabolism
-after major injury:
-reduced available T3 and circulating TSH:
-d/t inhibitory effects of cortisol and conversion of T4 to rT3 (inactive)
-“euthyroid sick syndrome or non-thyroidal illness”
57
-thyroid hormone alteration in systemic inflammation not mediated by endogenous IL-1
-in severely injured or critically ill patients, a reduced free T4 concentration predictive of high mortality
-experiments have shown that thyroid hormone depletion significantly decreases cellular and humoral immunity
-repletion is associated with enhancement of both types of immunity
Growth Hormones:
-GHRH stimulates pituitary release of GH in pulsatile fashion during sleeping hours
-GH release also affected by:
-autonomic stimulation, thyroxine, ADH, ACTH, alpha-melanocyte stimulating hormone, glucagon, and
sex hormones
-physical exercise, sleep, stress, hypovolemia, fasting hypoglycemia, decreased circulating fatty acids, and
increased amino acid levels
-inhibited by:
-hyperglycemia, hypertriglyceridemia, somatostatin, beta-adrenergic stimulation, cortisol
-function:
-promote protein synthesis while enhancing mobilization of fat stores
-hepatic ketogenesis
-inhibits insulin release and decreases glucose oxidation elevated glucose levels
-role of GH during stress:
-promote protein synthesis while enhancing mobilization of fat stores
-direct stimulation
-potentiation of adrenergic lipolytic effects on adipose stores
-promote hepatic ketogenesis
-inhibit insulin release and decrease glucose oxidation
-protein synthesis:
-mediated by secondary release of insulinlike growth factor-1 (IGF-1)
-promotes amino acid incorporation and cellular proliferation
-attenuates proteolysis in skeletal muscle and liver
-IGFs:
-mediators of hepatic protein synthesis and glycogenesis
-adipose tissue: increases glucose uptake and lipid synthesis
-skeletal muscles: increases glucose uptake and protein synthesis
-promote incorporation of sulfate and proteoglycans into cartilage skeletal growth
-associated decrease in protein synthesis and observed negative nitrogen balance attributed to reduction in
IGF-1 levels
-IGF produced predominantly in liver; dysfunction may contribute to negative nitrogen balance after injury
-GH and IGF-1 are immunostimulatory and promote tissue proliferation
Somatostatin:
-potent inhibitor of GH, TSH, renin, insulin, and glucagon release
-may regulate excessive nutrient absorption and activities of GH and IFG during convalescence form injury
Gonadotrophins and Sex Hormones:

-GnRH (hypothalamus) stimulates FSH and LH release from anterior pituitary
-release can be blocked by CRH, prolactin, estrogen, progestins, and androgens
-FSH and LH release suppressed after injury, stress, or severe illness (d/t inhibitory activity of CRH)
-estrogens:
-inhibit cell-mediated immunity, NK cells activity and neutrophil function
-stimulatory for antibody-mediated immunity
-androgens:
-predominantly immunosuppressive
58
Prolactin:
-GnRH and dopamine suppresses PRL secretion from anterior pituitary
-stimulants: CRH, TRH, GHRH, serotonin, VIP
-elevated levels seen after injury
-may account for amenorrhea frequently seen in women after injury or major operations
-has immunostimulatory properties
Endogenous Opioids:
-beta-endorphins attenuate pain perception; capable of inducing hypotension through a serotonin-mediated pathway
-enkephalins produce hypertension
-in GI tract: reduces peristaltic activity and suppresses fluid secretion
-in glucose metabolism:
-B-endorphins and morphine induce hyperglycemia, but also increase insulin and glucagon release by
pancreas
-endorphins influence immune system by increasing NK cell cytotoxicity and T-cell blastogenesis
-IL-1 activates release of POMC
-opioids compromise natural and specific immune system:
-inhibit proliferation and differentiation of lymphocytes and monocytes/macrophages
! ( ! ! ! )! * +)
Arginine Vaspressin (or ADH):

-synthesized in anterior hypothalamus and transported by axoplasmic flow to posterior pituitary for storage
-release stimulated by:
-elevated plasma osmolality (via sodium-sensitive hypothalamic osmoreceptors)
-changes in effective circulating volume (~10%)
-release enhanced by beta-adrenergic agonists, angiotensin II stimulation, opioids, anesthetic agents, pain,
and elevated glucose concentrations
-release inhibited by:
-alpha-adrenergic agonists and atrial natriuretic peptide (ANP)
-function:
-promotes reabsorption of water from distal tubules and collecting ducts
-mediates vasoconstriction peripherally:
-may cause trauma-induced ischemia/reperfusion phenomenon that precedes gut barrier
impairment
-stimulates hepatic glycogenolysis and gluconeogenesis hyperglycemia that increases osmotic effect
-elevated secretion is another characteristic of trauma, hemorrhage, open-heart surgery, and other major operations
-SIADH:
-low u/o, highly concentrated urine, and dilutional hyponatremia
-plasma osmolality < 275 mOsm/kg H2O and urine osmolality > 100 mOsm/kg H2O
-commonly seen in pts with head trauma and burns
-Diabetes Insipidus:
-voluminous output of dilute urine
-seen in comatose patients
Oxytocin:
-role in injury response unknown
-stimulates contraction of lactating mammary glands and induces uterine contractions in parturition
59
! &
Catecholamines:
-hypermetabolic state observed after severe injury has been attributed to activation of adrenergic system
-norepinephrine: from synaptic leakage during sympathetic nervous system activity
-epinephrine: from secretions of chromaffin cells of adrenal medulla
-functions:
-promotes stress-induced hyperglycemia
-liver: promotes glycogenolysis, gluconeogenesis, lipolysis and ketogenesis
-pancreas: decreased insulin secretion and increased glucagon secretion
-adipose: increases lipolysis
-skeletal muscle: inhibits insulin-facilitated glucose uptake
-other:
-thyroid: increase secretion of PTH, T4, T3
-secretion of renin
-inhibits release of aldosterone
-immune function:
-enhances leukocyte demargination with resultant neutrophilia and lymphocytosis
-lowers ratio of CD4 to CD8 T-cells
Aldosterone:
-mineralocorticoid
-synthesized, stored, and released in adrenal zona glomerulosa
-release induced by: AT II, hyperkalemia, and aldosterone stimulating factor (ASF) from pituitary
-ACTH is most potent stimulus for aldosterone release in injured patient
-function:
-maintain intravascular volume by conserving sodium and eliminating potassium and hydrogen ions
-early distal convoluted tubule: increases Na, Cl reabsorption and excretion of H+
-late distal convoluted tubule: Na reabsorption with excretion of K
-major effect on kidneys, but also acts on intestines, salivary glands, sweat glands, vascular endothelium,
and brain
Renin-Angiotensin:
-renin synthesized and stored in renal juxtaglomerular apparatus
-activation and release by:
-ACTH, AVP, glucagon, prostaglandins, potassium, magnesium and calcium
-barorecepors in JGA sense decrease in BP increase secretion
-angiotensin:
-angiotensinogen synthesized by liver
-renin converts angiotensinogen to angiotensin I
-angiotensin-converting enzyme on pulmonary endothelial surfaces converts AT I to AT II
-AT II:
-potent vasoconstrictor that stimulates aldosterone and vaspressin synthesis
-stimulates heart rate and myocardial contractility
-potentiates release of epinephrine by adrenal medulla, increases CRH release, and activates
sympathetic nervous system
-can induce glycogenolysis and gluconeogenesis
Insulin:
-derived from pancreatic beta islet cells
-released by certain substrates, autonomic neural input, and other hormones
-glucose major stimulant of insulin secretion
-others: amino aids, free fatty acids, and ketone bodies
-inhibition of release:
60
-epinephrine and sympathetic stimulation
-glucagon, somatostatin, GI hormones, beta-endorphins, IL-1
-function:
-global anabolic effect: promotes hepatic glycogenesis and glycolysis, glucose transport into cells, adipose
tissue lipogenesis, and protein synthesis
-in injured patient, biphasic pattern of insulin release observed:
-first phase: few hours after injury
-relative suppression of insulin, reflecting influence of catecholamines and sympathetic
stimulation
-later phase:
-return to normal or excessive insulin production with persistent hyperglycemia d/t
peripheral resistance to insulin
-ratio of insulin to glucose is used as a predictor of mortality and survival
-enhances T-cell proliferation and cytotoxicity
Glucagon:
-product of pancreatic alpha islet cells
-stimulants of secretion: plasma glucose concentrations and exercise
-function:
-stimulates hepatic glycogenolysis and gluconeogenesis
-promotes hepatic ketogenesis and lipolysis in adipose
-release after injury is initially decreased, but returns to normal 12 h later
'' #
, ' () (
-cytokines are produced by diverse cell types at site of injury and by systemic immune cells
-activity exerted locally via cell-to-cell interaction (paracrine)
-small polypeptide or glycoprotein; modulate gene transcription
-may be pro- or anti-inflammatory
-direct inflammatory response to infection and injury; actively promotes wound healing
-responsible for:
-fever, leukocytosis, hyperventilation, tachycardia (systemic inflammatory response syndrome SIRS)
-hemodynamic instability characteristic of septic shock
-metabolic derangements of injured patients (eg. muscle wasting and cachexia)
-contribute to end-organ injury multiple organ failure; death
Tumor Necrosis Factor-alpha:

-earliest and one of most potent mediators of injury/infectious response
-source: monocytes/macrophages, T-cells
-release is rapid and short-lived
-presence of effective endogenous modulators, which serve to prevent any propagation of unregulated
TNF-a activity
-major cytokine related to muscle catabolism and cachexia during stress
-amino acids mobilized from skeletal muscles and shunted toward hepatic circulation as fuel substrates
-other functions:
-coagulation activation
-promoting release of PGE2, PAF, glucocorticoid, eicosanoids
Interleukin-1:
-TNF-a induced synthesis of IL-1 by macrophages and endothelial cells
-types:
-IL-1a: cell membrane-associated; exerts influence via cellular contact
61
-IL-1b: in circulation in greater quantities; induces characteristic systemic derangements after injury
-synergistic and similar effects to TNF-a
-half-life (~6 min) less than TNF-a
-effects:
-induces classic inflammatory febrile response to injury: stimulates local prostaglandin activity in anterior
hypothalamus
-anorexia effect on satiety center
-augments T cell proliferation by enhancing IL-2 production
-may influence skeletal muscle proteolysis: cachexia
-decrease pain perception: promote release of endorphin, increasing number of central opioid-like
receptors
-potent stimulant for ACTH and GC release via hypothalamus and pituitary gland
-regulated by IL-1 receptor antagonists (IL-1ra): competes for IL-1 receptor binding
Interleukin-2:
-promotes T-cell proliferation, immunoglobulin production, and gut barrier integrity
-not readily detectable in circulation during acute injury
-secretion impaired in: cancer and AIDS
-attenuated IL-2 expression contributes to transient immunocompromised state of the surgical patient
Interleukin-4:
-glycoprotein molecule
-produced by activated TH2 cells
-functions include:
-induction of B-lymphocyte proliferation
-enhances macrophage MHC class II (HLA-DR and LHA-DP) expression and adhesion molecules
-induces class switching in differentiating B-lymphocytes IgG4 and IgE
-also a potent anti-inflammatory cytokine:
-down-regulates effects of IL-1b, TNF-a, IL-6, IL-8, and superoxides production
-induce apoptosis in inflammatory macrophages (abrogated by IFN-gamma)
Interleukin-6:
-used frequently as an indicator of SIRS and predictor of preoperative morbidity
-levels proportional to extent of tissue injury during an operation
-induced by TNF-a and IL-1
-long half-life
-functions:
-with IL-1, important mediator of hepatic acute-phase protein response
-enhances C-reactive protein, fibrinogen, haptoglobin, amyloid A, a-1-antitrypsin, and
complement production
-induces PMN activation; may delay the phagocytic disposal of senescent or dysfunctional PMNs
-anti-inflammatory effects:
-attenuates TNF and IL-1 activity while promoting release of sTNFRs and IL-1ra
-prolonged and persistent expression of IL-6 associated with immunosuppression and postop
infectious morbidity
-can reduce plasma glutamine
Interleukin-8:
-has been proposed as an additional biomarker for the risk of multiple organ failure
-serves a PMN activator and potent chemoattractant
-does not produce hemodynamic instability characteristic of TNF-a and IL-1
Interleukin-10:
-important endogenous regulatory mediator during inflammatory response
62
-modulates TNF-a activity: reduces TNF-a levels and associated deleterious effects
-may promote sTNFR and IL-1ra production
Interleukin-12:
-promotes differentiation of TH1 cells and production of IFN-gamma
-prevents apoptosis in certain T-lymphocyte populations after their activation
Interleukin-13:
-pleiotropic cytokine sharing may properties of IL-4
-produced during TH2 responses
-with IL-4, modulates macrophage function, but no effects on T-cells
-can upregulate macrophage MHC class I and II antigens and other surface antigens, such as CD23
-can inhibit NO production and expression of proinflammatory cytokines; can enhance production of IL-1ra
-net effect of IL-13, along with IL-4 and IL-10 is anti-inflammatory
Interferon-gamma:
-TH cells activated by the bacterial antigens IL-2 or IL-12 readily produce IFN-gamma
-conversely, IFN-gamma can induce production of IL-2 and IL-12 by TH cells
-important role in activating circulating and tissue macrophages
Granulocyte/Macrophage-Colony Stimulating Factor:

-GM-CSF production induced by IL-2 and endotoxins
-prominent role in delaying apoptosis of macrophages and PMNs
-promotes maturation and recruitment of functional leukocytes necessary for normal inflammatory cytokine
response, and potentially in wound healing
* +) & &+) ) ! ++" )
Programmed Cell Death:

-apoptosis is the principal mechanism by which senescent or dysfunctional cells, including macrophages and PMNs,
are systematically disposed of without activating other immunocytes or the release of proinflammatory contents
-several proinflammatory cytokines delay the normal temporal sequence of macrophage and PMN apoptosis in vitro:
-TNF, IL-1, IL-3, IL-6, GM-CSF, G-CSF, and IFN-gamma
-IL-4 and IL-10 accelerate apoptosis in activated monocytes
-failure of apoptosis of inflammatory immunocytes may perpetuate and augment the inflammatory response,
precipitating multiple organ failure in severely injured and critically ill patients
TNF Receptor-Mediated Programmed Cell Death:

-TNFR activation induce specific cell responses that may include initiation of apoptosis
-two specific transmambrane TNFRs (type I, p55; and type II, p75)
-p55:
-induces apoptosis, cytotoxicity, expression of adhesion molecules on endothelial cells, and
activation of sphingomyelin pathway and nuclear factor-kappa B
-p75:
-induces proliferation of T cells, fibroblasts, NK cells, and proinflammatory cytokine release
-during sepsis, down-regulation of TNFR activity may delay apoptosis of inflammatory macrophages and PMNs,
prolonging the inflammatory response
Fas/CD95 Receptor-Mediated Programmed Cell Death:

-along with p55 TNFR, Fas receptors exhibit similar cytoplasmic sequence motifs, known as “death domains”
-FasR predominantly expressed in liver, lung, heart, intestine, skin, and lymphocytes
-when triggered by FasL (specific ligand) apoptosis
-only known role of the Fas receptor
63
-while induction of apoptosis via Fas/FasL cross-linking in activated immunocytes may be advantageous during
systemic inflammation, this activity at the tissue level may be detrimental to the host
! ) ( , !)
Cortisol/Glucocorticoids:
-glucocorticoid administration before or concomitantly with endotoxins infusion in healthy human beings is able to
attenuate the symptoms, catecholamine response, and acute phase response, but it increases IL-10 release
-increased IL-10 release may contribute to acute anti-inflammatory effect of glucocorticoid
-the proinflammatory cytokine IL-1 and TNF and IL-6 can activate the HPA axis and induce the release of CRH and
ACTH increased circulatory GC levels inhibit endotoxins-induced production of TNF at the level of mRNA
translation
-dexamethasone inhibits neutrophil apoptosis and prolongs their functional responsiveness
Catecholamines:
-inhibit endotoxins-induced macrophage production of TNF-alpha
-endogenous epinephrine or exogenous administration as a component of sepsis treatment may serve to limit
excessive proinflammatory effects of the cytokine network during the early phase of systemic infection
' " #
( +)+ ++' ( ) !
Endothelial Cell Function:

-in a paracrine fashion, local mediators (eg. TNF-a, IL-1, endotoxins, thrombin, histamine, and IFN-g) are capable
of stimulating or activating the endothelial cell during local tissue injury
-endothelial cell can release several mediators:
-IL-1, PAF, PGI2 and PGE2, GM-CSF, growth factors, endothelin, NO, and TxA2
-modulate CV and renal function and influence the HPA axis
-collagenase secretion to permit neovascularization and vascular remodelling
-ACE convert AT I to AT II potent regulator of vascular tone
-if activated, up-regulates expression of leukocyte adhesion receptor molecules:
-E-selectin (requires stimulation of TNF-a and IL-1), P-selecting, ICAM-1, ICAM-2
-local injuries and inflammatory mediator stimulation promote the marination of circulating PMNs to endothelial
surfaces
-rolling, diapedesis
-activated PMNs and the subsequent release of inflammatory mediators and reactive oxygen metabolites
are implicated in capillary leakage, acute lung injury, and postischemic injury
Endothelium-Derived Nitric Oxide:

-EDNO can be released in response to ACh stimulation, hypoxia, endotoxins, cellular injury, or mechanical shear
stress from circulating blood
-induction of SMC relaxation by EDNO via activation of soluble guanylate cyclase and cGMP within the myocytes
-EDNO induces vasodilation and platelet deactivation
-formed from oxidation of L-arginine
Prostacyclin:
-PGI2 an important endothelium-derived vasodilator synthesized in response to vascular shear stress and hypoxia
-derived from arachidonic acid
-causes vasorelaxation and platelet deactivation by increasing cAMP
64
Endothelins:
-produced by endothelial cell in response to:
-injury, thrombin, TGF-beta, IL-1, AT II, ADH, catecholamines, and anoxia
-potent vasoconstrictor properties
-ET-1 most biologically active and potent vasoconstrictors known
-increased serum levels of ET are correlated with the severity of injury after major trauma, major surgical
procedures, and in cardiogenic or septic shock
Platelet-Activating Factor:
-phopsholipid constituent of cell membranes that can be induced by TNF, IL-1, ADH, and AT II
-stimulates production of TxA2 promotes platelet aggregation and vasoconstriction
-increases glucagon and catecholamine activity experimentally
-can induce hypotension, increase vascular permeability, hemoconcentration, pulmonary hypertension,
bronchoconstriction, primed PMN activity, eosinophil chemotaxis/degranulation, and thrombocytopenia
-alters shape of endothelial cells, causing them to contract and increase permeability
-chemotactant for leukocyte adherence to vascular wall and facilitates migration out of vascular compartment
Atrial Natriuretic Peptides:

-released by CNS and by specialized endothelium found in atrial tissues in response to wall tension
-potent inhibitors of aldosterone secretion and prevent reabsorption of sodium
!) ++ +)! ' ( ) !
Heat-Shock Proteins:
-production induced by heat, hypoxia, trauma, heavy metals, local trauma, and haemorrhage
-presumed to protect cells from traumatic stress
-function intracellularly in the assembly, disassembly, stability, and transport of proteins
Reactive Oxygen Metabolites:

-cause tissue injury by peroxidation of cell membrane unsaturated fatty acids
-cells are not immune to damage by their own ROMs but are generally protected by oxygen scavengers that include
glutathione and catalases
-activated WBCs are potent generators of reactive oxygen metabolites
-ROMs can induce apoptosis
! &+) ) ! ' () !
Eicosanoids:
-oxidation derivatives of arachidonic acid
-secreted by virtually all nucleated cells except lymphocytes
-phospholipids –(PLP-A2) arachidonic acid
-two major pathways:
-cyclooxygenase: production of all prostaglandin and thromboxanes
-lipoxygenase: production of leukotrienes and HETE
-synthesis stimulated by:
-hypoxic and ischemic injury, direct tissue injury, endotoxins, norepinephrine, ADH, AT II, bradykinin,
serotonin, ACh, and histamine
-function:
-diverse effects systemically on endocrine and immune function, neurotransmission, and vasomotor
regulation
-major components of the inflammatory response in injured tissue, characterized by vascular permeability,
leukocyte migration, and vasodilation
65
Kallikrein-Kinin System:
-bradykinins are potent vasodilators produced through kininogen degradation by the serine protease kallikrein
-release stimulated by hypoxic and ischemic injury
-kallikrein activated (from prekallikrein) by:
-Hageman factor, trypsin, plasmin, factor XI, glass surfaces, kaolin, and collagen
-function:
-increase capillary permeability and tissue edema, evoke pain, and increase bronchoconstriction
-increase renal vasodilation and reduce renal blood flow
-increase glucose clearance by inhibiting gluconeogenesis
-may also increase nitrogen retention
Serotonin:
-tryptophan derivative found in enterochromaffin cells of intestine and platelets
-stimulates vasoconstriction, bronchoconstriction, and platelet aggregation
-also capable of acting as a myocardial chrono- and inotrope
Histamine:
-derived from histidine and stored in neurons, skin, gastric mucosa, mast cells, basophil, and platelets
-release activated by increased calcium levels
-H1 receptor binding:
-increased histamine precursor uptake (l-histidine)
-bronchoconstriction, intestinal motility, and myocardial contractility
-H2 receptor binding:
-inhibits histamine release
-both: induces vasodilation and increased vascular permeability
-hypotension, peripheral pooling of blood, increased capillary permeability, decreased venous
return, and myocardial failure
' - #
' ). + ) *
Substrate Metabolism:
-healthy 70 kg adult expends 1700-1800 kcal/day of energy
-sources: lipid, carbohydrate, protein
-obligate glycolytic cells (eg. neurons, leukocytes, erythrocytes)
-require 180 g glucose per 24 h for basal energy needs
-hepatic glycogen ~75 g glucose
-skeletal muscle:
-cannot directly release free glucose d/t lack of glucose-6-phosphatase
-fasting decreased serum glucose net effect of body to increase glucose production
-decrease insulin release
-increased glucagon and more transient elevations of GH, catecholamines, ADH, and AT II
-glucagon and epinephrine enhance cAMP promotes glycogenolysis
-cortisol and glucagon promote gluconeogenesis
-norepinephrine, ADH, ATII –(PIP3+Ca++) promote glycogenolysis
-reduction in anabolic growth factors (eg. IGF-1)
-gluconeogenesis:
-mainly by liver, but also by kidneys (up to 45% in late starvation)
-precursors: lactate, glycerol, amino acids (eg. alanine and glutamine)
-lactate sources:
-skeletal muscles via glycogenolysis and glycolysis
-erythrocytes and WBCs after aerobic glycolysis
66
-lactate converted to glucose in liver via Cori cycle
-protein metabolism:
-75 g protein must be degraded (mostly from skeletal muscle) daily during fasting and starvation to provide
gluconeogenic amino acids to liver
-proteolysis (results from insulin and cortisol) BUN excretion
-after 5d, rate diminishes to 15-20 g/day
-occurs as CNS and other tissues adapt to ketone oxidation as predominant energy source
-amount of protein required for GNG significantly reduced
-lipid metabolism:
-160 g TG provides energy requirements for GNG and basal enzymatic and muscular function
- insulin, glucagon and catecholamines promotes lipolysis
- free fatty acids and glycerol
-FFA and ketone bodies (from liver) source of energy for heart, kidney, muscle, and liver
-lipid stores provide up to 40% of caloric expenditure during starvation
-lipid oxidation reduces glucose requirements:
-decreased amount of mandatory glycolysis, which requirements for GNG and protein
degradation
-once initial obligatory neuroendocrine stress hormone response recedes, whole-body energy expenditure also
decreases during prolonged fasting
' ). + & ! !
Energy Balance:
-associated increase in energy expenditure and increased oxygen consumption
-d/t increased sympathetic activity
-may be related to influences on cell membrane sodium permeability the energy required for ion pump
action to maintain normal transmembrane concentrations
Lipid Metabolism:
-FFA principle sources of energy after injury
-lipolysis enhanced:
-d/t ACTH, cortisol, catecholamines, glucagon and GH; insulin; sympathetics
-hormone-sensitive lipase stimulated by catecholamines
-FFA can be oxidized by cardiac and skeletal muscle to produce energy
-lipoprotein lipase (clears plasma TG):
-suppressed in adipose tissue after trauma, but not in muscle
-suppressed in both in sepsis
-ketogenesis:
-decreased after major injury, severe shock, and sepsis
-suppressed by insulin and other energy substrates, uptake and oxidation of FFA
-increased after minor injury or mild infection
Carbohydrate Metabolism:
-systemic glucose intolerance after injury state of relative insulin resistance
-increases in plasma glucose levels proportional of severity of injury; correlated to survival
-d/t increased hepatic production and peripheral insulin resistance
-deprivation of glucose to non-essential organs (eg. skeletal muscles and adipose) mediated via catecholamines
-mediator-induced reduction of skeletal muscle pyruvate dehydrogenase AcetylCoA for TCA cycle
results in shunting of pyruvate to liver for GNG
-glucose provided for inflammatory and healing cells in the wound environment
Protein and Amino Acid Metabolism:

-daily protein intake ~ 80-120g or 13-20 g of nitrogen
67
-loss of lean tissues after significant injury:
-skeletal muscle is depleted while visceral tissues (eg. liver and kidney) are relatively preserved
-severe trauma, burns, and sepsis are associated with increased whole-body protein turnover and increased
net protein catabolism
-accelerated proteolysis and GNG persist after major injury and during sepsis
-after trauma, substrate cycling of amino acid occurs b/n skeletal muscle, liver, and the wound:
-major source is skeletal muscle
-proteolysis enhanced by:
-oxidative species and diminished antioxidant activities
-increased ubiquitin-dependent proteolytic pathways
-glutamine and alanine released:
-glutamine: major energy source for lymphocytes, fibroblasts, and GI tract
!* ! / !) )/
Catabolic Phase:
-adrenergic-corticoid phase:
- glucagon, GC and catecholamines with insulin
-rates of GNG, acute phase protein production, and immune cell activity are all still altered during the
catabolic phase
-administration of glucose produces little or no change in rate of protein catabolism
-glucose turnover increased
-Cori cycle activity stimulated: 3C intermediates glucose by pyruvate carboxylase and PEP carboxylase
-lipolysis and FFA oxidation
Early Anabolic Phase:

-corticoid-withdrawal phase:
-within 3-8 days after uncomplicated elective surgery or after weeks in patients with extensive cross-
sectional tissue injury, sepsis, or ungrafted thermal injury
-characterized by sharp decline in nitrogen excretion and restoration of appropriate potassium-nitrogen
balance
-early acute phase reactants are supplanted by tissue repair and anabolic factors (eg. IGF-1)
-clinically: initial diuresis of retained water and renewed interest in oral nutrition
-synthesis of proteins (positive nitrogen balance):
-rapid progressive gain in weight and muscular strength
-gain of over 100 g of lean body mass/day
-rate of gain much slower than rate of initial loss
Late Anabolic Phase:

-may last from several weeks to several months after severe injury
-gradual restoration of adipose stores and positive nitrogen balance declines to normal
-weight gain is much slower because of high caloric content of fat
) ( 0 !
-history: -presence of weight loss and chronic illnesses or dietary habits influencing the quantity an quality
of food intake
-physical: -assess loss of muscle and adipose, organ dysfunction, and subtle change in skin, hair, or
neuromuscular function
68
-biochemical: -creatinine excretion, albumin, transferring
-fundamental goals of nutritional support:

-meet energy requirements of metabolic processes, core temperature maintenance, and tissue repair
-Basal Energy Expenditure (BEE):

-estimated with Harris-Benedict equations:
BEE (men) = 66.47 + 13.75(W) + 5.0(H) - 6.76(A) kcal/day
(women) = 65.51 + 9.56(W) + 1.85(H) - 4.68(A) kcal/day
W = weight (kg); H = height (cm); A = age (years)
-meet substrate requirements for protein synthesis

-dependent on degree of insult, source and amount of exogenous protein, previous nutritional
status
-maintain calorie-nitrogen ratio of 150-200:1
-precluding renal or hepatic dysfunction, ~ 0.25-0.35 g of nitrogen/kg daily should be provided
-vitamins usually not given in absence of preoperative deficiencies

-pts maintained on elemental diets or parenteral hyperalimentation require complete vitamin and mineral
supplementation
-intravenous feeds require all micronutrients to prevent development of deficiencies:
-eg. vit K, B12, folic acid, trace minerals, essential fatty acids
( ) ) (' ( &! ! )+ !
-reasonably well-nourished and otherwise healthy individual who undergoes an uncomplicated major operative
procedure has sufficient body fuel reserves to withstand the catabolic insult and partial starvation for at least 1 week
-requires: IV fluids /w min of 100 g glucose daily to minimize protein catabolism
-defined formula diets and TPN are unnecessary
-during early anabolic phase, pt needs adequate caloric intake of proper composition to meet energy needs
of the body and to allow protein synthesis
-chronically debilitated preoperatively from diseases or from malnutrition and patients who have suffered trauma,
sepsis, or surgical complications cannot maintain adequate caloric intake
-should receive consideration of nutritional support early
-in general, the indications for preoperative nutritional support appear largely confined to patients with
evidence of more severe erosion of lean body mass and adipose tissue stores
-enteral route should always be used when possible because it is considered to be more economical and well
tolerated in many patients
-NG, gastrostomy, and jejunostomy tube feedings for those with normal GI tract but cannot or will not eat
-ability to tolerate enteral feeds depends on:
-rate of infusion
-osmolality of feeds
-chemical nature of the product
-usually start with 30-50 cc/h then increased by 10-25 cc/h/d until optimal volume is delivered
-after full volume is attained, concentration is increased slowly to desired strength
-measure gastric residuals to monitor risk of aspiration
-decrease rate if abdo cramps or diarrhea occurs
-parenteral route used for supplementation in pt with limited oral intake or for complete nutritional management in
the absence of oral intake
-potentially enhances the magnitude of macroendocrine and microendocrine mediator responses to an
antigenic challenge
-loss of intestinal barrier function occurs
69
-experimental approaches for preserving GI mucosa integrity and gut mass:
-luminal stimulation by digestible or nondigestible substrates, and infusion of critical
intestinal fuel sources (eg. glutamine or short-chain fatty acids)
!)+ ( *
Nasoenteric Tube Feeding:

-contraindications for nasoesophageal or gastric tube feeding:
-unconsciousness or lack of protective laryngeal reflexes
-nasojejunal tubes to bypass dysfunctional gastric stomas and high GI fistulas
-infusion pumps:
-decrease incidence of GI side effects induced by overly rapid delivery of hyperosmolar solutions
-allows safer administration of larger daily volumes of nutrients; minimizes gastric distention
Gastrostomy Tube Feeding:

-for pts with chronic GI lesions arising at or above the cardioesophageal junction
-contraindicated for mentally obtunded pts with inadequate laryngeal reflexes
-used only in alert patients or in patients with total obstruction of distal esophagus
-feeding mixture may be pureed foods
-hyperosmolarity of the feeding formula is not generally a problem as long as pylorus is intact
Jejunostomy Tube Feeding:

-for pts in which nasoesophageal or gastrostomy tube feedings are contraindicated:
-comatose pts
-pts with high GI fistulas or obstructions
-pts in whom a nasojejunal feeding tube cannot be placed
-types:
-Roux-en-Y (permanent)
-Witzel (temporary):
-insertion of 18 Fr. rubber catheter into proximal jejunum ~30 cm distal to ligament of Treitz
-if tube is accidentally removed, pt should be observed for peritonitis for 12-18h after feedings restarted
-feedings are safely begun 12-18h after jejunostomy construction
-if the pt /w jejunostomy has proximal bowel or biliary fistula draining > 300 cc/d for prolonged period, fistular
drainage may be collected by sump suction, cooled, and promptly re-fed in small increments throughout the day
" & ( ! +) "

-useful for patients with depleted protein reserves secondary to GI tract disease (eg. UC, malabsorption syndrome)
and for pts with only partial function of the GI tract (eg. short bowel syndrome or gastric or small-bowel fistulas)
-contents include:
-baseline electrolytes, water, fat-soluble vitamins, and trace minerals
-no bulk minimal residuals
-no lactose
-partially hydrolysed or completely hydrolysed proteins
-complications:
-nausea, vomiting, and diarrhea d/t high osmolarity
-hypertonic nonketotic coma may occur in presence of excessive water losses or if diets are administered at
concentrations above those recommended
-hyperglycemia and glycosuria
70
)! !)+ + )
-continuous infusion of hyperosmolar solution containing carbohydrates, proteins, fat, and other necessary nutrients
through indwelling catheter into SVC
-ratio of calories to nitrogen must be at least 100-150 kcal/g nitrogen and the two materials must be infused
simultaneously in order to maximize nitrogen use
Indications for the Use of Intravenous Hyperalimentation:

-exclusively for intravenous nutrition:
-newborns with catastrophic GI anomalies (eg. tracheoesophageal fistula, gastroschisis, omphalocele, massive intestinal atresia)
-infants who fail to thrive nonspecifically or secondarily to GI insufficiency associated with short bowel syndrome, malabsorption,
enzyme deficiency, meconium ileus, or idiopathic diarrhea
-might be appropriate for enteral or parenteral nutrition:
-adults with short bowel syndrome secondary to massive resection or fistulas
-high alimentary tract obstructions without vascular compromise (achalasia, stricture, esophageal/gastric ca, pyloric obstruction)
-prolonged paralytic ileus after major operations, multiple injuries, blunt or open abdominal trauma
-malabsorption secondary to celiac disease, hypoproteinemia, enzyme or pancreatic insufficiency, regional enteritis or UC
-functional GI disorders such as esophageal dyskinesia after CVA, idiopathic diarrhea, psychogenic vomiting
-etc. etc.. see Schwartz pg. 43
-contraindications to hyperalimentation:
-lack of specific goal for pt management, or when instead of extending a meaningful life, inevitable dying
is prolonged
-period of cardiovascular instability or severe metabolic derangement requiring control or correction before
attempting hypertonic intravenous feeding
-feasible GI tract feeding
-patients in good nutritional status, in whom only short-term parenteral nutrition support is required or
anticipated
-infants with less than 8 cm of small bowel, since virtually all have been unable to adapt sufficiently
despite prolonged periods of parenteral nutrition
-patients who are irreversibly decerebrate or otherwise dehumanized
Preparation and Administration of Solutions:

-basic solution:
-20-25% dextrose
-3-5% crystalline amino acids
-vitamin supplementation:
-vitamin K (10 mg) and folic acid (5 mg) IM once weekly and B12 once a month b/c these are unstable in
hyperalimentation solution
-essential fatty acid deficiency: dry, scaly dermatitis and loss of hair
-prevented by periodic infusion of fat emulsion at rate equivalent to 10-15% of total calories
-trace mineral deficiencies (seldom seen, usually in pts with extended TPN use):
-zinc: eczematoid rash diffusely and at intertriginous areas
-copper: microcytic anema
-chromium: glucose intolerance
-insulin may be required for glucose intolerance
-administration of adequate amounts of K is essential to achieve positive nitrogen balance and to replace depleted
intracellular stores
-hypokalemia may cause glycosuria, which would be treated with potassium, not insulin
Fat Emulsions:
-derived from soybean or safflower oils are widely used as an adjunctive nutrient to prevent development of
essential fatty acid deficiency
-major energy source in TPN, but no evidence of enhanced metabolic efficacy if greater than 10-15% of calories is
provided as lipid emulsions
-pts with abnormal fa transport or metabolism, lipid nephrosis, coagulopathy, or serious pulmonary disease should
71
not receive fat emulsions
-limit administration to between 2.0-2.5 g/kg TBW/d
Special Formulations:
-renal failure patients (oliguric):
-final dextrose concentration of 40-45% and only essential L-amino acids
-hepatic failure:
-solutions contain increased levels of branched-chain amino acids and decreased concentrations of
aromatic amino acids to decrease encephalopathy
-cardiac cachexia:
-highly concentrated dextrose and amino acid formula that are low in sodium
Complications:
-sepsis secondary to contamination of CV catheter
-earliest signs: sudden development of glucose intolerance in a patient previously been maintained on
parenteral alimentation w/o difficulty
-if suspected, remove and culture catheter; replace at a different site
-problems with catheter placement:
-pneumothorax, hemothorax, or hydrothorax
-subclavian artery injury
-cardiac arrhythmia
-air embolism
-cardiac perforation and tamponade
-hyperosmolar nonketotic hyperglycemia:
-may occur with normal rates of infusion in patients with impaired glucose tolerance or in any pt if the
hypertonic solutions are administered too rapidly
-must monitor urine and blood glucose levels and electrolytes
-tx: volume replacement with correction of electrolyte abnormalities and administration of insulin
-excess calorie infusion may result in:
-carbon dioxide retention and respiratory insufficiency
-hepatic steatosis or marked glycogen deposition
72
! " #$ !
% & &
% '
-50-70% TBWt; ~ 60% (M), 50% (F)
-greater proportion of water in lean individuals
-newborns: 75-80% TBWt
-30-40% TBWt; largest proportion in skeletal muscle

-principal cations: potassium and magnesium
-principle anions: phosphates and proteins
(
-20% TBWt plasma (5% TBWt) + interstitial (15% TBWt)
-transcellular fluid (CSF, synovium) ~ 10% ECF = 1-2% TBWt
-principle cation: sodium
-principle anion: chloride and bicarbonate
)" ))
-proteins in plasma primarily responsible for effective osmotic pressure b/n plasma and interstitial fluid colloid
oncotic pressure
* & &
' ($ !
-normal individual consumes ~2000-2500 ml H2O/day; ~1500 ml by mouth
-daily water loss: 250ml stool, 800-1500 ml urine, ~600ml insensible loss
-insensible loss: skin (75%) and lungs (25%); by hypermetabolism, hyperventilation and fever
-can exceed 250ml/day per degree of fever
-unhumidified tracheotomy up to 1500ml/day
-gain in water: excessive cellular catabolism (up to 500ml/day)
)) )
-50-90 mEq (3-5g) as sodium chloride
-kidneys excrete excess salt
-gastrointestinal losses usually isotonic or slightly hypotonic
% & &
+ " $ ! )
-diagnosed by clinical examination
-indirect measurements:
-BUN rises with ECF deficit of sufficient magnitude to reduce GFR
-hematocrit: with ECF deficit; with excess
-[Na] NOT related to volume status of ECF
73
(1) Volume Deficit:
-most common causes of ECF deficit are GI losses from vomiting, NG suction, diarrhea, fistular drainage
-also sequestration of fluid in soft tissues injuries and infections, intraabdominal and retroperitoneal
inflammatory processes, peritonitis, intestinal obstruction, burns
(2) Volume Excess:

-iatrogenic
-secondary to renal insufficiency, cirrhosis, or CHF
$ ! )
-sodium primarily responsible for osmolarity of ECF
-clinical signs of hypo- or hypernatrema are not present until changes are severe
(1) Hyponatremia:
-acute symptomatic hyponatremia (<130) CNS signs of ICP; tissue signs of intracellular water
-risk of oliguric renal failure which may not be reversible if treatment delayed
(2) Hypernatremia:
-CNS and tissue signs characterize acute symptomatic hypernatrema
( + " , " )
-ECF deficit and hyponatremia:

-continuing to drink while losing large volumes of GI fluids
-post-op replacement of GI losses with hypotonic fluids
-ECF deficit and hypernatremia:
-loss of large amount of hypotonic salt solution (eg. sweat) in absence of fluid intake
-ECF excess and hypernatremia:
-prolonged administration of excessive sodium salts with restricted water intake
-ECF excess and hyponatremia:
-excessive administration of water or hypotonic salt solution in pt with oliguric renal failure
"- ) $ ! )
./0 % ) %
-buffers: (1) proteins; (2) phosphates; (3) bicarbonate-carbonic acid system

-carbonic acid excreted by lungs as CO2; inorganic acid anions excreted by kidneys with hydrogen or as ammonium
salts
pH = pK + log [BHCO3/H2CO3] = 6.1 + log [20/1] = 7.4
Respiratory Acidosis:
-associated with retention of CO2 secondary to decreased alveolar ventilation
-inadequate ventilation:
-airway obstruction, atelectasis, pneumonia, pleural effusion, pain from upper abdominal incision,
abdominal distention
-narcotic use
Respiratory Alkalosis:
-hyperventilation secondary to apprehension, pain, hypoxia, CNS injury, assisted ventilation
74
-PaCO2 should not be allowed to fall below 30 mmHg
-dangers related to potassium depletion ventricular arrhythmias and fibrillation, particularly in
patients who are digitalized or have preexisting hypokalemia
-d/t entry of K+ into cells in exchange for H+; excessive urinary K loss in exchange for
Na
-shifting oxyhaemoglobin dissociation curve to left limits unloading of oxygen
-tetany and convulsions if ionized calcium significantly depressed
Metabolic Acidosis:
-retention or gain of fixed acids (DKA, lactic acidosis, azotemia)
-loss of base bicarbonate (diarrhea, small bowel fistula, renal insufficiency)
-develops when capacity of kidneys for handling a large chloride load is exceeded (biliary, pancreatic,
small-bowel secretions) and are maintained on parenteral fluids for an extended period
-use of Ringer’s solution indicated
-non-anion gap: loss of bicarbonate or gain of chloride acid (eg. administration of ammonium chloride)
-most common cause of elevated anion gap: shock or inadequate tissue perfusion
-common causes of severe metabolic acidosis in surgical patients: acute circulatory failure with
accumulation of lactic acid
-used of Ringer’s solution does not accentuate lactic acidosis
-indiscriminate use of bicarbonate during resuscitation of patients in hypovolemic shock is
discouraged:
-citrate in transfused blood and lactate in Ringer’s solution are metabolized to
bicarbonate by liver severe metabolic alkalosis can result if excessive bicarbonate
administered
-treatment: correct underlying disorder when possible
-indication for bicarbonate administration: severe metabolic acidosis after cardiac arrest
Metabolic Alkalosis:
-loss of fixed acids or gain of bicarbonate
-aggravated by any preexisting potassium depletion
-majority of pts have some degree of hypokalemia: influx of K+ into cells, efflux of H+ into serum
-hypochloremic, hypokalemic metabolic alkalosis:
-persistent vomiting or gastric suction in pt with pyloric obstruction
-results in urinary bicarbonate excretion net H+ resorption by renal tubular cells, with
K+ excretion
-volume deficit aldosterone mediated Na+ resorption with K+ excretion
-hypokalemia excretion of H+ paradoxic aciduria
-treatment: replace ECF volume with NS + KCl
.0 )) " , " )
-normal dietary intake: 50-100 mEq/d

-majority excreted in urine
-90% of potassium within ICF (~150 mEq/L); major intracellular cation
-critical to cardiac and neuromuscular function
Hyperkalemia:
-signs:
GI: nausea, vomiting, intermittent intestinal colic, diarrhea
Cardiac: ECG high peaked T waves, widened QRS, depressed ST segments
-disappearance of T waves, heart block, diastolic cardiac arrest
-treatment:
-1g of 10% calcium gluconate temporary suppression of myocardial effects
75
-bicarbonate/glucose/insulin (45 mEq NaHCO3 in 1000 ml D10W with 20 u regular insulin)
promotes cellular uptake of potassium
-cation exchange resins: Kayexalate
-dialysis
Hypokalemia:
-more common problem in than hyperkalemia:
1. excessive renal excretion
-occurs with respiratory and metabolic alkalosis
-K+ in competition with H+ for renal tubular excretion in exchange for Na+
-increased K+ excretion in alkalosis in exchange for Na+ permits H+ conservation
-hypokalemia may produce metabolic alkalosis: increased excretion of H+ when [K+] in
tubular cells is low
-renal tubular excretion of K increased when large quantities of sodium are available
2. movement of potassium into cells
3. prolonged administration of potassium-free IV fluids
4. TPN with inadequate potassium replacement
5. loss in gastrointestinal secretions
-signs:
-related to failure of normal contractility of skeletal, smooth and cardiac muscle
-flaccid paralysis, DTR, paralytic ileus
-sensitivity to digoxin, with cardiac arrhythmias and ECG signs of low voltage, flattening of T
waves, depression of ST segments
-treatment:
-prevention
-no more than 40 mEq/L; rate should not exceed 40 mEq/h
-potassium should not be given to the oliguric patient or to patients during first 24h after severe
surgical stress or trauma
.10 " , " )
-total body calcium = 1000-1200 g

-majority found in bone as calcium phosphate or carbonate
-normal daily intake: 1-3g
-most excreted via GI tract; 200 mg excreted in urine daily
-~45% of serum calcium is ionized; ~50% bound to plasma proteins
-related to pH: acidosis Ca++; alkalosis Ca++
Hypocalcemia:
-symptoms: numbness/tingling of circumoral region and tips of fingers and toes
-signs: DTR, +Chvostek’s sign, muscle and abdominal cramps, tetany with carpopedal spasm,
convulsions, prolongation of QT interval on ECG
-common causes:
-acute pancreatitis
-massive soft tissue infections (necrotizing fasciitis)
-acute and chronic renal failure
-pancreatic and small-bowel fistulas
-hypoparathyroidism
-other causes: severe magnesium depletion
-treatment:
-correction of underlying cause and repletion of deficit
-IV calcium gluconate or chloride
-majority of patients receiving blood transfusion do not require calcium supplementation; binding
76
of ionized calcium by citrate generally compensated by mobilization of calcium from body stores
-for rapid transfusion: 500 ml q5-10min 2ml 10% calcium chloride for every 500 ml
Hypercalcemia:
-symptoms: vague GI, renal, MSK, CNS origin
-easy fatigue, lassitude, weakness, anorexia, nausea, vomiting, weight loss coma
-severe headaches, pains in back and extremities, thirst, polydipsia, polyuria
-major causes:
-hyperparathyroidism
-cancer with bony metastasis: most frequently seen in patient with metastatic breast cancer
receiving estrogen therapy
-other causes: sarcoidosis, myelomas, lymphomas, leukemias
-treatment:
-IV fluids +/- furosemide administration
.20 ! ) " , " )
-total body content: ~2000 mEq; ~ half incorporated into bone

-serum [Mg] = 1.5-2.5 mEq/L
-normal dietary intake: ~20 mEq (240 mg) daily
Magnesium deficiency:
-causes:
-starvation, malabsorption syndromes
-protracted losses of GI fluid
-prolonged IV therapy with Mg free fluids
-TPN with inadequate Mg
-other causes:
-acute pancreatitis
-treatment of DKA
-primary aldosteronism
-chronic alcoholism
-amphotericin B therapy
-protracted course after thermal injury
-functions: requirement for most enzyme systems
-signs and symptoms similar to calcium deficiency
-treatment:
-IV magnesium sulfate or magnesium chloride
-calcium chloride or calcium gluconate available to counteract any adverse effects of rapidly rising
serum magnesium level
Magnesium excess:
-commonly seen with severe renal insufficiency
-retention and accumulation of magnesium with impaired glomerular or renal tubular function
-other causes:
-magnesium-containing antacids and laxatives
-early thermal injury
-massive trauma or surgical stress
-severe ECF volume deficit
-severe acidosis
-signs and symptoms:
-lethargy and weakness with progressive loss of DTR
-ECG: PR interval, widened QRS, elevated T waves
77
-coma and muscular paralysis
death by respiratory or cardiac arrest
-treatment:
-correct co-existing acidosis
-ECF volume replenishment
-withholding exogenous magnesium
-acute symptoms temporarily controlled with IV 5-10 mEq of calcium gluconate
-peritoneal dialysis or hemodialysis if elevated levels persist
& &
Ringer’s Lactate:
-for replacement of GI losses and ECF deficits
-physiologic
-Na: 130 mEq; Cl: 109 mEq; lactate: 28 mEq
-minimal effects on body fluid composition and pH
Normal Saline:
-Na: 154 mEq; Cl: 154 mEq
-may induce dilutional acidosis by decreasing bicarbonate relative to carbonic acid
-ideal in correcting ECF deficit in presence of hyponatremia, hypochloremia, and metabolic alkalosis
0.45% NaCl: D5W:

-reasonable solution to use for maintenance requirements postoperatively in patients with no complications
who requires only a short period of parenteral fluids
- 3 $ -
(1) Correction of Volume Changes

-depletion of ECF without changes in concentration or composition is a common problem
-volume deficits:
-external loss of fluids
-internal redistribution (“third spacing”)
-massive ascites, burns, crush injuries, massive infection of subcutaneous tissues
-a slight increase in thickness from sequestration of fluid in the peritoneum may result in
a functional loss of several litres of fluid
-mild loss ~ 4% TBWt; moderate loss ~ 6-8% TBWt; severe loss ~ 10% TBWt
-prompt fluid replacement with balanced salt solution should be started
-reversal of signs of volume deficit, combined with stabilization of BP and pulse and an hourly
urine output of 30-50 cc are used as general guidelines
-rate of fluid administration:
-most severe volume deficits may be safely replaced initially with isotonic solutions at rates up to
2000 cc/h, with the rate reduced as the fluid status improves
(2) Correction of Concentration Changes

-Hyponatremia:
-Na deficit (mEq) = 0.6 Wt (140 - [Na])
-initially up to ½ of calculated amount of sodium administered slowly
-only to relieve acute symptoms; further correction is facilitated when renal function is
78
restored by correction of volume deficit
-if hypervolemic, then water restrict patient
-Hypernatremia:
-if symptomatic, D5W infused slowly until symptoms relieved
-if ECF osmolarity reduced too rapidly convulsions and coma
-ideally correct with ½ NS
- 3 ! "
-blood should be replaced to maintain an acceptable RBC mass irrespective of any additional fluid and electrolyte
therapy
-replacement of ECF should begin during the operative procedure
-balanced salt solution needed during operation is approximately 0.5 to 1 L/h, but only to a maximum of 2-3 L
during a 4h major abdominal procedure, unless there are other measurable losses
) - 3 ! "
(1) Immediate Postoperative Period

-initial fluid orders are written to correct any existing deficit, followed by maintenance fluids
-it is unnecessary and probably unwise to administer potassium during the first 24 h after operation unless
a definite potassium deficit exists
-if renal failure develops, the administration of small quantities of potassium may be detrimental
(2) Later Postoperative Period

-replacement of sensible and insensible losses
-insensible losses ~ 600 cc/day; increased by fever, hyperventilation, hypermetabolism 1500 cc/day
-replaced with D5W
-daily maintenance fluid given at steady rate while losses are incurred
-if given over shorter period, renal excretion of excess salt and water may occur while normal
losses continue over the full 24 h period
-potassium replacement: 40 mEq daily for renal excretion; ~20 mEq/L for replacement of GI
losses
(3) Special Considerations in the Postoperative Patient
Volume Excesses:
-earliest sign of volume overload is weight gain during the catabolic period, when the patient should be
losing 1/4 to ½ lb/day
-circulatory and pulmonary signs appear late and represent a massive overload
Hyponatremia:
-hyponatremia associated with surgical procedures and traumatic injury is prevented by the replacement of
extracellular fluid deficits
-hyperglycemia may cause a dilutional hyponatremia
-endogenous water release: without adequate caloric intake, cellular catabolism causes pt to gain up to 500
cc/day of water between the fifth and tenth days
-intracellular shifts: bacterial sepsis precipitous drop in serum sodium concentration
Hypernatremia:
-high serum sodium level may indicate a significant deficit of total body water
-often the result of excessive or unexpected water losses
79
a. Excessive Extrarenal Water Losses:
-sweat; tracheotomy; burns etc..
b. Increased Renal Water Losses:
-hypoxic damage to distal tubules and collecting ducts or loss of ADH stimulation from damage to
CNS large volumes of solute-poor urine
c. Solute Loading:
-high protein intake increased osmotic load of urea excretion of large volumes of water
-prevent by an intake of 7 ml of water per gram of dietary protein
-excessive glucose administration, osmotic diuretics
(4) Acute Renal Failure

-prerenal, renal or postrenal
-most common cause is sequestered or third-space loss in area of surgical procedure
-common intrarenal causes: endotoxemia, trauma, drugs (aminoglycosides), myoglobinuria, destabilized
haemoglobin
-postrenal causes: obstruction of ureter, bladder or urethra
Biochemical Abnormalities:
1. Metabolic acidosis results from failure of renal excretion of fixed acids and the inability to maintain respiratory compensation
2. Hyperkalemia d/t large amounts of intracellular potassium released in acute renal failure
3. Hyponatremia d/t production of metabolic water from metabolism of nutrients and liberation of water from intracellular
breakdown
4. Hyperphosphatemia and hypocalcemia d/t inadequate excretion and excessive release from injured tissue
5. Hypermagnesemia: kidney is the major organ for regulating magnesium balance
Predisposing Factors:
-Trauma:
-hypovolemic shock, myoglobinuria from rhabdomyolysis, intravascular haemolysis and
hemoglobinuria from transfusions
-Sepsis:
-endotoxins releases TNF produce renal failure
-Cardiopulmonary Bypass: hypoperfusion of kidneys
-Renal Transplantation:
-problems with renal artery, obstruction of urinary flow
-Urologic Surgery:
-obstruction in kidney, ureter, bladder, or urethra
-Vascular Disease:
-blood flow to kidney interrupted during clamp times of vascular surgeries
-Preexisting Renal Disease:
-nephrosclerosis, diabetes, chronic glomerulonephritis, chronic tubular interstitial nephritis
-Radiographic contrast agents
-Drugs:
-aminoglycosides, cyclosporine, amphotericin B, NSAIDs
Laboratory Studies:
-Urinalysis
-Urine osmolarity
-Urine urea and creatinine ratio:
-most useful in diagnosing acute renal failure postoperatively:
< 20 acute renal failure
> 40 prerenal azotemia
-Urine sodium:
-the underperfused kidney is sodium retaining, and a low urine sodium concentration is
characteristic of prerenal azotemia
80
Management of the Patient with Established Acute Renal Failure:
-correct reversible causes
-fluid and electrolyte management:
-treat hyperkalemia
-fluid intake should be restricted to replacing measured fluid losses plus 500-600 cc/d of
insensible losses
-hyponatremia: if below 120, dialysis is the only therapeutic endeavour that corrects
-metabolic acidosis
-use of dialysis:
-best initiated before the occurrence of life-threatening complications of acute renal failure such
as hyperkalemia, severe acidosis, uremic encephalopathy, or uremic pericarditis
-four forms:
-hemodialysis, peritoneal dialysis, continuous arterial-venous dialysis, continuous
venovenous ultrafiltration
81
! "# #" # $ #
! %
-endothelial cells prevent clotting by:

-inactivating adenosine diphosphate (ADP) interfering with platelet recruitment
-provide environment for antithrombin III inactivates thrombin
-release thrombomodulin decreases coagulation process
-Physiologic events in hemostasis: (1) vascular constriction; (2) platelet plug formation; (3) fibrin formation; (4)
fibrinolysis
& # #
-initial vascular response to injury
-vasoconstrictors:
-thromboxane A2 (TXA2) - powerful
-serotonin (5-hydroxytryptamine, 5-HT)
-bradykinin and fibrinopeptides
-contribution of pressure provided by surrounding tissues
-low perivascular pressures increased persistent bleeding:
-muscle atrophy accompanying aging, pts on steroids, Ehlers-Danlos syndrome
# #
-life span is 7-9 days
-Primary Hemostasis
-platelet plug formation on damaged intima within 15s of traumatic event
-requires vWF
-not affected by heparin
-principle mediators: ADP and serotonin
-plug process inhibited by cAMP
-Platelet release reaction stimulated by:
-ADP
-platelet factor 4
-trace thrombin on platelet surface
-Ca++, Mg++
-Release factors promote recruitment and aggregation and result in formation of amorphous plug:
-ADP, K+
-PDGF
-serotonin
-platelet factor 3:
-contributes phospholipid to several stages of coagulation cascade
-activates X (with IXa, VIII, and Ca++)
-activates II (with Xa, V, and Ca++)
-platelet factor 4 and B-thromboglobulin:
-inhibit heparin and modify fibrin formation
-Platelets provide lipoprotein surface:
-for conversion of prothrombin to thrombin
-initial activation of XI and XII
-Release inhibitor of plasminogen activation
82
#
-prothrombin thrombin: proteolytic enzyme which cleaves fibrinogen fibrin stabilizes platelet plug
-Intrinsic Pathway:
-starts with XII
-IXa + VIII + Ca++ (platelet surface): X Xa
-Xa + V + Ca++ (platelet surface): II (prothrombin) IIa (thrombin)
-Extrinsic Pathway:
-initiated by tissue lipoprotein
-thromboplastin + VII + Ca++: X Xa
-thromboplastin + Xa + V + Ca++: II (prothrombin) IIa (thrombin)
-Thrombin:
-activates XIII (fibrin stabilizing factor)
-cleaves fibrinopeptides A and B from fibrinogen fibrin
-makes VIII more potent
-XIIIa: cross-links fibrin monomers stable clot
-Actions of thrombin prevented by:
-antithrombin: binds thrombin to thrombomodulin on endothelium, preventing cleavage of fibrinogen
-activation of protein C: inactivates V and VIII
-circulating protease inhibitors
-Factors not synthesized by liver:
-thromboplastin, Ca++, most of factor VIII
-Vitamin K dependent: II, VII, IX, X
' # (
-dependent on plasmin
-lyses fibrin
-lyses others: fibrinogen, V, VIII
-split products interfere with normal platelet aggregation
-larger fragments incorporate into clot and form unstable clot
% )
#* #
(1) Autosomal dominant: von Willebrand’s disease, hereditary haemorrhagic telangiectasia, XI deficiency
(2) Autosomal recessive: deficiencies in factors X, V, VII, I
(3) Sex-linked recessive: hemophilia A (VIII) and B (IX, Christmas disease)
) $ #
-production: hereditary thrombocytopenia
-destruction: Wiskott-Aldrich syndrome
-von Willebrand disease: missing vWF
-Bernard-Soulier syndrome: normal vWF - missing glycoprotein I complex on platelet membrane receptor for vWF
-Glanzmann’s thrombasthenia: failed aggregation in presence of ADP; impaired mediation of factors in clot
retention
-Congenital afibrinogenemia: fibrinogen required for platelet aggregation
-Hermansky-Pudlak syndrome: storage pool disease platelets cannot store ADP
-oculocutaneous albinism, ceroidlike deposits in macrophages, bleeding diathesis
83
# # ) $ $ #
+, & ) $ # (- .* /
-male; sex-linked recessive; spontaneous mutations in 20%
-incidence 1:10000 to 1:15000
Clinical Manifestations:
-severity based on degree of deficiency: >5% of normal levels VIII: mild; 1-5%: moderately severe
-bleeding into joints (hemarthrosis), epistaxis, hematuria
-intracranial bleeding (trauma in 50% of cases): 25% of deaths
-vascular and neural compromise from pressure secondary to bleeding into soft-tissue closed space:
-Talipes equines contracture deformity: bleeding into calf
-Volkmann’s, flexion contractures of knees and elbos
-retroperitoneal bleeding: Psoas sign, hypovolemic shock
-intramural intestinal haematoma:
-n/v, crampy abdo pain, fever, WBC, “picket fence/stack of coins” appearance on UGI series
Treatment:
Replacement Therapy:
-half-life of VIII is 8-12h
-1 unit = amount present in 1 ml of normal plasma; FFP contains 0.6 u/ml; cryoprecipitates contain 9.6 u/ml
-minimum hemostatic level of VIII:
-mild haemorrhages: 30%
-joint and muscle bleeding and major haemorrhages: 50%
-major surgery and life-threatening bleeding: 80-100% pre-op and maintained > 30% x 2weeks
-amount given:
R = pt’s weight x [desired rise of VIII (% average normal)]/[total units of VIII in dose]
-half of R is subsequently administered q4-6h to maintain a safe level
-DDAVP in mild hemophila A and mild vWD:

-effects a dose-dependent increase of all VIII activits and release of plaminogen activator
-reduces blood loss associated with major surgical procedures by 40%
-continue replacement of VIII for at least 10 days after surgery
-for complications: avoid fasciotomy, aspiration of hemarthrosis, operations in general; mainstay of treatment is to
give coagulation factors
0, 1 ) $ # (- * ) /
-X-linked recessive; accounts for 20% of hemophiliacs
-severe (50% of cases), moderate, mild forms according to level of IX
-prolonged PTT
Treatment:
-FFP or rarely, IX concentrates
-levels of 20-50% for severe haemorrhage for 3-5days then maintain at 10-20% for 10 days
-daily dose: 30-50 u/kg followed by 20 u/kg/d
-levels of 50-70% if operation required
-development of antibodies is a serious complication of treatment (10% of pts)
, 2 #3 ' #"4 ) 5
-autosomal dominant
-diminution of VIII:C (procoagulant) activity; variation in level may be noted
-prolonged bleeding time, prolonged aPTT
84
-mild bleeding, epistaxis, menorrhagia
-serious bleeding after dental extractions, tonsillectomy
Treatment:
-cryoprecipitate (VIII R:vWF): 10-40 u/kg/12h
-replacement therapy should be begun 1 day pre-operatively
-aspirin must be avoided 10 days before operative procedure
) $ # $ #
-Factor XI (Rosenthal’s syndrome): no significant bleeding

-Factor V deficiency (parahemophilia): rare; significant bleeding in homozygotes; tx with FFP
-Factor VII deficiency: significant bleeding in homozygotes
-Factor X (Stuart-Prower) deficiency: associated with amyloidosis and familial carotid body tumours
-Factor II (prothrombin) deficiency: rare
+, #* " ' # # '# 5

-rare; fewer than 200 cases reported; autosomal recessive
0, # # 1 ) $ # (5
-rare autosomal recessive
-manifested by umbilical bleeding in the newborn and slow wound healing after an operation
-tx is FFP, cryoprecipitate, or XIII concentrates
6 ) % )
'#
-thrombocytopenia: most common abnormality of hemostasis that results in bleeding in surgical patient
-causes:
-disease processes: ITP, TTP, SLE
-hypersplenism/splenomegaly: sarcoid, Gaucher’s dz, lymphoma, portal hypertension
-reduced production in marrow: leukemia, uraemia, pts on cytotoxic therapy
-massive blood transfusion
-heparin induced: 0.6% of patients; after 4-15 days in pts given heparin for the first time
-impaired function: uraemia, thrombocythemia, PCV, myelofibrosis
-drugs: ASA, indomethacin, ibuprofen, dipyridamole, phenothiazine, penicillins, chelating agents,
lidocaine, dextran, beta-blockers, nitroglycerin, furosemide, antihistamines
-acute alcoholism
-viral infection
-vitamin B12 or folate deficiency
-no therapy for counts greater than 50000/mm3
-steroid therapy or plasmapheresis for idiopathic thrombocytopenia or SLE
-platelet transfusion:
-one unit = 5.5x1010 platelets: increases count by about 10x109/L
-4 to 8 units should be sufficient for adequate hemostasis
85
7 " (. $' # #
+, ) $' # # (#" 5
-Disseminated intravascular coagulation (DIC)
-caused by the introduction of thromboplastic materials into the circulation
-patchy necrosis of skin, hematuria and oliguria, confusion 2o cerebral ischemic, GIB, haemorrhage into adrenal
cortex acute hypotension
-causes: -retained dead fetus, premature separation of placenta, amniotic fluid embolus
-complication of dialysis, head trauma, mucin-producing and disseminated carcinoma, lymphomas,
thrombotic thrombocytopenia, rickettsial infection, snakebite, burns, aortic surgery, and shock from any
cause
-gram negative sepsis
-no lab test to confirm or exclude diagnosis; highly suggestive with combination of:
-low platelet count
-positive plasma protamines test presence of fibrin monomer-fibrinogen complexes
-reduced fibrinogen (<100mg/dL)
-context of patient’s underlying disease
Treatment:
-treat cause; supportive measures
-IV fluids + vasodilators
-plasma expanders if increased viscosity of blood
-active bleeding treated with FFP, cryoprecipitate (for fibrinogen), and platelet concentrates
0, ' # ( 5
-may occur in patients with metastatic prostatic carcinoma, shock, sepsis, hypoxia, neoplasia, cirrhosis, portal
hypertension, cardiopulmonary bypass
%( . $ 2 )
-major surgical risk for patients with marked thrombocytosis
-spontaneous thrombosis a complication of PCV: increased blood viscosity, platelet count and stasis
-myeloid metaplasia frequently represents part of the natural history of PCV
Treatment:
-thrombocyosis reduced with alkylating agents (eg. busulfan, chlorambucil)
-delay elective surgical procedures weeks to months after treatment
-emergency procedures: reduce RBC/plts by phlebotomy and replacement with RL
* )
-advanced cirrhosis:
-deficiencies in factors II, V, VII, X and XIII
-failure for liver to clear plasminogen activators increased fibrinolysis
-macroglobulinemia: abnormal production of proteins coat platelets
-multiple myeloma: cryoglobulins bind certain blood-clotting factors
# # #" ! "#
-spontaneous bleeding as a complication of anticoagulant therapy
-ecchymoses, petechia, or haematoma
86
+, " . # ( !(. *
-complications:
-overheparinization, heparin rebound, inadequate protamines neutralization, protamines excess,
thrombocytopenia
-two factors most important in triggering excessive bleeding: excessive fibrinolysis and platelet function
defects
-management:
-6 to 8 units of platelets
-if overheparinized: protamines
-excess fibrinolysis: EACA
% ) ! )
Platelet Count
-spontaneous bleeding only rarely for counts greater than 40000/mm3
-counts of 60000-70000/mm3 sufficient for hemostasis in surgery and trauma
Bleeding Time
-assessment of interaction b/n platelets and damaged blood vessel and formation of platelet plug
-abnormal in:
-thrombocytopenia
-qualitative platelet disorders
-vWD
-some patients with Vdeficiency or hypofibrinogenemia
-ASA ingestion
Prothrombin Time
-measures speed of the Extrinsic Pathway
-will detect deficiencies of factors II, V, VII, X and fibrinogen
Partial Thromboplastin Time

-screening test for Intrinsic Pathway
-sensitive to VIII, IX, XI, and XII as well as II, V, VII, X
Thrombin Time
-detects qualitative abnormalities in fibrinogen
-detects circulating anticoagulants and inhibitors of fibrin polymerization
-clotting time of pt’s plasma measured after thrombin added
Tests of Fibrinolysis
-fibrin degradation products (FDPs) measured immunologically
-euglobulin clot lysis time, dilute whole-blood or plasma-clot-lysis time: more sensitive, rapid evaluation of
fibrinolysis
& % 8
. 2 2 # $
-History:
-prolonged bleeding or swelling after biting lip or tongue
-bruises without apparent injury
87
-prolonged bleeding after dental extraction
-excessive menstrual bleeding
-bleeding problems associated with major and minor operations
-medical problems within past 5 years
-medications including aspirin within past 10 days
-relative with a bleeding problem
-Preoperative assessment:
Level 1: -negative history, minor procedure
-no screening test needed
Level 2: -negative history, major procedure
-platelet count, PTT
Level 3: -history suggestive, procedure where hemostasis is impaired (eg. cell savers)
-procedures where minimal bleeding could be injurious (eg. intracranial bleed)
-platelet count, bleeding time, PT/PTT
Level 4: -highly suggestive history
-hematologist consult, platelet count, bleeding time, PT/PTT
2 # $ 9 2 # . 2 $ . 2 ! "#
-May be due to:

-ineffective local hemostasis
-complications of blood transfusion
-previously undetected hemostatic defect
-consumptive coagulopathy
-fibrinolysis
-Operations on prostate, pancreas and liver: operative trauma ma stimulate local plasminogen activation and lead to
increased fibrinolysis on the raw surface
-Transfusion purpura:
-uncommon cause of thrombocytopenia; considered if bleeding follows transfusion by 5-6 days
-donor platelets are of uncommon PlA1 group sensitize recipient to make antibody to foreign platelet
-antibody then destroys recipient’s own platelets
-usually self-limited
-Be aware of DIC, gram-negative sepsis (endotoxins-induced thrombocytopenia)
-Complications of biliary tract surgery in cirrhotic patients:
-related to portal hypertension and coagulopathy associated with chronic liver disase
-tx: vasopressin IV to reduce portal HTN; EACA to correct increased fibrinolysis
% * # "
-digital pressure
-haemostat and subsequent ligation with sutures or clips
-non-absorbable sutures evoke less tissue reaction and absorbable materials
-non-absorbable material in an infected wound can lead to extrusion or sinus tract formation
-cold packs promote hemostasis by inducing vascular spasm and increasing endothelial adhesiveness
* #
-heat denatures protein which results in coagulation of large areas of tissue
-advantage: time; disadvantage: more tissue is necrose
88
* #
-epinephrine: induces vasoconstriction; used on oozing sites in mucosa areas
-gelatin foam (Gelfoam), oxidized cellulose (Oxycel), oxidized regenerated cellulose (Surgicel), and micronized
collage (Avitene)
-fibrin glue (Tisseal)
* $ . # * .(
Banked Whole Blood

-rarely indicated and rarely available
-shelf life 40 +/- 5 days
-changes in red cell: reduction of intracellular ATP and 2,3-DPG decreases oxygen transport function
-poor source of platelets
-within 21 days: pH to 6.68, lactic acid, K, NH3
Typing and Crossmatching

-crossmatching between donor’s red cells and recipient’s serum
-Rh negative ~ 15% of donor population
-Rh-positive blood should not be transfused to Rh-negative females who are capable of child-bearing
-emergency blood transfusion with type O blood
-cryoglobulins in patients with malignant lymphoma and leukemia: blood administered through blood warmer
Packed Red Cells and Frozen Red Cells

-provides oxygen carrying capacity
-reduced amount of sodium, potassium, lactic acid
-frozen red cells not available for use in emergencies: often used in pts previously sensitized; cells have been
selected for lack of certain antigens
Leukocyte-Poor Washed Cells

-aspiration of buffy coat and passing them through white-cell filter
-red cells washed with sterile isotonic solution
-for patients with demonstrated hypersensitivity to leukocytes or platelets
Platelet Concentrates
-indications:
-thrombocytopenia due to massive blood loss and replacement with platelet-poor products
-thrombocytopenia due to inadequate production
-qualitative platelet disorders
-may transmit infectious diseases and account for allergic reactions
-transfuse to elevate platelet levels to range of 50,000 to 10,000/mm3 for surgeries
-isoimmunity most important factor limiting usefulness
Frozen Plasma and Volume Expanders

-FFP: provide factors V and VIII
-RL, dextran, albumin: rapid plasma expansion
-prolongation of bleeding time and haemorrhage can occur with amounts of dextran exceeding 1L/day
Concentrates
-antihemophilic concentrates
-albumin: 25 g osmotic equivalent of 500 ml of plasma; hepatitis free product
89
#" # $ . # $! " #
Improvement in Oxygen-Carrying Capacity

-no correlation however between anemia and dehiscence or severity of post-operative infection
Volume Replacement
-restore circulating blood volume
-measurement of haemoglobin and hematocrit can be misleading and do not reflect severity of blood loss
-in OR: blood loss up to 20% replaced with crystalloids; above 50%, replaced with crystalloids, RBC, and albumin
or plasma +/- FFP if continued bleeding
Replacement of Clotting Factors

-treatment of certain haemorrhagic conditions
. $ #" #
Massive Transfusion
-single transfusion greater than 2500 ml or 5000 ml transfused over a period of 24h
-complications:
-circulatory overload or DIC may occur
-dilutional thrombocytopenia, impaired platelet function, deficiencies of V, VIII, XI
-citrate toxicity: excessive binding of ionized calcium; rarely have a significant effect
-reduced 2,3-DPG increased affinity of RBC for O2 and less efficient delivery
-hypothermia decreases CO and rate
-hemolytic transfusion reaction
-infectious diseases
% * " $ " # # ! "
Routine Administration
-usually 5 ml/min for 1 min then 10-20 ml/min
-with marked oligemia: 500 ml over 10 min, second 500 ml over 10 min
-no practical advantage in intraarterial transfusion
Other Methods
-intraperitoneally: 90% enter circulation but uptake not complete for at least 1 week
-via medullary cavity of sternum and long bones: painful; limited rate
-cell saver: 250 ml in 5-6 min
-hemodilution: remove blood and maintain intravascular volume with crystalloids or colloid; removed blood may be
then retransfused
. #
(1) Hemolytic Reactions

-incidence of non-fatal reactions: 1 per 6000 units
-incidence of fatal reactions: 1per 100,000 units
-clerical or laboratory errors account for reactions d/t incompatibility of A,B,O and Rh groups
-haptoglobin binds haemoglobin complex is cleared by reticuloendothelial system
-free haemoglobin combines with albumin to form methemalbumin
-red cell stromal lipid; antibody-antigen complexes activating XII end complement may initiate DIC
90
Clinical Manifestation:
-pain, sensation of heat along vein; facial flushing, lumbar pain, constricting chest pain
-chills, fever, respiratory distress, hypotension, tachycardia
-if anaesthetized: abnormal bleeding and continued hypotension
-fall in platelet count, increased fibrinolysis, consumption of coagulation factors (esp V, VIII)
-Rudowski: oliguiria 56%; hemoglobinuria 56%; hypotension 50%; jaundice 40%; n/v 30%; flank pain 25%;
cyanosis and hypothermia 22%....
Treatment
-immediately stop transfusion
-send sample of patient’s blood to blood bank for comparison with pretransfusion samples
-determine bilirubin levels
-foley hourly urine measured
-initiate diuresis and alkalinize urine (mannitol or furosemide, 45 mEq bicarbonate)
-maintain hydration
(2) Febrile and Allergic Reactions

-occur in 1% of transfusions
-urticaria, fever within 60-90 min
-caused by transfusion of antibodies from hypersensitive donors or transfusion of antigen
-tx: antihistamines, epinephrine, steroids
(3) Bacterial Sepsis

-gram-negative, esp Pseudomonas are most common cause
-shock: administration of adrenergic blocking agents, oxygen, antibiotics
(4) Embolism
-normal adult generally can tolerate embolism of 200 ml of air
-venous air embolism:
- venous pressure, cyanosis, “mill wheel” murmur over precordium, hypotension, tachycardia and
syncope
-tx: left lateral decubitus position in Trendelenburg
-arterial air embolism: dizziness and fainting, LOC, convulsions; air may be visible in the retinal arteries
(5) Thrombophlebitis
-discontinue transfusion and compress locally
(6) Overtransfusion and Pulmonary Edema

-rise in venous pressure, dyspnea, cough
(7) Transmission of Disease

-malaria, Chaga’s disese, brucellosis, syphilis
-viral hepatitis: most common fatal complication; risk 0.035% per unit blood
-AIDS: one case per 225,000 patients transfused
91
-pathophysiologic condition: state of inadequate tissue perfusion
!"
-return of venous blood to heart produces ventricular end-diastolic wall tension, a major determinant of cardiac
output
-veins in skeletal muscles respond to external factors: gravitational forces and muscle pump
-exercise and increased sympathetic reflexively decrease the splanchnic capacitance
-salt and water balance from the kidneys via hormonal effects of renin, angiotensin and antidiuretic hormone
# $! !
-Frank-Starling curve: force of contraction dependent on initial muscle length
-affected by variety of disease states: MI, valve dysfunction, cardiac hypertrophy
!"
-force acting to resist myocardial work during contraction
-arterial pressure is the major component that influences the ejection fraction
-determined by precapillary smooth muscle sphincter
-in normal heart, stroke volume maintained in lieu of increased afterload by increased reload
# %
-decreased circulating or effective intravascular volume

-increased peripheral vascular resistence to protect blood pressure in compensation for falling CO
-differential increases in skin, gut, and kidney to protect other vital organs
&' (! ) (' ((
1. -increased vascular tone elevates PVR redistribution of blood flow among organ systems
-“autoregulated” organs (heart, brain) preferred
2. -increased sympathetic activity

-diminished vagal inhibition of rate and force of cardiac contraction greater contractility and enhanced venous return CO,
myocardial O2 consumption
3. -decreased capillary hydrostatic pressure transcapillary influx of extravascular ECF

-this intravascular volume and blood viscosity by dilution
4. -increased tissue extraction of oxygen by presence of acidosis and 2,3-DPG

-rightward shift of oxyhaemoglobin dissociation curve
-hypoxia hyperventilation resp. alkalosis increased rate of erythrocyte synthesis of 2,3-DPG
5. -diminished renal flow afferent and efferent arterioles stimulated

-u/o decreases as H2O and sodium are retained
6. -increased release of catecholamines by adrenals

-produce vasoconstriction and tachycardia
-glycogenolysis, lipolysis, skeletal muscle breakdown stimulated, insulin release inhibited promote glucose mobilization, protein
catabolism, and negative nitrogen balance
-retention of sodium and water in proximal tubule of nephron
92
7. -ACTH released (stimulated by various stresses)
-cortisol potentiates actions of epinephrine and glucagon, further stimulates mobilization of amino acids from skeletal muscle, and
results in renal sodium and water retention
8. -insulin secretion diminished
9. -ADH secreted in response to increased serum osmolarity and hypovolemia

-potent splanchnic vasoconstrictors
-increases water permeability and passive sodium transport in the distal nephron tubule
-Renin-angiotensin system activated
-response to sympathetic stimulation of juxtaglomerular cells (B-adrenergic action), renal perfusion pressure, and
compositional changes in tubular fluid
-Angiotensin II:
-powerful arterial and arteriolar vasoconstrictors
-stimulates renal prostaglandin production
-stimulates release of aldosterone and ACTH
-Aldosterone: increases sodium resorption in exchange for potassium and hydrogen ions in distal nephron
-Prostaglandins (esp PGE2), kallidreins produced in kidney dilate renal vessels and increase renal blood flow
$& !) ! * & (
-Acute Respiratory Distress Syndrome (ARDS)

-hypoxia (despite oxygen therapy), decreased pulmonary compliance, diffuse infiltrates on CXR, non-
pulmonary edema
Etiology
-ARDS is the final common pathway to various pulmonary insults
-initiation of inflammatory mediators increases microvascular permeability proteinaceous fluid deposition in
alveolar epithelial and pulmonary capillary endothelial interface V/Q mismatch
-fluid overwhelms pulmonary lymphatic clearance
-pulmonary edema refractory to diuretics and fluid restriction; colloid administration not useful
Diagnosis
-clinical suspicion
Therapy for ARDS

-maintain tissue oxygenation: PaO2 > 65 mmHg
-volume ventilator with tidal volume and rate set to allow adequate CO2 exchange
-PEEP initiated at 5 cmH2O; used to maintain oxygenation at nontoxic (50% or less) levels
-set ventilator at 100% O2; increase PEEP by increments of 2.5 allowing at least 30 min for equilibration
-measure arterial and mixed venous blood gases, PCWP, and CO
-increase PEEP to as much as 20 without compromise of CO
-decrease O2 incrementally but keep PaO2 of 65 mmHg
-PEEP can then be decreased if oxygenation maintained by increments of 2.5 q12h
-potential risks of PEEP are exacerbated by hypovolemia: intrathoracic pressure and venous return CO
)' + &
$" ($( !
Composition of Resuscitation Fluids
1. Ringer’s Lactate:
93
-lactate content will not aggravate lactic acidosis
-safe inexpensive, equilibrates rapidly throughout ECF
2. Colloid solutions:
-raise intravascular colloidal pressure intravascular influx of interstitial fluid
-more expensive, may bind and decrease ionized serum calcium, decrease circulating immunoglobulins,
decrease immune reaction to tetanus toxoid, decrease endogenous production of albumin
-may not necessarily be better for fluid resuscitation over crystalloids
-no clinical evidence that appropriate resuscitation with balanced slat solution is associated with
any harmful effects on pulmonary function
3. Hypertonic Saline:
-can be effective initial resuscitative solution but requires close monitoring of electrolytes to prevent
hypernatrema and hyperosmolar coma
-long-term benefits not established
4. Hetastarch:
-slow equilibration can lead to rapid fluctuations in CVP
-mild and transient coagulopathies noted
5. Dextran:
-greater risk of anaphylaxis; has produced coagulation defects and immunoglobulin depression
6. Blood substitutes:
-stroma-free haemoglobin (SFH) eliminates side effects secondary to erythrocyte stromal elements
-high affinity for oxygen, short plasma half-life, available only from human sources
-not a practical substitute
-perfluorodecalin:
-require emulsification to be water soluble
-use requires higher inspire oxygen concentrations
-effective substitute for haemoglobin
",$+! !')
(1) Vasopressors
-may elevate BP at expense of further PVR and tissue perfusion
-do not substitute for adequate fluid resuscitation
(2) ATP
-in experimental models, found to improve survival rates in potentially lethal shock (in combination with fluids)
-limited usefulness in clinical treatment since may result in marked homodynamic instability in hypovolemic pt
(3) Positioning
-Trendelenberg may interfere with respiratory exchange
-preferred position is elevation of both legs while maintaining head, trunk and arms supine autotransfusion of
pooled blood in venous circulation
(4) MAST Garment

-resultant increase in total PVR may elevate sBP while CO and peripheral perfusion
-may compress IVC and impair venous return and increase venous resistance
-risk of reperfusion injury
-of value only as temporizing device or as specific treatment of bleeding pelvic fractures
94
(5) Pulmonary Support
-beneficial in patients with abnormal oxygen saturations: eg. PTX, pulmonary contusion, aspiration, a/w
obstruction, COPD etc..
(6) Antibiotics
-no support for protective mechanism against ravages of hypovolemia
-use in patients with open or potentially contaminated wounds
(7) Analgesics
-if causative injury produces severe pain, control of pain becomes mandatory
-small doses of narcotics should be given intravenously to prevent profound sedation
(8) Steroids
-specific instances, steroid depletion with hypovolemic shock may occur:
-elderly patient
-Addison’s disease, post-adrenalectomy, adrenal suppression with exogenous steroids
-IV hydrocortisone desirable in these cases
-steroids not indicated in trauma patient with hypovolemia
(9) Monitoring
-CVP:
-normal to depressed despite administration of fluids continuing hypovolemia
-elevated or rapid rise impairment of pumping mechanism
-if shock is refractory to treatment, must look for:
-continuing blood loss into chest or abdomen
-inadequate volume replacement
-inadequate clotting
-multisystem trauma with occult thoracic injuries (cardiac tamponade, hemopneumothorax)
-myocardial insufficiency (contusion or hypoperfusion)
!" *
-heart unable to generate sufficient cardiac output to maintain adequate tissue perfusion
-hypotension in the face of adequate intravascular volume
Pathophysiology
-secondary to valvular heart disease, cardiomyopathy, myocardial contusion
-AMI most frequent cause; fatal if >40% loss of left ventricular mass
-complications:
-papillary muscle dysfunction, ischemic ventricular septal defects, massive LV infarction,
arrhythmia
-vicious cycle created: increased myocardial oxygen demand, hypotension, shortened diastole, increased PVR and
afterload
Treatment
-initial therapy: optimizing ventricular reload by manipulating filling pressure, decreasing afterload in patient with
adequate sBP, correcting arrhythmia, improving contractility to sustain vital organ perfusion
1. Monitoring and Volume Management:

-supplemental oxygen, pain relief and sedation, continuous ECG
-Foley catheter for urine output, art line, oximetry, Swan-Ganz
-small increase in LV filling pressure by volume infusion may maximize CO via Frank-Starling mechanism
-must r/o mechanical obstruction such as tamponade or embolism
95
-watch for pulmonary edema intubation and ventilation will myocardial oxygen demand from increased
work of breathing
2. Inotropic Agents:
-beta1-adrenergic receptors increased contractility and CO
-increases myocardial oxygen demand
-Dopamine:
- may reverse life-threatening hypotension and restore MAP to about 80 mmHg
-low doses:
2-5 ug/kg/min splanchnic, coronary, renal vasodilation
5-8 ug/kg/min adrenergic-mediated in contractility and heart rate
-high doses:
alpha-adrenergic effects: CVP and coronary vasoconstriction
-variable increase in heart rate
-can precipitate other arrhythmia
-Dobutamine:
-synthetic catecholamine with predominantly inotropic effect
-Digitalis:
-controversial; useful in supraventricular arrhythmia
-increased MO2: adds very little homodynamic benefit relative to therapy the sympathomimetic
agents
3. Vasodilator Agents:
-some patients with low CO and high filling pressures have near-normal arterial blood pressures
-systolic ventricular wall stress is high, and reducing afterload should increase cardiac output and decrease
myocardial work therefore can use nitroprusside, but with extreme caution in hypotensive patients
4. Mechanical Support
-intraaortic balloon pump: unloading LV and reduce myocardial work
-elevates diastolic BP: increases pulmonary perfusion, decreases myocardial work, increases
cardiac output distal to ventricle
-unclear if improves long-term survival
-good bridge until surgically correctable problems are addressed
-left ventricular assist devices: currently limited to cardiac surgery patients
5. Arrhythmias
-decreased ventricular EDP from decreased filling time
-digoxin drug of choice for atrial fibrillation or flutter - cardioversion if hypotension or hypoperfusion
-verapamil for tachyarrhythmias of atrial origin
-propranolol for sinus tachycardia
-defibrillation for ventricular fibrillation
-lidocaine for premature ventricular complexes which may lead to ventricular tachyarrhythmias
-bradyarrhythmias: electrical pacing
$ *
-occurs after serious interference with the balance of vasodilator and vasoconstrictors influences to the arterioles
and venules
-clinical syncope
-paralysis of vasomotor influences; eg. high spinal anaesthesia, spinal cord injury
-reflex interruption of nerve impulses: acute gastric dilatation
-low BP, low pulse rate, dry, warm, flushed skin
-decreased CO, decreased PVR
96
-can result in kidney failure and brain damage
Treatment
-gastric dilation NG tube insertion
-high spinal anaesthesia fluids, vasopressor (Neo-synephrine)
-spinal trauma maintain normal CVP that rises slightly with rapid fluid administration and using a vasopressor
judiciously to support arterial pressure
'
-most frequent causative organism: gram-negative bacteria, occasionally gram-positive bacteria

-most common source is GU system; second is respiratory, then GI
Clinical Manifestations
-normovolemic but has hypotension despite increased CO and good filling pressure
-paradoxical “warm shock”
-high CO associated with decrease in oxygen utilization and narrowed arteriovenous oxygen difference
-thrombocytopenia may be early indicator of gram-negative sepsis
-systemic illness may result form inappropriate systemic effects of mediators used to contain local infection
-myocardial depression despite hyperdynamic CO
Pathophysiology
-TNF is a central and proximal mediator of the host response to endotoxemia and bacteremia
-produced predominantly by cells of macrophage lineage
-reduction in membrane potential preceded onset of hypotension
-TNF-alpha:
-capable of inducing membrane depolarization in vitro
-important mediator of septic shock
-induces synthesis and secretion of secondary mediators: cytokines, PG, leukotrienes,
PAF, complement, coagulation cascade
-may synergise with lipopolysaccharide to induce many toxic effects mediated by TNF-alpha
-naturally occurring inhibitors of TNF-alpha activity: extracellular type I and II TNF receptors
shed from cell surface in response to inflammatory stimuli
-Interleukin-1
-key mediators of host response to infection, inflammation and injury
-IL-1 receptor antagonist (IL-1ra) blocks many functions of IL-1:
-lymphocyte proliferation, increased adhesion of endothelial cells for neutrophils and
eosinophil; synthesis of IL-1, TNF-alpha, IL-6, and IL-8 by monocytes; nitric oxide
production in SMC
-anti-endotoxins antibodies fail to confirm beneficial effects
-other potential mediators of septic shock: linins, endogenous opiates, other recently purified cytokines
Therapy
-antibiotics and early surgical debridement or drainage of abscess
-fluid therapy, vasoactive drugs as adjuncts
-broad spectrum should include anaerobic coverage
-steroids offer no advantage; use only in hypoadrenalism and stress coverage in those already taking steroids
1. Pharmacologic support
-dopamine: improves hypotension
-dobutamine: may not be tolerated by hypotensive patients
-use of pressors is primarily for transient support while primary definitive therapy with antibiotics and
drainage of surgical infection are being instituted
97
2. Manipulations of Humoral Responses
-difficult because of the complex and ill-defined interactions among a large number of mediators
-only a few showed statistical benefits in studies: HA-1A (human monoclonal IgM against lipid A of
endotoxins), E5 (murine monoclonal IgM against lipid A)
98
!
-infections requiring operative treatment:

1. necrotizing soft tissue infections
2. body cavity infections (eg. peritonitis, suppurative pericarditis, empyema)
3. confined tissue,organ, joint infection
4. prosthetic device-associated infections
" # "$
-operative treatment generally required when host defences cannot function properly or when continuing
contamination with microorganisms
! %
(1) Microbial Pathogenicity:

-thick capsules in bacteria and fungi resistant to phagocytosis
-resist intracellular killing (phagocytosis by lysosome):
eg. Mycobacterium tuberculosis, Aspergillus flavus, Toxoplama gondii
-exotoxins: eg. Clostridium sp., Staph. aureus, Strep. pyogenes
-neurotoxins: Clostridium tetani, Clostridium botulinum
-endotoxins: lipopolysaccharide-protein complexes (gram negative bacteria)
(2) Host Defenses:

-Local Host Defenses:
-epithelium
-lack of moisture (skin), flushing action of tears and urine, cilia (trachea, bronchi), peristalsis,
mucous, pH, local immunity (IgA)
-Systemic Host Defenses:
-phagocytic cells, immune system, molecular cascades (complement, coagulation, kinin)
-Macrophages: liver (Kupffer cells), spleen, lymphoid tissue, lung, grain (glial cells), connective
tissue (histiocytes), pleura and peritoneum
(3) Local Environmental Factors:

-phagocytic cells do not function effectively in the presence of devitalized tissue or foreign bodies
-fluid collections and edema inhibit phagocytosis
-peripheral vascular disease and shock prevent blood (and hence cells and mediators) to reach sites of
microbial contamination
-lowered tissue oxygen tension inhibits function of phagocytic cells; promotes growth of anaerobes
(4) Surgical Technique:

-important determinant of postoperative wound infection
99
&' ( $% "#
-cellulitis:
-spreading infection of skin and subcutaneous tissues
-local pain/tenderness, edema, erythema
-usually indistinct borders
-+/- systemic symptoms
-caused by: Strep. pyogenes, Staph. aureus, Strep. pneumoniae, Haemophilus influenzae, other
streptococci, aerobic and anaerobic gram-negative bacteria
-erysipelas:
-caused by strep. pyogenes
-intense erythema with sharp line of demarcation
-lymphangitis:
-inflammation of lymphatic channels
-presents as visible red streaks
)' *
-carbuncle:
-subcutaneous abscess from confluent infection of multiple contiguous hair follicles
-most commonly Staph. aureus
-felon:
-purulent collection in distal phalanx
-intense pain and pressure in compartment; treat with lateral incision
-breast abscess:
-usually Staph. aureus
-treat with incision and drainage and antibiotics
-perirectal abscess:
-infection of crypt glands that extends into perirectal space
-aerobic and anaerobic gram-negative bacteria
+' ,
-most caused by mixed aerobic and anaerobic gram-negative and gram-positive bacteria
-Clostridium sp. (C. perfringens, C. novyi, C. septicum) - gram positive rods
-most common, most dramatic infections, rapid progression, high mortality
-“gas gangrene”
-subcutaneous emphysema: anaerobic bacterial metabolism hydrogen, nitrogen, methane
-Strep. pyogenes
-Vibrio
-fungi necrotizing infections progress more slowly than bacterial infections
-surgical treatment requires debridement of all necrotic tissue
-hyperbaric oxygen: inhibits production of alpha toxin in Clostridia
-no improvement in patients with nonclostridial infection
-complications: middle ear injury, trauma to sinus, PTX, air embolism
-'
-caused by Clostridium tetani
-majority of cases appear after punctures, lacerations, and abrasions
-two toxins:
-tetanospasmin
-actons on anterior horn cells of spinal cord and brainstem
100
-blocks inhibitor synapses muscle spasms and hyperreflexia
-testanolysin
-cardiotoxic and causes haemolysis; not thought to be of major clinical importance
-generalized muscle spasms generalized convulsions
-orthotonos, opisthotonos, emprosthotonos
-spasm of laryngeal and respiratory muscles fatal acute asphyxia
-mortality rate can exceed 50%
-diagnosis on clinical grounds; laboratory investigations not helpful in diagnosis
Treatment:
-tetanus immune globulin (TIG) 500-10,000 units ASAP
-ICU admission intubation, ventilation, paralytic drugs
-mild cases: sedation, muscle relaxants, analgesics
-(hyperbaric oxygen is ineffective)
-treat wound to remove C.tetani and nonviable tissue +/- antibiotics
Prevention:
Summary of Recommendations for Tetanus Prophylaxis in Routine

Wound Management
History of Clean Minor Wounds All Other Wounds*
Adsorbed
Tetanus
Td TIG Td TIG
Toxoid (Doses)
Unknown or < Yes No Yes Yes

3 doses
> 3 doses No No No No
(Yes if > 10y (Yes if > 5y
since last dose) since last dose)
*such as, but not limited to, wounds contaminated with dirt, feces, soil, or saliva; puncture wounds;
avulsions; and wounds resulting from missiles, crushing, burns, or frostbite
. ($ / $
&' ( *( % *
-Primary peritonitis: caused by single organism; commonly seen in pts with ascites or renal failure on PD
-Secondary peritonitis:
-defect in GI tract
-requires operative intervention; antibiotics against aerobic and anaerobic enteric bacteria
-Tertiary peritonitis:
-peritonitis-like syndrome as a result of a disturbance in host’s immune response
-peritonitis without evidence of pathogens
-may also be caused by fungi or low-grade pathogenic bacteria
-Intraabdominal abscess: percutaneous or operative drainage along with Abx therapy needed
)' % "$ %
-causes:
-pneumonia (most common), pulmonary infact, septic embolic to lung, tracheal or bronchial
fistula, leaking esophageal anastomosis, hepatic abscess, subphrenic abscess, trauma, leaking
bronchial closure, infected hemothorax, paravertebral absces
101
-chronic empyema: dyspnea, fatigue, anemia, debility, clubbing of fingers
-treated with chest tube; may be converted to open drainage after 2 to 3 weeks
-open drainage if multiple pus pockets, thick pus, or inadequate drainage via CT
# ( " (
-septic arthritis
-suppurative pericarditis
# ! / (
-cardiac valves, pacemakers, vascular grafts, artificial joints
-total removal to eradicate infection
" 0 (1 % 2
-urinary tract infections (most common), wound infection, lower respiratory tract infection, bacteremia, cutaneous
infection
&' 3 (
Classification:
Classification of Operative Wounds in Relation to Contamination and Increasing Risk of

Infection
Clean (1.5-3.9% infection rate)

-elective, primarily closed, undrained
-non-traumatic, uninfected
-no inflammation encountered
-no break in asepsis
-respiratory, alimentary, genitourinary, or oropharyngeal tracts not entered
Clean-contaminated (3-4% infection rate)

-alimentary, respiratory, or genitourinary tracts entered under controlled conditions
and without unusual contamination
-appendectomy
-oropharynx entered; vagina entered
-GU entered in absence of culture-positive urine
-biliary tract entered in absence of infected bile
-minor break in technique
-mechanical drainage
Contaminated (8.5% infection rate)

-open, fresh traumatic wounds
-gross spillage from gastrointestinal tract
-GU or biliary tracts entered in presence of infected urine or bile
-major break in technique
-incisions where acute non-purulent inflammation present
Dirty (28-40%)
-traumatic wound with retained devitalized tissue, FB, feces, delayed treatment
-perforated viscus
-acute bacterial inflammation with pus encountered during operation
102
Definition of Surgical Wound Infection:
Superficial:
-infection occurs at incision within 30 days after operation
-involves skin or subcutaneous tissue above fascial layer with any of the following:
-purulent drainage
-organism isolated from culture
-wound opened deliberately by the surgeon
Deep:
-infection occurs at incision within 30 days after operation (no prosthesis); within 1 year of an implant
-infection beneath fascial layer and any of the following:
-wound spontaneously dehisces or deliberately opened when T>38 and/or pain
-abscess seen on direct examination, operation, or histopathologic examination
-surgeon diagnoses infection
)' "#$ 4
Operating Room Environment:

-air filtration to reduce number of microbes
-positive pressure relative to air
Instruments and Drapes:
-proper sterilization; drapes should be kept as dry as possible
Hand Washing:
-washing for 5 minutes sufficient
-hexachlorophene, povidone-iodine, chlorhexidine commonly used
Gloves:
Other Barriers:
-caps to prevent hair and skin scales falling into wounds
-masks prevent droplets entering wounds
-no data that demonstrate unequivocally reduction of infection rate
Preoperative Stay
-longer preoperative hospitalization more likely to have post-operative wound infections
-may acquire more virulent or antibiotic-resistant bacteria
-compromised host defences
Remote Infections:
-can triple rate of infection; due to moisture
-elective operations should be delayed until infection eliminated
Hair removal:
-nicks and cuts from shaving: sites where bacteria can proliferate
-clipping preferred; shaving done in operating room to prevent bacterial proliferation
Skin Preparation:
Reduction of Colonic Bacteria:
-enemas before colonic surgery
-oral antibiotics: neomycin and erythromycin
Improving host Defenses:
-correct malnutrition, obesity, abnormal physiologic states
-smoking cessation
Surgical Technique:
-minimize injury to tissue and prevent accumulation of agents that facilitate bacterial growth or
inhibit host defences
-latex rubber drains leads to a higher wound infection rate than not using a drain
103
Prophylactic Antibiotics:
-Principles:
1. Choose Abx effective against most likely pathogen
2. Abx with low toxicity
3. Give single, fully therapeutic dose IV 30-60 minutes preoperatively
4. Give second dose if surgery > 4h or twice half-life of Abx
5. Give 2-3 doses post-op; no need to extend beyond 24h
6. Use of Abx appropriate when infection frequent or when consequences of infection
unusually severe
-cephalosporins most commonly used because of broad spectrum
)' # " 0 (
Urinary Tract Infection:

-40% of hospital-acquired infections
-from operations of lower urinary tract, instrumentation of the bladder, or catheterization
-higher risk in pregnant women, elderly or debilitated pts, urologic abnormalities
-indwelling catheter: 5-10% risk/d
Lower Respiratory Tract Infection:

-third most common nosocomial infection
-risks factors:
-aspiration
-pain from thoracic or upper abdo surgery and trauma atelectasis predispose to infection
-pulmonary edema: fluid in alveoli inhibits phagocytic capacity of pulmonary macrophages
-tracheotomies and respiratory care devices
-causative organisms:
-Staph. aureus, Pseudomonas aeruginosa, Klebsiella sp., E.coli, Enterobacter sp.
Vascular Catheter-Related Infection:

-central lines > peripheral lines; polyethylene > silastic
-mostly from skin organisms at skin exit site: Staph. aures and S. epidermidis
-hematogenous: yeast, gram-negative enteric bacteria
5 .
&' % /
Staphylococcus
-facultative anerobes
-found on moist areas of body, anterior nares, mucous membranes
(1) Staph. aureus:

- most common pathogen in wound infections
-pathogenic factors:
-coagulase: major factor in its pathogenicity
-cell wall and capsules inhibit opsonization and thus phagocytosis
-enterotoxin food poisoning
-epidermolytic toxin exfoliative bullae (Scalded Skin Syndrome)
104
-TSS toxin-1 toxic shock syndrome
-catalase: resists H2O2-mediated intracellular killing
(2) Staph. epidermidis:

-thought to be commensal
-causes infection in presence of FB (eg. plastic catheters, ventricular shunts, prosthetic joints,
valves)
Streptococcus
-S. pyogenes, S. pneumoniae
-viridans group: S. mutans, S. mitior, S. salivarius, S. sanguis, S. milleri
-grouped according to:
a. Lancefield classification: cell surface antigens
b. Hemolytic ability on blood agar:
-alpha haemolysis: zone of green discolouration around colonies; intact RBC
-beta haemolysis: complete clearing of area around colonies; destroyed RBC
-gamma haemolysis: no haemolysis
(1) Group A Streptococci:

-Strep. pyogenes: GABHS
-pathogenic factors:
-cell surface M protein and capsule resistant to phagocytosis
-hyaluronidase and streptokinase promote spread of infection
-streptolysin O and streptolysin S: hemolysins
-proteinases tissue invasion
-pyogenic exotoxins
Manifestations:
-pharyngitis scarlet or rheumatic fever
-erysipelas
-cellulitis, wound infection, endocarditis, UTI, bacteremia
-primary necrotizing soft tissue infections (although S. pyogenes an uncommon cause) and abscesses
)' * ( / $ * % / .
-Escherichia, Klebsiella, Proteus, Enterobacter, Serratia, Providencia

-Vibrio: in marine and water bacteremia and necrotizing soft tissue infections
-Pseudomonas: obligate aerobes; frequently found in immunologically compromised patients
-cause necrotizing infections, esp pneumonia and vasculitis
-Ecthyma gangrenosum: cutaneous manifestations of necrotizing vasculitis d/t Pseudomonas
-due to resistance, frequently treated with two antibiotics
+' * .
-found in mouth, vagina, and GI tract; infections usually endogenous

-low redox potential common to all anaerobic infections
-factors for predisposition:
-vascular disease, cold, shock, edema, trauma, devitalized tissue, operation, foreign bodies, malignant
disease, growth of aerobic microorganisms
-examples:
-Bacteroides fragilis, Fusobacterium, Peptostreptococcus
-Clostridium:
-produce exotoxins: C. perfringen, C. septicum, C. novyi
105
-enterotoxins: C. difficile, C. perfringins
-neurotoxins: C. tetani, C. botulinum
-primary pathogens: cause disease in immunocompetent pts

-Histoplasma, Coccidioides, Blastomyces
-opportunists: cause disease in immunocompromised pts
-Candida, Cryptococcus, Aspergillus, phycomycetes (Mucor, Absidia, Rhizopus)
-treatment consists of:
-stopping antibiotics, correcting host defences, therapy with amphotericin B or one of the azole antifungal
agents
6
-Herpesvirus family: CMV, HSV, VZV, EBV
-CMV: -causes most viral infections in organ transplant recipients
-ulcerative lesions of the GI tract bleeding or perforation
-EBV: -polyclonal B-cell lymphoma in transplant recipients
% %% ( $6
-retrovirus of lentivirus family
-RNA virus with cylindrical core containing RNA, RNA-dependent DNA polymerase (reverse transcriptase), and
core proteins
-GP-120: affinity for CD4+ receptor on TH cells
-infected CD4+ cells cannot carry immune functions opportunist infections, Kaposi’s sarcoma
and primary CNS lymphomas
-CD4 count < 200/mm3 = AIDS
Surgery in HIV-Infected Patients:

-HIV related problems:
-peritonitis secondary to bowel perforation due to CMV infection
-GI obstruction from Kaposi’s or lymphoma of GI tract
-intestinal haemorrhage d/t CMV, lymphoma, Kaposi’s
-intraabdominal or retroperitoneal infection by mycobacterial and other opportunistic organisms
5 .
! * % *
-need adequate concentration delivered to site of infection

-should exceed minimum inhibitory concentration (MIC)
-pharmacokinetics dependent on protein binding of drug and lipid solubility
(1) Blood:
-concentration determined by rapidity of excretion and protein binding
-highly protein-bound antibiotics not excreted as rapidly do not have to be given as frequently
(2) Urine:
-sulfonamides, penicillins, cephalosporins, aminoglycosides, tetracyclines, quinolones, azoles
-excreted principally in urine and achieve high concentrations
(3) Bile: -besides urine, only bile regularly has antibiotic concentrations higher than serum levels
106
(4) Interstitial Fluid and Tissue:
-high, prolonged serum concentration and low protein binding favourdiffusion from serum into
extravascular tissue
(5) Abscesses:
-reduced antimicrobial efficacy d/t:
-acidic pH
-low redox potential
-large numbers of microbial and tissue products that can bind antibiotics
-drainage is key
* $
Prophylactic Antibiotics:
-discussed earlier
-administer to all patients with previously placed prosthetic devices such as cardiac valves or artificial
joints who are having any operation or dental procedure
Therapeutic Use of Antibiotics:

a. Empiric Therapy:
-intraabdominal surgical infections and necrotizing soft tissue infections: mixed gram-negative
and gram-positive aerobic and anaerobic bacteria
b. Definitive Therapy
! (%
Route: intravenous
Duration: most surgical infections can be treated effectively in 5-7 days of antibiotic therapy
Treatment Failure:
-wrong antibiotic, intraabdominal abscess, resistant bacteria, other causes (other sites of infection)
-inadequate dose, inappropriate route
Drug Toxicity:
-in renal failure, give a first dose of 80-100% then estimate timing and amount of second dose according to
various schedules based on the normal half-life of the antibiotic
107
-depth of injury proportionate to temperature applied, duration of contact and thickness of skin
(1) Scald Burns:

-hot water most common cause of burns
-60oC deep dermal or full-thickness burn in 3s
-69oC 1 s
-exposed areas tend to be burned less deeply than areas covered with thin clothing
-immersion scalds are always deep, severe burns
-deliberate scalds commonest form of reported child abuse (~5% of admission to burn centers)
-most common in children < 8 y
(2) Flame Burns:

-second most common burn
(3) Flash Burns:

-third most common burn
-explosions of natural gas, propane, gasoline
-mostly dermal; generally heal without requiring extensive skin grafting
(4) Contact Burns:

-usually limited in extent but invariably very deep
!"!
-critical legislative actions have decreased burns and burn mortality

-smoke detectors, maximum temperature for home and public hot water heaters
Burn Severity and Classification:

-severity of injury proportionate to:
-size of total burn
-depth of burn
-age of patient
-associated medical problems or injuries
-ABA and ACSCT classification:
a) Minor:
-superficial burns < 15% TBSA
b) Moderate:
-superficial burns 15-25% TBSA in adults; 10-20% TBSA in children
-full thickness burns < 10% TBSA
-burns not involving eyes, ears, face, hands, feet or perineum
c) Severe
108
Burn Center Referral Criteria:
1. Second- and third-degree burns > 10% TBSA in pts under 10 or over 50 yoa
2. Second- and third-degree burns > 20% TBSA in other age groups
3. Second- and third-degree burns involving face, hands, feet, genitalia, perineum, and major joints
4. Third-degree burns > 5% TBSA in any age group
5. Electrical burns, including lightning injury
6. Chemical burns
7. Inhalation injury
8. Burn injury in patients with preexisting medical disorders that could complicate management, prolong
recovery, or affect mortality
9. Any burn patients with concomitant trauma where burn injury poses greatest risk of morbidity or
mortality
10. Burn injury in children admitted to a hospital without qualified personnel or equipment for pediatric
care
11. Burn injury in patients requiring special social, emotional, and/or long-term rehabilitative support,
including cases involving suspected child abuse, substance abuse, etc.
# ! # $! %! !
(1) Airway:
-secure airway
-if suspicion of smoke inhalation 100% oxygen by mask
-endotracheal tube for unconscious patients
(2) Cold Application:

-smaller burns application of cold water
-does not prevent further tissue damage, but delays edema formation probably by reducing initial
thromboxane production
-ice water should never be used associated cutaneous vasoconstriction can extend thermal damage
(3) Emergency Room Care:

-careful search for other life-threatening injuries is first priority
-burn is attended to after ABC’s
(4) Emergency Assessment of Inhalational Injury:

-suspect if flame burn or anyone burned in enclosed space
-hoarseness and expiratory wheezes signs of potentially serious airway edema or smoke poisoning
-elevated carboxyhemoglobin is presumptive evidence of associated smoke poisoning
-decreased P/F ratio (arterial PO2/FIO2)
-400-500 is normal
-< 300 in patients with impending pulmonary problems
-< 250 indication for aggressive pulmonary support
-bronchoscopy to assess edema of upper airway
(5) Fluid Resuscitation in the Emergency Room

-systemic inflammatory response
-capillary leak: loss of fluid and protein into extravascular compartment
- CO d/t peripheral resistance
- flow to skin may convert zone of stasis to one of coagulation increases depth of burn
-inadequate fluid resuscitation end organ damage
-begin with 1000 cc/h Ringer’s solution in adults; 20 cc/kg in children
109
-CVP monitoring in pts with burns 50% TBSA, associated medical problems, very young or very old,
smoke inhalation
-Swan-Ganz catheters in pts with > 65% TBSA b/c of homodynamic instability
(6) Tetanus
-burns are tetanus-prone wounds
(7) Gastric Decompression

-tube feeding to protect stomach from stress ulceration
(8) Pain Control

-morphine 2-5 mg IV until pain control adequate
(9) Psychosocial Care

-social worker
%$# & # ' #% &
Chest Escharotomy:
-early respiratory distress may be due to compromise of the ventilatory function caused by a cuirass effect
related to a deep circumferential burn wound of the chest
-escharotomy: anterior axillary line bilaterally
Escharotomy of Extremities:
-circumferential burn wounds of extremities may lead to permeant, serious neurologic and vascular deficits
-intramuscular compartment pressure: treat if > 30 mmHg
-local anaesthesia unnecessary because 3rd degree eschar is insensate
-incisions along mid-medial or mid-lateral aspect of extremity; should extend to subcutaneous fat
-burn patients are at risk for developing compartment syndrome up to 72 h postinjury frequent
assessment of involved extremity needed
-burn extent, patient age, and depth of burn are primary determinants of mortality
Burn Size:
-Rules of Nines:
-upper extremity: 9% TBSA x 2 = 18%
-lower extremity: 18% TBSA x 2 = 36%
-anterior and posterior trunk: 18% TBSA each = 36%
-head and neck: 9% TBSA = 9%
-perineum 1% TBSA = 1%
TOTAL = 100%
-Hand ~ 2.5% TBSA: dorsal surface 1% TBSA, palmar surface 1%, vertical surface 0.5%
-infants: head almost 20% TBSA
Burn Depth:
-primary determinant of long-term appearance and function
-healing from remaining epithelium lined skin appendages: sweat glands, hair follicles with attached
sebaceous glands
110
-deeper the burn fewer appendages longer burn takes to heal
-burns taking > 3 weeks to heal often produce hypertrophic scars, functional impairment, and thin fragile
epithelial cover
-these burns should be treated surgically
-depth dependent on:
-heat of burn source
-thickness of skin
-duration of contact
-heat-dissipating capability of skin (blood flow)
(1) Superficial (Shallow) Burns:
First Degree Burns:

-involve only epidermis
-erythema d/t dermal vasodilation
-painful
-desquamation at ~ day 4
Superficial Dermal Burns (Second Degree):

-include upper layers of dermis
-blisters with fluid collection at interface of epidermis and dermis
-usually heal spontaneously in 3 weeks if no infection
-usually no scar formation
(2) Deep Burns:
Deep Dermal Burns (Second Degree):

-extend into reticular layers of dermis
-blisters, wound surface mottled pink and white colour; blanche with pressure
-discomfort rather than pain
-will heal in 3-9 weeks if no infection
-will invariably have scar formation; joint function at risk if no physiotherapy
Full-Thickness Burns (Third Degree):

-involve all layers of dermis
-heal only by wound contracture, epithelialization from wound margin, or by skin graft
-white, cherry red, or black +/- deep blisters; do not blanche with pressure
-leathery and firm; insensate
Fourth Degree Burns:

-involve subcutaneous fat and deeper structures
-Systemic Inflammatory Response Syndrome (SIRS) commonly seen in burn patients
$ %*
-hypovolemic shock and tissue trauma formation and release of local and systemic mediators vascular
permeability or in microvascular hydrostatic pressure
-Histamine:
-involved only in the very early increase in permeability
-released by mast cells immediately early after injury increased capillary permeability
111
-increased intravascular junction space in venules
-Serotonin:
-released immediately upon postburn platelet aggregation
-increases pulmonary vascular resistance
-indirectly amplifies vasoconstrictive effects of norepinephrine, histamine, angiotensin II, PG
-Prostaglandins:
-contribute to formation of burn edema
-PGE2 and PGI2 (prostacyclin) arterial dilatation in burn tissue blood flow and hydrostatic
pressure accentuate edema process
-Proteolytic cascades:
-coagulation, fibrinolysis, kinins, complement system
-Bradykinins: increase vascular permeability in the venule
-reduction of CO after burn injury is a result of hypovolemic and cellular shock, increased systemic vascular
resistance due to sympathetic stimulation and hypovolemia
-after successful resuscitation, CO normalizes after 18-24h and increases to supernormal levels during wound-
healing phase
! #+ % !, ! -
Hypermetabolism:
-glucose:
-metabolism elevated
-gluconeogenesis from alanine and glycogenolysis are increased
-plasma insulin levels elevated; hepatic insulin resistance basal rate of glucose production
elevated despite normal or elevated insulin level
-protein:
-excreted primarily as urea progressive depletion of protein stores
-proteolysis increased increased efflux of amino acids (particularly alanine)
-increased gluconeogenesis from amino acids makes them unavailable for reincorporation
of body protein
-wound repair requires amino acid protein synthesis and increased immunologic activity and may
require accelerated protein synthesis
-recommended protein intake: 1-2 g/kg/d
-fatty acids:
-released at rates in excess of requirement of fatty acids and energy substrates
-not oxidized but re-esterified into TG fat accumulation in liver
Neuroendocrine-Mediator Response:
-catecholamines are the major endocrine mediators of hypermetabolic response in thermally injured
patients
-thyroid hormonal serum concentrations not elevated in patients with large burns
Immune Response to Burn Injury
Cytokine Cascade:
-after injury, a number of cytokines are induced rapidly, including TNF, IL-1 and IL-6
-TNF-alpha detectable early in burn shock; maximum level is of prognostic significance
-IL-1 and IL-6 are up regulated in inflammatory sites inducing PMN chemoattraction
-IL-2, a key cytokine in cellular immune response, is significantly suppressed in pts with large burns
-IL-6 induces hepatic synthesis of acute phase response proteins (eg. alpha-glycoprotein, C3, fibronectin)
112
Arachidonic Cascade:
-PGE2: major product after thermal injury
-produced by macrophages
-immunosuppressive effect by:
-inhibition of lymphocyte IL-2 production and T-cell activation
-down-regulation of IL-6
-massive increases in thromboxane B2
-leukotriene B4 is a potent neutrophil chemotactin produced after thermal injury
Cell-Mediated Immunity:
-impaired after burn injury
-functional capacity of T cels to perform their normal physiological response is impaired
Macrophages:
-function impaired after thermal injury
-products suppress mitogenic responsiveness in normal lymphocytes
Neutrophils:
-decreased Fc receptor expression, depressed intracellular killing capacity, and leukocyte chemotaxis
-CD16 (FcR, Fc, IgG receptors) and CD11 (adhesion molecules) on neutrophils is impaired
-baseline granulocyte oxidative activity is increased
Humoral Immunity:
-marked diminution of total serum IgG concentration
-levels return to normal between 10-14 days postburn
-low levels of IgG predictive of poor prognosis
-classical and alternative complement pathways are depleted
-production of GCSF and GM-CSF also impaired
Pathophysiology of Burn Shock:

-resuscitation complicated by obligatory burn edema and voluminous transvascular fluid shifts
-increase in total body capillary permeability
-maximal edema formation b/n 8-12 h postinjury in smaller burns; 12-24 h in major burns
-burns greater than 30% TBSA systemic decrease in cell transmembrane potential, involving non-
thermally injured cells
-d/t increase in intracellular [Na] secondary to decreased Na-ATPase activity
-fluid resuscitation only partially restores membrane potential and intracellular [Na]
Resuscitation from Burn Shock:

-primary goal is to replace fluid sequestered as a result of thermal injury
-massive fluid shifts can occur even though total body water remains unchanged
(1) Crystalloid Resuscitation:

-RL most popular resuscitation fluid
-Parkland Formula:
-4 ml/kg/%burn in first 24 h
-one-half over 8 hours; other half over then next 16 h
-Modified Brooke formula:
-2 ml/kg/%burn in first 24 h
113
(2) Hypertonic Saline:
-results in less edema because of smaller total fluid requirements
-advantages over RL controversial
(3) Colloid Resuscitation:

-Evans Formula:
-1 ml/kg/%burn for colloid and RL over the first 24 h
-Brooke Formula:
-0.5 ml/kg/%burn for colloid; 1.5 ml/kg/%burn for RL
-Slater Formula:
-RL 2L/24 h; FFP 75 ml/kg/24 h
-restoration and maintenance of plasma protein content are not effective until 8 h postburn, when
adequate levels can be maintained with infusion
(4) Dextran
Special Considerations in Burn Shock Resuscitation:
Fluid Resuscitation in the Thermally Injured Pediatric Patient:

-children have limited physiologic reserve require proportionately more fluid for burn shock resuscitation
than adults
-~5.8 ml/kg/%burn
-Cincinnati Shriners Burns Institute:
-4 ml/kg/%burn + 1500 ml/m2 BSA for the first 24 h
-Galveston Shriners Burns Institute:
-5000 ml/m2 %burn + 2000 ml/m2 BSA for the first 24 h
Inhalational Injury:
-increases fluid requirements
-require 5.7 ml/kg/%burn
Rate of Administration:
-volume infused should maintain urine output of 30-50 cc/h in adults and 1 cc/kg/h in children
Fluid Replacement Following Burn Shock Resuscitation:

-burn edema at 24 h postburn is near maximal, and the interstitial space may well by saturated with sodium
-additional fluid requirements depend on type of fluid used during initial resuscitation:
-if hypertonic solutions initially free water will be needed to restore iso-osmolar state
-if colloid was not used protein repletion frequently needed:
Brooke Formula: 0.3-0.5 ml/kg/%burn of 5% albumin during second 24h
Parkland Formula: replace (circulating plasma volume x 20%) with colloid
-maintenance fluids:
Total maintenance fluid = (1500 ml/m2 TBSA) +
evaporative water loss[(25+%burn) x m2 TBSA x 24]
-use 50% normal saline with potassium supplements

-after initial 24-48 h, adult patients with major thermal injuries require a urine output of 1500-2000 ml/24h;
children require 3-4 ml/kg/h
114
)
./0 # + 1 '!
-60-70% of deaths from house fires attributed to CO poisoning
-affinity for haemoglobin 200 times greater than oxygen and interferes with oxygen delivery:
1. prevents reversible displacement of oxygen on haemoglobin
2. shifts oxygen haemoglobin dissociation curve to the left decreasing oxygen unloading from at tissue
level
3. CO inhibits cytochrome oxidase a3 complex less effective cellular respiration
4. CO may bind to cardiac and skeletal muscle, causing direct toxicity
-COHb levels:
-< 10%: no symptoms
-20%: headache, nausea, vomiting, loss of manual dexterity
-30%: weak, confused, lethargic
-40-60%: coma
->60%: death
-half-life of COHb: room air 4-5 h; 100% O2 45-60 mins; HBO at 2 atm 30 min; HBO at 3 atm 15-20 min
-use of hyperbaric oxygen still controversial
.20 $! & # 3# -
-usually limited to upper airway:
-nasopharynx and oropharynx: very effective mechanism for heat exchange d/t relatively large surface area
and associated air turbulence, as well as their mucosa water lining that acts as a reservoir
-sudden exposure to hot air reflex closure of vocal cords reduces potential for lower airway injury
-greatest risk in those injured in an explosion and those who have been unconscious in a fire
-presence of significant intraoral and pharyngeal burns early intubation ETT for 3-5 days
.40 & *! $# #
-hydrogen cyanide: more effective inhibitor of cellular respiration than CO
-inhalation of aldehydes and caustic acids and bases mucosa coagulation and liquefaction necrosis
-direct epithelial damage: loss of bronchial epithelial cilia and decreased alveolar surfactant
-increase in bronchial blood flow with stimulation of alveolar macrophages
-airway edema, sloughing of necrotic epithelial mucosa, impairment of mucociliary clearance of secretions airway
obstruction V/Q mismatch hypoxia
-in the presence of burns, smoke poisoning approximately doubles the mortality from burns of any size
Diagnosis:
-anyone with flame burn and anyone burned in an enclosed space should be assumed to have smoke
poisoning until proved otherwise
-physical examination
-edema, strider, soot impaction smoke inhalation
-wheezing or rhonchi on chest auscultation injury to lower airways
-LOC decreased with hypoxemia, CO poisoning, or cyanide poisoning
-neurological deficits CO poisoning
-carboxyhemoglobin levels, ABG (to get P/F ratio)
Treatment:
(1) Upper Airway:
-in the presence of increasing laryngeal edema, nasotracheal or orotracheal intubation is indicated
-tracheotomy should never be used as an emergency procedure
-treatment of postextubation strider includes administration of racemic epinephrine and Heliox
(2) Lower Airway and Alveolar Damage:
-tracheobronchitis wheezing, coughing, retained secretions
115
-supplemental oxygen immediately
-efficacy of bronchodilators is questionable
-presenting sign of lower airway damage is hypoxemia
-treatment for smoke poisoning is supportive maintain ventilation with PEEP and oxygenation
until lung heals itself
-tracheotomy for those requiring long term ventilation (performed b/n 3 and 30 days after
intubation)
-anterior neck burns require excision and grafting 5-7 days prior to creation of
tracheotomy
./0 # 1% # ' #6
-for deeper burns, the eschar is surgically removed and the wound closed, with grafting techniques and
procedures for immediate placement of flaps tailored to meet patients’ individual needs
-early wound closure shortens hospital stay and duration of illness
.20 ! # 65 ' #!
Evidence Based Conclusions:
1. Small (<20%) full-thickness burns, and burns of indeterminate depth, if treated by an experienced surgeon, can be safely
excised and grafted with a decrease in hospital stay, cost to the patient, and time away from work or school
2. Early excision and grafting dramatically decreases the number of painful debridement required by all patients
3. Patients with burns between 20-40% TBSA will have fewer infectious wound complications if treated with early excision and
grafting
4. In animals with experimental burns, the depressed immune response and hypermetabolism associated with burns can be
ameliorated by early burn wound removal
Clinical Impressions:
1. Scarring is less severe in wounds closed early, leading to better appearance and fewer reconstructive procedures
2. Mortality from wound infection is lower in patients with major burns after early excision
3. Mortality from other complications of major burns may be lower with early excision and grafting
.40 !%$ %# '! #

-Tangential (Sequential) Excision:
-shaving very thin layers of burn eschar sequentially until viable tissue is reached
-if bed does not bleed briskly, another slice of the same depth is taken until a viable bed of dermis
or subcutaneous fat is reached
-Fascial Excision:
-reserved for patients with very deep burns or for patients with very large, life-threatening, full-
thickness burns
-advantages:
-results in reliable bed of known viability
-tourniquets can be routinely used for extremities
-operative blood loss less than sequential excision
-less experience is required to ensure an optimal bed
-disadvantages:
-operative time longer
-may be severe cosmetic deformity
-higher incidence of distal edema
-damage to superficial tendons and nerves
-cutaneous denervation
-skin graft loss from relatively vascular fascia over joints can lead to an ungraftable bed
and require eventual flap coverage
116
-Early Reconstruction:
-skin graft junctures should be avoided over joints, and grafts should be placed transversely when
possible
-thick skin grafts yield a better appearance than thin skin grafts:
-used for face, neck and other cosmetically important areas
-adjacent pieces of skin graft should be approximated carefully
-Donor Sites:
-with early excision the patient was spared the painful daily debridement, and with burn pain
diminished, patients concentrated on donor site pain
-all dressing seem to work, and difference in healing time are only 1 or 2 days
-complications: hypertrophic scarring, changed pigmentation, blistering, infections
-infections treated with systemic antibiotics and continuously moist dressings or silver
sulfadiazine
Cultured Epidermal Autograft

-in vitro culturing of epidermal cells (keratinocytes)
-bacterial contamination and colonization of the grafted bed results in rapid CEA disappearance from the
site
-persistent fragility of CEAs is related to the delayed formation of rete ridges
1. Cultured keratinocytes can be grown within 3 weeks and can be grafted successfully on a viable, non-infected excised burn
wound bed. For a massive burn with few or no available donor sites, this may be life-saving, especially in children
2. Take varies from poor to fair, with an optimistic range of 30-40%
3. Because epidermal cells lack a dermis, in early stages of wound healing, CEAs can provide only a barrier function to prevent
fluid exudation and bacterial invasion
4. The cover is fragile and must be protected from mechanical disruption for months, limiting daily activities and vigorous
physical and occupational therapy
5. CEAs are a temporary measure, permitting survival in the patients with massive burns.
Dermal Substitutes
-bovine collagen matrix with fiber size and distance similar to that of dermis, with a ground substance,
chondroitin 6-sulfate, filling the pores
-provides template on which native fibroblasts, endothelial cells, and macrophages can replace the collagen
with a dermal matrix resembling dermis
./0 # % !8 !& !
-hypermetabolism and hypercatabolism are universal consequences of injury
-magnitude of increase in metabolic rate is directly proportional to the size of burn injury
-requirements estimated from the Harris-Benedict equation
-routine determination of resting energy expenditure (REE) conducted at least twice weekly on burn patients for
proper adjustments of caloric needs
-caloric goal should be calculated at 120-130% of the measure REE
Carbohydrates:
-glucose is the best source of non-protein calories in the burn patient
-peripheral amino acids (alanine, glutamine and other glycogenic amino acids gluconeogenesis) and
wound lactate (glucose production by the Cori cycle) account for approximately one-half to two-thirds of
new glucose produced by the liver
-depletion of body protein during period of starvation leads to energy deficits and malfunctioning of
glucose-dependent energetic processes at the cellular level
117
Protein:
-energy and protein cooperatively contribute to improvement in protein conservation
-amino acid administration promotes synthesis of visceral and muscle protein without affecting the rate of
protein breakdown
-glucose retards whole-body protein breakdown and decreases the total amino acid pool, but exerts little
effect on protein synthesis
-both mechanisms improve nitrogen balance
-glutamine an important energy source for GI tract; broken down to alanine used in gluconeogenesis
-arginine may diminish protein catabolism and has secretagogue activity on pituitary and pancreatic
hormones improves immune function
Fat:
-appears to be a poor calorie source for the maintenance of nitrogen equilibrium and lean body mass in
hypermetabolic patients with large burns
-enthral tube feeding products are largely devoid of omega-3 fatty acids; alpha-linolenic deficiency has
been demonstrated in patients on long-term tube feedings.
.20 ( #& # ' !#

-All vitamins should be supplemented
-ascorbic acid has an essential role in wound repair, and plasma levels are frequently depressed in burn patients
-supplement 250-500 mg of vitamin C daily
-frequent determinations of Na, K, Cl, Ca, Mg, and PO4 are best guides to electrolyte replacement
-Zinc: important cofactor in enzymatic function and wound repair; deficiency documented in burn patients
.40 ! 6 '& #
-seems to influence outcome
-TPN used only when patient’s needs cannot be wholly met by enteral route
-functionally intact alimentary tract always should be used
-safest route for infusion of nutrients is distal to the ligament of Treitz
-advantages of enteral route over TPN:
-maintains integrity of GI tract
-increased hepatic protein synthesis may reduce incidence of bacterial translocation from the gut
-preserves gut mucosa mass and maintains digestive enzyme content
-stimulates trophic hormones, particularly gastrin
-initiate greater insulin release and promotes anabolism
-blunts intensity of hypercatabolic response and more effectively maintains preinjury weight
-prolonged postresuscitation ileus, overuse of narcotics, and constipation are frequently causes of failure of
successful enteral alimentation
-sepsis is associated with ileus and severe glucose intolerance
Composition of Enteral Nutrition:

-specialized feeding regimens improve disease-related metabolic derangements while enhancing nutritional
status
-in burn patients, significant amounts of omega-3 fatty acids should be used
.90 % # # ,, !# !
-burn patients require higher ambient temperatures for comfort because of the apparent change in the hypothalamic
set point of thermal neutrality
-warming burn patients to 38.2oC decreases the metabolic rate and corresponding energy requirements
-warming blankets, and heat lamps may be required
-administration of narcotics reduces metabolic rate associated with pain
-systemic infection requires additional calories to maintain nitrogen balance
-vigorous physical therapy promotes preservation of muscle bulk and must be provided on a daily basis to all
patients requiring prolonged hospitalization
118
-burns cause severe immunosuppression that is directly related to the size of the burn wound
!' % 6 6!%
-extent of burn injury is one of the major demographic predictors of outcome
-presence of inhalation injury correlates highly with infection and mortality
-burns involving less than 10-20% TBSA in otherwise healthy burn patients are almost never associated with life-
threatening infection
%# # 6! #
-diagnosis remains one of infection because many of the cardinal signs of sepsis are also present in uninfected burn
patients
-thrombocytopenia is one of the major manifestations of infection
-a precipitant onset of hyperglycemia, fall in blood pressure, and decrease in urinary output should suggest the
possibility that the patient is becoming unstable
-if associated with hypothermia, leukopenia, and falling platelet count, the patient is probably developing
sepsis
5 ' 6!%
-gram-negative bacteria (Pseudomonas species) is the dominant organism causing fatal wound infections
-pathological feature of burn wound sepsis is invasion of the organisms into viable tissue
spread to perivascular structures capillaritis and vascular occlusion haemorrhagic necrosis
-likelihood of septicaemia increases in proportion to the size of the burn wound
! & #
-respiratory tract most common locus of infection
-diagnosis confirmed by presence of characteristic CXR patterns, and presence of offending organisms and
inflammatory cells in sputum
-damaged lung tissue from inhalational injury can become infected
-antibiotic prophylaxis only selects resistant organisms and does not reduce the incidence of pneumonia
,, # "! $ & + ,$ !+
-major cause of sepsis in burn patients in up to 5% of major burns
-associated with use of IVcatheters
#% ! # ' %# '
-should be suspected in patients with positive blood cultures and no other identifiable source of bacteremia
-systemic antibiotic therapy should be instituted and continued for at least 4 weeks
# #% 6!%
-the majority of patients with positive urine cultures do not require antimicrobial treatment
-candiduria in the absence of signs of systemic infection can be treated with bladder irrigations with amphotericin B
$ ' 6 $! #
-rare complications
-a conservative approach with drainage of the helix centrally, in an attempt to preserve the out cartilages, is usually
successful
!# & ! 6 6!%
-definitive treatment of the septic burn wound is the expeditious excision of the wound
119
Topical Antimicrobial Therapy:
-proved wide-spectrum antimicrobial activity:
-silver nitrate:
-associated with electrolyte imbalances and methemoglobinemia (unusual)
-mafenide acetate:
-able to penetrate eschar; only agent capable of suppressing dense bacterial proliferation
beneath eschar surface
-disadvantage is strong carbonic anhydrase inhibition interferes with renal buffering
mechanisms
-silver sulfadiazine: most common agent used
Silver Nitrate Mafenide Acetate Silver Sulfadiazine

Active Component 0.5% in aqueous solution 11.1% in water miscible base 1.0% in water miscible base
Spectrum of Antimicrobial Gram (-) - good Gram (-) - good Gram (-) - variable
Activity Gram (+) - good Gram (+) - good Gram (+) - good
Yeast - good Yeast - poor Yeast - good
Method of Wound Care Occlusive dressings Exposure Exposure or single-layer

dressings
Advantages -Painless -Penetrates eschar -Painless

-No hypersensitivity reaction -Wound Appearance readily -Wound appearance readily
-No gram-negative resistance monitored monitored when exposure
-Dressings reduce evaporative -Joint motion unrestricted method used
heat loss -No gram-negative resistance -Easily applied
-Greater effectiveness against -Joint motion unrestricted when
yeasts exposure method used
-Greater effectiveness against
yeasts
Disadvantages -Deficits of sodium, potassium, -Painful on partial-thickness -Neutropenia and

calcium, and chloride burns thrombocytopenia
-No eschar penetration -Susceptibility to acidosis as a -Hypersensitivity - infrequent
-Limitation of joint motion by result of carbonic anhydrase -Limited eschar penetration
dressings inhibition
-Methemoglobinemia - rare -Hypersensitivity reactions in
-Argyria - rare 7% of patients
-Staining of environment and
equipment
Subeschar Clysis and Surgical Treatment:

-when burn wound sepsis has developed, the probability of survival is less than 10%
-injection of semi-synthetic penicillins beneath the infected eschar is associated with markedly improved
survival
-generalized wound sepsis in stable patients should be treated by surgical excision
Antibiotics:
-indiscriminate use of multiple agents promotes overgrowth of Candida species, enterococci, and multiple-
antibiotic-resistant organisms in the patient and in the burn center
-infection caused by an identified organism is treated by a single antibiotic
-altered pharmacokinetics of antibiotics in burn patients result in lowered serum drug levels when the usual
recommended dose is used inappropriate peak levels should prompt alterations in the dosage
120
!% %#
Care at the Scene:

-rescuer must avoid touching patient until current can be turned off
-ventricular fibrillation is common
-once ABCs completed, a careful search must be made for associated life-threatening injuries
-intense tetanic muscle contractions associated with electrocution can fracture vertebra or cause major joint
dislocations
Acute and Definitive Care:

-electric current is converted to heat in direct proportion to the amperage of the current and the electrical resistance
of the body parts through which it passes
-smaller the size, the more intense the heat and the less the heat is dissipated: fingers, hands, forearms,
feet, and lower legs are frequently totally destroyed
-massive underlying tissue destruction may be present
-myoglobinuria frequently accompanies severe electrical burns
-cardiac damage may be present; normal cardiac function on admission generally means that subsequent cardiac
dysrhythmia is unlikely
-nervous system is particularly sensitive to electricity
-severe brain damage or spinal cord injury is possible
-delayed transverse myelitis can occur days or weeks after injury
-damage to peripheral nerves common permanent dysfunction
-posttraumatic stress disorders are much more frequent after electrical burns than after thermal burns
-cataracts are a well-recognized complication of electrical contact burns
-frequently bilateral; often occur within a year or two of injury
Wound Management:
-early surgical treatment indicated:
-massive deep tissue necrosis which will not clear up with standard resuscitation techniques, major
debridement and/or amputation may be necessary
-compartment syndrome
-otherwise definitive surgical procedures can be done between days 3 and 5, before bacterial contamination occurs
and after the tissue necrosis is delineated
$!& %#
Emergency Care:
-involved clothing should immediately be removed and the burns thoroughly flushed with copious amounts of water
-will limit severity of the burn
-neutralizing agents may cause burns themselves; they frequently generate heat while neutralizing the offending
agent
-chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue, or diluted
by flushing with water
-chemical burns considered deep dermal or full-thickness, until proven otherwise
-phenol: can have severe systemic effects
-hydrofluoric acid: may cause death from hypocalcemia
121
)
# # !& ! 6
Treatment at the Scene of the Accident:

-place in tepid water rather than ice water
-wrap in clean cloth and victim taken to an emergency facility
-chemical burns irrigated with copious amounts of water
Initial Medical Management:

-determine if there is any possibility of smoke inhalation injury
-tetanus prophylaxis given
-cleanse wound with bland soap and water
-shave hair in areas of and adjacent to burns
-removal of tar and asphalt Medisol (citrus and petroleum distillate)
-chemical burns irrigated with water for 20 mins; neutralizing agent should not be applied
-blisters (options):
-left intact and underlying wound allowed to heal
-fluid evacuated and overlying skin allowed to cover underlying wound
-debridement
Follow-up Wound Care:

-problems of immunosuppression, hypermetabolism, and increased susceptibility to infection are not associated with
minor burns
-keep wound clean and in a moist environment
-systemic antibiotics rarely indicated; may predispose wound to later opportunistic infection
-follow-up care (do twice daily):
1. washing wound with bland soap and water
2. patting wound dry with a clean towel
3. applying a bland ointment
-vigorous program of ROM exercise: prolonged edema retards wound healing and is minimized with physical
therapy
-usually wound will totally epithelialize in 2-3 weeks
-wounds not healing within 14 days, then primary excision and grafting should be performed
-examine superficial partial-thickness wounds at 6 weeks for hypertrophic scarring
-use compression dressings if hypertrophic; worn ~12-18 months
-avoid sun exposure until wound is completely healed hyperpigmentation may occur; sun block recommended
Alternative Methods of Wound Management:

-Biobrane and OpSite: prosthetic skin substitutes in the treatment of partial-thickness outpatient burns
Management of Critical Areas:
Face: -should be left exposed; washed regularly
Ears: -treated with bland ointment
Eyes: -confirm corneal burns with fluorescein

-treat similarly to corneal abrasions
Hands: -elevate hand for 24-48h to minimize swelling

-circumferential burns may require hospitalization for observation
-ROM as soon as possible
122
Feet: -ROM important
-elevate feet when not walking
Perineum:
-require hospitalization for 24-48h for observation of urinary obstruction secondary to edema
Complications:
-most complications in small burn injuries result from overtreatment:
-too-vigorous dressing changes that pull off newly formed epithelium, or the use of a variety of topical and
systemic antibiotics that can cause secondary infection or formation of a pseudomembrane
# # !& ! 6 '! # ! #-
Medical Criteria for Outpatient Management:

1. No existing complications of thermal injury, such as inhalation injury
2. Fluid resuscitation completed
3. Stabilized hospital course
4. Adequate nutritional intake
5. Adequate pain tolerance
6. No anticipated septic complications
Outpatient Treatment Program:

-two phases of treatment:
-home-treatment:
-wash wound twice daily etc..
-exercise every hour
-physical therapy:
-hydrotherapy, debridement of burn wounds, and a supervised exercise regimen
-treatment reviewed and modified if necessary
-pharmacological modalities:
-hypnotics and analgesics: morphine, methadone, codeine, acetaminophen, NSAIDs
-anesthetic agents: ketamine, fentanyl
-antianxiety drugs, major tranquillizers and antidepressants
-non-pharmacological modalities:
-verbal and/or physical comfort
-relaxation therapy
!$#+ #
Inpatient Therapy:
-maintaining function and preventing the complications of prolonged immobility are the specific goals of the
rehabilitative treatment of burn patients
-position of maximal comfort promotes the formation of scar contractures
-edema is reduced by compression and elevation
-active and passive exercises implemented
-scar hypertrophy can be retarded by the use of custom-fitted pressure garments over healed scars
123
Outpatient Therapy:
-continuous follow-up of persisting functional deficits
-evaluation for corrective surgical procedures
-modification and evaluation of rehabilitation therapy
Psychological Support:
-anxiety, depression, denial, withdrawal, regression
-post-traumatic stress disorder:
-in nearly half of older children and adults suffering burn injury
-recurrent intrusive recollections, avoidance of circumstances that invoke memories of event, loss of
interest in daily activities, feelings of isolation, hyperalertness/vigilance, memory impairment, sleep
disturbances
-psychosocial support is critical for the burn patients for the duration of the course of treatment and follow-up
$ % + !&
Hypertrophic Scar and Keloid Formation:

-hypertrophy typically develops in deeper partial-thickness injuries and third-degree burns allowed to heal by
primary intention
-keloids overgrows the original dimensions of the initial injury and hypertrophic scar develops in the bed of the
injured tissue and is confined to its original anatomic boundaries
-hypertrophic scars flatten with time; keloids do not
-other forms of therapy for hypertrophic scarring: radiotherapy, cryotherapy, and reexcision and wound closure
-most successful approach is initial pressure therapy until wound matures, followed by subsequent excision
and application of skin grafts
-for keloids, excision alone has a recurrence rat > 50%
-intralesional injection of corticosteroids may reduce the bulk of keloid and hypertrophic scar mass
-acts by decreasing collagen synthesis and increasing collagen degradation through the collagen
inhibitors a2-macroglobulin and a1-antitrypsin
-major side effects are hypopigmentaion and atrophy of the skin surrounding the keloid
Marjolin’s Ulcer:
-chronic ulceration leading to malignant degeneration
-squamous cell carcinoma is most common
-rare tumours: malignant fibrous histiocytoma, sarcoma, neurotropic malignant melanoma
-chronic breakdown of a healed burn wound scar should lead to suspicion of malignant degeneration
-~30% of burn scar carcinomas occur in the head and neck
-adjuvant radiotherapy improves survival
Heterotopic Ossification:
-occurs in up to 13% of burn patients; ossification of soft tissue
-most commonly involves patients with full-thickness burns greater than 20% TBSA, and is found adjacent to the
involved joint 1-3 months after injury
-elbow most commonly affected joint
-limited physical activity precedes radiographic evidence of calcification
Fractures:
-up to 10% of burn patients have associated fractures
-treated with splints and traction until resuscitation complete
124
!" # !
-acute: “normally proceed through an orderly and timely reparative process that results in sustained restoration of
anatomic and functional integrity”
-chronic: “wounds that have failed the above”
$% !
Primary Closure:
-approximates the acutely disrupted tissue with sutures, staples, or tape
Delayed Primary Closure:
-approximation of wound margins is delayed for several days after the wound has been created
-prevents infection in wounds in which there is significant bacterial contamination, foreign bodies,
or extensive tissue trauma
-during the time the wound is open, events occur that will significantly decrease the chances of
wound infection after closure
Secondary Wound Closure:
-margins of the open wound move together by the biologic process of contraction
& "' ( ) )
Epithelialization:
-keratinocytes migrate and then divide to resurface partial-thickness loss of skin or mucosa
Contraction:
-spontaneous closure of full-thickness skin wounds or constriction of tubular organs after injury
Connective tissue matrix deposition:
-fibroblasts are recruited and produce a new connective tissue matrix
' !
*+, #
-damaged vessels and lymphatic trigger a cascade of events:
-vasoconstriction; mast cell release of vasoactive compounds: bradykinin, serotonin, histamine;
diapedesis of cells into wound; hemostatic clot of platelets
-platelets release clotting factors to produce fibrin; also produce several essential cytokines which modulate
the subsequent wound healing events
*-, ! (( #
-migration of leukocytes into the wound
-24h: predominantly PMNs, then by macrophages
*., / %
-fibrous protein collagen is synthesized
-cross-linking of collagen provides strength and integrity
-increased synthesis within 10h of injury
-synthesis peaks after 5-7 days and then declines gradually
(4) Remodelling
-acute and chronic inflammatory cells diminish gradually, angiogenesis ceases, and fibroplasias ends
-equilibrium between collagen synthesis and collagen degradation is gradually restored
125
$# 0
Cytokine Source Functions
Platelet Derived Growth Platelets, macrophages, -chemotactic for PMNs, macrophages, fibroblasts, and SMCs
Factor (PDGF) including endothelial cells, keratinocytes, -activates PMNs, macrophages, and fibroblasts
isoforms AA, AB, and BB smooth muscle cells -mitogenic for fibroblasts, endothelial cells, and SMCs
-stimulates production of MMPs, fibronectin, and HA
-stmulates angiogenesis and wound contration
-remodelling
-inhibits platelet aggregation
-regulates integrin expression
Transforming Growth Platelets, T lymphocytes, -chemotactic for PMNs, macrophages, lymphocytes, fibroblasts, and SMC
Factor Beta (TGF-B) macrophages, endothelial cells, -stimulates TIMP synthesis, keratinocyte migration, angiogenesis, and
including isoforms b1, b2, keratinocytes, SMCs, fibroblasts fibroplasias
b3 -inhibits production of MMPs and keratinocyte proliferation
-regulates integrin expression and other cytokines
-induces TGF-B production
Epidermal Growth Factor Platelets, macrophages, saliva, -mitogenic for keratinocytes and fibroblasts
(EGF) urine, milk, plasma -stimulates keratinocyte migration and granulation tissue formation
Transforming Growth Macrophages, T lymphocytes, -similar to EGF

Factor Alpha (TGF-A) keratinocytes, and many tissues
Fibroblast growth factor-1 Macrophages, mast cells, T -chemotactic for fibroblasts

and -2 family (FGF) lymphocytes, endothelial cells, -mitogenic for fibroblasts and keratinocytes
fibroblasts, and many tissues -stimulates keratinocyte migration, angiogenesis, wound contraction and
matrix deposition
Keratinocyte growth factor Fibroblasts -stimulates keratinocyte migration, proliferation, and differentiation
(KGF; aka FGF-7)
Insulin-like Growth Liver, macrophages, -stimulates synthesis of sulfated proteoglycans, collagen, keratinocyte
Factor-1 (IGF-1) fibroblasts,a nd others migration, and fibroblast proliferation
-endocrine effects similar to growth hormone
Connective tissue growth Endothelial cells, fibroblasts -chemotactic and mitogenic for various connective tissue cells
factor (CTGF)
Vascular endothelial cell Keratinocytes -increases vasopermeability

growth factor (VEGF) -mitogenic for endothelial cells
Tumour Necrosis Factor Macrophages, mast cells, T -activates macrophages

(TNF) lymphocytes -mitogenic for fibroblasts
-stimulates angiogenesis
-regulates other cytokines
Interleukins (IL-1 etc..) Macrophages, mast cells, -chemotactic for PMNs (IL-1) and fibroblasts (IL-4)
keratinocytes, lymphocytes, and -stimulates MMP-1 synthesis (IL-1)
many tissues -angiogenesis (IL-8)
-TIMP synthesis (IL-6)
Interferons (IFN-a etc) Lymphocytes and fibroblasts -activates macrophages

-inhibits fibroblast proliferation and synthesis of MMPs
-“wound hormones” that can be endocrine, paracrine, autocrine, intracrine

-functions of cytokines:
-regulate cell proliferation:
-competence factors: get cell into G1 phase (eg. PDGF)
-progression factors: promote the cell through the proliferation cycle (eg. IGF-1)
-chemotaxis
-direct production of specific components needed for matrix repair
126
PDGF: platelet derived growth factor
-initiates many wound healing events and stimulates production of several other cytokines
-chemotaxis for fibroblasts, neutrophils, macrophages, SMC
-stimulates production of fibronectin and hyaluronic acid
-may stimulate wound contraction
TGF-beta: transforming growth factor

-increases collagen synthesis by specifically enhancing matrix gene expression and by inhibiting
collagenase production and activity
-isoforms:
TGF-B1: most abundant
TGF-B2: found in amniotic fluid, saliva, breast mild, aqueous and vitreous humour of eye
TGF-B3: least studied
FGF: basic fibroblast growth factor (bFGF):

-potent angiogenic factor
-causes increased epithelial cell migration
-hastens wound contraction
EGF: epithelial growth factor

-stimulates epithelial migration and mitosis
1# " & # 1& # / (
-collagen is the major component of the extracellular matrix of all soft tissues, tendons, ligaments, and bone
-matrix also contains glycosaminoglycancs, proteoglycans, fibronectin, laminin, elastin
Synthesis:
-transcription mRNA translation on RER proline hydroxylation glycosylation (galactose/glucose)
procollagen (soluble) secretion into extracellular matrix cross-linking (lysyl oxidase) and cleavage of
amino and carboxyl terminals (procollagen peptidase) collagen (insoluble)
-three polypeptide chains: glycine-proline-X
-hydroxyproline important for collagen stability; ascorbic acid and oxygen required for
hydroxylation process
Degradation:
-breakdown mediated by matrix metalloproteinases (MMPs)
-MMPs synthesized by variety of cells: inflammatory cells, fibroblasts, epithelial cells
-MMP-1, 8, and 13: initiate degradation of collagen by splitting molecule into specific 3/4 and 1/4
fragments (TCA and TCB fragments)
-after this initial split, other nonspecific proteases further degrade collagen
-MMPs are zymogens which are activated by other proteases such as plasmin
-MMPs inhibited by alpha-2-macroglobulins and tissue inhibitors of metalloproteinases (TIMPs)
Ground Substance:
-proteoglycans and glycosaminoglycans
-molecular “shock absorbers”, provide for moisture storage, and also sequester cytokines
# "#
Mechanism:
-myofibroblasts: peak during and after the process of wound contraction
-extracellular matrix also important in contraction process
127
-precise mechanism of contraction not fully understood
Clinical Approaches:
-for scar revision, must assess maturity of scar:
-mature scar: soft and pliable
-skin graft may be used to correct contracture
-FTSG contracts much less than STSG
-splinting of wound required
-immature scar: stiff, indurated, hypertrophic, tender
-still contains inflammatory cell components and myofibroblasts that contribute to
contracture
-use musculocutaneous flap to fix defect or wait until scar matures
% #' 2#
-epidermis provides barrier protection from external environment

-collagen rich dermis provides all the strength attributed to skin
-basement membrane provides structural support for the epidermis and attaches it to dermis
Mechanism:
-healing by migration and mitosis
-epithelial destruction scab for dermal protection
-migration of cells from margins of wound and from hair follicles and sebaceous glands
-cells flatten out and send cytoplasmic projections into surrounding tissue
-epithelial cells, secrete proteases and migrate as a sheet of cells
-fibronectin and vitronectin support migration
-move by actin-myosin contractile system
-mitosis begins when there are not enough cells for further migration
-factors involved:
-bFGF, PDFG, TGF-a and EGF stimulate keratinocyte migration and mitosis
-TGF-B inhibits epidermal cell proliferation but stimulates motility
##
-nutrition important for collagen synthesis and immune response

-Ascorbic acid:
-essential; lack is most common cause of wound healing deficiency
-deficiency = scurvy
-co-factor in hydroxylation of proline; essential for addition of molecular oxygen
-60 mg/day RDI; up to 1 g/day recommended in trauma patients
-iron: required for prolyl hydroxylation
-calcium and magnesium: required for collagenase activity and protein synthesis in general
-oxygen: required for hydroxylation and energy needed for bacterial killing and cell viability
(( %%
-only a small number of immunosuppressed patients actually manifest clinical wound healing problems
-chemotherapeutic anticancer drugs inhibit healing
-malignancies deplete nutrients and also inhibit wound healing directly
128
#" ! "#) & #/ (
(1) Osteogenesis Imperfecta

-mutation in genes for Type I collagen
-four types: mild to lethal
-brittle bones, dermal thinning, increased bruisability
-normal scarring and skin extensibility
(2) Ehlers-Danlos Syndrome

-joint laxity, skin hyperextensibility and fragility, poor wound healing, vascular rupture
-ten types each with different enzyme or biochemical defects
-patients at risk for surgical vascular complications
(3) Marfan’s Syndrome

-tall stature, arachnodactyly, lax ligaments, myopia, scoliosis, pectus excavatum
-dissecting aneurysm of the root and ascending portions of the aorta
-defects in collagen structure; abnormal fibrillin in elastin
(4) Epidermolysis Bulla

-blistering and ulcerations
-excessive production of MMPs by fibroblasts; abnormal matrix adhesion to epidermis and associated
basement membranes
-complications: stenosis and strictures in GI tract surgery
-phenytoin decreases collagenase activity in fibroblasts; has been used to treat patients with recessive
dystrophic epidermolysis bulla
"# #' # !! "#
Factors that Affect Healing in Surgical Practice Factors that Contribute to Wound Infection
Local Factors General Factors Surgeon
Surgical technique
Blood supply Age Devitalized tissue
Denervation Anemia Impaired local circulation
Hematoma Anti-inflammatory drugs Hematoma
Infection (local) Cytotoxic drugs Foreign body
Mechanical stress Hormones Organism
Protection (eg. Dressings) Infection (systemic) Infective nature
Surgical technique Jaundice Source: (a) Endogenous, eg. skin, biliary, colorectal
Suture material and technique Malignant disease (b) Exogenous (cross-infection)
Type of tissue Malnutrition Patient
Obesity Disease: eg. DM, neoplasia, malnutrition, anemia,
Temperature chronic granulomatous disease
Trauma, hypovolemia, hypoxia Medications: eg. steroids, cytotoxics, intensive antibiotic
Uremia therapy, radiotherapy
Vitamin deficiency Immune response of individual
Trace metal deficiency Remote active infection
3 &
# # # "#
Anatomy:
-inner mucosa layer for absorption
129
-outer muscularis mucosa layer for motility
-both wrapped by serosa layer
Layers:
-Epithelium: one-cell thick; regenerates q8days
-Laminia propria: collagen types I, III, and V and elastin
-Muscularis mucosa
-Submucosa
-Muscularis propria: densely packed SMC with types I and III collagen
-Serosa
Injury and Repair:

-quality of healing determined by depth of injury and chronicity of injury
-inflammation and erosion healing w/o scar
-no mesenchymal cell response if injury confined to mucosa
-penetration of submucosa mesenchymal cell repair response: SMC migration and collagen production
-if acute ulcer normal architecture of intestine eventually restored
-if chronic ulcer stricture and obstruction can ensue as scar accumulates
-Crohn’s Disease:
-inflammation of submucosa to serosa
-increased collagen Type I and Type V
-therefore causes symptoms of intestinal obstruction
-Ulcerative Colitis:
-inflammation limited to mucosa
-thinning of matrix perforation rather than stricture
-Radiation Injury:
-extensive and progressive submucosa, muscularis, and serosa fibrosis
-Lye ingestion:
-mucosa penetrated fibrosis and stricture occur
Keloids and Hypertrophic Scars:

-Hypertrophic Scars:
-remain within boundaries of original wound
-almost always regress over a period of time
-Keloids:
-extend beyond the boundaries of the original wound
-usually do not regress
-usually recur after excision unless additional therapy provided
-overabundant collagen deposition and decreased degradation:
-increased mRNA for Type I collagen; keloids may contain increased TGF-B
-keloid tissue contains more soluble collagen and greater water content
-collagenase inhibitor a2-macroglobulin abundant in keloids and hypertrophic scars
-current treatments not consistently effective
-surgical excision
-intralesional injection of triamcinolone 40 mg/ml, no more than 2 ml q6-8weeks to avoid
systemic side effects
-adverse effects: local atrophy, depigmentation, telangiectasia
-keloids have increased histamine containing mast cells itching: oral antihistamine for relief
Factitious Wounds:
-self-mutilation
130
Marjolin’s Ulcer:
-nonhealing wound in an area of previous trauma may represent squamous cell carcinoma
-normal immunologic surveillance decreased because of dense scar unable to destroy malignant
transformation within scar
-type I collagen with significant amount of proteoglycan

-meticulous technique and early mobilization required for repair of flexor tendons in fibrous flexor sheaths
-preservation of vincula (which supplies blood to the tendon) needed to prevent ischemic and scarring
-early motion provides stress forces to lengthen and remodel scar; enhances lubrication from synovial fluid
3
-injury haematoma formation, edema, and pain
-migration of cells into and neovascularization into fracture site
-formation of soft callus: fibrocartilaginous splint of granulation tissue and cartilage
-endochondral ossification over 6-8 weeks by osteoblasts from periosteum and medullary canal
-remodelling over years
-rigid internal fixation: no soft callus formation direct bone to bone healing across injury without endochondral
ossification
-delayed union of nonunion (factors):
-site of fracture, presence and degree of soft-tissue injury, bone loss, inadequate reduction, inadequate
immobilization, infection, previous radiation, malignant growth at the fracture site, poor blood supply to
the fracture
-bone grafts:
-Osteogenesis: formation of new bone by cells that survive in the graft
-Osteoconduction: blood vessels and cells from the surrounding tissue grow into the bone graft scaffold
-osteoinduction: transformation of local, undifferentiated cells into bone-forming cells
#
-has little propensity to heal
-deep injury to articular cartilage that goes into subchondral bone produces exuberant inflammatory and healing
response fibrocartilage intermediate hyaline cartilage formed over time
' "
Pathophysiology:
-arise form physical and biochemical insults of extended duration
-prolonged inflammatory stage of wound repair extensive tissue damage and impaired healing by PMNs
-products released by PMNs continue to degrade extracellular matrix and prevent or impair the migration
of other reparative cells in to the wound
Venous Stasis Ulcers:

-result of deep venous obstruction or valvular incompetence
-typically occur superior to or near the medial malleolus
-tend to be large and irregularly shaped
-perivascular “fibrin cuffs”
Pressure Ulcers:
-pressure and hear forces over bony prominences cell death in least vascularized tissues
-can be complicated with osteomyelitis
-Marjolin’s ulcers rarely occur in these chronic ulcers
131
-spinal cord injury patients at risk: do not have normal leukocyte response to injury below level of
enervation
-fecal and urinary incontinence maceration and skin breakdown
-antibiotics should not be used to treat these wounds unless they are causing systemic toxicity
Classification:
Stage I: Non blanchable erythema of intact skin, the heralding lesion of skin ulceration
Stage II: Partial-thickness skin loss involving epidermis and/or dermis
Stage III: Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend
down to, but not through, underlying fascia
Stage IV: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle,
bone, or supporting strictions (eg. tendon, joint capsules, etc..)
Diabetic Ulcers:
-typically present as foot ulcers
-neuropathy is most important causative element
-tissue trauma and pressure are promoting factors
-lack of sensation results in increased mechanical stress, prevents timely detection of skin
punctures, or improper shoes, or the detection of foreign bodies in shoes
-angiopathy: capillaries are thicker and more permeable
Mechanisms Involved in the Healing of Chronic Ulcers:

-pressure and diabetic ulcers heal mainly by contraction
-venous ulcers heal mainly by epithelialization
Chronic Wound Care:

-most wounds regardless of cause will heal by secondary intention only if the underlying cause is corrected
-tissue perfusion and cellular oxygenation are important factors for chronic wound repair
-no evidence however that hyperbaric oxygen can improve the healing (with the exception of
osteoradionecrosis)
-debridement to remove damaged and necrotic tissue often helps to accelerate healing
-disinfectants should be avoided since they may injure normal tissue
Factors that Influence Healing of Chronic Wounds

Pressure Smoking
Ischemia Cancer
Age Radiation
Nutrition Distant malignancy
Perfusion Chemotherapy
Metabolism (diabetes) Hereditary healing disorders
Infection Glucocorticoid steroid treatment
-partial-thickness wounds require semiocclusive dressings to provide moist environment for epithelialization
-combining an absorbent dressing material with the polyurethane film or hydrocolloid alleviates the
problem of excess wound fluid
-occlusive/semiocclusive dressings may exacerbate infection when covering areas in which the bacterial count is
higher than 100,000/g of tissue.
-dressings are used to deride:
-exposed tendon: slower more gentle process needed use hydrogens to keep wound moist
-eschar use hydrocolloid; debridement through autolysis
132
&
-tissue reactivity to particular sutures and its significance in the healing process has never been validated
-woven suture material should not be used in the closure of contaminated wounds
-more likely to facilitate infection than a smooth suture
-staples must be removed within a few days if permanent skin marks are to be avoided
-tape strips may be used to substitute dermal sutures as long as wound edges are well approximated
-fetal wound repair is characterized by a significantly reduced inflammatory response

-fetal platelets have different aggregative characteristics and reduced cytosine release
-instead of collagen, the major component of the wound matrix is hyaluronic acid
-amniotic fluid may inhibit fetal wound contraction, but the mechanisms and component(s) remain unclear
133
-orthotopic transplantation: graft placed into its normal anatomic location (eg. heart transplant)
-heterotopic transplantation: graft placed in a different site (eg. kidney transplant)
-syngeneic: transplantation b/n individuals of identical genetic strain
-allogeneic: transplantation b/n genetically different members of same species
-xenogeneic: transplantation b/n different species
-autotransplant: one site to different site within same individual
! "#
-epitope: molecular unit of specific immune recognition (carbohydrate/peptide moiety)
-antigen: epitope containing molecules that can be bound by T-cell receptors or antibodies of B-cells
-may contain several epitopes
-major histocompatibility complex (MHC):
-cluster of genes on chromosome 6
-known as human leukocyte antigen (HLA)
-polymorphic gene: differ in detail while conforming to the same basic structure
$ $ % &!!' #
-innate vs. acquired immunity:

-innate: non-specific
-acquired: specific recognition; based on antigen receptors
-immunological memory
-mediated by lymphocytes, T cells (cellular immunity) , and B cells (humoral immunity)
Cellular Immunity:
-TCR recognizes processed peptide antigens bound to MHC molecules
-parenchymal cells express class I MHC molecules
-display peptides from within (eg. viral replication)
-bind to T-cells /w CD8 molecule
-hematopoeitic cells express class II MHC molecules
-display peptides that have been phagocytized from surrounding extracellular spaces
-bind to T-cells /w CD4 molecules
-CD4+ T-cells are first alerted of an invasion of the body by antigen presenting cells (APCs) and activate CD8+ T-
cells to search the body for cells that have been infected by this invader
Humoral Immunity:
-B cells bind soluble antigens and secrete soluble forms (Abs) to bind these foreign molecules
-material bound by Ab is opsonized for destruction by cells of the innate system of immunity
-ie. macrophages, monocytes, PMNs
-activate complement system membrane destroyer
-Cytokines amplify response of one cell to one antigen

-prototypical cytokine of T-cell activation is IL-2
134
( ) '( ' * ( ( & "
-antigens responsible for human allografts rejection are encoded by HLA region of chromosome 6
-class I molecules (HLA-A, B, and C)
-class II molecules (HLA-DR, DP, and DQ)
-other genes encoded by HLA:
-TNF-alpha and beta
-components of complement cascade (class III molecules)
-heat-shock protein (HSP-70)
-peptide transporter proteins TAP 1 and TAP 2; proteosome proteases LMP 2 and LMP 7
-other polymorphic transplant antigens: ABO blood group
-Class I molecule:
-single polymorphic gene + nonpolymorphic protein B2-migcroglobulin (from chr 15)
-30-50 alleles per locus
-structure:
-expressed as single MHC-encoded, transmembrane alpha chain (/w 3 domains alpha 1, 2 and 3),
in combination /w B2M
-binding via groove made by alpha 1 and alpha 2 domains
-binds peptides synthesized in the endoplasmic reticulum
-found on all nucleated cells except neurons
-Class II molecule:
-two chains: alpha and beta
-differ by alleles represented at each locus and in number of loci present in HLA class II region
-structure:
-formed by two MHC-encoded chains (alpha and beta) each /w two domains
-binding site via alpha 1 and beta 1 domains
-binds peptides derived from endocytosed proteins
-found primarily on cells of the innate immune system (phagocytes, macrophages, monocytes)
-can be upregulated to appear on other parenchyma cells by cytokines
-inheritance of HLA genes follows simple Mendelian genetics:

-25% offspring HLA identical
-50% haploidentical
-25% nonidentical
+ "# & "
-physiologic role of MHC molecules:

-provide mechanism for T-cell inspection of parenchyma cells (class I)
-provide interface between innate immune cells and T-cells (class II)
-in transplant, T-cell responses to either class can generate a rejection episode
-T-cells can recognize foreign MHC molecules and activate
-CD8+ T-cells:
-if self-peptides are presented to T-cells, then no activation occurs
-alterations in peptide content (eg. viral replication), causes activation immune response
-enhanced cytotoxic capabilities for infected cell destruction
-CD4+ T-cells:
-can activate CD8+ T-cells and Ab-producing B-cells
-release of cytokines to recruit CD8+ T-cells
-B cells are stimulated to release Ab
-release of INF-gamma induces expression of class II molecules on local cells and increase expression of
class I molecules locally
135
-matching donors and recipients /w regard to HLA type has been shown to improve outcome after kidney, heart, and
pancreas transplantation
-no such correlation for liver transplantation
-matching may reduce overall survival:
-HLA compatibility potentiates the inflammation during viral reinfection after
transplantation for viral hepatitis and increases the chances for clinical recurrence of the
original disease
( & & "

-historically MHC polymorphism defined by:
-lymphocytotoxicity assay and MLC
-both assays only define MHC epitopes but not the entire molecule
-lymphocytotoxicity assay:
-donor serum /w anti-MHC Ab of known specificity; mix /w recipients lymphocytes
-if Ab binds to MHC activates complement (rabbit) recipients lymphocytes stained /w blue dye
-MLC assay:
-incubate recipient T-cells /w irradiated donor T-cells in presence of 3H-thymidine
-recipient cells proliferate if they differ from donor cells increased radionuclide uptake
-prospective typing assay limited to living-related donors
-other methods:
-restriction fragment length polymorphism (RFLP)
-oligonucleiotide hybridization
-polymorphism-specific amplification (PCR-SSP): most commonly used for class II typing
-sequence polymorphism that do not alter the TCR:MHC interface are unlikely to affect allografts survival;
enhanced precision of molecular typing may provide more information than is clinically relevant
( ) '( ' * ( ( & " (
T-Cell Receptor:
-T-cells formed in fetal liver and bone marrow
-migrate to thymus during 1st trimester
-at thymus, a series of DNA rearrangement and recombination occurs (V, J, D and C regions)
-individual cells recombine to express a single TCR /w a single specificity
-results in population of T-cells capable of binding 109 different specificities: essentially all
combinations of MHC and peptide
-now also able to express CD4 and CD8
-after recombination, thymic selection occurs to avoid “self-destruction”
-cells initially interact /w MHC-expressing cortical thymic epithelium
-first positive selection occurs: if no binding cells are useless (unable to function in
periphery) apoptosis occurs
-then negative selection: surviving cells move to thymic medulla
-lose either CD4 or CD8
-if binding to self-MHC occurs apoptosis results
-only cells released into periphery are those that can bind self MHC /wout activation
Antibody:
-maturation occurs in the bone marrow
-two light-chain loci (kappa and lambda) each /w V, D, J, and C regions
-types: IgM, IgG, IgA, IgE, or IgD; defined by heavy chain usage
-Fc portion: binds cells of the innate system
136
-in IgM and certain classes of IgG can activate complement
-isotype switching: alteration of heavy-chain gene usage from IgM to either:
-IgG: significant soluble mediator of opsonization
-IgA: mucosa immune responses
-IgE: mast-cell mediated immunity
-IgD: primary cell-bound Ab
-affinity maturation:
-D and J regions undergo random additions resulting in clones that have altered antigen affinity
-those /w increased affinity are retained for future encounters; will have a more vigorous response
+ "# & " ( " ) '(
T-Cell Activation:
-initial binding to APC or endothelial cell is non-specific and mediated by adhesion molecules (eg. ICAM-
1, VCAM-1, LFA-1)
-MHC recognition:
-single interaction of TCR /w an MHC is not sufficient for activation
-~8000 TCR ligand interactions /w same antigen must be reached
-initiation of a series of intracytoplasmic protein tyrosine kinases (PTK)
activation of phosphokinase C-gamma hydrolysis of PIP2 IP3 + DAG
-IP3 binds to ER release of Ca++ induces calmodulin to bind to and activate
calcineurin initiate transcription of IL2
-IL2 autocrine activation of T-cell potentiates DAG activation of protein
kinase C (PKC) gene regulatory steps in cell cycle
-also requires second confirmatory signal by binding CD28 (on T-cell) /w B7 molecules (on
APC) potentiates the TCR-initiated tyrosine phosphorylation
-reduces the number of binding events of TCR-MHC from 8000 to 1500
T-Cell Amplification:
-cytokines (particularly IL-2 and IFN-gamma) recruit other T-cells
-T-cells develop one of two phenotypes:
-Th1 cells:
-mediate cytotoxic responses (eg. delayed-type hypersensitivity)
-express IL-2, -12, -15, and IFN-gamma
-Th2 cells:
-support the development of humoral or eosinophilic responses
-express IL-4, -5, -10, and -13
-immunosuppression produces artificial patterns of gene expression, resulting in nonphysiologic patterns of
cytokine secretion
-in the late phases of rejection, the inflammatory response recruits cells /w nonspecific cytotoxic activity to
the organ
-IL-8, released by activated macrophages and T cells, also recruits PMNs to the scene to remove necrotic
tissue
T-Cell-Mediated Cytotoxicity:
-amplification generally performed by CD4+ T-cells: best suited to interact /w class II expressing APCs
-cytotoxicity best mediated by CD8+ T-cells
-in the artificial situation of transplantation, both CD4+ and CD8+ mediate cytotoxicity
-Ca++ mediated exocytosis of cytolytic granules: contain perforin and serine proteases called
granzymes
-T-cells can also induce apoptosis
-after activation, non-MHC-restricted, T-cell-mediated cytotoxicity occurs other T-cells /wout the
specific TCR can participate in cytotoxicity
137
-T-cells expressing the gamma-delta TCR are prominent effector of non-MHC-restricted cytotoxicity
-this is induced by high levels of IL-2
B-Cell Activation and Clonal Expansion:

-surface Ab cross-linking by antigen leads to B-cell proliferation and differentiation into a plasma cell
-B-cells can also internalize antigens bound to surface Ab and process them for presentation to T-cells
-can bind antigen in circulation and initiate a T-cell response
-Plasma cells hypertrophied Golgi apparatus
-secrete large amounts of monoclonal Abs
-antigen exposure generally leads to B-cell affinity maturation and isotope switching, and produces high-
affinity IgG Ab
Antibody-Mediated Cytotoxicity:
-Ab serves as anchoring site for complement C1q:
-Classical Complement Activation Cascade:
-two Fc bind C1q and activate it C3 activation formation of membrane attack
complex (MAC) of polymerized C5, 6, 7, 8, and 9
-results in disruption of cell membrane and cell lysis
-several byproducts of C3 cleavage serve as chemoattractant to phagocytic cells and as
opsonins potentiating antigen phagocytosis
-Ab can act as opsonin
-phagocytic cells have receptors for Fc portion of IgG Ab-dependent cellular cytotoxicity
-Ab binding to endothelium complement activation on endothelial cell cellular retraction and exposure
of underlying matrix potentiates platelet activation and aggregation
microvascular thrombosis, a hallmark of the tow Ab-mediated graft rejections: hyperacute
rejection and acute vascular rejection
( ,( # ) !
Hyperacute Rejection (HAR):

-caused by presensitization of recipient to antigen expressed by donor
-develops minutes to hours following graft reperfusion
-initiates complement-mediated lysis and induces immediate graft thrombosis
-exposure usually d/t prior transplant, transfusion, or pregnancy
-no treatment, but can be prevented by preoperative screening (prevents HAR in 99.5% of transplants):
-lymphocytotoxic crossmatch
-mix donor (nonactivated T-cells) /w serum from recipient in the presence of complement
-lysis indicates presence of Abs directed against donor
-detection of IgG Abs directed against class I MHC molecules represents a positive test
and a contraindication to transplantation
-ABO typing
-vascular rejection; a delayed variant
-mediated by humoral factors
-occurs when offending alloantibodies exist in circulation at levels undetectable by crossmatch
assay
-re-exposure leads to restimulation of memory B-cells responsible for donor-specific Abs
-initial graft function followed by deterioration ~ POD#3
-can occur through de novo Ab synthesis spurred by T-cell-dependent B-cell activation
Acute Rejection:
-caused primarily by T-cells
-evolves over days to weeks; most common in the first 6 months
-T-cells bind antigen via TCR (either directly or after phagocytosis of donor tissue and re-
138
presentation of MHC peptides by self APC) cell activation
-results in massive infiltration of graft of T-cells, /w destruction of the organ
-incidence of acute rejection declines /w decreasing MHC disparity, but any mismatch can cause T-cell
mediated destruction. Therefore T-cell specific immunosuppression required
-treatment leads to graft restoration in 90-95% of cases
-monitoring for acute rejection mus be intense, particularly during the first year after transplantation
-unexplained graft dysfunction should prompt biopsy and evaluation for lymphocytic infiltration
and graft parenchyma necrosis characteristic of acute rejection
Chronic Rejection:
-poorly understood
-insidious onset: months to years
-pathophysiology undefined, untreatable
-heightened immunosuppression not effective in reversing or retarding progression
-characterized by parenchymal replacement by fibrous tissue /w a relatively sparse lymphocytic infiltrate
-direct cell-mediated tissue destruction is not a primary mechanism
-requires re-transplantation
!!' '
-the event occurring at the time of transplantation are the most critical in establishing the state of immune
unresponsiveness necessary for long-term graft survival
-immunosuppression is extremely intense in the early post-op period and subsequently tapers
-induction immunosuppression: usually involves deletion of T-cell response completely and
cannot be maintained indefinitely /wout lethal consequences
-maintenance immunosuppression: well tolerated if dosed appropriately
-rescue agents: immunosuppressant used to reverse an acute rejection episode (same as agents
used for induction)
Corticosteroids:
-used in conjunction /w other agents, improves graft survival
-can contribute significantly to the morbidity of transplantation
-anti-inflammatory agent
-bind to an intracellular receptor after nonspecific uptake into the cytoplasm
-prevents the function of NF-KB, a key activator of proinflammatory cytokines
-prevents the primary mechanism by which lymphocytes amplify their responsiveness
-block transcription of IL-1 and TNF-alpha and IFN-gamma production, PMN migration, and
lysosomal enzyme release by PMNs
-inhibits PLA2 and arachidonic acid cascade
-mutes upregulation of MHC
-do not have a significant influence on Ab production
-most commonly used is prednisone or methylprednisolone
-effects of steroids:
-suppressed HPA axis
-need coverage /w steroid preparation in the amount equal to their endogenous adrenal
capacity; should not exceed 50 mg hydrocortisone q8h
-impaired glucose tolerance
-delayed wound healing
-salt and fluid retention
-hypertension
-CNS effects (insomnia, depression, nervousness, euphoria)
-chronic effects:
-Cushing’s syndrome, cataracts, muscle wasting, and growth retardation n prepubertal
139
children
-peptic ulcers
-osteoporosis (inhibition of bone matrix formation and intestinal absorption of calcium)
-HLA-identical donors: no need for steroids
-pts who have survived a year /wout a rejection episode can be considered for /wdrawal from steroids
Antiproliferative Agents:
Azathioprine:
-hepatic conversion azathioprine 6-mercaptopurine (6-MP) 6-thio-inosine monophosphate (6tIMP)
-inhibits DNA synthesis by alkylating DNA precursors and inducing chromosomal breaks through
interference /w DNA repair mechanisms
-inhibit conversion of IMP to AMP and GMP
-effects are nonspecific
-effectively inhibits rejection as a maintenance agent but, has no value as a rescue or induction agent
-1-3 mg/kg/day
-toxicity: bone marrow, gut mucosa, liver
-decrease dose as total WBC or leukopenia (< 0.3)
-hold in the presence of infection
-hepatotoxin: rarely used in liver transplantation
Mycophenolate Mofetil (MMF):

-noncompetitive, reversible inhibitor of IMP dehydrogenase
-prevents a critical step in RNA and DNA synthesis by limiting GTP and dGTP production
-there is a “salvage pathway” for GMP production in most cells except lymphocytes
-therefore has selective immunosuppressive effects
-blocks proliferative response of both T and B lymphocytes
-inhibits Ab formation
-prevents generation of cytotoxic T-cells
-advantages over azathioprine:
-does not cause nephrotoxicity or hepatotoxicity
-less bone marrow suppression
-reduces the rate of rejection/treatment failure from 48% to 31%
-effective as rescue agent
-may interact /w tacrolimus, potentiating the effect and possibly the side effects of this drug
Calcineurin Inhibitors:
Cyclosporine:
-mainstay immunosuppressant in most maintenance regimens
-mechanism of action:
-binds to cytoplasmic cyclophilin (cis-trans peptidyl-prolyl isomerases critical for protein folding)
-does not effect immunosuppression but is related to toxic side effects
-cyclosporin-cyclophilin complex binds to calcineurin-calmodulin complex
-prevents Ca++-dependent phosphorylation and activation of transcription-regulating
factor NF-AT
-prevents transcription of IL-2 and other genes critical for T-cell activation
-reversible inhibition of T-cell-mediated immune responses, but does not prevent antigen recognition by T
cells. Effects can be overcome /w exogenous IL-2
-ineffective as rescue agent b/c effects are abolished in the presence of IL-2
-metabolised by cytochrome P-450 of liver:
-concentrations increased by inhibitors (eg. ketoconazole, erythromycin, CCBs)
-concentrations decreased by inducers (eg. rifampin, phenobarbital, phenytoin)
-side effects:
140
-renal:
-causes dose-related nephrotoxiciy d/t vasoconstrictors effect on proximal renal arterioles
-idiosyncratic reaction producing hemolytic uremic syndrome
-hyperkalemia
-hypertension
-neurologic:
-tremors, paresthesia, headache, depression, confusion, somnolence, seizures
-hypertrichosis
-gingival hyperplasia
-hepatotoxicity: increased LFTs
Tacrolimus (FK506):
-macrolide produced by Streptomyces tsukubaenis
-blocks NF-AT arrests T-cell activation
-intracellular target is an immunophilin distinct from cyclophilin
-100x more potent in blocking IL-2 and IFN-gamma production than cyclosporine
-mainly maintenance agent; has shown promise as rescue agent
-side effects:
-similar to cyclosporine wrt renal and hepatic toxicity
-tremors and mental status changes
-diabetogenic effect
-effective in liver transplants (drug of choice)
Antilymphocyte Preparations:
Antilymphocyte Globulin (ALG):

-targets central mediator of acute rejection, the T-cell, by coating multiple epitopes on this cell type and
promoting their clearance through complement-mediated lysis, opsonin-induced phagocytosis, and
internalization of key surface receptors
-thrombocytopenia may be a problem (cross-reactivity to platelets)
-dose 10-20 mg/kg/day IV for 10-14 days
-commonly used as part of multidrug induction immunosuppression protocol in renal transplantation /w
cyclosporine, azathioprine or MMF and prednisone
-side effects:
-fever, chills
-skin rash
-thrombocytopenia and leukopenia (require an alteration in treatment)
-daily CBC required
-reactivation of CMV, HSV, EBV and VSV
OKT3:
-murine monoclonal Ab to the signal transduction subunit on human T cells (CD3)
-binds to CD3 and prevents signal transduction of T-cell receptor antigen binding event and
arrests amplification of a rejection episode
-downregulates TCR complex “blind” T-cell
-blocks cytotoxic activity of already activated T cells through inappropriate activation and
degranulation
-dose 5 mg/day for 10-14 days
-pre-treat /w methylprednisolone to prevent adverse reactions
-monitor /w flow cytometry to measure percentage of CD3+ cells
-good rescue agent (better than steroids) but limited to steroid-resistant rejection b/c of side effects
New Immunosuppressive Agents:
141
Rapamycin:
-macrolide antibiotic derived from Streptomyces hygroscopicus
-similar to tacrolimus; have been shown to antagonize each other
-interacts /w FK-BP but does not affect calcineurin activity
-does not inhibit expression of NF-AT or IL-2, but impairs signal transduction by the IL-2
receptor
-prevents T-cells from entering the S phase of cell replication
-advantage: interrupts T-cell activation even if IL-2 is present from an exogenous source or ongoing
rejection
-hypertriglyceridemia may be a significant side effect
Deoxyspergualin:
-isolated form Bacillus laterosporus
-has the strongest antiproliferative properties via anti-monocyte-anti-macrophage effect
-prevents the nuclear translocation of NF-KB
-inhibit antigen presentation or the costimulatory function of APCs
-effective in prolonging allografts survival in animal models of renal, pancreas, liver, and heart transplant
-side effects:
-GI disturbances
-headache, fatigue, perioral numbness, decreased white blood cell and platelet counts and
hematocrit
-synergistic /w cyclosporine
Brequinar:
-selectively inhibits T- and B-cell proliferation
-inhibits enzyme dihydro-rotate dehydrogenase interferes /w pyrimidine synthesis
-inhibits lymphocyte DNA synthesis and interrupts rejection process at level of clonal expansion
-synergistic /w cyclosporine
-side effects: leukopenia
Anti-IL-2 Strategies:
-high-affinity IL-2 receptor is dependent on up-regulation of 55-kD subunit Tac
-induction /w anti-Tac Abs has prevented and reduced frequency of early rejection when used in
combination /w cyclosporine
-synergistic /w cyclosporine, may reduce the dose of cyclosporine
-other Abs: 33B3.1, BT563
Costimulation Blockade:
-interruption of the CD28 pathway of costimulation may selectively energize only those cells undergoing
binding to the allografts, leaving non-reactive cells unaffected
-agents under investigation include Abs directed against B7-1 and B7-2, CD28, CD40, gp39, and fusion
protein, CTLA4-Ig
Concordant Xenografts:
-derived form closely related species, such as Old world monkeys and apes
-most of the critical molecular elements responsible for antigen presentation and T-cell-mediated rejection
are revolutionarily conserved in mammals
-feasible /w available immunosuppressive pharmaceutical agents
-widespread application of concordant xenografts would quickly deplete the supply of nonhuman primates
-concern that zoonotic transfer of disease would put the pt and the public at undue risk
142
Discordant Xenografts:
-rapid HAR, generally from IgM Abs directed against atypical carbohydrate residues
-intervention at all levels of innate and acquired immunity will be required for successful engraftment
-transgenic alteration of pigs to express human proteins is the key for future clinical applications of
discordant xenografts
. .
-Vascular grafts
-used as autografts
-replacement of damaged or atherosclerotic arteries
-vein grafts (eg. saphenous) are optimal conduits for CABG
-autografting of arteries used occasionally for arterial replacement of diseased renal artery (hypogastric
artery)
-allogenic arterial conduits are the ideal replacement material for transplant renal artery stenosis
-Nerve grafts
-serves as a route along which the pt’s own nerve can regenerate
-prevention or amelioration of systemic complications may be possible by achieving more precise glucose control
-most successful approach to restoring normal long-term glucose homeostasis in Type I diabetes is whole-organ
pancreas transplantation
Historical Background:
-using a whole pancreaticoduodenal allografts /w anastomosis of the duodenal segment to the bladder is the safest
and most popular method of handling exocrine secretions
Indications:
-Type I insulin-dependent diabetics younger than 45 years
-no significant CAD
-no major amputations or severe visual impairment
-contraindications: untreated malignancy, active infection, HIV seropositivity
-three circumstances:
-pancreas transplantation alone (PTA) - in the non-uremic pt /w normal kidney
-pancreas transplantation after successful kidney allografting (PAK)
-offered to young diabetics /w tow ore more end-organ complications, who have undergone prior
living-related or cadaveric renal transplantation
-simultaneous pancreas-kidney transplant (SPK) - in uremic pt
-~90% are SPK
Operative Procedure:
-most widely used duct management technique of pancreas transplantation is bladder drainage, in which a
duodenal segment is anastomosed side-to-side to the dome of the bladder
-advantages of bladder drainage:
-urinary amylase determinations as screening test for rejection
-avoidance of enteric anastomosis and spillage of bowel contents
-reduced potential for peripancreatic infections
-advantages of enteric drainage:
-avoidance of post-operative urologic complications
-avoidance of chronic dehydration and need for bicarbonate replacement
143
-early removal of foley
-technique:
-vascular reconstruction of pancreatic blood supply is performed /w donor iliac artery “Y” graft to
donor splenic artery and superior mesenteric artery
-duodenum segment is shortened to approximately 10-12 cm
-spleen removed by ligating splenic artery and vein
-intraabdominal placement of graft
-pancreas usually is placed into the right iliac fossa, and the kidney, if transplanted
simultaneously, is implanted on the left side
-venous anastomosis performed: portal vein of graft to distal inferior vena cava or iliac
vein
-arterial anastomosis: iliac “Y” graft /w recipient iliac artery
-bladder drainage side-to-side anastomosis of duodenal segment to dome of bladder
-enteric drainage side-to-side anastomosis to ileum
-generous IV doses of mannitol and albumin administered to limit reperfusion injury and tissue
edema
-irrigation /w antibiotic solution, including amphotericin B, miconazole, and cephalothin, to
minimize risk of peripancreatic infection, abscesses, and mycotic aneurysm
Postoperative Management:
-quadruple drug regimen: ATGAM or OKT3, MMF, cyclosporine or tacrolimus, and steroids
-antibiotic therapy for 10-14 days post-op
-acute rejection in 70-80% of pts, usually in the first year
-rescue: high-dose steroids x 2 days; if no response, OKT3 or ATGAM
-/w early treatment, 90% reversible
-lymphocytic infiltrates initially involve exocrine portion of gland; islet cells removed later
-monitor exocrine secretions of amylase in urine; a consistent drop > 25% strongly suggests possibility of
rejection, but it is not a reliable indicator of rejection
-obtain biopsies (gold standard) b/c only 55% of hypoamylasuria have biopsy evidence of rejection
-diagnosis of rejection after SPK transplantation relies almost entirely on serum creatinine and renal biopsy since
rejection of pancreas graft alone is unusual
Complications:
-urologic complications most common
-hematuria:
-early: usually mild and self-limiting
-late: d/t suture granulosa, urinary tract infection, or ulceration of duodenal segment
-if persists despite appropriate therapy, conversion to enteric drainage indicated
-postoperative urinary leak:
-three sites: urethral implantation site, duodenocystostomy anastomosis, duodenal segment
-early: usually located in bladder-duodenum suture line
-late (> 4 weeks): lateral duodenal staple lines or as the result of an ulcer /win duodenal segment
-significantly elevated serum amylase and development of pancreatic ascites discernible on CT
scan are highly suggestive
-diagnosis /w voiding cystourethrogram (VCUG)
-tx: Foley catheter bladder decompression for 2-3 weeks
-may require re-exploration and conversion to enteric drainage
-urinary tract infections:
-d/t alkalinization of urine secondary to bicarbonate and exocrine secretions, presence of a
diabetic neurogenic bladder /w incomplete emptying, mucosa injury at the bladder anastomosis,
and prolonged catheter drainage
-persistent urethritis:
-digestive action of pancreatic enzymes on urothelium
-treat /w Foley drainage for several weeks; may require conversion to enteric drainage
144
-early postoperative hyperamylasemia:
-may cause ARDS from preservation-induced pancreatitis
-late graft pancreatitis:
-sudden-onset lower abdo pain; elevation of serum amylase; absence of leak; evidence on
CT scan of gland edema and retroperitoneal inflammation and peripancreatic
inflammation, /wout evidence of abscess or fluid collections; resolution of symptoms
/win 24h of Foley catheter drainage
-metabolic acidosis:
-result of excessive urinary loss of bicarbonate-containing exocrine fluids
-tx /w oral replacements and fluids
-peripancreatic fluid collections:
-drained if suspicion of infection
-exocrine secretions of the pancreas transplant must be converted from bladder drainage to enteric drainage in 10-
25% of pancreas transplant recipients
-common indications are persistent hematuria and urinary leaks from the duodenal segment
Results:
-two most significant factors affecting graft survival are the circumstances in which the pancreas transplant occurs
and the duct management technique used
-good pancreatic graft survival: > 75% 1-year graft survival
Effect of Pancreas Transplantation on Secondary Complications of Diabetes

-enhanced quality of life, reversal of neuropathies, prevention of diabetic nephropathy, amelioration or stabilization
of diabetic retinopathy
-a functioning pancreas graft prevents the recurrence of diabetic nephropathy in the renal transplant
-subjective improvement of neuropathic symptoms: requires tight control of glycemic index
-transplant of small intestine resulted in unacceptable morbidity and mortality rates

-TPN has been shown to be an excellent treatment modality that has allowed many pts /w intestinal failure to
survive /w reasonable quality of life
Potential Candidates:
-pts /w short-bowel syndrome
-Crohn’s disease, mesenteric thrombosis, trauma (adults)
-Necrotizing enterocolitis, intestinal pseudoobstruction, gastroschisis, volvulus, intestinal atresia (children)
Operative Procedures:
-three methods:
-pts w/o liver failure isolated intestinal grafting
-/w liver failure combined liver intestine transplant
-multivisceral procedure
Donor Issues:
-most clinicians consider an identical ABO blood type mandatory b/c of previously reported hemolytic reactions
-a limiting factor is the required size match between donor and recipient (for children)
Management and Pretreatment:

-mechanical cleansing as well as antibiotic decontamination /w erythromycin and neomycin
-ALG/ATG or OKT3 has been used to pretreat donor in order to prevent graft-versus-host disease; however donor
pretreatment is not used routinely
145
Preservation:
-University of Wisconsin solution used for preservation
-intestines more sensitive to ischemia and reperfusion injury
-good results for up to 16h cold ischemic time
-it is recommended that the intestine be transplanted /win 12h of retrieval
Immunology:
-problems /w graft-versus-host disease (GVHD) and host-versus-graft disease (rejection)
-reducing the number of lymphocytes by using shorter segments, irradiation, or poly/monoclonal Abs affects the
severity of GVHD and possibly reduces its incidence
-cyclosporine or tacrolimus has been used
-prednisone and azathioprine insufficient; tacrolimus significantly improved the out come after intestinal
transplantation
Diagnosis of rejection:
-symptoms: fever, abdo pain, elevated WBC, ileus, increased stomal output, gastrointestinal bleeding, positive
blood cultures
-intestinal biopsies: cryptitis, shortening of villi, mononuclear infiltrate, mucosal sloughing
-immunopathology: increased class II or IL-2 receptor expression
-Loss of mucosal integrity: measures of intestine permeability: 99mTc-DTPA po and urinary excretion measured
value greater than 5% indicates increased permability and possibly an acute rejection
Results:
-1-year graft survival: 65%
-3-year graft survival: 29%
Indications:
-indicated for treatment of irreversible liver failure from acute or fulminant disease or chronic liver disease
-fulminant disease: cause usually unknown, but may be secondary to viral hepatitis, Wilson’s disease, hepatotoxins,
or alcoholic hepatitis
-posthepatitic cirrhosis resulting from hepatitis B or C is associated /w the risk of recurrence of viral hepatitis and
cirrhosis in the transplanted liver.
-strategies to prevent recurrence of hep B: hep B hyperimmune globulin, interferon, lamivudine
-tranplant for PBC associated /w high success rate; primary dz may recur and is difficult to distinguish from chronic
rejection
-PSC should be treated before cholangiocarincoma develops
-alcoholic liver disease account for 75% of liver failure; a period of abstinence and evidence of family and social
support are required before the candidate can be eligible for transplantation
-tranplantation for cancer is controversial; immunosuppression usually favors the reemergence of underlying
malignancies
Preoperative Evaluation:
-signs and symptoms of liver failure
-pts /w stage IV coma must be managed aggressively to prevent cerebral edema or hemorrhage
-increased INR and thrombocytopenia: bleeding should be treated /w FFP and platelets
-GIB related to underlying portal hypertension constitutes an indication for liver transplantation
-ascites: diuretics and paracentesis
-hepatorenal failure, is reversible after liver transplantation; search for any underlying cause of renal dysfunction
-pts /w liver failure are immunocompromised; SBP can be treated /w antibiotics
-patient /w advanced cirrhosis often have a substantial loss of their non-parenchymal liver mass and
reticuloendothelial system, rendering them highly susceptible to sepsis, particularly by translocation across
146
the gut
-hyperdynamic state: elevated CO and low systemic vascular resistance; pulmonary hypertension may develop
risk for cardiac-related intraoperative death
Contraindications:
-multisystem organ failure
-sepsis outside the liver, although pts /w a septic focus /win the liver may appropriately be treated /w liver
transplantation
-noncompliance /w medical therapy (eg. Active alcohol or drug abuse)
-severe cardiac or pulmonary disease
-disseminated cancer
Immunologic Considerations:
-graft failure more frequently due to primary nonfunction, recurrence of original disease, or biliary and vascular
complications; usually not d/t immunologic rejection
-rejection episodes common during first 3 months posttransplant
-ABO blood groups compatibility is required, but this is not absolute; ABO-incompatible liver transplants have been
performed successfully
-ABO compatible but non-identical liver (eg. blood type O donor to type A recipient) may be associated /w a self-
limited graft-versus-host reaction, leading to haemolysis of recipient RBCs
-HLA matching is not a consideration in liver transplantation b/c the shorter preservation times required make it a
practical impossibility
Donor Procedure, Procurement, and Preservation:

-all hepatic arteries must be preserved and reconstructed as necessary in order to avoid infarction of the transplanted
liver
-preferred technique is aortic and portal vein flushing /w University of Wisconsin (UW) solution prior to
hepatectomy, followed by ex vivo portal vein, celiac axis, and superior mesenteric artery flushing and cold storage
on ice
-liver then biopsied:
-presence of more than 40% macrovesicular fat replacing hepatic parenchyma, severe microvesicular fat, or
severe hydropic change predictive of primary non-function
-increased incidence of biliary strictures and primary nonfunction can occur /w long preservation times
Recipient Operative Procedure:

-begins /w native hepatectomy followed by implantation of donor liver
-requires occlusion of IVC and portal vein simultaneously during anhepatic phase may lead to hemodynamic
instability
-venovenous bypass was developed to limit this instability
-“piggyback” technique: venovenous bypass rarely needed
-a donor liver procured from an adult may be reduced in size as necessary for transplantation to a pediatric recipient
-split-liver techniques can be used to supply one liver to two pts
-heterotopic and auxiliary liver transplantation have been used; advantage is that, should the native liver recover, the
pt can be weaned from immunosuppressive drugs, allowing the transplanted liver to atrophy or be removed
surgically
-avoidance of vasoconstrictive inotropic agents, such as epinephrine, norepinephrine, phenylephrine, or high-dose
dopamine will reduce blood flow to the liver
-prostaglandin E1 infusions may be useful for increasing renal and hepatic perfusion in the immediate postoperative
period
-diuretics in the first 24-48 h to help mobilize fluids sequestered as a result of cirrhosis
-maintenance immunosuppression: cyclosporine or tacrolimus
147
-tapering steroids also used
-induction /w ALG or OKT3 is optional; may be useful in pts recovering form hepatorenal failure allows a delay
in starting nephrotoxic agents such as cyclosporine or tacrolimus
-elevations in LFTs prompt percutaneous liver biopsy
-rejection typically responds to bolus steroid therapy; steroid-resistant rejection treated /w ALG or OKT3
Complications:
-primary nonfunction: high INR, low fibrinogen level, high ammonia level in first several days posttransplant
-pts develop hepatic encephalopathy progressing to coma
-urgent transplant required
-portal vein thrombosis:
-rare complication
-marked rise in serum ammonia level or variceal bleeding
-diagnosed by Doppler ultrasonography
-required thrombectomy, restoration of portal flow, and evaluation of the cause of thrombosis
-hepatic artery thrombosis:
-5% in adults; higher incidence in pediatric liver transplantation
-early: d/t technical problems; late: immunologic injury of hepatic arterial tree
-results in ischemic changes of bile ducts leading to plugging and obstruction biloba formation liver
abscess and sepsis
-mx: retransplant or observation
-bilomas can be drained percutaneously, and strictures of the common bile duct can be treated /w
resection and Roux-en-Y drainage
-bile leaks:
-must be treated immediately may lead to peritonitis, sepsis and graft loss
-tx /w operative intervention or by ERCP /w papillotomy and temporary stenting of the CBD
-recurrence of original disease: PBC, Hep B and C
-hepatoma or cholangiocarcinoma recurring in a transplanted liver contraindicates retransplantation
-posttransplant lymphoproliferative disorder (PTLD)
Results:
-certain indications, such as PBC in adults and biliary atresia in children, are associated /w higher-than-average
success rates
Preoperative Considerations for Cardiac Transplantation:
Recipient Selection:
-long waiting lists; ~15-20% mortality rate among pt on the waiting list
Indications:
148
General Indications Warranting Consideration for Adult Cardiac
Transplantation
Severe cardiac disability despite maximal medical therapy
-History of recurrent hospitalization for CHF
-New York Heart Association functional class III or IV
-Peak metabolic oxygen consumption <15 mL/kg/min
Symptomatic cardiac ischemic refractory to conventional treatment
-Unstable angina not amenable to coronary artery bypass grafting or PTCA /w left
ventricular ejection fraction < 30%
-Recurrent symptomatic ventricular arrhythmias
Exclusion of all surgical alternatives to cardiac transplantation
-Revascularization for significant reversible ischemic
-Valve replacement for critical aortic valve disease
-Valve replacement or repair for severe mitral regurgitation
-most cardiac transplant recipients suffer from end-stage, inoperable coronary artery disease (38%) or
idiopathic cardiomyopathy (40%)
-other diagnoses: defined cardiomyopathy (eg. viral, postpartum, familial), congenital anomalies, and
valvular disease
-peak oxygen consumption, a function of peak cardiac output and peripheral oxygen extraction, correlates
well /w functional class and is an independent predictor of outcome in heart failure pts
-if < 15 mL/kg/min (< 50% normal), then 1 -year mortality rate exceeds 50%; these pts would
benefit from transplantation
Contraindications:
-advanced age, irreversible hepatic, renal, or pulmonary dysfunction, active or extrapulmonary infection,
severe peripheral or cerebral vascular disease, unresolved malignancy, severe, pulmonary hypertension,
psychiatric illness or history of medial noncompliance, drug or alcohol abuse, current tobacco use, and
cachexia or morbid obesity
-studies demonstrated that older pts (>60years):
- more likely to die of late infectious complications or malignant disease after transplantation
-higher risk for developing steroid-induced diabetes and clinically significant osteoporosis
-severe COPD: FEV1 < 1L or 50% or predicted
-chronic infective agents (eg. hep Ba nd C, HIV) preclude transplant
-previous malignancies < 5 years of cure (except SCC of skin)
-severe fixed pulmonary hypertension: increased incidence of posttransplant RV failure
-higher mortality rates /w transpulmonary pressure gradient > 15 mmHg
-these pts should be considered for combined heart-lung transplantation
Evaluation and Management of Pts Awaiting Cardiac Transplantation:
Candidate Evaluation and Listing:

-Status I:
-require an ICU setting receiving parenteral inotropic drugs or mechanical device support
-less than 6 months old
-Status II: all other waiting pts
-selected tests are performed, particularly peak oxygen consumption and hemodynamic measurements
(repeated every 6 months)
Medical Management:
-goal: relieve debilitating symptoms; preserve organ function and optimize pt’s condition for
transplantation
-usually treated /w digoxin, diuretics, vasodilators, and ACEi +/- anticoagulants
-amiodarone has improved survival in pts /w end-stage heart failure /wout increasing perioperative risk
149
Mechanical Support:
-intraaortic balloon pump (IABP)
-improves coronary perfusion and reduces afterload and mitral regurgitation
-cannot be used for extended periods of time
-ventricular assist system (VAS)
-intermediate ro long-term circulatory support for pts in severe ventricular failure
-considered when:
- CI < 2.0 L/min/m2 BSA
-ventricular filling pressure > 20 mmHg
-u/o < 20 cc/h
-systemic vascular resistance is > 2100 dynes sec/cm-5
-reduced mortality rates in those awaiting cardiac transplantation
Donor Selection and Management:
Criteria:
-irreversible brain death
-tests: ECG, ABG, echo, serologic screening (eg. HIV, hepatitis, HBsAg, hep C Ab, HSV, CMV,
toxoplasma), pancultures
-normal cardiac function and absence of significant cardiac history and significant coronary atherosclerosis
-absolute contraindications:
-severe coronary or structural disease, prolonged cardiac arrest, prior MI, CO-Hb > 20%, SaO2 <
80%, metastatic malignancy, HIV+
Management:
-maintenance of hemodynamic stability
-IV fluids to maintain CVP b/n 5-12 mmHg
-DI is common and requires IV vasopressin (0.8-1.0 U/h)
-dopamine, alpha agonists may be used judiciously
-blood tranfusion sparingly to maintain Hb ~ 10g/dl
-avoid hypothermia
Donor-Recipient Matching:
-parameters include ABO compatibility and body size
-ABO mismatch hyperacute rejection
-size matching and graft ischemic time particularly important for recipients /w elevated pulmonary vascular
resistance
-grafts from donors whose weight is < 80% of that of recipient or /w ischemic times longer than 2 h are avoided
-no upper donor size limit in adults
-recipient is screened for preformed Abs against a standardized panel of random donors
Operative Procedures:
Procurement:
-median sternotomy pericardial well created
-heart inspected and palpated for contusions, perforations, thrills, and CAD
-intravenous heparin administered at a dose of 300 u/kg and allowed to circulate for 3-5 min
-ligation and division of vessels
-hyperkalemic cardioplegic solution at 2-4oC rapidly infused into aortic root @ 150 mmHg arrest in
diastole
-cold saline at 4oC poured onto heart and into pericardial well
-remainder of pulmonary vessels divided
-heart removed and placed in cold saline medium
150
Orthotopic Transplantation:
-pt prep: CV access via (L) IJ vein; sparing right for future endomyocardial biopsies
-median sternotomy; routine cannulation of aorta and vena cavae
-see Fig 10-23
Heterotopic Transplantation:
-operative technique bypasses the left heart and involves anastomoses between the left atria, aorta,
pulmonary arteries, and donor superior vena cava to recipient right atrium
-indications:
-irreversible severe pulmonary hypertension
-diminished donor heart function anticipated b/c of size mismatch or prolonged ischemic time
Early Postoperative Period:

-monitor cardiac rhythm and arterial and central venous pressures
-primary objective is to maintain adequate perfusion while minimizing cardiac work
-10-20% have some degree of transient sinus node dysfunction (usually sinus bradycardia)
-usually resolves /win a week
-persistent dysfunction in <5% permanent pacemaker
-heart rate maintained b/n 90-110 bpm (temporary pacing or isoproterenol)
-sBP maintained b/n 90-110 mmHg (using nitroglycerin or nitroprusside if necessary)
-renal dose dopamine (3-5 ug/kg/min) used to augment renal blood flow and u/o
-cardiac function normalizes /win 3-4 days wean parenteral inotropes and vasodilators
-optimize pulmonary function:
-FIO2 100%, tidal volume of 10-15 ml/kg, rate of 10-14 bpm, PEEP of 3-5 cmH2O
-adjust settings q30min to achieve PaO2 > 75% mmHg /w FIO2 40%, PaCO2 30-40 mmHg, pH
7.35-7.45
-weaning when pt deemed stable, awake and alert
-expedient removal of vascular lines to reduce incidence of line-related infections
-pacing wires removed after 7-10d if pacing not required
-in cardiac surgery ward: immunosuppressant dosage adjustment, initial endomyocardial biopsy, and early
rehabilitation
-second endomyocardial biopsy and baseline coronary arteriogram ~ 2weeks post-op
Graft Physiology:
-de-nervated heart (from sympathetic and parasympathetic plexus) is isolated from normal autonomic
regulatory mechanisms
-resting HR higher b/c of absence of vagal tone, sinus arrhythmia and carotid reflex bradycardia
-increased sensitivity to catecholamines increased B-adrenergic receptor density and loss of
norepinephrine uptake in postganglionic sympathetic neurons
-cardiac output at low end of normal range
-delayed increase in heart rate
Immunosuppression:
-“triple drug” combination: cyclosporine, azathioprine, glucocorticoid
-high dose, then taper
-cyclosporine:
-inhibits T lymphocyte activation (blocking release of IL-2 from helper T cells)
-trough serum concentration of 150-250 ng/ml x first few weeks 50-150 ng/ml
-side effects: nephrotoxicity, hypertension, hepatotoxicity, hirsutism, increased incidence of
lymphoma
-azathioprine:
-cytotoxic agent and bone marrow suppressant
151
-dosed to maintain WBC < 5000 mm3
-side effects: generalized bone marrow depression (leukopenia, anemia, thrombocytopenia)
-glucocorticoid:
-potent immunosuppressive effects by inhibiting leukocyte elaboration of inflammatory mediators
-methylprednisone bolus 500 mg IV then 125 mg IV q8h x 24h
-then 1.0 mg/kg/day during first week 0.2 mg/kg/day if no acute rejection
-side effects: cushingoid features, hypertension, diabetes, osteoporosis, peptic ulcer disease
-addition of OKT3 to triple-drug regimen over first 10 post-op days has delayed time to first rejection and
has reduced early rejection rates, but has not resulted in significant differences in overall recipient survival
-side effects: hypotension, bronchospasm, fever
-premeditate /w acetaminophen, antihistamines, corticosteroids
-most side effects are manageable or reversible /w dose reduction
Postoperative Complications:
Acute Rejection:
-major cause of death after cardiac transplantation
-highest incidence during first 3 months
-using OKT3 /w triple therapy reduces rejection from 84% to 75%
-after 3 months: incidence ~ 1 episode per pt a year
-endomyocardial biopsy is gold standard for diagnosis
-acute rejection characterized by:
-lymphocytic infiltration and myocytic necrosis
-treatment:
-severe or moderate in early posttransplant period: pulsed steroid dosing
-methylprednisone IV @ 1000 mg/d x 3d
-subsequent severe or moderate rejection episodes on routine surveillance:
-steroid pulsing or by po prednisone to 100-200 mg/day x 3d taper over 2 weeks
-mild rejection not treated unless persistent
-refractory rejection to steroids:
-ATG or OKT3
-MTX and total lymphoid irradiation
-repeat biopsy q 10-14 days after antirejection therapy
Chronic Rejection:
-accelerated atherosclerosis major limiting factor
-may lead to arrhythmias, MI, sudden death, or impaired LV function and CHF
-angina not experienced b/c graft is de-enervated
-risk factors for developing CAD:
-older donor age
-older recipient age
-incompatibility at HLA-A1, A2 and DR loci
-hypertriglyceridemia
-frequent acute rejection episodes
-recipient CMV infection
-elevated levels of antiendothelial Abs correlate /w graft CAD
diffuse vascular narrowing; concentric intimal proliferation /w SMC hyperplasia
-coronary angiograms on a yearly basis; intracoronary ultrasonography is a sensitive test for graft
atherosclerosis
-tx: PTCA or CABG for proximal lesions; retransplantation for diffuse disease
Infection:
-leading cause of morbidity and mortality
-risk peaks during first few months after transplantation
152
-early infections (first month after transplantation)
-bacterial (gram negative bacilli)
-pneumonia, mediastinitis, catheter sepsis, urinary tract and skin infections
-late infections:
-opportunistic viral, fungal, and protozoan pathogens
-CMV infection most common viral infection (73-100% transplant pts)
-reactivation ~ 1-4 months after transplant
-donor organ though to be most common vector of primary CMV infections
-leukopenia /w fever, pneumonia, gastroenteritis, hepatitis, and retinitis
-CMV pneumonitis most lethal (13% mortality)
-retinitis most refractory to treatment
-trigger for accelerated graft CAD and inhibitor of cell-mediated immunity
-tx: ganciclovir (DHPG) and hyperimmune globulin
-fungal infection:
-tx: amphotericin B, fluconazole and flucytosine
-infection prophylaxis:
-vaccinations: pneumococcal, hepatitis B and DPT boosters; annual influenza vaccine
-in children, MMR before transplantation
-perioperative antibiotics: cefazolin
-long-term prophylaxis: nystatin for thrush, SMX-TMP for opportunistic bacterial and
Pneumocystis carinii infections, and antiviral agents such as acyclovir or ganciclovir
Neoplasm:
-recipients predisposed to skin cancer, B-cell lmphoproliferative disorders, carcinoma in situ or cervix,
carcinoma of vulva and anus, and Kaposi’s sarcoma
-appear ~ 5 years after transplantation
-lymphomas frequently seen in recipients < 20 ya
-thought to be d/t EBV infection in setting of T-cell suppression
-tx /w reduction in immunosuppression and antiviral agent (acyclovir or ganciclovir)
Retransplantation:
-indications are graft failure from accelerated graft CAD or recurrent acute rejection
) ( ) (
-indications:
-acquired dilated cardiomyopathy
-congenital heart disease
-blood type and donor size are most important considerations in donor-recipient matching
-moderate oversized heart grafts are preferred for recipients /w and elevated pulmonary vascular resistance
-immunosuppression therapy similar to adults; steroids are tapered more quickly to minimize growth retardation
and infectious complications
-acute rejection treated /w pulsed steroids; antilymphocyte preparations, total lymphoid irradiation, and methotrexate
reserved for refractory cases
153
' " ) ' "
Preoperative Considerations:
Recipient Selection Criteria:

-Single-Lung Transplantation:
-pulmonary fibrosis
-emphysema
-bronchopulmonary dysplasia
-primary pulmonary hypertension w/o significant right heart dysfunction
-post-transplant obliterative bronchiolitis
-Bilateral Single-Lung Transplantation: (avoids risk for infection from retained native lung)
-cystic fibrosis/bronchiectasis w/o cardiac decompensation
-emphysema/COPD w/o cardiac decompensation
-Heart-Lung Transplantation:
-severe primary pulmonary hypertension /w RV decompensation and/or cardiomyopathy
-severe Eisenmenger’s syndrome /w RV decompensation or uncorrectable congenital heart disease
(eg. truncus arteriosus, large septal defect)
-intercurrent cardiac and pulmonary disease
-contraindications similar to those in cardiac transplantation

-upper age limit 50-60 years
-systemic disease /w significant renal or hepatic dysfunction, acute illness, unresolved malignancy, or
psychiatric illness
Evaluation and Management of Pts Awaiting Lung or Heart-Lung Transplantation:

-cardiac function:
-ECHO, doppler and saline-contrast flow studies, radionuclide angiography, Holter monitoring,
cardiac catheterization
-treatment of heart failure: dietary restrictions, diuretics, vasodilators
-treatment of pulmonary hypertension: supplemental oxygen therapy to eliminate stimuli for hypoxic
pulmonary vasoconstriction and secondary erythropoiesis
-if severely ill, prostacyclin may reduce PA pressures, but this is only temporary
-interstitial lung disease:
-corticosteroids are used to treat, but interfere /w tracheal healing significant dose reductions
needed in anticipation of heart-lung transplantation (prednisone to less than 0.1 mg/kg/day)
Donor Selection and Management:

-same criteria as for heart transplantation
-donor PaO2 should exceed 100 mmHg on FiO2 30% and 400 mmHg on FiO2 100%
-peak inspiratory pressures should be < 30 cmH2O
-donors should receive broad-spectrum antibiotics for infection prophylaxis before explanation
-severe coronary or structural heart disease
-prolonged cardiac arrest
-prior MI
-CO-Hb > 20%
-SaO2 < 100%
-active malignancy
-significant smoking history (> 5 pack years or 1 ppd over past year)
-HIV
-primary objective is maintenance of hemodynamic stability and pulmonary function
-to maintain adequate perfusion pressures, dopamine is the standard inotropic agent used
-avoid FiO2 levels in excess of 40% may be toxic to enervated lung
154
Donor-Recipient Matching:
-parameters include ABO compatibility and body size
-matching donor and recipient height seems to be the most reproducible method of selecting
appropriate donor lung size
-donor lungs should not be > 4 cm over similar measurements
-panel-reactive Abs (PRA) level greater than 50% prompts prospective specific crossmatch between the
donor and recipient
Operative Techniques:
-see Schwartz pg. 413-415
Management of Recipients:
Early Postoperative Period:

-ischemic and reperfusion injury result in increased vascular permeability and impaired mucociliary
clearance mechanisms
-lower tidal volumes and flow rates may be necessary to limit peak airway pressures to less than 40 cmH2O
-most pts are extubated /win 3 days and weaned from supplemental oxygen by 10 days after
transplantation
-“reimplantation response”: graft edema due to inadequate preservation, reperfusion injury, or early
rejection
-judicious administration of fluids and loop diuretics is required
Immunosuppression:
-protocols similar to those used in cardiac transplantation
-induction therapy /w anti-lymphocytic Ab preparations can be used
Postoperative Complications:
-early morbidity and mortality most commonly caused by infection, graft failure, and heart failure
-mortality after 1 year caused most commonly by obliterative bronchiolitis, infection, and malignancy
-majority of acute rejection occurs in first 3 months
-fever, dyspnea, impaired gas exchange: PaO2, FEV1, interstitial infiltrate on CXR
-dx /w bronchoscopy /w transbronchial parenchyma lung biopsy and BAL
-lymphocytic perivascular infiltrates
-tx /w IV steroid boluses; persistent rejection treated /w ATG or OKT3
-pulmonary and cardiac rejection present asynchronously in most cases
-transbronchial biopsy: 89% sensitivity in predicting cardiac rejection
-endomyocardial biopsy: 34% sensitivity in predicting lung rejection
-chronic lung rejection:
-obliterative bronchiolitis (OB): dense eosinophilic submucosa scar tissue that partially or totally
obliterates lumina of small airways
-decreases in PaO2 and FEV1
-no effective treatment; augmentation of immunosuppression
-dx in 20-50% of long-term lung transplant survivors
Infection:
-bacterial, viral, fungal infections leading causes of M+M
-bacteria:
-gram-negative: predominate during early post-op period
-lack of cough reflex in denervated lung, abnormal mucociliary clearance mechanisms, and
deficiencies in lymphatic drainage predispose grafted lungs to infection
-invasive infections caused by organisms cultured form donor
-viruses:
-CMV most common and clinically significant
155
-b/n 2 weeks and 100 days after transplant
-primary infection in previously seronegative recipients more serious than reactivation in
seropositive pts
-dx /w BAL or transbronchial biopsy
-tx /w ganciclovir
-prophylaxis: ganciclovir, acyclovir, and polyvalent immune globulin
-Herpes Simplex pneumonia: tx /w acyclovir
-risk of developing lymphoproliferative disease; in association /w EBV infection
-treat by lowering immunosuppression and administering acyclovir
-fungal infections:
-peak in frequency b/n 10 days and 2 months posttransplant
-Candida albicans and Aspergillus
-tx /w fluconazole, itraconazole or amphotericin B
-prophylaxis: inhaled amphotericin B
-Pneumocystis carinii: prophylaxis /w oral TMP/SMX or inhalational pentamidine
-most common airway complications are partial anastomotic dehiscence and stricture
-dx during bronchoscopic examination
-tx: dehiscence: reoperation or close observation and supportive care
stricture: laser ablation or dilation /w rigid bronchoscopy or balloon and bougie dilators
) ( ' " ) ' "
-indicated for children /w end-stage pulmonary vascular or parenchyma disease:

-pulmonary hypertension and cystic fibrosis
-potential recipients generally have a life expectancy of less than 1 year, have normal hepatic and renal function, are
free of active systemic infection, and are in a stable psychosocial environment
-blood group and lung size are primary criteria for donor-recipient matching
Preoperative Management:
Transplant Recipient Evaluation:

-history, physical
-labs: CBC, lytes, BUN, creatinine, urinalysis, serologic studies for hepatitis B and C, CMV, HIV
-CXR, ECG
-metastatic workup for pt /w remote history of malignancy
Indications and Contraindications:

-Absolute:
-recently treated cancer (other than BCC or SCC of skin)
-HIV
-hepatitis /w evidence of cirrhosis or chronic hepatitis on biopsy
-severe IHD not amenable to CABG or PTCA
-Relative:
-obesity, noncompliance /w medical therapy, hx of tuberculosis, several renal diseases (eg.
oxalosis and sickle cell disease)
Histocompatibility Testing:
-blood group typing and HLA typing
156
-for living donor transplants, exception is ABO subtype A2 less antigenic
-/w plasmapheresis and preoperative preparation, an A2 donor kidney can be transplanted into a
non-A2 recipient
-HLA-typing:
-lymphocytotoxic serologic test
-potential recipient’s cells are tested against a battery of sera (from multiparous women or as
monoclonal Ab preparations)
-all cadaveric and potential living donors are HLA typed as well
-class I antigens HLA-A,B and C and class II antigens HLA-DR, DP, and DQ
-not necessary to type every antigen in a living-related donor situation b/c all HLA
antigens are found together on chromosome 6
-HLA-A,B and DR is sufficient
-siblings: zero-, one- or two-haplotype match
-parents and children: always one haplotype match
-two-haplotype matched living donor kidneys have near 100% graft survival /w extremely low rate
of acute rejection
-if a healthy donor is available that is blood-group-compatible, the pt should be considered even
/w a poor HLA match
-one year survival advantage for six-antigen matches over completely mismatched cadaveric
transplants is ~5%
-serum screening for anti-HLA Abs
-multiparous women who have lost a transplant are at highest risk for sensitization
-test pt’s serum against a panel of lymphocytes selected to represent the known HLA antigens
-an important factor in predicting the likelihood of finding a suitable donor for a given recipient:
-if panel reactive Abs (PRA) > 90% will likely have reactivity against 90% of potential
donors
-final crossmatch
-cells from potential donor and serum from recipient incubated together
-Ab binding detected using a cytotoxic technique or flow cytometry or antihemophilic globulin
(AHG) est
-performed before proceeding /w transplantation
-a positive T-cell crossmatch is considered an absolute contraindication to transplantation
-along /w blood typing, the final crossmatch constitutes the most important histocompatibility test
and is mandatory before all renal transplants
Renal Donor:
Evaluation of the Living Donor:

-advantages of live donation:
-excellent immediate graft function and avoidance of posttransplant dialysis
-better short-term and long-term results
-preemptive transplantation
-avoidance of waiting time for a cadaveric kidney
-reduction of immunosuppressive therapy (in HLA-identical transplants)
-risks to donor:
-1/10,000 risk of death and 10% or less risk of morbidity
-contraindications (inappropriate donors)
-presence of DM, HTN, Ca, significant cardiopulmonary disease, hx of renal dz, > 65 years
-proteinuria > 250 mg/24h, creatinine clearance < 80 ml/min, significant urologic abnormalities
-further donor evaluation:
-CT of collecting systems, ureter and bladder
-if minor urologic abnormalities detected in one kidney chosen for donation
-kidney /w the fewest number of renal arteries usually is chosen; left kidney is preferable b/c of longer
renal vein
157
Evaluation of the Cadaver Donor:
-account for ~ 75% of all kidney transplants
-marginal donors may be used:
-older and may have other dz not affecting kidneys, including low-grade brain tumours
-mild renal dysfunction or acute tubular necrosis
Donor Nephrectomy:
-most common complications after live donation: UTIs, wound infections, and PTX
Organ Preservation:
-hypothermia is the cornerstone of organ preservation
-however, hypothermia induced cell swelling may occur b/c Na-K pump is slowed
-mechanisms of preservation injury:
-loss of energy-generating capabilities resulting from mitochondrial damage b/c of loss of precursors for
ATP regeneration
-oxygen free radicals in reperfusion injury
-activation of catabolic enzymes
-activation of arachidonic acid cascade and production of cytotoxic products such as thromboxane and
leukotrienes
-two basic methods of preservation: cold storage and machine perfusion
-majority of kidney transplant centers still cold-store kidneys
Surgical Procedures:
Preoperative Preparation:
-cardiac stress testing or cardiac catheterization:
-for long-standing diabetes, hx of cardiac dz, age > 50
-bilateral native nephrectomy before transplantation:
-poorly controlled hypertension, chronic pyelonephritis and hydronephrosis
-polycystic kidney disease: if pain, hematuria, and UTI accompany disease
-cystoscopy, cystometrogram or VCUG may be required for those /w urologic history
-pts /w hx of pancreatitis: pancreatic U/S or CT scan and w/u for hyperparathyroidism
-cholecystectomy before transplant in pts /w symptomatic cholelithiasis
-pretransplant sigmoid colectomy: hx of diverticulitis, esp. pts /w PKD (higher incidence of diverticulosis)
-active hepatitis or chronic liver diseases and cirrhosis are not candidates
-but, those /w hepatitis B who are HbeAg negative and /w chronic persistent hepatitis C may be considered
Anesthesia:
-Swan-Ganz catheter and art line for older pts and those /w significant hypertension, diabetes, or previous CABG
-avoid succinylcholine in hyperkalemic pts: may exacerbate hyperkalemia and result in cardiac arrest
-renal-dose dopamine may be used to enhance renal transplant perfusion
-pts usually are given methylprednisolone, mannitol, and furosemide before removal of vascular clamps and
reperfusion of the kidney
Postoperative Care:
Immediate Care:
-u/o (from obligatory diuresis) usually is replaced /w half-normal saline solution /w 5% dextrose /wout potassium
-replace u/o plus 30 ml/h (insensible losses) not exceeding 200 ml/h
-early delayed graft function occurs in approximately 25% of cadaveric transplants
-fluid replacement linked to u/o will help to prevent fluid overload and the need for urgent hemodialysis
-anuria/oliguria in live donor kidney should alert to serious problem b/c these are expected to function immediately
-assess for any blood clots in Foley – irrigate or replace FC
158
-assess volume status; if CVP < 12 mmHg – give fluid bolus (500 cc) until CVP rises
-trial of furosemide (up to 200 mg) if no response from fluid boluses
-if no change in u/o despite above, then doppler U/S of kidney to assess blood flow
-if blood flow ok, then obstruction or urine leak (usually at UV junction) assessed /w U/S or
nuclear scintigraphy
-delayed graft function if above evaluation unremarkable: managed /w hemodialysis
Technical Complications:
-early: graft thrombosis, urine leaks, bleeding, wound infections
-late: lymphoceles, ureteral strictures, renal artery stenosis
-graft thrombosis:
-arterial or venous thrombosis
-technical in origin
-abrupt cessation of u/o
-dx on U/S
-early post-op bleeding:
-dysfunctional platelets in uremic pts
-DDAVP at time of operation to help /w platelet function if operative field not dry
-urine leaks:
-at UV junction most commonly
-usually technical failure, but also occur b/c of distal ureteral slough from inadequate blood supply
-dx: decreasing u/o, lower abdo pain, scrotal or labial edema, and rising serum creatinine
-U/S: fluid collection; renal scan: extravasation of radioisotope beyond collecting system
-tx: early exploration and repair
-UV leaks: reimplantation
-bladder leaks: primary closure
-lymphoceles:
-perinephric collections of fluid in ~5% transplants
-result of excessive iliac dissection and failure to ligate lymphatics overlying iliac artery
-may present as swelling over transplant, unilateral leg edema from iliac vein compression, increased
creatinine level from ureteral compression
-dx: aspiration: high protein content and creatinine concentration equal to serum
-drainage if symptomatic (ie. Causing compression)
-options: sclerosis /w tetracycline or peritoneal window for intraabdominal drainage
-renal artery stenosis:
-in 10%; usually in first 6 months
-primarily presents /w HTN
-may also have fluid retention, bruit over transplanted kidney
-worsening renal function when ACEi are used to treat HTN
-dx: angiogram; U/S and MRI angio may be used as screening tools
-may occur distal to anastomosis from rejection, atherosclerosis, and clamp or perfusion cannula injury
-more common if end-to-end anastomosis used vs end-to-side
-tx: >80% can be corrected /w balloon angioplasty at time of angiography; else repaired surgically
-ureteral obstruction:
-rising Cr /w hydronephrosis
-d/t lymphocele or stricture in distal ureter
-strictures d/t ischemia and sometimes rejection;
-dx: antegrade pyelogram
Immunosuppression:
-antithymocyte globulin (ATG), OKT3, cyclosporine, tacrolimus, azathioprine, mycophenolate mofetil, prednisone
-numerous protocols for cadaveric transplants
-triple therapy:
159
-azathioprine (or MMF), cyclosporine and prednisone
-cyclosprine 5-8 mg/kg po bid
-MMF 1000 or 1500 mg po bid (watch for GI sxs and leukopenia)
-prednisone 500-1000 mg IV then rapid taper to 5-10 mg od after 3-6 months
-steroids usually for life
-quadruple therapy:
-addition of ATG or OKT3
-to avoid nephrotoxic effects of cyclosporine and tacrolimus
-cyclosporine or tacrolimus not given until Cr level < 3.0 mg/dL; overlapped /w ATG or OKT3 until target
cyclosporine levels achieved
-two-haplotype living-related protocols:
-cyclosporine-based protocol /w azathioprine or MMF; steroid /wdrawal
-one-haplotype and living-unrelated protocols similar to cadaveric protocols
Treatment of Rejection:
-rejection occurs in 40-50%
-first line: high-dose steroids (usually methylprednisolone 500-1000 mg for 3-5 days)
-second line: OKT3 effective in reversing 90%
-polyclonal preparations such as ATG used in those /w Abs to OKT3 or serious side effects from OKT3-
induced cytokine release
-OKT3 as first line if biopsy-proven vascular rejection
-if rejection, then switch pt to MMF
-if refractory to steroids and OKT3, then treat /w tacrolimus (reversal in 75% of pts on tacrolimus)
Long-term Complications:
-most common causes of death: cardiovascular disease, infectious disease, malignancy
-noncompliance responsible for 10-15% of late graft losses
-recurrence of disease
-cardiovascular dz more common in pts /w DM, HTN, elevated serum cholesterol and triglyceride levels, and
smokers
-risk of IHD 3-4x greater in posttransplant pts than general population
-prevention is key:
-reduce hyperlipidemia /w diet and weight loss +/- statins
-minimized use of steroids, treatment of HTN, exercise
-hepatic dysfunction:
-common after transplantation; may be secondary to hep B, C, or drug toxicity (azathioprine, cyclosporine)
-hep B: progression to cirrhosis accelerated /w immunosuppression: may enhance viral replication
-hep C: more common than hep B; causes chronic liver disease in majority of pts
-hepatotoxicity from azathioprine/cyclosporine uncommon
-azathioprine: cholestatic pattern (d/c drug)
-cyclosporine: increased bilirubin and transaminase levels (usually responds to decreasing dose)
-may also be caused by pancreatitis, cholelithiasis and choledocholithiasis
-bone and mineral metabolism:
-hypophosphatemia and hypercalcemia (may be from persistent hyperparathyroidism)
-subtotal parathyroidectomy if: severe mental status changes, renal stones, fractures, pancreatitis, serum
calcium > 12.5 mg/dl after 1 year
-severe osteopenia or osteonecrosis
-minimize steroid dosage and correct hyperparathyroidism
-estrogen and calcium supplements in post-menopausal women
-may require etidronate and nasal calcitonin
-hyperglycemia:
-secondary to steroids: increase glucose production, impair peripheral use, and increase glucagon levels
-cyclosporine and tacrolimus decrease beta cell excretion and cause peripheral insulin resistance
-malignancies:
160
-lymphomas (1-2%)
-carcinoma of colon, rectum, prostate, breast and lung NOT increased
-skin cancer (esp. SCC) up to 20x higher
-higher incidence of Kaposi’s sarcoma and genital neoplasm (eg. Vulvar, vaginal, and cervical carcinomas)
-Posttransplant lymphoproliferative disease (PTLD):
-driven by EBV
-polymorphic B-cell hyperplasia nuclear atypia malignant monoclonal B-cell lymphoma
-occurs more frequently in those who have received antilymphocyte preparations (eg. ALG, ATG, and
OKT3)
-tx by lowering or stopping immunosuppression
-may respond to antiviral treatment /w acyclovir or ganciclovir
Special Problems:
Diabetes:
-diabetics at higher risk for HD and PVD
-all should have noninvasive cardiac evaluation for ischemia
-transplantation contraindicated if diffuse coronary disease (not amenable to surgery) /w LV dysfunction
-diabetic candidates for renal transplantation should be evaluated for combined kidney-pancreas transplantation
-juvenile diabetics /w transplants have 5 year survival rates ~80% (vs ~30% in non-transplanted pts on dialysis)
Pediatric Pts:
-pediatric pts /w functioning kidneys grow more normally, have significant catch-up growth, and potentially can
have more normal lifestyles
-work-up similar to adults, but less need for evaluation for comorbid conditions
-look for urologic as well as neurologic (eg. spina bifida) abnormalities
-recommended that pts < 1 year be allowed to grow before consideration for transplant
-pediatric pts have poorer overall graft survival than adult pts, particularly in cadaveric tx
-outcome better /w living-donor transplants
-high risk of non-compliance
Retransplant Pts:
-retransplant recipients have poor overall graft survival compared to first transplant recipients
-factors which increase graft loss in retransplant:
-extremely short survival of first transplant d/t acute rejection in < 6 months
-high PRA levels: generalized sensitization from a previous failed graft
-best outcomes have been demonstrated /w induction therapy, and the use of OKT3 or ATGAM can be
recommended for these pts
-acceptable preservation times vary with organ

-heart: within 5h
-kidney: 40-50h
-pancreas: 10-20h
-liver: within 6-12h
-injury to organ could occur because of cardiovascular instability and hypotension
-goal is to reduce warm ischemic time, cool organ rapidly via flushout of vascular system
-hypothermia (4oC) and composition of preservation solution are key factors in successful preservation
-flushout should remove blood as completely as possible at an acceptable pressure (60-100 cmH2O)
-warm ischemic depletes ATP and redistributes electrolytes across cell membrane
-degradative reactions continue (accumulation of lactic acid, pH, proteolysis, and lipolysis) causes
structural alterations in membranes that may be irreversible
161
-ideal preservation solution:
-presence of impermeant molecules that suppress hypothermically induced cell swelling
-ion pumps slow down, loss of electrical potential across membranes, and entry of Cl down its
chemical gradient leads to accumulation of water in cell swelling organ damage
-appropriate biochemical environment
-University of Wisconsin (UW) solution:
-lactobionic acid as primary impermeant:
-large MM (358 kD)
-negatively charged
-also contains raffinose, hydroxyethyl starch, adenosine (stimulates ATP synthesis during reperfusion of
the organ)
-machine perfusion for kidneys decreases delayed graft function (<10% vs 25-30% seen in simple cold storage)
-gluconate is used in place of lactobionic acid
162
! "
-sum total of abnormalities of all organ systems and their interactions that determine the outcome of an operation
#$ % &
-estimation using Goldman’s cardiac risk index
-risk of surgical cardiac death:
-no previous MI: 1.0-1.2%
-MI > 6 months: 6.0%
-MI (transmural) < 3 months: 16-37%
-predisposing factors for perioperative cardiac death:

1. infarction within 6 months
2. congestive heart failure
3. arrhythmias
4. aortic stenosis
5. emergency or major surgery
6. age greater than 70 years
7. poor medical condition
-ECG and hematocrit level are significant

-stress test indicated to identify patients at risk
-positive if any or all of the following:
-ST depression > 0.2 mV, inadequate heart rate response to stress, or hypotension
-delay surgery (if possible) to > 6 months after MI

-angioplasty or CABG may be necessary before any major surgical procedure
-treat CHF and a-fib
#'$ ( &
-risk factors:
1. smoking
2. obesity
3. advanced age
4. industrial exposure
5. PCO2 > 45 mmHg diffusion defect
6. abnormal PFTs:
-FVC < 70% predicted
-FEV1 < 2.0L or < 70% predicted
-PEFR < 200 L/min
-FEV1/FVC < 65%
7. PAP > 30 mmHg
-exercise oxygen consumption (prior to thoracotomy) (VO2) > 20 ml/kg/min less likely to have post-op pulmonary
complications
-8 weeks smoking cessation prior to surgery beneficial
#)$ * &
-serum abnormalities of BUN and Cr are not manifest until > 75-90% of renal reserve lost
-creatinine clearance (ml/min) = [1.23 x weight (140-age)]/creatinine in umol/L
163
-correct reversible causes: infection, uncontrolled hypertension, obstruction, and dehydration
-peritoneal, hemodialysis, or continuous ultrafiltration occasionally required
#+$ * &
-patients with cirrhosis
-Child-Pugh criteria: based on presence of ascites, bilirubin, encephalopathy, nutritional status, albumin
-class A < 5%; B 5-10%; C 20-50% mortality following non-cardiac surgery
-generally die of high-output CV failure and low peripheral resistance
-see Table 11-4
-measures that can be taken:
-abstinence from alcohol important prior to elective procedures
-improve protein tolerance by use of branched-chain amino acid
-control ascites:
-spironolactone and lasix combined with fluid restriction to 1500 ml/day
-limit sodium to 2g/day
#,$ * & see Chap. 3
#-$ . */*
-difficult to assess
-severely malnourished patient:
-weight loss > 15% over previous 3-4 months
-serum albumin < 3.0 g/dL
-energy to injected skin-test antigens
-serum transferring level < 200 mg/dL
-if severely malnourished, then enteral or parenteral (only if severe) nutrition for 4-5 days preop
-normalize retinol binding protein, thyroxin-binding prealbumin, and transferring
#0$ ! &# 1 2 * 2 $
-no definite guidelines
-see appendix
. 3 4
Pathophysiology:
-lack of metabolically effective circulating insulin
-deficient utilization of glucose by peripheral tissues
-increased output of glucose by liver
-increased fatty acids ketones urine
-glycosuria osmotic diuresis loss of sodium and potassium
-anaesthetic agents can cause an exaggerated hyperglycemic epinephrine response and an increased
resistance to exogenously administered insulin
-stress of operation aggravates hyperglycemia
-epinephrine: glycogenolysis
-glucocorticoid: mobilized protein, anti-insulin effect
-growth hormone
Management:
-DM pts should have preference on operative schedule to minimize effects of fasting and ketosis
-mild DM frequently do not require insulin; dietary control sufficient
-pts using OHA should continue their use until day before operation
164
Insulin Therapy:
-see appendix for protocols
Ketoacidosis:
-IV hydration, insulin therapy, and electrolyte replacement (potassium)
-need for potassium usually does not exceed 80 mEq
Nonketotic Hyperglycemic Hyperosmolar Coma:

-relatively uncommon
-usually occurs in elderly diabetic or nondiabetic obese patients and those receiving TPN
-treat with large amounts of hypotonic solutions and intravenous insulin (est dose of 10 U)
Pathophysiology:
-disorder of normal body thermoregulation
-controlled by anterior hypothalamus
-?protective mechanism to combat infection
-all pyrogens evoke common mediator IL-1 (endogenous pyrogen)
-alters activity of temperature-sensitive neurons raises set-point increased body temperature
-vasoconstriction chills, shivering
Perioperative Fever:
-fever in the immediate postoperative period usually is not serious, is not very high, and is self-limited
-usually ascribed to atelectasis
Malignant Hyperthermia:
-incidence ~ 1/100000 general anaesthetic procedures
-succinylcholine, halothanes metabolic acidosis and electrolyte imbalances
-hypercalcemia, hypotonicity, hyperthermia (~40OC), oxygen denaturation, hypercapnia, cardiac
dysrhythmia
-treat with dantrolene IV 1 mg/kg, repeat to total dose of 10 mg/kg prn
-supportive measures; ventilation/oxygenation, treatment of possible myoglobinuria
Fever within 24 Hours:

-usually due to atelectasis or failure to clear pulmonary secretions
-unnecessary to do extensive tests at this point
-if high fevers with rigours, hypotension, and changes in mentation: consider severe wound complications
such as necrotizing fasciitis or intestinal leak
Fever at 24-48 Hours:

-usually respiratory complications
-catheter related problems - UTI
-inspect wound for cellulitis, necrotizing fasciitis, or clostridia myositis
Fever after 48-72 Hours:

-thrombophlebitis
-most common cause of fever after 72h is wound infection
-also suspect UTI
-less common infections: pneumonitis, acute cholecystitis, idiopathic postoperative pancreatitis
-drug allergy
-candidiasis may complicate IV TPN tx with amphotericin B
-fever after 1 week leaking anastomosis, abscess, deep wound infection
165
5 . 4
5 % /*
-staphylococcus aureus most frequently involved offending organism
-enteric organisms in bowel surgery; other less common pathogens: enterococci, Psedomonas, Proteus,
Klebsiella
-hemolytic strep responsible for 3% of wound infections
Classification of Operative Wounds

Class Wound Description Examples Incidence of
Infection
I Clean Nontraumatic, uninfected operative wounds 1.5-3.9%

in which the respiratory, alimentary, or
genitourinary tract is not entered. Usually
closed without drains
II Clean-contaminated Respiratory, alimentary, or genitourinary 3-4%

tract is entered with only minimal
contamination
III Contaminated Fresh traumatic wounds; wounds with a 7.4-8.5%

major break in sterile technique; wounds
encountering non-purulent inflammation;
wounds made in or near contaminated skin
IV Dirty Purulent infection is encountered 28-40%
Factors: -type of operative wound

-age: 15-24 years (4.7%); > 65 years (10%)
-diabetes: not an independent risk factor when adjusted to age
-steroids: increase rates from 7 to 16%
-obesity: doubles rate
-remote infection
-duration of operation: < 30 min (3.6%); > 6 hours (18%)
-malnutrition
-others (see Table 11-9)
Prevention:
-skin preparation: -clipping (2% infection rate) preferred over shaving (5%) of hair
-bowel preparation: -clear liquids, cathartics, antibiotic regimens
-prophylactic antibiotics
-maintenance of temperature: -warming blankets, warm fluids
-meticulous technique: -gentle handling of tissue, hemostasis
-appropriate drainage
-infections usually evident between 5th and 8th POD; may manifest after weeks if pt on antibiotics
-necrotizing fasciitis or clostridia myositis can occur within 24 hours
Management:
-open incision and pack wound with gauze
-cellulitis and edema add antibiotics; Gram stain may help guide treatment
-if hemolytic strep penicillin for 1 week
-clostridia myositis/necrotizing fasciitis surgical debridement
166
-Fournier’s gangrene: necrotizing fasciitis of perineum or groin in diabetic patients
-30-70% mortality rate
5 % *
-inadequate hemostasis
-provide good culture medium for bacteria
-early haematomas return to OR ligate responsible vessel primary closure of wound
-late haematomas manage patient expectantly with hope that haematoma has not become contaminated
5 % *
-lymph collections
-aspiration and pressure dressings
-continuous closed-suction drainage
5 % . *1 * *
-< 45ya: 1.3%; > 45ya: 5.4%
-generally caused by a technical factor
-contributory factors:
-malnutrition, hypoproteinemia, morbid obesity, malignancy with immunologic deficiency, uraemia,
diabetes, coughing with increased abdominal pressure, remote infection
-local factors: hemorrhage, infection, excessive suture material, poor technique
-monofilament sutures have lower incidence of disruption than braided sutures
-vitamin C deficiency: 8x increase in wound dehiscence
-zinc deficiency associated with poor healing
-steroids interfere with wound healing; use vitamin A to counteract these effects
-chemotherapeutic agents inhibit wound healing
-usually wait 1-2 weeks post-op before chemotherapy started
-radiation causes obliteration of small vasculature and fibrosis
-salmon-coloured fluid draining from wound at 4th or 5th POD (85% of the time)
Treatment:
-depends on pt’s condition
-if no evisceration non-operative treatment with sterile occlusive wound dressing and binder
-evisceration moist sterile towels applied and pt returned to OR
-perioperative broad-spectrum antibiotics should be given
4 4
( **
-requires release of alpha-adrenergic receptors in SMC of bladder neck and urethra and parasympathetic stimulation
to contract bladder
-stress, pain, spinal anaesthesia, and various anorectal reflexes conspire to increase alpha-adrenergic stimulation
-if retention urinary catheter used
* * *
Etiology:
-inadequate resuscitation: -sympathetics decreases renal blood flow; RAA system will shunt blood away
from afferent arterioles
167
-drug toxicity: aminoglycosides, vancomycin, amphotericin B, high doses of penicillin G or sulfonamides
-see Table 11-12 for other nephrotoxic drugs
Pathophysiology of Renal Dysfunction:
Prerenal:
-BUN/Cr 20:1
-commonly observed with dehydration
-hepatorenal syndrome:
-two mechanisms: hypovolemia (type I) and maldistribution of blood flow (type II)
-Type I: deficiency in intravascular volume secondary to blockage of liver outflow ascites
-Type II: failing liver, elevated bilirubin, other stigmata of cirrhosis; CO and low PVR
-kidneys are normal; recovery is rare and depends on recovery of intrinsic liver disease
Intrinsic Damage:
-acute tubular necrosis:
-most common cause in surgical setting is renal perfusion d/t prolonged and sustained
hypotension (from sepsis, blood los, hypovolemia, dehydration, or myocardial infarction)
-mechanism:
-kidney tries to maintain glomerular blood flow afferent dilatation and efferent
constriction of arterioles
-perceived hypoperfusion angiotensin by RAA system afferent constriction
- sympathetics norepinephrine afferent constriction
-this results in tubular ischemic and hypoperfusion of renal cortex ATN
-myoglobinuria and transfusion reaction (free Hb) may complicate renal injury
-other causes:
-radiocontrast dyes with dehydration
-atheromatous embolic during aortic vascular surgery
-clamping of renal artery
Postrenal Failure:
-ureteral clots or stones; BPH
Prevention of Acute Renal Failure:

-chronic UTI treat with Abx
-BPH TURP or balloon dilation
-chronic renal impairment ensure adequate hydration
-in low flow states, mannitol, bicarbonate, and diuresis induced by furosemide should be used
-mannitol increases renal corticla blood flow and produces an osmotic diuresis
Manifestations:
-oliguria with u/o of 0.4-0.5 cc/kg/h in adult
-anuria: uncommon; usually from ATN as a result of renal artery thrombosis or obstructive uropathy
-fractional excretion of sodium (FENa) = [UNa / PNa] / [UCr/PCr]
-if > 1% intrinsic renal damage
-UNa < 10 mEq/L prerenal cause or intrinsic liver disease
-intrinsic UNa > 40 mEq/L, FENa > 3%
Management:
-if diagnosis is uncertain:
-volume challenge if suspect hypovolemia
-once adequate volume status established furosemide (20-40 mg) to improve u/o
-stop nephrotoxic drugs
-established renal failure:
168
-treat hyperkalemia: infusion of calcium, hypertonic dextrose solution, and insulin then resins
-maintenance of nutrition in patients with ATN: enterally or parenterally
-IV “Giordano-Giovannetti diet” of essential AA and hypertonic dextrose, with minimum
of fat, decreases mortality in patients with ATN
-dialysis for critical ionic excesses, volume overload, or BUN concentration > 80-100 mg/dl
Pathophysiology:
-VC and FRC may be reduced after upper abdominal surgery (50-60% and 30% respectively)
-postoperative pain alters mechanics of respiration
-closing volume (lung volume at which airway closure is first detectable) decreases in the postoperative
period
-other physiologic causes of insufficiency: diffusion defects, abnormalities in V/Q, reduction in CO with
persistent shunt, alterations in Hb level and persistent shun, and shunting that is anatomic or related to
atelectasis
Smoking: -must abstain at least 8 weeks to achieve any demonstrable benefit

Age: -must look at physiologic age rather than chronological age
Obesity: -related to underlying pulmonary dysfunction characteristic of this patient population
-decreased FRC d/t chest wall compliance
COPD: -ensure adequate pain control
-use gastrostomy tube rather than NG found to statistically decrease incidence of
respiratory complications
Cardiac dz: -beware of pulmonary edema in CHF patiens
**
-collapse of alveoli resulting from anaesthesia, diaphragmatic dysfunction, postoperative incisional pain, and patient
positioning
-prevention is key:
-coughing and deep breathing, chest physiotherapy, incentive spirometry,
-intermittent positive pressure breathing, and CPAP
-medication for prophylaxis:
-expectorants: provide more liquid secretions
-detergents and mucolytic solutions: alter surface tension of secretions and render their elimination more
likely
-bronchodilators: eliminate bronchospasm
*
-third most common nosocomial infection (after wound and UTI)
-pathogens include Psueudomonas, Serratia, Klebsiella, Proteus, Enterobacter, Streptococcus
-use of H2-blockers may breakdown acid barrier, allowing overgrowth and colonization of the stomach by intestinal
flora (gram negatives)
-fever, productive cough, dyspnea, pleuritic chest pain, and purulent sputum
-if hypotensive, consider gram negative pneumonia
169
Management:
-cultures obtained via routine ETT suctioning have little predictive benefit in correctly identifying the
pathogen responsible for noscomial pneumonia
-empiric therapy with aminoglycoside and antipseudomonal penicillin initiated until definitive culture
results obtained (via BAL ideally)
-most likely setting is during emergency induction of anaesthesia, particularly in pts with GERD or hiatal hernia
-presence of gastric contents in mouth followed by wheezing, hypoxia, bronchorrhea, and cyanosis
-CXR: progression of local damage and infiltration accute respiratory failure results
-causes chemical pneumonitis that results in bacterial colonization with subsequent development of
pneumonia
Management:
-prevention: empty stomach and neutralization of gastric contents
-suction then ETT to complete clearance of tracheobronchial tree
( %*
-pulmonary-capillary hydrostatic pressure exceeds plasma oncotic pressure
-most common causes: fluid overload or myocardial insufficiency secondary to MI
-others: sepsis, valvular dysfunction, neurogenic stimulation, and hepatic failure
-increased capillary permeability:
-sepsis, ARDS, acute pancreatitis
-two peak phases:
-during resuscitation if too aggressive with fluid replacement
-post-operative when fluid mobilization occurs
-rales, distended neck veins, cyanosis, peripheral pitting edema
-CXR: vascular redistribution, septal lines (Kerley’s B lines), peribronchial and perivascular cuffing
Management:
-depends on inciting cause
-for overload:
-pulmonary catheter may aid diagnosis and management
-PAWP 18-25 mmHg; CI decreased with increased PVR
-if PAWP normal or low, look for other causes
-?ARDS
-ECG look for evidence of pump failure
-treat with diuretics, IV nitroglycerin ( venous capacitance and preload)
-dobutamine or amrinone may improve cardiac output
-consider afterload reduction with nitroprusside if above maneuvers fail to produce a sufficient CI
2 ( % *
-fat embolism extremely common pathologic finding after trauma
-26% in patients with single fracture to 44% in patients with multiple fractures
-fat embolism syndrome with pulmonary dysfunction, coagulopathy, and neurologic disturbances associated with
increased circulating fat globules is ncommon
170
Pathophysiology:
-long bone fractures with release of marrow fat into circulation
-respiratory insufficiency
-CXR shows characteristic bilateral alveolar infiltrates
-may evolve into ARDS
-CNS involvement in 86% confusion and disorientation with eventual progression to coma
-characteristic petechial rash occurs in axillae, neck , and skin folds
-fat globules in urine not specific for fat embolism syndrome
-associated findings:
-unexplained drop in hct, thrombocytopenia, hypocalcemia, and hypoalbuminemia
Management:
-immobilize any long bone fracture
-early surgical fixation decreases incidence of pulmonary complications of fat embolism
-oxygenation and supportive measures
* * (. * ( % *# . $
-pt incapable of maintaining adequate oxygenation, adequate ventilation, adequate tissue delivery, or some
combination of these defects
-syndrome that includes:
-lung injury, acute in nature
-bilateral infiltrates on frontal chest radiograph
-PaO2/FIO2 < 200
-PCWP < 19 mmHg with no evidence of CHF
-may be due to specific single cause or may represent endpoint of a poorly understood pathway with a common final
denominator of lung damage and subsequent decompensation of oxygenation and ventilation
Etiology and Pathophysiology:

-abnormal cytokine response to injury:
-activation of complement cascade, activtionof thromboxane-leukotrienes pathway, disorders in
NO production, degranulation of neutrophils, production of increased permeability factors by
macrophages
transudation of fluid and reactive materials into alveoli
-causes V/Q mismatch
-CXR shows “whiteout”; CT scan demonstrate regional changes in lung function
-volutrauma: maldistribution of inspired tidal volume secondary to PPV and the heterogeneous nature of
lung injury in ARDS
-overdistention of alveolus beyond its normal maximum
Management:
-reduce volutrauma:
-early use of PEEP adjusted to the inflection point (as seen on pressure-volume curve)
-pressure-limited ventilation with plateau pressures less than 35 cmH2O
-permissive hypercapnia
-use of inhalational NO
-PEEP has remained the mainstay of treatment of ARDS
-recruits collapsed alveolar units
-attenuates lung injury associated with PPV
-may prevent loss of FRC and prevent alveolar collapse at end-expiration
-permissive hypercapnia limits potentially detrimental effects of increased peak airway pressures, the
number of breaths necessary per minute, which reduces the risk of barotrauma and volutrauma
171
-inhalation of NO at mall doses has reduced pulmonary hypertension and improved oxygenation in a
variety of patients
-newer modalities using partial liquid ventilation (PLV) and perfluorocarbon-assisted gas exchange
(PAGE)
. 4
4( % /
-mortality from perioperative MI ranges from 54% to 89%
-presence of coronary artery disease: risk of perioperative MI increased from 0.1-0.7% to 1.1%
-patients over 40: infarction rate is 1.8%
-previous MI: infarction rate 27% (within 3 months); 11% (b/n 3 and 6 months); 5% (> 6 months)
Identification of the Patient at Risk:

-Goldman index
-look for cardiac signs, symptoms and risk factors
-most cases occur on operative day or during first 3 PODs
-most important precipitating factor is shock risk of coronary thrombosis and myocardial ischemic
-chest pain only in 27% of patients b/c may be masked by narcotics
-may manifest as a sudden appearance of shock, dyspnea, cyanosis, tachycardia, arrhythmia, or CHF
-evaluate with ECG, serial cardiac enzymes, ABG (rule out respiratory causes)
Management:
-pre-operative:
-optimize CHF (digitalization for pts with enlarged hearts)
-treat anemia
-optimize fluid and electrolyte balance
-continue beta-blockers until morning of operation
-operation after 6 months of an MI
-intra-operative:
-regulation of BP important
-avoid hypoxia, hypotension, haemorrhage, dehydration, electrolyte disturbance and arrhythmias
-treatment:
-+/- monitoring in ICU
-pain relief: morphine and sedation
-+/- heparin, ASA; nitro and beta-blockers
-hypoxia relief: oxygen
-shock treated by vasopressor agents
-early emergency cardiac catheterization, angioplasty, or stenting may reverse an evolving MI
1( 1
-sinus tachycardia (not an arrhythmia) is the most common disturbance of rhythm, followed by PVC and sinoatrial
arrhythmia
Etiology:
-intrinsic cardiac disease
-perioperative release of catecholamines d/t stress or pain
-organ manipulation that stimulates reflex response
-electrolyte abnormalities and metabolic disturbances:
172
-hypokalemia PACs and PVCs
-hyperkalemia conduction abnormalities
-hypocalcemia QT interval ventricular arhythmias
-hypercalcemia bardycardia and heart block
-cardiac medications:
-digitalis toxicity supraventricular-atrial flutter with varying block, PVCs, VT or VF
-antihypertensive meds sinus bardycardia or induction block
-anaesthetic agents:
-halothanes ventricular dysrhythmias
-parasympathetic stimulation (neostigmine, physostigmine, succinylcholine) bardycardia
-other factors:
-hypercapnia may suppress sinoatrial node function ectopic pacemaker or aberrant reentry
mechanisms
-thyrotoxicosis atrial fibrillation
-pheochromocytoma
Management of Preexisting Arrhythmias:

-digoxin for patients with supraventricular tachycardia
-reversible causes, such as electrolyte disturbances, drug toxicity, hypoxia, etc. should be controlled
-cardiac pacing for significant conduction defects:
-third degree AV block
-Mobitz II block
-sick sinus syndrome
Management of New-onset Arrhythmias:

-ECG:
-P waves present supraventricular origin
-variable morphology ectopic focus, MAT or SVT
-P waves absent A-fib
-QRS narrow supraventricular origin
-QRS wide ventricular origin or supraventricular with aberrant conduction, conduction block
-Acute tachyarrhythmias with hypotension cardioversion (100 360J)
-Symptomatic bradycardia 0.5mg atropine IV q5min to max of 0.04 mg/kg
-consider transcutaneous pacing
Sinus Tachycardia:
-find and treat cause: pain, hypovolemia, hypoxia, acidosis, sepsis, CHF, hypoperfusion, hypercapnia
Paraoxysmal Supraventricular Tachycardia:

-re-entry tachycardia
-rates between 150 and 250 bpm
-primary treatment with
-adenosine 6 mg IV; repeat with 12 mg after 1-2 min
-then verapamil 2-5 mg IV with second dose after 15-30 min
-may consider cardioversion
Atrial Fibrillation:
-lack of “atrial kick” may result in 10-15% decrease in cardiac output
-causes:
-thyrotoxicosis, valvular heart disease, hypertension, CAD, PE, MI
-common after pneumonectomy
-cardioversion if hemodynamically unstable
-anticoagulate if long standing A-fib
-control rate (eg. with CCB, BB) and rhythm
173
Sustained Supraventricular Tachycardias:
-may be a result of digitalis toxicity
-obtain serum potassium and digitalis levels
Atrial Flutter:
-if unstable cardioversion
-digitalis used to maintain heart rate once controlled
Ventricular Tachycardia and Fibrillation:

-if pulseless precordial thump and immediate defibrillation at 200 J
-(review ACLS protocols)
( * *
Preoperative Hypertension:
-preoperative hypertension that is untreated or poorly controlled does increase the risk of perioperative
blood pressure lability, which may result in increased incidence of stroke, TIA, arrhythmias, post-op MI,
and possibly post-op renal failure
-postpone operation until hypertension controlled if:

-previous hypertension with diastolic pressure > 110
-new-onset hypertension
-sudden increases in hypertension
-recent deterioration in critical end-organ status
-delay operation in patients with mild or moderate hypertension with:

-ECG changes of MI or ischemic
-new-onset dysrhythmias
-emergence of LVH on ECG
-new onset or unstable angina
-CHF, whether established or new
-recent neurological deficit
-new onset of high-grade hypertensive retinopathy
-continue antihypertensive medications until day of operation
Postoperative Hypertension:
-systolic pressures > 200 mmHg result in bleeding from suture line, haemorrhagic cerebral infarction,
myocardial ischemic or infarction, and acute renal failure
-~ 80% of post-op HTN episodes occur within first 3 h of emergence form anaesthesia
-d/t ETT, inadequate analgesia, acute bladder distention, fluid overload
-tracheal stimulation, hypothermia, hypercapnia, hypoxemia
-if uncontrollable sodium nitroprusside or labetalol is given
-late post-op:
-d/t hypervolemia 2o fluid mobilization into intravascular space, inadequate analgesia, or failure to
resume previous antihypertensive medications
174
3
6 *% ( * 2* *
Lupus Anticoagulant Factor (Anticardiolipin Syndrome):

-antibodies that interfere with in vitro PTT by prolonging phospholipid-dependent clotting factors
-increased risk of arterial and venous thrombosis
-patients normally do not require anticoagulation therapy
-those undergoing major procedures should receive prophylactic anticoagulation therapy and mechanical
prophylaxis
Heparin-Induced Thrombocytopenia:
-form of consumptive platelet activation
-not dose dependent
-mechanism: autoantibody formation directed toward heparin and platelet surface antigens
-mild: occurs 2-4 days after heparin exposure
-severe: 6-12 days after exposure and associated with thrombosis
-arterial thrombosis common
-significant mortality rate
-phlegmasia cerulea dolens amputation rate up to 30%
-treatment: stop heparin; +/- surgical thrombectomy; Greenfield filter, anticoagulation with warfarin
1* *% 1 2 . %*
Antithrombin-III Deficiency:
-AT-III the most important inhibitor of coagulation
-inactivates thrombin, Xa, IXa, XIa, plasmin, kallikrein, XIIa
-deficiency is autosomal dominant
-recurrent thrombosis in 60%; pulmonary embolus in 40%
-treatment: heparin; if OR FFP to raise level of AT-III
Protein C Deficiency:
-Protein C: vit K-dependent inhibitor of procoagulant system
-inactivates V and VIII
-seen in 4-5% of patients < 45y with unexplained venous thrombosis
-deficiency is autosomal dominant: (CRM-: lack of protein; CRM+: dysfunctional protein)
-significant when serum activity < 70%
-treatment: warfarin
Protein S Deficiency:
-Protein S: vit K-dependent; produced by hepatocytes and megakaryocyte
-cofactor for Protein C
-significant when serum activity < 60%
!
-associated with high mortality related mainly of primary disease
-75% of pts are > 70y
-causes: poor oral hygiene, dehydration, use of anticholinergic agents, lack of oral intake
-staphylococci infection via probable transductal inoculation of parotid gland
-routes of spread for suppurative parotitis:
-downward into deep fascial planes of the neck
-backward into external auditory canal
175
-outward into skin of face
-swollen tender parotid
-may progress rapidly to severe cellulitis on affected side of face and neck
-may require tracheotomy if airway compromised
Management:
-prophylaxis: adequate hydration, good oral hygiene
-start with broad spectrum Abx against staph; take C+S of pus
-surgical drainage; should not be delayed beyond 5th day
Prognosis:
-mortality approximated 20%, but his was frequently related to the patient’s basic disease
* % 3 7* 2
-small bowel normally does not manifest ileus post-op, because it continues to function throughout and after
operation
-tube feedings may start almost immediately after operation
-if inflammation or several anastomoses in small bowel 24h ileus might be experienced
-gastric ileus: 24-48h
-colonic ileus: 3-5 days
-caused by:
-surgical manipulation, inflammation, peritonitis, blood in peritonem
-blood in retroperitoneum
-hypokalemia, hypocalcemia, hyponatremia, hypomagnesaemia
-opiates and phenothiazine
-treatment:
-correct underlying disorder, if any; mostly supportive treatment
-long tube decompression
-measure serum albumin prolonged ileus in hypoalbuminemic patients
-12.5g q8-12h to raise albumin > 3.0 mg/dL often results in return of bowel function
* & %
General Considerations:
-factors that increase likelihood of anastomotic leakage:
-emergency procedures, poorly prepared patients, inadequately resuscitated patients, prolonged
intraoperative hypotension, hypothermia
-etiological factors: poor surgical technique, distal obstruction, inadequate proximal decompression
Duodenal Stump Blowout:

-disastrous complication with a high mortality
-complications: peritonitis, subhepatic abscess, pancreatitis, sepsis, establishment of an external fistula wit
fluid, and electrolyte abnormalities
-most likely to occur between 2nd and 7th POD
-adequate drainage required: incision below (R)CM and insertion of large sump catheter
-fluid and electrolyte therapy, TPN instituted
176
Intestinal Leaks and Fistulas:
Leaks: -fever, leukocytosis, unexplained ileus in absence of intestinal obstruction, complicated post-op course
-if patient is in jeopardy, sepsis uncontrolled, no effective drainage abdomen re-explored
-anastomosis must be resected and redone
-if hemodynamically unstable separation of both ends and diversion should be done
Fistula: -increased wound pain and redness/drainage on POD #4-5
-usually result from operations involving inflammatory bowel disease, cancer, or lysis of adhesions
-allow fistula to close spontaneously
Therapy of an Established Fistula:

-five phases: stabilization, identification and diagnosis, decision, operation, healing
1. Stabilization:
-resuscitation using crystalloids, RBC, and albumin
-Abx only if septic
-sump-type drain placed around skin; skin protected with Stomadheisve and ion exchange paste to keep
pH acidic and prevent activation of pancreatic enzymes that require basic pH
-TPN: 5-6% AA, 15-25% dextrose, 20% fat
-nutrition can be monitored with RBP, TBP, transferring
-enteral feeds may be attempted but they must be supplemented with TPN
2. Identification and Diagnosis:

-obtain fistulogram/sinogram
-degree of bowel continuity, size and depth of defect, presence of distal obstruction, nature of bowel
adjacent to fistula, presence of large abscess
-fistulas unlikely to close spontaneously:
-ileal, gastric, fistulas at ligament of Treitz
-total anastomotic disruption; partial disruption with adjacent abscess; lateral fistula with distal
obstruction; fistula in strictured intestine; end fistula with no distal communication
-local sepsis or systematic sepsis
-spontaneous closure usually within 5 weeks of adequate nutrition support in a patient w/o sepsis
3. Decision:
-somatostatin used to promote closure
-if short-turnover protein levels are increasing, the serum albumin concentration is approaching 3.0 g/dl,
and the patient is maintaining the albumin level without infusions of exogenous albumin, operation can
take place
-failure to maintain or increase in levels of transferring, retinol-binding protein, and thyroxin-binding
prealbumin indicative of mortality
4. Operation:
-mortality ~10-11% if operated during first 10 days or after 4 months; ~20% between 10 days and 4months
-resection and end-to-end anastomosis; protection with omentum onlay
-for duodenal fistula: vagotomy and gastrojejunostomy, feeding jejunostomy and gastrostomy, area of
fistula drained
-chronic pancreatic fistula:
-excise fistula down to pancreas, identify leak, distal pancreatectoy and splenectomy
-Roux-en-Y anastomosis can be used to provide internal drainage for the pancreatic fistula
5. Healing:
-feeding delayed 7-10 days
-difficulties eating:
-lack taste sensation: use zinc sulfate or lactate
-may be necessary to allow alcohol to induce eating
177
Colocutaneous Fistulas:
-fluid and electrolyte abnormalities and skin digestion are rare, but infectious complications are significant
-percuaneous drainage of intraabdominal abscesses and local care of wound infections
-antibiotics as indicated
-spontaneous closure likely
-persistence if sepsis, distal obstruction, anastomotic dehiscence, Crohn’s disease, or carcinoma present
-lack of spontaneous close by 5 weeks surgical repair
-resection of fistula and affected colonic segment with primary anastomosis and temporary
diversion of the fecal stream by colostomy
* ( ( % *
Dumping:
-loss of pyloric valve that normally prevents hyperosmolar material from entering duodenum and small
bowel
-d/t pyloroplasty, pyloromyotomy, gastrojejunostomy, gastric resection, Billroth I or II anastomosis
-results in release of vasoactive substances:
-serotonin, bradykinin, substance P, peptides (VIP, pancreatic polypeptide, insulin, glucagon,
neurotensin, enteroglucagon)
-results in decreased plasma volume hypotension; hypokalemia
-symptoms:
-early postprandial bloating, borborygmus, cramps, sensation of light-headedness, palpitations,
sweating, hypotension
-eating solids at meal and drinking liquids afterwards diminishes symptoms
-avoid carbohydrates which are more likely to provoke dumping
-in severe cases, long-acting octreotide may oppose some of the action of released peptides and ameliorate
the symptoms
-surgical treatments: conversion of BII to BI; 6 cm reverse loop of jejunum to slow transit of hypertonic
solution
Postvagotomy Diarrhea:
-5-20% of patients have troublesome diarrhea post-truncal vagotomy
-factors:
-dysmotility or dysfunction of small bowel motility stasis and overgrowth of bacteria,
malabsorption of fat, increased and incoordinate bile flow into small bowel
-treatment difficult:
-antibiotics have little success
-10-cm reversed jejunal loop 100 cm distal to ligament of Treitz has been advocated
Afferent Loop Syndrome:

-syndrome almost always occurs when the afferent loop is anastomosed to the greater curve after a BI
gastrectomy
-obstruction of afferent loop from adhesions, kinking, intussusception, volvulus of afferent loop, stomal
ulcer, or obstruction of the efferent limb
-duodenal secretions increases in afferent loop regurgitated into stomach
-haemorrhagic pancreatitis or perforation can occur
-symptoms:
-eating is regularly followed by RUQ epigastric distention and pain, borborygmus, and cramps
relieved by projectile vomitus of clear bile that is never mixed with food
-operation require for relief of these symptoms:
-afferent loop is anastomosed into Roux-en-Y efferent loop ~60 cm downstream to prevent reflux
of bile into stomach
-vagotomy to prevent marginal ulcer
178
Alkaline Reflux Gastritis:
-stomach sensitive to bile; eating associated with burning epigastric pain
-large amounts of bile emanating form afferent loop
-acute and chronic inflammation, evidence of decreased parietal cells, and increase in mucous-secreting
cells, and intestinalization of the gastric glands
-most effective treatment: cholestyramin and sucralfate
-if medically unmanageable: Tanner-19 procedure with vagotomy and long bile-containing loop
anastomosed 60 cm down stream
Nutritional Complications:
-fat malabsorption chronic nutritional deficiency, failure of absorption of fat-soluble vitamins, chronic
bile salt diarrhea
-iron and calcium absorbed primarily in duodenum
-after BII many pts hypocalcemic and iron-deficiency anemic
-loss of intrinsic factor monthly B12 injections required
-may require conversion of BII to BI
Recurrence of Disease:
-complications for ileostomies: ulcerative colitis 4%; Crohn’s disease 30%
-Crohn’s: granulomatous, ulcerations; peristomal fistulas
-ciprofloxacin and metronidazole should be initiated
-no point in resiting stoma recurrence will likely happen again
Stomal Necrosis and Retraction:

-necrosis or retraction superficial to fascia no immediate action required
-necrosis extends below fascia immediate laparotomy and reconstruction of stoma
-retraction below level of fascia immediate laparotomy to prevent further fecal contamination of
peritoneal cavity
Skin Complications:
-usually result of siting and inability to obtain appropriate seal around stoma
-Caraya powder, ion exchange paste, +/- nystatin powder and systemic fluconazole (if yeast) are helpful
-cellulitis requires antibiotics
Stomal Stricture:
-development of serositis in immediate postoperative period
-most common cause of stricture is necrosis or retraction, resulting in mucocutaneous separation, exposure
of the serosa, and subsequent serositis
-tx: stoma separated from skin, skin opening enlarged, new maturation performed
-if stricture at fascial level, fascial opening enlarged
Peristomal Hernias and Prolapse:

-prolapse occurs when there is vigorous peristalsis and insufficient fixation of bowel to underside of
anterior abdominal wall
4 3 4
( % * / * * * / % * *# . $
-most common metabolic complication after surgery
179
-may result in CNS damage, seizures and death
-secretion of ADH is more prolonged or more intense than after normal operative procedures
-management:
-if slight edema and [Na] ~125-130 fluid restriction is all that is required
-if CNS disturbance:
-symptoms not severe mannitol given slowly provokes diuresis of excess water secreted with
minimum of sodium; furosemide can be added
-if severe 3% saline; small increments 50-100 ml over 3-4 hours
-permanent CNS damage can occur if rapid correction of hyponatremia
-prevention: avoid overresuscitation of patients; limit free water
. %* / 1( %4* 2
Thyroid Storm:
-mortality of 10-20%
-occurs in patients with existing thyrotoxicosis that is unrecognized or uncontrolled
-any traumatic event, such as surgery, infection, or embolism, may complicate thyrotoxicosis and provoke
thyroid storm
-once hypotension supervenes, it is a preterminal event
-irreversible cardiac failure usually is the mode of death
-tx: -control of catecholamine-induced cardiac symptoms: propranolol IV 1mg/min to max of 10 mg
to control HR
-dobutamine may be necessary
-PTU 200 mg and KI 5-10 gtts given to decrease T3 and T4 release
-hydrocortisone 200 mg IV followed by 100 mg q8h diminishes thyroid hormone release
Myxedema Coma:
-pts with chronic hypothyroidism that is unrecognized or inadequately controlled; provoked by stress of
operation
-inciting factors: trauma, infection, GIB, surgery, narcotics and phenothiazine
-tx: -warming, hydration, assisted ventilation
-L-thyroxine 300-500 mg IV then 50-100 mg/d
%* // * (
-d/t suppression of pituitary-adrenal axis by previous administration of steroids or destruction or exhaustion of
adrenal glands
-in patients with carcinoma, bilateral adrenal metastasis may occur
-symptoms:
-unexplained hypotension, fever, abdominal pain, light-headedness, weakness, palpitations, mental status
changes, nausea, and vomiting
-lab findings:
-hypoglycemia, hyponatremia, occasionally hyperkalemia
-tx: -measure serum cortisol and initiate treatment
-hydrocortisone 200 mg IV
-hypotension should resolve in 1-2h if dx is correct
-400 mg hydrocortisone in divided doses over 24h should b given if hypotension not resolved
8* *
-most common cause is pre-existing liver disease
-cirrhosis, alcoholic hepatitis, fatty infiltration
-general anaesthesia should be avoided in patients with established liver dz:
-portal vein’s contribution is diminished and hepatic artery supplies at least 50% of hepatic flow
180
-splanchnic vasoconstriction of hepatic artery markedly decreases hepatic flow
-therefore, regional or epidural anaesthetic is preferred
-liver failure usually on 3rd or 5th POD
-somnolence, jaundice, u/o, ascites
-treatable reversible causes:
-hypovolemia, hypokalemia, hypomagnesaemia, GIB, constipation, remote infection
-must r/o SBP
-tx: -correct lytes, administration of neomycin, cathartic, or lactulose, and provision of nutritional support
-enteral feeds preferred:
-modified low aromatic, high branched-chain amino acid formulation
-hepatorenal syndrome type II can complicate hepatic failure; if liver does not recover post-op death
-delirium (20%), depression (9%), dementia (3%), functional psychosis (2%) of elderly post-op patients
-manifestations are extremely variable
-delirium: occurs most commonly in elderly patients and those who are immobilized for long periods
-depressive reactions: pt characteristically uncooperative or recovery may be impeded by listlessness,
anorexia, and disinterest
-suicide a major risk in pts with depressive reaction
-paranoid psychotic disorder
Management:
-efforts should be directed at removing toxic causes of the acute brain syndrome, removing unnecessary
stimuli without isolating the patient, and providing psychologic or pharmacologic tranquillization
-consultation with psychiatry is indicated in the case of any acute and severe emotional disturbance
.* * * % 1* /. *
-delirium usually follows operation within 48h but may be delayed
-hyperactivity with irritability, delusions, hallucinations, restlessness, and agitation
-cause is multifactorial
-Haldol 2-15 mg PO bid or 1-5 mg IV followed by 5-10 mg/h may help agitation
-prophylactic medication with lorazepam should be administered in the perioperative period to patients with severe
alcoholic histories who are candidates for DTs
.* *
-characteristically occurs late in the post-op period
-use of SSRIs are useful
*
-very yound gan old patients are particularly vulnerable to the development of psychiatric complications after
surgical treatment
Pediatric Surgery:
-severe anxiety states may be precipitated by the shock of operation
-emotional needs must be attended to
-maturity is important and decreases post-op anxiety reactions
181
Surgery in the Aged:
-more prone to become emotionally disturbed when confronted with new situations, esp. if inadequate
comprehension and generalized feeling of insecurity
Gynecologic and Breast Surgery:

-high incidence of depression, anxiety and sexual difficulties
-contact with other mastectomy patients expedites psychologic rehabilitation
-the more the procedure antedates menopause, the greater the likelihood of associated psychologic
disturbance (ie. hysterectomy)
Cancer Surgery:
-two major threats: disease and extensive surgical treatment
-depression is related to an anticipated interference with valued activities
-tendency toward seclusion, withdrawal, and nonparticipation
-depression frequent
Cardiac Surgery:
-serious psychiatric disturbances observed with considerable frequency afte mitral valvulotomy and open-
heart surgery
-manifestations usually after initial lucid interval of 3-5 days; resolve shortly after transfer from CICU to
ward
-postoperative incapacitation and increased time on heart-lung machine are factors increasing the
likelihood of delirium ?organic brain damage from operation
Dialysis and Transplantation:

-suicide rate is 300 times greater in dialysis and transplantation patients
-uraemia, debilitating disease, and the undergoing of repeated procedures are contributing factors
182
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Indications:
1. Continuous monitoring of blood pressure
-shock, acute hypertensive crisis, use of potent vasoactive or inotropic drugs, high levels of
respiratory support, high-risk patients undergoing extensive operations, controlled hypotensive
anaesthesia, rapidly changing cardiac function
2. Frequent sampling of arterial blood
-any acute illness involving cardiovascular or respiratory dysfunction
-contraindications of specific sites of catheterization:

-severe occlusive arterial disease with distal ischemic, presence of a vascular prosthesis, and local
infection
Clinical Utility:
-observation of arterial pressure waveform may permit a qualitative assessment of cardiovascular status
Sites of Catheterization:
-radial artery:
-mean and end-diastolic radial pressures usually accurate estimates of aortic pressure
-systolic pressure often much higher than that of aorta d/t overshoot caused by resonant behaviour
of radial artery
-test collateral supply with Allen’s test (6s return of blood or less)
-axillary artery:
-long-term direct arterial pressure monitoring
-better representation of aortic pressure waveform and minimal systolic pressure overshoot
-because of extensive collateral circulation, thrombosis will not lead to compromise in distal arm
-femoral artery:
-easier localization and cannulation
-dorsalis pedis artery:
-relatively small size and overestimation of systolic pressure at this level
-superficial temporal artery:
-surgical exposure required for cannulation
-risk of cerebral embolization has been reported in infants
-brachial artery is not used often because of high complication rate:
-may lead to loss of forearm and hand if collateral flow is not sufficient
Complications:
-failure to cannulate, haematoma formation, disconnection from monitoring system with bleeding
-increased of radial artery occlusion:
-female gender, low CO states, vasoconstrictors drugs, severe PVD, small wrist circumference,
insertion by surgical cut-down, multiple puncture attempts, haematoma formation, and increased
duration of cannulation
-increased risk of infection:
-placement > 4 days, insertion by surgical cut-down, local inflammation
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Indications:
-secure access for fluid therapy
-drug infusions
-parenteral nutrition
-CVP monitoring
-other: aspirate air embolism, placement of cardiac pacemakers or IVC filters, hemodialysis access
-contraindications for specific sites of catheterization:

-vessel thrombosis, local infection or inflammation, distortion by trauma or previous surgery
Clinical Utility:
-CVP:
-can differentiate pericardial tamponade from hypovolemia
-tracing:
-absent a-wave: A-fib
-prominent v-wave: tricuspid insufficiency
-used to measure RAP; indirectly measures RVEDP, and estimates RVEDV
-cannot be used to assess LV function
Sites of Catheterization:
-subclavian vein:
-easiest to cannulate, but risk of PTX and inability to compress vessel if bleeding occurs
-internal jugular vein:
-lower risk of PTX; good compressibility
-risk of arterial puncture
-external jugular vein:
-high incidence of failure
-femoral vein:
-risk of infection and thrombosis continue to limit general acceptance of long-term cannulation
Complications:
-long-term: infection or thrombosis
-three types of thrombi:
-mural thrombus
-catheter thrombus
-sleeve thrombus
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Indications:
-in general, a PA catheter indicated whenever the data obtained will improve therapeutic decision making
without unnecessary risk
-see Table 12-1
Clinical Utility:
-measures directly:
- CVP, PADP, PASP, MPAP, CO, PAWP, mixed venous blood gases, continuous mixed venous
oximetry
-others:
-LAP:
-PAWP is a reliable index of LAP even in the presence of elevated pulmonary vascular
184
resistance
-if measuring in West’s Zone I or II, then PAWP may reflect alveolar pressure and not
LAP (esp. if low pulm. vasc. pressures or high PEEP)
-must be in West’s Zone III (catheter should be below LA in supine position) to
accurately measure LAP
-LVEDP:
-in absence of MV dz or premature MV closure d/t AR, LAP reflects LVEDP
-LVEDV:
-if no alterations in LV compliance, LVEDP will reflect LVEDV
-intrathoracic pressures introduces artifact that affects all intrathoracic vascular pressures:
-if respiratory insufficiency:
-“stiff” lungs do not transmit alveolar pressure as readily to pulmonary circulation
-PEEP artifact should not exceed 1 mmHg for every 5 cmH2O PEEP applied
-hypovolemic patients:
-may cause greater discrepancy higher measured PAWP than actual
-intravascular measurements should be performed at end-expiration and obtained from a calibrated
oscilloscope rather than digital display which may average artifact
-cardiac output: via thermodilution method

-CO is inversely proportional to area under thermodilution curve
-measures in reality RV CO - in the absence of intracardiac shunting, (R) and (L) CO are
equivalent
Catheter Insertion:
-mean PAWP should be lower than the MPAP and lower than or equal to the PADP
Complications:
-development of dysrhythmias (up to 50% of patients, but <1% are serious)
-RBBB seen in 3-6%, therefore need for transvenous pacemaker on standby
-coiling, looping or knotting in RV
-infections
-thromboembolism
-pulmonary artery rupture:
-more likely in elderly patients and those with hypertension
-other: thrombocytopenia, cardiac valve injuries, catheter fracture, balloon rupture
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-Cardiac output (CO)

-preload: changes in PAWP frequently are used as an estimate of changes in LV preload (preload ~
LVEDV ~ LVEDP ~ PAWP)
-afterload: SVR most commonly used measure of ventricular afterload
-methods to increase stroke volume (SV):
-increase preload by augmentation of intravascular volume
-a major increase in PAWP during infusion suggests poor ventricular compliance, exhausted
preload reserve, and increased risk of pulmonary edema with further volume loading
-if PAWP rises modestly, if CI improve, and if PAWP returns to within several mmHg of the
original value within 10 min of stopping infusion, additional fluid can be given w/o high risk of
exacerbating pulmonary venous congestion
-if inadequate tissue perfusion after volume infusion:
-increase myocardial contractility with inotropic drugs and/or ?decreasing ventricular afterload
with vasodilators
185
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Lung Volumes:
-Tidal volume (VT): volume of air moved in or out of lungs in any single breath
-Vital capacity (VC): maximal expiration following a maximal inspiration
-reduced in diseases involving respiratory muscles or their neural pathways, obstructive and
restrictive ventilatory impairment, and in pts who fail to cooperate fully
-Minute volume (VE): total volume of air leaving lung each minute
-increase in VE required to maintain normal PaCO2 suggests increased dead space relative to VT or
an abnormally high CO2 production
-Dead space (VD): portion of tidal volume that does not participate in gas exchange
-the VD/VT ratio ~ 0.33-0.45 in healthy subjects
-increased in ARDS, emphysema, PE, shock with low CO, PPV with excessive PEEP
-if > 0.6, usually wearable from ventilator
Pulmonary Mechanics:
-Maximal inspiratory force: maximal pressure below atm exerted against an occluded airway
-more negative than -20-25 cmH2O used as one clinical parameter to confirm recovery from NM
block after general anaesthesia
-more negative than -30 cmH2O predict successful weaning from mechanical ventilation
-limited power in predicting weaning outcome; assess only strength without taking into account
the demands placed on respiratory muscle pump
-Compliance:
-change in volume divided by a change in pressure
-decreased values are observed with disorders of the thoracic cage or a reduction in the number of
functioning lung units (resection, bronchial intubation, PTX, atelectasis, pulmonary edema)
-Work of breathing:
-measure of the process of overcoming the elastic and frictional forces of the lung and chest wall
Blood-Gas Analysis:
-pulmonary and cardiac function must be assessed to evaluate any given set of ABGs accurately
-a decreasing PaO2 without a change in PaCO2 suggests that blood oxygenation is deteriorating
despite constant alveolar ventilation
-usually attributable to V/Q imbalance or intrapulmonary shunting
-oxyhaemoglobin dissociation curve:
-right shift: increased DPG, temperature, PCO2; decreased pH
-left shift: carboxyhemoglobinemia; decreased temperature and PCO2; increased pH
-little evidence that shifts of oxyhaemoglobin dissociation curve are clinically significant in the
majority of patients
-hypercapnia ( PaCO2):
-d/t hypoventilation (ie. CNS depression), increased CO2 production (eg. hyperthermia,
hyperthyroidism), increased physiologic dead space
-mixed venous blood:
-mixture of all blood that has traversed the capillary beds capable of extracting oxygen
-reflects total body balance between oxygen delivery and oxygen consumption of perfused tissues
Parameters Derived from Blood-Gas Analysis:

-see Table 12-3
186
Capnography:
-patients with COPD and other derangements associated with increased dead space have increased arterial
to end-tidal CO2 gradient [P(a-ET)CO2]
-PETCO2 (end-tidal CO2 gradient):
-determine proper ETT placement
-in CPR an increase from zero (circulatory arrest) provides an immediate bedside validation of the
efficacy of CPR; provides earliest evidence of successful resuscitation
-detection of increased CO2 production in malignant hyperthermia
-detection of disconnection or malfunction of anaesthesia breathing circuit
Pulse Oximetry:
-in the presence of elevated carboxyhemoglobin or methemoglobin levels, SPO2 overestimates fractional
saturation at all saturation values
-methemoglobinemia maybe induced by a large number of drugs, including local anesthetics (prilocaine,
benzocaine), NTG, phenacetin, phyenytoin, Pyridium, and sulfonamides
Continuous Mixed Venous Oximetry:

-helpful in assessment of oxygen supply-demand relationship in critically ill pts
-SVO2 (mixed venous saturation) will decrease if:
-increase in oxygen consumption; decrease in cardiac output or haemoglobin
-normal range: 0.6-0.8
-below normal range:
-increased oxygen consumption:
-fever, shivering, seizures, exercise, agitation
-decreased oxygen delivery:
-low cardiac output, anemia, arterial Hb denaturation
-above normal range:
-increase in oxygen delivery relative to consumption:
-hyperdynamic phase of sepsis, cirrhosis, peripheral left-to-right shunting,
general anaesthesia, cellular poisoning, marked arterial hyperopia
-uses:
-indicator of adequacy of oxygen supply-demand balance of perfused tissues
-may function as early warning signal of untoward events
-may improve the efficiency of the delivery of critical care by providing immediate feedback as to
the effectiveness of interventions
-Gastric tonometry has been propsed as a relatively noninvasive monitor of the adequacy of aerobic metabolism in
organs whose superficial mucosa lining is extremely vulnerable to low flow and hypoxemia and in which blood
flow is sacrificed first in both shock and the systemic inflammatory response syndrome
-intramucosal pH (pHi) is measured
Clinical Utility:
-in critically ill patients, used as predictor of organ dysfunction and mortality
-better predictor of mortality than base deficit, lactate, oxygen delivery, and oxygen consumption
-can provide metabolic end point of resuscitation
RENAL MONITORING
-kidneys are excellent monitors of the adequacy of perfusion
187
Glomerular Function Tests:
-BUN:
-affected by GFR and urea production
-may be increased in UGIB, catabolic states induced by trauma, sepsis, or steroids
-may be lowered during starvation and in advanced liver disease
-not a reliable monitor of renal function in critically ill patients
-Creatinine:
-inversely related to GFR
-not influenced by protein metabolism or the rate of fluid flow through the renal tubules
-plasma creatinine level will double with a 50% reduction in GFR (constant production of Cr)
-acute reductions are not immediately reflected, 24-72h required for equilibration to
occur
-CCr = (140-age) x weight in kg / 72 x PCr multiply by 0.85 for females
Tubular Function Tests:

-with prerenal azotemia, the tubules can appropriately reabsorb sodium and water
-in intrinsic renal failure, tubular function is markedly compromised, and the ability to reabsorb sodium and
water is impaired
-FENa appears to be the most reliable for distinguishing prerenal azotemia from acute tubular necrosis
-in an oliguric patient, a value <1% is usually d/t a prerenal cause
->2-3% tubular cause
-correct interpretation is not possible if the patient had received diuretics in the 6-12h preceding the test
Intracranial Pressure Monitoring:

-CPP = MAP - ICP
-CPP may be insufficient if ICP > 20 mmHg
-aim to keep CPP level of at least 70 mmHg
-common indication for monitoring: severe head injury
-others: subarachnoid haemorrhage, hydrocephalus, postcraniotomy, Reye’s syndrome
-methods: ventricular catheter, subarachnoid bolt, epidural bolt, fiberoptic catheter
-complications: infection, haemorrhage, malfunction, obstruction, malposition
Electrophysiologic Monitoring:
-EEG used in:
-CEA, cerebrovascular surgery, open heart surgery, epilepsy surgery, induced hypotension for a
variety of surgical procedures
-somatosensory evoked potentials:
-reflect integrity of dorsal spinal columns and sensory cortex
-useful for monitoring during resection of spinal cord tumours, spine instrumentation, CEA, and
aortic surgery
-brainstem auditory-evoked potentials:
-reflect integrity of CN VIII and auditory pathways
-monitoring for surgery in posterior fossa
-visual evoked potentials:
-monitor optic nerve and upper brainstem
-pituitary surgery
Transcranial Doppler Ultrasonography:

-used to monitor cerebral blood flow
-may detect vasospasm following spontaneous or traumatic subarachnoid haemorrhage and can help
identify hyperemic or low-flow states
188
Jugular Venous Oximetry:
-invasive method of continuously monitoring jugular venous bulb oxyhaemoglobin saturation
-provides a measure of the relationship b/n total cerebral blood flow and total cerebral oxygen consumption
Assessment of Caloric Expenditure:

-Basal energy expenditure (BEE) can be estimated with the Harris-Benedict equation
-Resting energy expenditure (REE) can be approximated form the BEE by increasing it by 10%
-must find balance:
-certain conditions (eg. trauma, burns, sepsis etc.) increases caloric requirements
-however excessive caloric administration is potentially detrimental
excess calories converted to fat CO2 production
-liver may develop fatty infiltration resulting in hepatic dysfunction
Measurements:
-the ratio of CO2 production to oxygen consumption is the respiratory quotient (RQ)
-average ~ 0.8
-monitoring oxygen consumption and CO2 production and calculating the RQ provide inferences into the
adequacy of total calories as well as the mixture of substrates:
-prolonged starvation fat metabolism: RQ ~0.6-0.7
-excessive carbohydrate administration RQ > 1.0
-no great method of measuring this all prone to errors
189
Notes and points from previous exams
Anatomy and Physiology
1. Testes does not drain into inguinal lymph nodes.

2. Intercostobrachial nerve innervates skin on inner side of upper arm.
3. Left recurrent laryngeal nerve loops around arch of aorta next to ligamentum arteriosum prior to heading
cephalad.
4. Superior laryngeal nerve provides sensation to supraglottic larynx (internal branch) and innervation to
cricothyroid muscle (external branch).
5. Recurrent laryngeal nerves provide sensation to subglottic larynx
6. Carotid sheath contains: common carotid artery, internal jugular vein, vagus nerve
7. Sympathetic chain: T1-L2
8. Anterior shoulder dislocation: axillary nerve injury (deltoid muscle)
9. Colles’ fracture numb thumb and index finger: median nerve injury
10. Injury to common peroneal nerve foot drop, deficit in tibialis anterior
11. Herniation of disc at L4-5 (L5 nerve root) loss of extensor hallucis longus and loss of sensation to dorsum
of foot
12. Contents of carpal tunnel: median nerve plus long flexor tendons
13. Horner’s Syndrome associated with injury at T1
14. Structures that traverse the parotid gland: CN VII, retromandibular vein
15. Sympathetic fibers exit the spinal cord through anterior roots
16. Decreased sensation to pain in left lower extremity right spinothalamic tract severed
17. Origin of vertebral artery: subclavian artery
18. Common association with Meckel’s diverticulum: ectopic gastric mucosa
19. Penis/clitoris supplied by pudendal artery
20. Small muscles of the hand are supplied by median and ulnar nerve
21. Cremaster muscle derived from internal oblique
22. Muscle contraction without joint movement isometric
23. Superior epigastric artery lies anterior to posterior rectus sheath and posterior to posterior rectus muscle
24. Circulation of lymph in vessels is by action of valves, muscles, gravity, intraabdominal pressure
25. Sensory supply to anterior 2/3 of tongue: V3
26. Taste to anterior 2/3 of tongue: VII
27. Sensory and taste to posterior 1/3: XI
28. Spinal cord ends at L2
29. Sigmoid colon is not a retroperitoneal structure
Anaesthesia
1. Succinylcholine contraindicated in major trauma in up to 60 days because of hyperkalemia secondary to

increased sensitivity of muscle cells to depolarising agents. Causes increased efflux of potassium out of
cells.
2. Local anaesthesia:
-all are alkaline
-toxicity decreased with epinephrine
-metabolized by liver
-CNS symptoms before cardiac (circumoral numbness, tinnitus, dysarthria, seizures)
3. Amides: lidocaine, prilocaine, etidrocaine, bupivicaine (two “i”s)
4. Esters: procaine, cocaine, tetracaine (one “i”)
190
-procaine allergy possible due to its preservatives

5. Lidocaine toxicity: 3-5mg/kg; 7mg/kg with epinephrine
-to determine amount contained, multiply % with amount in ml and add a zero
-eg. 5ml of 2% contains 100mg
6. Longest acting local anaesthetic: Tetracaine
7. Main risk of chronic exposure to inhalational agents: spontaneous abortion
8. Preferred anaesthetic agent with short duration for outpatient procedures: Propafol
9. Malignant hyperthermia:
-caused by succinylcholine and all inhalational agents (except N2O)
-earliest and most consistent sign: tachycardia and increased end-tidal CO2
-masseter muscle spasm in children
-dantrolene for treatment
10. Dantrolene: Ca release from sarcoplasmic reticulum inhibits contraction
11. Best post-op analgesia for obese patient with thoracotomy/abdominal surgery: epidural
12. ASA Classification:
I: normal
II: mild to moderate disease, not limiting activity (eg. HTN, DM)
III: severe disease limiting activity but not incapacitating (eg. heart disease that limits activity)
IV: severe disease that is life-threatening
V: moribund, little chance of survival
E: emergency surgery
13. Helium improves laminar flow
14. Ketamine: smooth muscle relaxer and bronchodilator
15. Appropriate size ETT in children = age/4 + 4
16. Safe agent to use in malignant hyperthermia: Thiopental
17. Patient given 15 mg morphine and gravol post-op, becomes somnolent and decreased RR. Best first action:
administer naloxone
18. General anaesthesia preferred for long cases
19. Patient hypotensive under anaesthesia (with spinal/epidural) after putting patient in reverse Trendelenburg:
loss of sympathetic tone
20. Long term steroid use about to have major surgery: hydrocortisone 100 mg 8h pre-op then q8h for several
days post-op
21. Elderly patient on chronic thiazide treatment for HTN going for surgery. Most important complication is
hypotension
22. Mortality from general anaesthesia in otherwise healthy patient: 1 in 100,000
23. Change in radius will result in the most significant change in flow
Pharmacology
1. Bethanacol contraindicated in CAD and bladder outlet obstruction
-negative inotrope and chronotrope
-smooth muscle constriction in bronhioles, bladder and uterus
2. Ciprofloxacin:
- theophylline levels
-s/e: n/v, diarrhea, headache, dizziness, insomnia
3. Ampicillin and amoxicillin ineffective in the presence of penicillinase
4. Penicillinase resistant: methicillin, nafcillin, oxacillin, cloxacillin
-others: clavulin, sulbactam, tazobactam, vancomycin
5. Vancomycin least likely to become resistant to bacteria producing penicillinase
6. Advantage of 3rd generation cephalosporins: better gram negative coverage and CSF penetration
7. Cephalothin (1st generation cephalosporin) most likely side effect: hypersensitivity
191
-others: phlebitis, painful IM, nephrotoxic with aminoglycoside

8. No dose adjustment needed in renal insufficiency for: erythromycin
9. Pharmacokinetic alterations in elderly patients are due to decreased renal clearance
10. Pharmacokinetic alterations in infants are due to immature hepatic function
11. Corticosteroids do not cause renal failure
12. ASA inhibits cyclooxygenase; decreases arachidonic acid to prostaglandins
13. Four year old male, 15kg post-op appendectomy; analgesia:
-morphine 0.05-0.10mg/kg: 1.5 mg IV q3-4h prn
14. Clofibrate can increase the effect of coumadin
15. Bacteriostatic antibiotics:
-erythromycin (50S)
-clindamycin (50S)
-chloramphenicol (50S)
-tetracyclin (30S)
-sulfonamides
16. Cocaine is a potent vasoconstrictor
17. Digoxin works in A-fib by slowing AV conduction
18. Barbiturate will reduce action of coumadin (by inducing cytochrome P450)
19. Acetazolamide: carbonic anhydrase inhibitor
-s/e: metabolic acidosis from HCO3 diuresis, increased excretion of Ca, K, Mg and Na; hyperglycemia,
hyperuricemia
20. Epinephrine: beta-effects at low doses, alpha-effects at high doses
21. Epinephrine from adrenal medulla; norepinephrine from sympathetic nervous system
22. Amikacin: synthetic aminoglycoside that does not develop antimicrobial resistance
23. 70 yo on methyldopa (s/e is hemolytic anemia) develops anemia with Hb 80 MCV 70. First priority is to
order Coomb’s test
24. Lasix can induce increased urine output with GFR. May be used in patients with GFR as low as 10cc/min
25. Antibiotic not associated with nephrotoxicity: erythromycin
26. Gentamicin does not cover for bacteroides
27. Gentamicin, ciprofloxacin are antipseudomonas antibiotic
28. Dilantin side effects: lymphadenopathy, rash, gingival hyperplasia
29. Anti-cholinergic effects: confusion, dilated pupils, dry mouth, anhydrosis, constipation
30. Penicillin resistance not seen in treponema pallidum
31. Least nephrotoxic aminglycoside: tobramycin
32. Antibiotics avoid in pregnancy: tetracyclin, ciprofloxacin, streptomycin
33. Antibiotics that interfere with bacterial cell wall synthesis: penicillins, cephalosporins, vancomycin
34. Cimetidine, erythomycin will increase serum dilantin by inhibiting P450
The Systemic Response to Injury
1. Mast cells are not phagocytes

2. Vasopressin can coronary vasospasm
3. Energy used for actin-myosin complex: ATP
4. NO:
-release from endothelial cells
-causes vasodilation and increased capillary permeability
-inhibition of platelet aggregation and monocyte adhesion to endothelial cells
-inhibition of smooth muscle proliferation
5. Bradykinin:
-vasodilation, increased vascular permeability, bronchospasm, pain, edema, inhibits gluconeogenesis
6. Growth hormone decreases insulin release, promotes protein synthesis, promotes mobilization of fat stores
192
7. Growth hormone during trauma: hyperglycemia

8. End product of anaerobic glycolysis: lactate
9. TXA2: vasoconstriction and platelet aggregation
10. PGI2: vasodilation and decreased platelet aggregation
11. Osteoclastic activity is responsible for bone remodelling after fracture
12. Anti-inflammatory cytokines: IL-4, 10, 13
13. Most important mediator in septic shock: TNF
14. Growth factors: promote growth of endothelium and are important mediators of inflammatory response
Fluid and Electrolyte Management of the Surgical Patient
1. Sodium deficit:
-Na = %body water x TBW(140-[Na])
-%body water = 50% female, 60% male (note previous exam may give volume of distribution of Na as
20%)
2. Plasma volume in 70kg male = 3.5L (5% body weight)
3. Blood volume is ~7% body weight (hct 40%, plasma 60% blood volume)
4. SIADH:
-hyponatremia, urine Na concentration, urine K, urine osmolality
5. Hypokalemia caused by all: lasix, hydrochlorothiazide, mannitol, ventolin
- except: metoprolol
6. Hypermagnesemia:
-hyporeflexia
-CNS: lethargy, coma, paralysis
-CVS: ECG changes and cardiac alterations similar to Ca
7. Hypomagnesemia:
-increased DTR, cardiac dysrhythmias, weakness, mental status changes, seizure
8. Patient with post-op, receiving only IV fluids: Na 112, Cl 105, K 3, BUN 12. Cause is dilutional
hyponatremia
9. Use calcium IV for cardiac effects of hyperkalemia
10. 70% of CO2 is transported in the blood as HCO3-
11. Most common cause of hypercalcemia:
-outpatient: parathyroid adenoma
-inpatient: metastatic disease (esp. breast cancer)
12. pH from 7.0 to 7.4, [H] less than half; from 7.4-7.0, [H] more than double
13. Pyloric stenosis: hypokalemic, hypochloremic, metabolic alkalosis
-signs and symptoms: projectile vomitting, non-bilous, olive mass, stomach peristalsis
14. Four year old boy with pyloric stenosis and 25% dehydration. Fluid for resuscitation: D5 0.45NS with 30
mEq Kcl at 25cc/h
15. Neonatal nutritional needs:
-90-120 kcal/kg/day
-Free H2O
-Na 3-5 mmol/kg/day
-K 2-3 mmol/kg/day
-protein 2-3.5 g/kg/day
16. When giving contrast dye, to avoid renal insufficiency: ensure patient is well hydrated
17. Ringer’s lactate: Na 130, Cl 109, Ca 3, K 4, HCO3- 28
18. Emphysema does not cause respiratory alkalosis
19. Urinary Na > 40 suggests renal cause to acute renal failure
20. Hypoaldosteronism (Addisonian crisis): everything decreased except K (will be )
21. Hyperaldosteronism: hypokalemia, hypertension, Na and H2O retention
193
22. Hyperadrenalism: hypokalemia, hypervolemia, hyperglycemia, hypernatremia, hypertension but NO delayed

closure of growth plates
23. Site of action of aldosterone: distal tubule
24. Diabetes causes polyuria with increased specific gravity
25. Mannitol: increased osmotic diuresis, hyponatremia, increased serum osmolality
-does not cause cellular overhydration
26. Renal clearance: removal of a substance for blood per unit time (Cx = UcV/Px)
27. Anion gap = Na - (Cl + HCO3); non-anion gap seen in diarrhea
28. Hyperkalemia does NOT cause paralytic ileus
29. Symptomatic hyponatremia < 120 treated with hypertonic saline
30. Most likely cause of hyperosmolar diuresis is DM
31. In DI, urine is most dilute in collecting ducts
32. Renin levels decrease in primary hyperaldosteronism
33. Albumin contributes to 70% of oncotic pressure; t ½ = 18-21 days
34. Albumin contributes to anion gap
35. Excretion of acids: 1/3 titratable acids and 2/3 ammonium
36. Main action of Ca is to muscle contractility
37. Patient with advanced cancer presenting with hypercalcemia. Initial treatment: normal saline with lasix
38. Bone fractures do not cause hypercalcemia
39. Patient with hyperkalemia. Treatments: insulin and dextrose, kayexalate, Ca gluconate, Lasix
40. Propranolol does NOT lower serum potassium
41. Suggestion of ATN:
-urine Na > 40
-FeNa > 2-3%
-urine osmolality < 350
42. PTH: net effect serum Ca and serum PO4
- Ca and phosphate absorption in intestine
- Ca and PO4 excretion in kidney
- Ca and PO4 resorption in bone
43. DI:
-central: failure to secrete ADH from hypothalamus
-nephrogenic: kidney unresponsive to ADH
44. Osteomalacia bone matrix and mineralization
45. Osteopenia bone matrix and normal mineralization
46. Characteristic radiologic finding in primary hyperparathyroidism: subperiosteal resorption of bone of the
radial aspect of middle ....?
47. Increased renin does not increase ADH
Nutrition
1. Salivary amylase inactivated by low pH in the stomach (optimal pH = 7)

2. Elevated LFTs with TPN
-not associated with any other abnormalities
-usually not clinically significant
-may occur regardless of patients’ nutritional status
-possibly due to excess lipids to glucose ratio
3. TPN solution of 20% dextrose and 5% amino acids infusing at 42 cc/h (1L/d):
-Daily non-protein calories: 720 kcal (dextrose = 3.4 kcal/g)
-Daily nitrogen load: 8g (6.25g AA = 1g nitrogen)
4. Carbohydrates in TPN at rate no greater than 5mg/kg/min
5. Fat administered in TPN at no more than 2.5g/kg/min
194
6. Complications of enteral feeding, except: hypoglycemia

7. Primary source of nutrition for enterocytes: glutamine
8. Arginine:
-improves wound healing
-improves macrophage function and enhances cellular immunity (antitumour)
9. Starvation:
-carbohydrates supply energy for >24h
-fat is anhydrous compared to proteins and carbohydrate stores and is more calorie dense (9.4 kcal/g)
-protein catabolism increased (10g of nitrogen per day)
10. Best/safest site for long-term TPN: subclavian vein
11. Patient on TPN with renal insufficiency. Best means to determine amount of proteins to be given: creatinine
levels
12. Best indication for TPN: severe pancreatitis
13. Free ammonia is formed from metabolism of cells in the gut; ?most derived from deamination of amino acids
in the liver
14. Patient with central line and TPN - 4 days later becomes febrile. Best initial management: draw blood culture
from line and from periphery
15. Best way to assess successful enteral feeding by ?BM <600cc/24h
16. Best time to start pre-op TPN: 2 weeks pre-op (Schwartz: 7-10days)
17. Serum creatinine is a reflection of skeletal muscle breakdown
18. Starvation does not increase metabolic rate
19. Action of lipoproteins: to carry cholesterol
20. Patient on TPN presents with Na 119, K3.5 Cl 140, BS 13. Likely situation: excessive H2O has been given
21. Best method to confirm dx of iron deficiency anemia: lack of stainable iron
22. Zinc deficiency: dermatitis, wound healing problems
23. Copper deficiency: microcytic anemia
24. Selenium deficiency: muscle pain, fatal cardiomyopathy
Hemostasis, Surgical Bleeding, and Transfusion
1. Best pre-operative screening for bleeding risk: history and physical (ie. prior bleeding problems)
2. Heparin actions:
-inhibition of antithrombin III
-increases PTT
3. Coumadin:
-vitamin K antagonist
-prevents carboxylation of factors II, VII, IX, and X (“1972")
4. Major crossmatch: mixing donor RBC with recipient serum
5. Minor crossmatch: mixing donor serum with recipient RBC
6. Patient with obstructive jaundice and hypoprothrombinemia: due to poor fat absorption (unable to absorb
vitamin K)
7. Acute DVT management: Heparin 5000u IV bolus followed by 800-1000u/h infusion
8. Most common cause of transfusion related death: Hepatitis C
9. Management of hemolytic transfusion reaction:
-most important: stop transfusion
-least important: Lasix
-others: IV hydration, alkalinization of urine, Lasix or Mannitol, Foley
10. Patient with VonWillebrand’s disease going for surgery:
-DDAVP prior to surgery
-if active bleeding, use cryoprecipitate
11. Woman with hypernephroma, on coumadin for MVP, presents with gross hematuria. 4 units PRBC given
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and she is now stable with INR 2.2, Hb 98. Next step is: give FFP
12. VonWillebrand’s disease: autosomal dominant, most common bleeding disorder (1% population), variable
expression
13. Risk of infection from donor increases with number of units transfused
14. Defect in CRF hemostasis: Quality of platelets bleeding time prolonged
15. Papaverine does not affect platelet function
16. Sickle cell disease: presence of fetal hemoglobin does not promote sickling
17. Side effects of protamine:
-hypotension (most common)
-pulmonary hypertension
-anaphylaxis, n/v
18. Most common complication of massive transfusion: dilutional thrombocytopenia/hypothermia
19. Most common coagulation defect: dilutional thrombocytopenia
20. Most common cause of asystole from massive transfusion: hypothermia
21. Most common cause of febrile transfusion reaction: WBCs in donor blood
22. Patient with hemophilia going for surgery. Need 30-60% factor VIII activity before, during and after surgery
for at least 2 weeks. Ideally for surgery, levels should be 80-100%.
23. Classical hemophilia: mild (>5% factor VIII activity); moderate (2-5%); severe (<2%)
24. Most characteristic in classical hemophilia: prolonged PTT (normal PT and bleeding time)
25. Platelet transfusion can transmit syphilis if stored at room temperature (should be stored at 4oC)
26. Albumin and plasma proteins do not transmit hepatitis and syphilis
27. Patient receiving transfusion intra-op begins bleeding from operative field and decreased urine output
-hemolytic transfusion reaction
-stop transfusion, infuse saline and mannintol/lasix etc.. (“all except: steroid”)
-check recent hemolytic reaction: urine free hemoglobin
28. Father with hemophilia: all his sons will be normal, his daughter will be carriers
29. Oral contraceptives predispose to DVTs by:
- antithrombin III levels
- protein S
- fibrinolytic activity
- coagulation factors (fibrinogen, VII, VIII, IX,X)
30. Platelets secrete:
-alpha granules: PDGF, TGF-B, IGF-1, fibronectin, fibrinogen, thrombospondin, vWF
-dense bodies: serotonin
-lysosomes: hydrolases and proteases
31. Heparin-induced thrombocytopenia:
-due to antibody formation directed towards heparin and platelet surface
-treatment: stop heparin (can use danaparoid, hirudin, or LMW heparin)
32. Post massive transfusion (48h): pCO2 40, CVP 15, pO2 50 on 100% most likely cause is pulmonary edema
33. Primary fibrinolysis: euglobin lysis time, fibrinogen, FDP
34. EACA inhibits plasminogen activation - for treatment of primary fibrinolysis
35. Factor VIII:C produced by endothelial cells (also in liver); other coagulation factors made by liver
hepatocytes
36. TTP improves with steroids and splenectomy; high success rate with plasmapheresis
37. Elevated PT in: coumadin use, extrinsic pathway defects, VII deficiency
38. DIC: diffuse bleeding, PT and PTT, fibrinogen, FDP; must treat primary cause
39. Blood volume increases with all except: hepatic venous congestion
40. Hypofibrinogenemia is associated with DIC, cancer of prostate, advance liver disease
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Surgical Infections
1. Clean contaminated operations:
-entering respiratory tract, GI, GU, gyne procedures
2. Antibiotics given 30 mins prior to incision
3. Endocarditis prophylaxis prior to GU procedure: Penicillin (Vancomycin if allergic) and Gentamicin
4. Best method to diagnose C.difficile colitis: C.difficile toxin
-tx: oral or IV metronidazole: oral vancomycin
5. Subcutaneous air NOT pathognomic for clostridial myonecrosis
6. Skin preparations:
-best for persistent effect: Chlorhexidine
-immediate reduction of bacterial counts: Alcohol
7. Shave 24 hours before surgery increases chance of wound infection
8. Tetanus:
-booster every 10 years
-2yo never vaccinated, with laceration: tetanus toxoid and TIG at different site (plus future doses)
9. Endocarditis prophylaxis required for esophagoscopy with sclerotherapy injection
10. Abscess secondary to Bacteroides fragilis, best Abx: Clindamycin
11. Parotitis: most common organinsm is Staph. aureus; best Abx is cloxacillin
12. Strep gives diffuse erythematous rash use penicillin
13. Central line infection, most likely organism: Staph. epidermidis
14. Pre-op antibiotics for inguinal hernia repair: 1st generation cephalosporin (Ancef)
15. Patient with chills and fever 6 hours after insertion of Foley catheter, first thing done: blood cultures
16. Most suitable agent to sterilize surgical instruments: glutaraldehyde
17. Rabies:
-single stranded RNA virus
-Boy bitten by neighbourhood dog, best management: quarantine dog for 10 days do not treat for rabies
-Treatment if not vaccinated: local wound management, HRIG 20IU/kg (½ in wound, ½ IM gluteal), and
vaccine (HDCV or RVA) 1.0 ml deltoid for 5 doses (days 0,3,7,14 and 28)
18. Most common etiology of CJD: corneal transplant
19. Post-splenectomy organisms: S. pneumonia, H. flu, Neisseria sp. (encapsulated organisms)
20. Punctured right index finger swollen finger: tenosynovitis
21. Most common etiology for isolated aortic regurgitation: Endocarditis
22. C-section: prophylactic antibiotics given after cord is clamped
23. Patient does not need prophylaxis for cardiac catheterization
24. Strep causes erythema with serous exudate, even with bacterial count of 103/gm tissue
25. Most likely cause of wound infection from domestic animal bite: Pasteurella multocida
26. Most likely cause of wound infection from human bite: Staph and strep; Eikenella corrodens (15%)
27. Least likely to require prophylactic antibiotics: history of rheumatic fever as child
28. Most common cause of empyema is pneumonia
29. Central line infection:
-staph epi: can use sterilized line again
-staph aureus: remove line, 48 hours w/o line, Abx for 6 weeks
30. Toxic shock syndrome staph aureus toxin
31. Most common nosocomial infection: UTI
32. Most common organism causing nosocomial pneumonia: gram negatives (pseudomonas)
33. Systemic candidiasis frequently seen in immune suppressed patients
34. Treatment of chlamydia: doxycyline
35. Pseudomembranous colitis associated with any antibiotics (esp. clindamycin, ampicillin, cephalosporins)
36. Patient with tissue expander, presents with redness and discharge from area. Management: remove expander
37. Patient had C-section, on 1st generation cephalosporin and develops temperature post-op. Additional
coverage for: ?gram-negatives vs. enterococcus
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38. Surgicele has bacteriocidal property

39. Maculopapular rash over V3 distribution treated with acyclovir
40. Bladder cancer does not increase the chance of UTI
41. Patient on TPN with episode of bacteremia. Most common source of infection: infection along outside of
catheter
42. Endotoxin released from cell wall
43. Mechanism of bacterial resistance to antibiotics is production of penicillinase, mutation..
44. Most common cause of adult bronchiectasis: childhood pulmonary infections
45. Gram positive cocci: staph aureus, staph epi, strep pyogenes, strep viridans, strep pneumonia, anaerobic strep
46. Gram negative cocci: moraxella cataralis, niesserria sp
47. Most common presenting symptom in otitis media: pain
48. Immune compromised patient with severe sepsis, best regimen: aminoglycoside and piperacillin
49. Least likely bacteria found in human bite: pseudomonas
50. Major constituent of stool bacteria: E.coli vs ?bacteroides
51. Cellulitis and lymphangitis: usual organism is streptococcus
52. Penicillin is the drug of choice for Corynebacterium and diptheria
53. Most common organism found in mouth: strep viridans
54. Health care worker with herpetic whitlow should be relieved of OR duties until lesion is healed
Infectious Disease in Surgery
1. Patient with mononucleosis like presentation in whom you suspect HIV:

-ELISA best screening test; Western blot best confirmatory test
2. Hepatitis B:
-65% of new infection will be subclinical
-10-15% will be chronic
3. Kaposi’s sarcoma:
-10% AIDS patients of those 10% will die 1% incidence of death by Kaposi’s sarcoma in AIDS
4. Best method for diagnosis pneumocystis carinii: BAL; second: lung biopsy
5. Most common infection transmitted to operating room personnel: HBV
6. Needlestick injury (risks of contracting diseases):
-HIV: 0.3% (~1/200)
-HCV: 3.3%
-HBV: 33.3%
7. HAV transmitted via fecal-oral route
8. HCV detected within 6 months of exposure
9. Best protection from contracting AIDS: universal precautions
10. HIV is least transmissible in saliva
11. CNS infections in AIDS: toxoplasmosis, CMV, herpes, cryptococcus, TB, progressive multifocal
leukoencephalopathy
Trauma
1. Basically intubate everyone with airway problems
2. Most common cause of hypotension post trauma: hypovolemia
3. Child with head injury, decision to sending patient home based on length of time he was unconscious
4. Child with poor IV access:
-percutaneous peripheral vein, saphenous vein, venous cut down
-intraosseus up to 6 years (emergency)
5. Aortic tear most commonly in decelerating injuries at the level of ligamentum arteriosum distal to left
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subclavian artery
6. 40yo male, MVA, HR 140 RR 40 deviation of trachea: 14 gauge needle to 2nd ICS followed by chest tube in
5th ICS AAL
7. Revised trauma score, Triage score and Abbreviated injury scale take all into account except: urine output
8. Hemotympanum: mostly associated with base of skull fracture
9. MVA, widened mediastinum and loss of left CVA aortogram
10. Complete tracheo-bronchial disruption presents as: Massive air leak in chest tube with no lung expansion
11. Signs of ruptured diaphragm: air fluid level in lower lung field with NG tube in lung on CXR
12. Woman 36 wks gestation involved in MVA. Abdominal pain, uterus hard tender, bleeding PV: abruption
13. Treatment of neurogenic shock does not include MAST pants
14. Management of patient with spinal cord injury. First thing to do is manage airway
15. Best time to get critical x-rays in trauma is: after primary survey
16. Pathophysiology of neurogenic shock: increased venous capacitance due to decreased peripheral resistance
17. Most common complication of CSF leak: meningitis
18. Patient with knee dislocation and absent distal pulses. After reduction, pulse returns but remains weak do
femoral angiogram
19. DPL positive except: amylase level 20IU (should be over 80IU)
-poor for assessing retroperitoneal hematoma
20. Goal of CPR: maintain cerebral perfusion
21. Carotid sheath exposed due to injury. Best managed by: primary closure
22. Know GCS scoring
23. Cephalic vein should be catheterized for hypotensive MVA patient
24. Pelvic fracture, still showing signs of hemorrhage despite volume resuscitation. Next step: apply external
fixator.
25. Chest tube drains 1200cc blood originally followed by 600cc in next 3 hours. Next step: thoracotomy
-most common source of bleeding: intercostal artery
-indications:
->1500 cc initially
->200cc/h for 4 hours
->100cc/h for 8 hours
26. Relief of symptoms immediate with aspiration of pericardial effusion
27. Spinal cord injury having intact sensation, flaccid paralysis in upper limbs and able to hold lower limbs
against gravity. Patient has: central cord injury
28. Patient with extensive facial fractures:
-fixation can be delayed until patient is more stable
-CT is best method for evaluation
29. Revised Trauma Score: GCS, RR, BP
30. Cranial nerve injury most commonly seen with intracranial injury: olfactory (I)
31. Cranial nerve injury most commonly seen with increased ICP: abducens (VI)
32. Compartment syndrome:
-most reliable sign: pain out of proportion to injury and on passive movement
-least reliable sign: absent pulses
33. Child with supracondylar fracture of humerus. Suspect Volkmann’s ischemic contracture. Confirm with:
pain on passive extension of fingers
34. Treatment for frostbite: rapid rewarming of extremities
35. Child presents with frost bite hands and feet, you should: elevate the core temperature if significantly reduced
36. Post MVA, bleeding at urethral meatus with comminuted fracture of pelvis: retrograde urethrogram
37. Common finding in IVP for trauma patient: decreased perfusino with renal contusion
38. Most sensitive indicator of pericardial tamponade is: ?pulsus paradoxus
39. The following ICP in trauma: hyperventilation, elevating HOB, loosen tight clothing around neck, mannitol
-except: steroids
40. Most common solid abdominal organ injured in blunt injury: spleen
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41. Most common viscus abdominal organ injured in blunt injury: duodenum
42. Most common organ abdominal injured in penetrating injury: liver
43. Coverage for distal 1/3 of tibia: musculocutaneous free flap
Burns
1. A man with 1st degree burns to face, 2nd degree burns to anterior thorax and abdomen, circumferential burns
to right thigh and lower leg. Body surface affected: 36%
2. STSG will have better take on contaminated surface than FTSG
3. Less contraction with FTSG, better cosmetic results (skin colour matching)
4. Respiratory complications most common cause of death in burn patients
5. Most common cause of pneumonia is via bronchoalveolar route (vs. hematogenous route)
6. Parkland formula for burns: 4cc/%burn/kg. 50% in first 8 hours and 50% in next 16 hours.
7. Patient with inhalational injury, first step in management: secure airway
8. Patient with inhalational injury, all execpt: tracheostomy
9. Unconscious patient with head injury in a house fire is most likely to have inhalational injury
10. Inhalational injury will require more fluids than calculated by Parkland formula
11. Most sensitive sign of inhalational injury: carbonaceous sputum
12. Severity of inhalational injury proportional to time of exposure, closed room
13. Most important s/e of silver sulfadiazine: leukopenia (neutropenia)
14. Alkali causes liquefaction necrosis; acids causes coagulation necrosis
15. 14 yo with 25% partial thickness burns to left side of face, chest and upper arm. Most appropriate initial
management: assessment and treatment of respiratory system
16. Patient with 3% full thickness burns secondary to molten metal in the middle of the back. Treatment of
choice: early excision and skin grafting
Wound Care and Wound Healing
1. Site of enzymes to destroy tissues during inflammation is: polymophonuclear neutrophils

2. Collagen:
-via fibroblasts
-begins depostion: 10 hours
-peak rate of synthesis: 6-7 days
-maximum content: 6 weeks (42 days); cross-linking: 6 weeks
-tensile strength:
-30% at 3 weeks
-most rapid increase in first 6 weeks
-maximum at 1-2 years - reaching only 80% of original skin strength
-rate limiting step in synthesis: hydroxylation of proline
3. Strength of incisional wound does not increase until collagen is deposited
4. Polypropyline suture:
-least reactive (amongst those listed in question)
-maintains tensile strength at 2 months (~90% one year)
5. Best property of dressing a wound: decreases disruptive physical forces
6. In musculocutaneous free-flap, skin is least sensitive to ischemia
7. Sutures provide the maximum strength of a wound at 3 days
8. Predominant cell type at 7 days: fibroblasts
9. Elastin:
-decreases with age, has elastic recoil, no effect on tensile strength, present in skin and blood vessels
-any defect of elastin in aorta dissecting aneurysm
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10. Keloids extend beyond the margins of the surgical wound; best treated by steroid injections; difficult to
distinguish microscopically from hypertrophic scars
11. Best moisture barrier: keratinocytes in epithelium
12. Effect of delayed wound healing due to radiation caused by: Damaged endothelium
13. Steroid effects:
-inhibit inflammatory response
-inhibit fibroblast proliferation
-inhibit protein synthesis in wound
-delays wound contracture
-alters t-cell function
-decreases tensile strength of closed wound
-retards epithelialization and angiogenesis
14. Chronic steroid use causes thinner dermis than normal with less collagen
15. Steroid effects can be reversed by: Vitamin A
16. Hypertrophic:
-increased water content, beta-growth factor
17. In urine, best indication of collagen breakdown: hydroxyproline
18. Donor site on thigh for STSG heals by epithelialization
19. Severity of contracture which could affect the patients function is influenced by: site and depth of the wound
20. Pyoderma gangrenosum:
-hypersensitivity vasculitis seen in Crohn’s, UC, RA, lymphoma, leukemia
-50% idiopathic
-tx: dapsone, steroid therapy and local wound care
21. Best indicator of muscle viability is bleeding after incision
22. Staples, suture and tape provide same strength to healing wound
23. Staples better than sutures when it comes to wound infection
24. Bone remodelling continues even after 6 months. Osteoclastic activity is the dominant force.
25. Regeneration can occur from cell of the following except: ?dermal papilla
26. Macrophages digests tissue within an abscess
27. Wound infection most likely to occur from normal flora of skin
28. Most important factor to prevent wound dehiscence is: surgical technique
29. Dermal papillae: basal cell layer; does not contribute to epithelialization
30. Repair of peripheral nerve, the least and last function to be retained: two point discrimination
31. Vitamin C required in hydroxylation of proline and lysine in collagen synthesis
Oncology
1. Transcription of mRNA from DNA occurs in the nucleus catalysed by RNA polymerase
2. Translation occurs on ribosomes; synthesis of protein from mRNA sequence
3. Most specific finding for malignancy histologically: mitotic figures and prominent nucleoli
4. Tumour arising from sympathetic nervous system in pediatric population: Neuroblastoma
-most common abdominal tumour in children between 2-4 years
5. Tumour associated with SIADH: small cell (oat cell) ca
6. Symptomatic malignant pericarditis: treat with intraoperative pericardial window
7. Alkylating agents: non-cell cycle specific
-cyclophosphamide, busulphan, cisplatin, dacarbazine, chlorambucil, mustard gas
8. Most serious side effect of 5FU (cell-cycle specific): myelosuppression
9. Most important side effect of bleomycin: pulmonary fibrosis
10. Most important effect of doxorubicin: cardiac toxicity
11. Vincristine (cell-cycle specific, m-phase):
-prolonged ileus, peripheral neuropathy, alopecia, mild myelosuppression, ADH effect, vesicant
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12. Cyclophosphamide:
-alkylating agent, non-cell cycle specific
-s/e: hemorrhagic cystitis, neutropenia, n/v, alopecia, infertility
13. Most likely tumour to cause hemorrhage after metastasis to brain: melanoma
14. Colon carcinoma least likely to metastasize to bone (PTBLK)
15. Aneuploidy:
-absence of normal complement of DNA
-most common genetic aberration seen in malignant cells
16. Brachytherapy gives least radiation to the skin
17. Multiple ports used in radiation therapy because it protects radiosensitive tissue
18. Molecular oxygen enhances the effects of radiation
19. Radiotherapy most dependant upon:
-adequate oxygen tension
-mitosis
-vascularity
-temperature
20. Most common neoplasm associated with Paget’s disease: Osteosarcoma
21. 35yo with previous history of radiation, has solitary asymptomatic thyroid nodule, cold on thyroid scan and
FNA consistent with thyroiditis. Next step: thyroidectomy
22. Sero-sanguinous discharge from single breast duct. Concerned about cancer.
23. Mortality from cancer in females: lung breast colorectal
24. Mortality from cancer in males: lung prostate colorectal
25. Incidence of cancer in males: prostate lung colorectal
26. Patient with lump in breast 2 cm in size, last month 3 cm in size. Next step: FNA
27. Patient with 2cm neck mass in upper cervical nodes of 2 months duration. Plan should be: examination of
aerodigestive tract first, then FNA
28. Pain control in cancer patients: use of ASA may potentiate the effect of narcotics
29. Fractionation of radiation allows normal tissue to heal between doses
30. Oncogenes: genes that, when expressed, contribute to the development of malignancy
31. Proto-oncogenes: genes found in normal tissues that, when activated may lead to transformation of the cell to
a malignant phenotype
32. Best method to perform anterior scalene lymph node biopsy: borders of dissection should include internal
jugular vein lateral, omohyoid muscle superior
33. Most common cause of SVC obstruction: small cell ca
34. Antidote to methotrexate: folinic acid (leucovorin)
35. Barrett’s esophagus: most predictive of malignancy in severe dysphagia
36. Pathological changes in radiation pneumonitis:
-1h-1day: immediate release of surfactant
-1-3 months: compensatory swelling of type II cell
->3 months: disappearance of type II cell and alveolar collapse
37. Malignant melanoma: ratio of white:black = 20:1
38. 2cm lesion on bone scan can been because of: osteoblastic activity
39. Nasopharyngeal carcinoma most commonly presents as: neck mass (60%)Changes in skin secondary to
radiation:
-end arteritis obliterans, atrophic skin changes, erythema, hyperpigmentation
40. Radiomimetic chemotherapy: alkylating agents
41. Anti-tumour agent produces its effect on tumour cells by decreasing the number of tumour cells by a constant
fraction
42. Neoadjuvant chemotherapy: chemo used prior to definitive tx (eg. surgery or radiation)
-benefits: size of tumour, determines response to chemo to predict the efficacy in an adjuvant setting
43. Lesions associated with malignant melanoma: Lentigo maligna, congenital nevus, dysplastic nevus
44. 40 year old asymptomatic, CT scan shows 2 cm adrenal mass. Most likely adenoma
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45. Pancreatic Ca:

-anatomic distribution: 70% head, 20% body, 10% tail
-LFTs: bili, ALP, sl. transaminases
-glucose intolerance
-occasional elevation of amylase, lipase
46. Prostate Ca does not metastasize to lung and brain
47. Tumours associated with increased alpha-fetoprotein: hepatocellular ca, choriocarcinoma, testicular teratoma,
endodermal yolk sac tumour of ovary
48. Alpha-fetoprotein: higher in cigarette smokers, useful in detecting recurrence of colon cancer
49. Clarke stage I melanoma with no inguinal metastasis. Management: 2 cm margins with no inguinal dissection
50. Metastatic spread to lymph nodes first to sub-capsular area
51. Rectal and anal tumour treatment: combination surgery and radiation therapy
Transplantation and Immunology
1. Apoptosis: programmed cell death (with reaction of T-cells)

2. Allograft: tissue from different individuals of same species
3. Hyperacute rejection:
-due to preformed antibodies
-characterized by PMN infiltration and complement-mediated injury to vascular endothelium
4. Acute rejection mediated by T-cells
5. Chronic rejection may be due to antibody response, cell-mediated response or combination of the two
6. T-cells: suppressor, helper and cytotoxic
7. Screening of donors for organ transplantation does NOT include Legionella
8. Variable portion of light and heavy chain confers specificity of antibody to antigen binding
9. OKT3 most antigenically specific agent in prevention of graft rejection
10. Highest immunogenicity: skin
11. HLA on chromosome 6
12. Class I antigen:
-encoded on chromosome 6
-expressed in all nucleated cells except neurons
-targets of CD8+ cells (cytotoxic cells)
13. Antigen present cells of skin: Langerhan’s cells
14. BCG: active, non-specific immunization
15. Cyclosporin:
-specific immunosuppressant
-s/e: hepatotoxic, nephrotoxic, neurotoxic, gingival hyperplasia, hypertrichosis, hypertension
-increased incidence of lymphoma, may be diabetogenic
16. CMV:
-DNA virus
-most common infection in transplant patients (esp. cardiac > renal)
17. Specific immunosuppressive effects: cyclosporin, OKT3, ALG
18. Tumours in immunosuppressed patients:
-epithelial tumours: SCC
-mesenchymal tumours: lymphoma (10-100x than general population)
19. Signs of renal transplant rejection:
-pain, fever, leucocytosis, proteinuria, hypertension, oliguria anuria, increase in graft size
20. Delayed hypersensitivity reaction:
-requires more than 5days to appear
-requires previous exposure at least once
21. Primary immunoglobuin response: IgM; secondary immunoglobulin response: IgG
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22. IgA released in aerodigestive tract and GI tract

23. Function of spleen is to produce gammaglobulins
24. Optimal immune response: B-cell, T-cell, macrophages
25. Most common cause of death in post-transplantation: infection
Surgical Complications
1. Contraindications to elective surgery: subendocardial MI one month ago (<6months)

-Goldman Index: S3 gallop, PVC > 5/min, non-sinus or PAC on last preoperative ECG, age > 70,
emergency operation, intrathoracic, intraperitoneal or aortic site, significant AS, poor general medical
condition
-highest risk for non-cardiac surgery: MI, unstable angina, CHF, arrhythmia, valvular heart disease
2. FEV1: objective means of assessing lung function pre-op
-increased risk if FEV1 <50% for thoracic procedures; <30% for other surgeries
3. Increased pulmonary complications of PaCO2 > 45 mmHg
4. Most common complication of popliteal aneurysm: Thrombosis (40%)
5. High output renal failure resolves spontaneously
6. Management of post-obstructive diuresis: replace 50% of urine output with D5W
7. A fistula in GI tract will not heal if there is 200cc/day output
8. Tracheostomy:
-1st ring: subglottic stenosis
-5th ring: tracheo-innominate fistula
9. Post-esophageal dilation esophageal rupture (pneumomediastinum, chest pain, subQ emphysema).
Management: OR for primary repair within 6 hours
10. Most common complication using cautery: cutaneous burns
11. Monopolar: more tissue injury vs bipolar
12. Venogram is gold standard in detecting DVT in lower limb
13. Insertion of IVC filter NOT indicated in streptokinase allergy
14. 6 hours post-splenectomy, patient develops fever of 39oC, most likely cause: atelectasis
15. Vertical incisions do not contribute to wound dehiscence in laparotomy
16. Post-thyroidectomy patient has acute airway compromise and swollen neck. Initial management: open the
incision and evacuate hematoma
17. Best test to assess tracheal function after repair of tracheal stenosis: Maximum expiratory flow
18. Testicular torsion presents with decreased epididymal flow on ultrasound
19. Acute onset of left testicular pain: emergent surgical exploration
20. Patient POD#4 abdominal surgery with left leg pain. Femoral pulse barely palpable, pedal pulse cannot be
felt, with leg cyanosed and pitting edema to mid-thigh: ?iliofemoral thrombosis vs femoral artery embolism
21. Patient with asthma on prednisone (20mg/day) for 10 days, if stopping drug: there would be no adverse effect
(has to be used at > 20mg/d for > 3 weeks for adrenal suppression)
22. Fat embolism:
-lipiduria, thrombocytopenia, respiratory failure, PCO2 due to hyperventilation
-symptoms usually 48-72h after insult
-radiographic finding most typically evidenced 24-48h
-most common cause of death: respiratory failure
23. Reflex sympathetic dystrophy:
-pain with emotion and temperature changes
-chronic pale and cool
-hyperhydrosis, smooth skin, ?osteoporosis
-relieved by regional sympathetic block
-mx: local heat, analgesia, physio, alpha-adrenergic blockade, sympathectomy
24. Following TAHBSO, patient found to have asymptomatic pelvic hematoma observe
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25. Most likely finding in patient with early ARDS: refractory hypoxia
26. Most common source of bleeding from tracheostomy: inferior thyroid artery
27. Most common source of massive bleeding from tracheostomy: innominate artery
28. Damage to thoracic duct NOT seen in catheterization of right IJ
29. PE causes less than 10% infarction
30. Cause of hypoxia in PE is due to no perfusion of ventilated alveoli
31. Least sensitive method of diagnosing DVT in legs: history and physical
32. Persanten is NOT and acceptable method for DVT prophylaxis
33. Platelet inhibitors are not effective in DVT prophylaxis
34. Pathophysiology of high output renal failure: retention of BUN
35. Best method to follow glucose levels in a diabetic patient post-op: blood sugar
36. Most likely cause of hypoxia post-op in patient with known IHD: pulmonary edema (2o CHF)
37. Patient with urinary retention, foley inserted giving 1300cc urine. Patient continues to have u/o, most likely
cause: post-obstructive polyuria
38. Patient administered penicillin and develops urticaria and faints. Initial management: epinephrine
39. Most common site for DVT: calf vein (soleus and posterior tibial and peroneal veins)
40. Steroid therapy produces muscle wasting seen first in: pelvic and shoulder region (proximal muscle
weakness)
41. Contrast reaction: urticaria, hypotension, chest pain, dyspnea
42. 30 year old with bilateral hilar adenopathy and non-caseating granulomas on mediastinosopic biopsy:
sarcoidosis
43. Most likely cause of acute scrotum in 30 year old: acute epididymal orchitis
44. ATN: secondary to ischemia, septicemia, tubular toxins (myoglobin, contrast, drugs), acute pancreatitis,
prolonged hypotension
45. All can cause paralytic ileus: peritonitis, retroperitoneal hematoma, opioids, myxedema
46. Gynecomastia caused by: renal failure, liver failure, Kleinfelter’s, adrenal cortical tumours, spironolactone
47. Superficial femoral embolism, definitive treatment is embolectomy
48. Least effective drug in preparing patient with thyrotoxicosis for surgery: phenylephrine
49. Air embolism:
-100-300cc produce typical features
-IV line can be used to release air; place patient in LLD position
-hypocapnic secondary to hyperventilation
50. Pathology seen in ARDS:
-small stiff wet lungs
-atelectatic changes
-patchy diffuse hemorrhages
-alveolar infiltrates
Critical Illness and Physiologic Monitoring of the Surgical Patient
1. PCWP reflects (L) atrial pressure

2. In a patient with PE all the following are present except: PCWP
3. Post-op patient with stable SVT unresponsive to carotid massage. Best drug: adenosine adenosine
verapamil
4. Cardiogenic shock management: start dopamine infusion (old)
5. CVP most accurately taken in a ventilated patient at: End-expiration
6. Arterial embolus most likely to have originated from left atrium
7. VC = TLC - RV
8. All increase shunt fraction except: decreased flow in the bronchiolar arteries
9. Multiorgan failure: each organ involved increases mortality rate by 30%
205
10. 57yo male has infected appendectomy. Several days later he is hypotensive with SVR 600 and CVP 8, most
likely diagnosis: Septic Shock
11. Patient with massive PE and in shock. What would suggest he is a candidate for thrombolytic therapy: he
requires inotropic support
12. Brain death: absence of cerebral blood flow on cerebral angiogram
13. Coronary blood flow is determined by myocardial oxygen demand
14. Diastolic blood pressure is dependent on peripheral vascular resistance
15. Phenylephrine acts on alpha-receptors to cause vasoconstriction
16. Intra-aortic balloon pump:
- MAP, coronary blood flow, peak diastolic pressure, afterload
-contraindicated in severe aortic regurgitation, aortic stenosis, ventricular aneursym, dissection of aorta,
ventricular septal defect, recent prosthetic graft in aorta within 12 months
17. Effects of PEEP:
-prevent alveolar collapse by maintaining FRC above critical closing volume; improves lung compliance
- V/Q mismatch
- venous return CO
- afterload
- EDV
- ICP, CVP
18. Young male with disappearance of distal pulses following exercise can best be explained by: redistribution of
peripheral vascular resistance
19. GFR affected by:
-arterial oncotic pressure, interstitial oncotic pressure, AV pressure difference, renal blood flow
-except: reflux
20. Oxygen dissociation curve:
-SaO2 vs oxygen tension
-right shift: T, [H], CO2, DPG
-left shift: T, [H], CO2, DPG, carboxyhemoglobin
21. ARDS: 4 stages:
-I: hypoxia and hypocapnia
-II: hypoxia and hypercapnia
-III: x-ray changes
-IV: massive x-ray changes
22. ARDS earliest and best indicator: refractory hypoxemia
-PaO2:FiO2 < 200
23. Best method to assess capillary perfusion in a patient with shock: urine output
24. Patient developed A-fib with rapid ventricular response, most effective treatment initially:
-unstable: cardioversion
-stable: digoxin (old)
25. Interstitial pulmonary disease: FEV1, pO2, pCO2, residual volume
26. Best indicator of alveolar ventilation: pCO2
27. Starling’s law: SV relationship to EDV
28. Best treatment for mild digitalis toxicity: stop the drug
29. Cerebral auto-regulation: regulation of brain blood flow according to variation in arteriovenous pressure
30. Best non-invasive test to differentiate primary pulmonary hypertension from thromboembolic pulmonary
hypertension: radioisotope perfusion/ventilation scan
31. At sea-level, mixed venous oxygen of 40 mmHg considered normal
32. One gram of 100% saturated Hb contains 1.39 ml of O2
33. Indications for artificial ventilation:
-PO2 < 70 on oxygen mask
-PCO2 > 50
-alveolar-arterial difference 60 after 100% O2
206
-RR > 25/min

34. Absence of DTR not required for declaration of brain death
Medico-legal/Ethics
1. Surgeon NOT liable when recurrence of breast malignancy occurs when patient enters a clinical trial of
adjuvant therapy
2. Informed consent: if patient decides not to undergo an operation you have to explain the risks of his decision
Statistics
1. Power is determined by Type II error

2. Case control: best retrospective study design to determine if a given result was due to specific intervention
3. Double blind: both investigator and patient do not know who is receiving placebo or drug
4. Standard deviation:
-1 SD = 66%
-2 SD = 95%
-3 SD =99%
207
Methods of Fractionation
Conventional Fractionation:
-1.8-2.2 Gy per day for 5 days/week for 5 weeks (45-55 cGy total)
Method Fractions Dose per Total Total Acute side Late side
per day fraction treatment treatment effects effects
dose time
Hyperfractionation increased decreased increased same increased decreased
Accelerated fractionation increased same decreased decreased increased decreased
Accelerated hyperfractionation increased increased increased decreased increased increased
Hypofractionation same increased same decreased increased increased
Other fractionation schemes include hyperfractionation, hypofractionation, and accelerated fractionation. In

hyperfractionated regimens, the goal is to deliver higher tumor doses while maintaining a level of long-term tissue
damage that is clinically acceptable. The daily dose is unchanged or slightly increased while the dose per fraction is
decreased, and the overall treatment time remains constant. The œ/ß for the tumor must be greater than that of the
dose-limiting tissue.
An additional rationale for hyperfractionation is to allow radiosensitization through redistribution. The greater the
number of fractions, the greater the likelihood that the tumor will be in a sensitive phase of the cell cycle at some
time during the treatment. This strategy invariably results in more intense acute reactions when compared to
conventional treatment.
In the accelerated fractionation schemes, the dose per fraction is unchanged while the daily dose is increased, and
the total time for the treatment is reduced. Three basic variations are possible.
Continuous hyperfractionated accelerated radiation therapy (CHART) is an intense schedule of treatment, where
multiple daily fractions are administered within an abbreviated period of time. An intense acute reaction develops in
most patients. This reaction usually limits the total dose.
In a concomitant boost technique, the first fraction of the day is administered in a larger volume, while the second
fraction is targeted to a reduced-boost field of treatment. The boost may be administered early in the course of
therapy or toward the end of treatment. This regimen is based upon the recognition that the treatment can induce an
accelerated repopulation of the tumor cells so that reduction of the overall treatment time results in improved
control.
Clinical trials are in progress with the goal of evaluating these various altered fractionation patterns and comparing
them to conventional treatment. Preliminary results from the recently completed randomized trial, RTOG-9003,
supports the benefit of altered fractionation over conventional treatment for head and neck cancer.
208
ANTIMICROBIAL TREATMENT GUIDELINES
FOR ACUTE BACTERIAL RHINOSINUSITIS 2004
Sinus and Allergy Health Partnership
ADULTS
Initial Therapy Clinical Bacterio- Switch therapy options (no

efficacy logic improvement or worsening
(%) efficacy after 72 hours)
(%)
Mild disease with no recent antimicrobial use (past 4-6 weeks)

Amoxicillin/clavulanate (1.75-4 g/250mg/d) 90-91 97-99
Amoxicillin (1.5-4 g/d) 87-88 91-92 Gatifloxacin, levofloxacin, moxifloxacin
Cefpodoxime proxetil 87 91 Amoxicillin/clavulanate 4g/250 mg
Cefuoxime axetil 85 87 Cetriaxone
Cefdinir 83 85 Combination Therapy
Beta-lactam allergic
TMP/SMX 83 84
Doxycycline 81 80 Gatifloxacin, levofloxacin, moxifloxacin
Azithromycin, claritromycin, erythromycin 77 73 Rifampin plus clindamycin
Telithromycin 77 73
Mild disease with recent antimicrobial use (past 4-6 weeks) or moderate disease
Gatifloxacin/levofloxacin/moxifloxacin 92 100
Amoxicillin/clavulanate (4 g/250 mg/d) 91 99 Reevaluate patient
Ceftrizxone 91 99
Combination therapy (high-dose amoixillin or clindamycin + cefixime or rifampin)
Gatifloxacin/levofloxacin/moxifloxacin 92 100 Reevaluate patient
Clindamycin and rifampin
F.Ling - Antibiotic Guideline for ABRS (1)
209
CHILDREN
Initial Therapy Clinical Bacterio- Switch therapy options (no

efficacy logic improvement or worsening
(%) efficacy after 72 hours)
(%)
Mild disease with no recent antimicrobial use (past 4-6 weeks)

Amoxicillin/clavulanate (90 mg/6.4 mg/kg/d) 91-92 97-99
Amoxicillin (45-90 mg/kg/d) 86-87 90-92 Cetriaxone
Cefpodoxime proxetil 87 92 Combination Therapy
Cefuoxime axetil 85 87
Cefdinir 84 86
TMP/SMX 83 84 Reevaluate patient
Azithromycin, claritromycin, erythromycin 77 73 Combination therapy
Mild disease with recent antimicrobial use (past 4-6 weeks) or moderate disease
Amoxicillin/clavulanate (90 mg/6.4 mg/kg/d) 91-92 97-99 Reevaluate patient
Ceftriaxone 91 99 Combination therapy
TMP/SMX 83 84 Reevaluate patient
Azithromycin, claritromycin, erythromycin 78 76 Combination therapy (clindamycin or

TMP/SMX plus rifampin)
Clindamycin 79 78
F.Ling - Antibiotic Guideline for ABRS (2)
210
OLFACTORY FUNCTION AND DYSFUNCTION
INTRANASAL CHEMOSENSATION
-adult humans possess at least three intranasal systems:

-CN 0 - nervus terminalis
-high gonadotropin-releasing hormone content (animals)
-CN I: main olfactory system
-CN V: trigeminal somatosensory system
-also: rudimentary vomeronasal organ
ANATOMY OF THE MAIN OLFACTORY SYSTEM
-First olfactory bulb layer:

-neuroepithelium: pseudostratified columnar epithelium situated on cribriform plate and segments
of superior septum and both superior and middle turbinates
-six different cell types:
-bipolar receptor cell
-ciliated cell projects from nasal cavity to brain
-sustentacular (supporting cell)
-microvilli rather than cilia
-insulate bipolar cells and regulate composition of mucous
-deactivate odorants and assist in protecting epithelium from foreign agents
-contain xenobiotic-metabolizing enzymes
-microvillar cell
-located at epithelial surface
-function not well understood
-cells lining Bowman glands
-responsible for most of mucus adjacent to olfactory neuroepithelium
-horizontal basal cells
-globose basal cells
-have potential for giving rise to neurons and nonneural cells
-1000 different receptor genes
-Second olfactory bulb layer (glomerular layer):

-each olfactory bipolar receptor neurons makes synapse with dendrites second order neurons
(mitral and tufted cells) within a glomerulus located within the olfactory bulb
-cells within this layer decrease with age
-Third olfactory bulb layer (external plexiform layer)

-contains the cell bodies of tufted cells
-sends axons through olfactory tract
-Fourth olfactory bulb layer (mitral cell layer)

-contains cell bodes of large mitral cells
-also sends axons through olfactory tract
-granule cells: maintain synaptic contact between tufted cells and mitral cells
F.Ling - Olfactory Function and Dysfunction (1)
211
OLFACTORY DISORDERS
Terminology
-anosmia: loss of ability to smell
-hyposmia or microsmia: decreased ability to smell
-total anosmia: inability to smell all odorants on both sides of nose
-dysosmia: distorted smell perception
Causes of Olfactory Loss (Anosmia and Hyposmia)

-types:
-sensorineural loss: eg. trauma
-conductive loss: eg. nasal obstruction from polyps
-obstructive nasal and paranasal sinus disease: most common

-upper respiratory infection: second most common
-head trauma: third most common
-2/3 of causes due to prior URI, head trauma, nasal and paranasal sinus disease; usually permanent
-other causes:
-congenital:
-familial dysautonomia
-Kallmann’s syndrome
-autosomal dominant
-hypogonadotrophic
-anosmia secondary to incomplete olfactory bulb and stalk, hypothalamus, or
olfactory epithelium -
-iatrogenic: septoplasty, rhinoplasty, turbinectomy, XRT
-intranasal neoplasms
-intracranial tumours
-olfactory groove meningiomas, frontal lobe glioma, pituitary adenoma, meningioma)
-epilepsy
-psychiatric disorders
-exposure to environmental chemicals, medications
-smoke, sulfur dioxide, putrid gases, cocaine, cadmium, heavy metals, radiation,
chemotherapy
Causes of Olfactory Distortions (Dysosmia)

-usually reflect dynamic elements associated with degeneration of the olfactory epithelium
-aura-like hallucinations
-psychiatric disorder
Causes of Heightened Smell Function (Hyperosmia)

-rare
-epilepsy
Influences of Aging on Ability to Smell

-decreases with age; between ages 65-80 ~50% have decreased ability to smell
-olfactory dysfunction maybe the first sign of AD and idiopathic PD
212
CLINICAL ASSESSMENT AND PATIENT MANAGEMENT
Olfactory Testing
-reliability of a number of olfactory tests is low
-UPSIT (University of Pennsylvania Smell Identification Test)
-4 booklets containing 10 odorants a piece
-multiple choice (forced choice) with 4 response alternatives
-chance performance = 25%
-very low scores reflect avoidance, and hence recognition of the correct answer
-high reliability
-Electrophysiologic Tests:
-still experimental
-OERPs: odor event-related potentials; not reliable, non-localizing
DETECTION OF MALINGERING
-suspected if pt reports smell loss yet a clear OERP is documented
PATIENT MANAGEMENT
Conductive Olfactory Loss

-allergy management, topical and systemic corticosteroid therapy, antibiotics, surgical intervention (ie.
FESS)
Sensorineural Olfactory Loss

-metabolic and regenerative activity in olfactory epithelium induced by environmental agents
-smoking cessation will improve smoking-induced anosmia
-no treatment for presbyosmia
213
NASAL FUNCTION AND EVALUATION
THE NASAL AIRWAY
Nasal Blood Vessels

-resistance vessels
-control blood flow: arterioles and precapillary sphincter
-exchange vessels (subepithelial capillaries)
-filtration and absorption of fluid: capillaries
-allow for transport of solutes and fluids
-capacitance vessels
-blood volume: venous sinusoids, veins
-arteriovenous anastomoses
-regulate nasal blood flow by allowing blood to flow directly from the resistance vessels to the
venous sinusoids
Vasomotor Control
Sympathetic
-norepinephrine (primary neurotransmitter)
-avian pancreatic polypeptide
-neuropeptide Y
Parasympathetic
-acetylcholine (primary neurotransmitter)
-vasoactive intestinal polypeptide
-peptide histamine isoleucine
Other
-substance P
-stimulation of smooth muscle, vasodilation and stimulation of nasal secretion
-H1 and H2 histamine receptor agonist vasodilator
-leukotriene D2 vasodilator
RESPIRATION
Nasal Airway Resistance

-accounts for more than 50% of total airway resistance
-three areas of resistance
-nasal vestibule
-aka: external nasal valve
-skin-lined region beginning anteriorly at nares and extending to level of caudal end of
upper lateral cartilage
-dilator nares muscles prevents collapse from negative inspiratory pressure
-potential cause of obstruction during inspiration
-nasal valve
-aka: internal nasal valve, limen nasi
-borders: nasal septum, caudal end of upper lateral cartilage, anterior end of inferior
turbinate, nasal sill
-narrowest segment of nasal airway (50% of total nasal resistance)
F.Ling - Nasal Function and Evaluation (1)
214
-nasal cavum
-region posterior to piriform aperture
-engorgement of inferior turbinates contributes to resistance
-resistance can change with posture, disease, physiologic state and psychologic factors
-major sites for regulation of airway resistance:
-dilator nares muscles
-venous sinusoids of nasal turbinates
Nasal Cycle
-intrinsic variability of nasal airway resistance that occurs in cyclic pattern in as may as 40% of persons
-duration 2-6 hours
-positional effect:
-congestion of nasal chamber in lower position
-d/t neural response to stimulation of pressure receptors on surface of body
EVALUATION OF THE NASAL AIRWAY
History
-character of nasal obstruction:
-onset and duration
-constant vs intermittent
-unilateral (tumours, normal nasal cycle) vs bilateral
-associated mouth breathing, snoring, anosmia/hyposmia/taste disturbances, tearing (nasolacrimal
duct obstruction or allergy)
-contributing factors:
-potential toxin and allergen exposure Common Classifications of Drugs that Cause
-known drug allergies Rhinorrhea and Nasal Congestion
-medications -antihypertensives
–history of immunodeficiency, asthma, sinusitis, -psychotropic medications
otitis media, allergy, sleep disturbances, facial -oral contraceptives
trauma or surgery -chronic nasal decongestants: rhinitis
medicamentosa
-associated symptoms: -cocaine: local vasoconstriction
-allergic component (sneezing, itchy and watery -tobacco: irritates mucosa and impairs ciliary
eyes, clear rhinorrhea) clearance
-antithyroid medication
-sinus involvement (facial pain, headaches)
-aspirin: activates peripheral chemoreceptors
-acute infection (fevers, malaise, purulent or -marijuana
odorous rhinorrhea, pain)
-other head and neck symptoms:
-sore throat, postnasal drip, cough, ear complaints, halitosis, ocular pain, hoarseness
Physical Exam
-external nasal exam:
-external deformities, nasal flaring, nasal airflow
-anterior rhinoscopy:
-examine with and without topical decongestion
-quality of turbinates, nasal mucosa
-nasal septum
-osteomeatal complex obstruction
-foreign bodies, nasal masses, choanal opening
-quality of nasal secretions:
-purulent or thick (infectious)
215
-watery and clear (vasomotor rhinitis, allergy)
-salty and clear (CSF leak)
-H&N exam:
-facial tenderness, tonsil and adenoid hypertrophy, cobblestoned posterior pharynx, cervical
adenopathy, otologic exam
Ancillary Test
-allergy evaluation
-paranasal plain films
-CT/MRI
-biopsy of nasal mass
-ciliary biopsy and mucociliary clearance tests
-nasal secretion protein and glucose (evaluate CSF leak if suspected)
-culture and sensitivity
-pulmonary function tests
-olfactometry
-rhinomanometry: provides an objective measurement of airway resistance, largely not utilized in clinical
practice since highly time consuming, not cost effective, and inaccurate
Rhinomanometry
-used to measure pressure needed to produce airflow through nasal airway ie. resistance
-does not measure location of nasal obstruction
-anterior rhinomanometry:
-measurement of transnasal pressure at anterior end of nose
-differential pressure transducer inserted into occluded nostril, difference between atmospheric
pressure and nasal pressure = pressure difference b/n nasopharynx and air = driving pressure for
airflow through unobstructed nostril
-limitations:
-cannot be used in cases of complete occlusion of one nasal passage
-septal perforation or marked flaccidity of septum
-posterior rhinomanometry:
-air pressure in nasopharynx measured with catheter placed in mouth
-interpretation:
-two major types of nasal obstruction: mucosal hypertrophy/congestion and structural deformity
-resistance measured before and after decongestion to determine relative importance of the above
two factors
-nasal resistance greater than 0.3 Pa/cm3/s usually symptomatic
-threshold for subjective obstruction varies
Unilateral Nasal Resistance:

-high variability between individuals
-no strict limits set
Total Nasal Resistance:

-less variable - not affected by nasal cycle
-better predictor of presence of obstructive symptoms
-pts treated for nasal obstruction with septal surgery are more likely to have subjective improvement if
initial nasal resistance is greater than 0.3 Pa/cm3/s
Effect of Decongestion:
-if decongestion causes less than 35% decrease in resistance, a structural cause can be inferred
-eg. septal deformity, conchal hypertrophy, stenosis, concha bullosa
216
Airway Collapse:
-typical rhinomanometric finding of collapse is an asymmetric nasal pressure-flow curve
-collapse only occurs during inspiration, therefore higher inspiratory resistance c/f expiratory resistance
Acoustic Rhinometry
-noninvasive measurement of cross-sectional area of regions of nasal airway
-can help identify location of flow-limiting segments in nasal airway
-results reproducible and accurate
-graph produced of nasal cross-sectional area as function of distance
-able to find narrow segments of airway
-acoustic pulse is introduced and reflected pulse measured
-does not measure effect of narrow regions on airflow dynamics or airway resistance
-area distal to severe constriction may not be accurately estimated
-Characteristics of Rhinograms:
-initial flat tracing = nosepiece
-first depression (I notch) = nasal valve
-second trough (C notch) after a small peak = head of inferior turbinate
-upward slope (climbing W) with small peaks and troughs = posterior nasal cavity and its
increasing cross-sectional area
-region of maximum narrowing ~1.73 cm = region of nasal valve

-vasoconstriction of nasal mucosa does not markedly change this region of narrowing
-subjects with subjective feeling of near total obstruction and objective severe septal deformity
had a mean MCA of 0.3 cm3
217
SINUS ANATOMY AND FUNCTION
EMBRYOLOGY AND DEVELOPMENT
-4th week gestation:

-frontonasal process identified, arises over developing forebrain
-ectodermal
-contributes to nasal capsule
-9th and 10th week gestation:
-nasoturbinals:
-become Agger nasi cells
-ethmoturbinals or basal lamellae
-six ridges on lateral wall numbered anterior to posterior direction; separated by furrows
-first becomes uncinate process
-furrow between first and second becomes ethmoid infundibulum
-second becomes anterior wall of bulla ethmoidalis
-third forms attachment of middle turbinate to lateral nasal wall
-fourth forms attachment of superior turbinate
-fifth to sixth coalesce and disappear by birth
-maxilloturbinal
-becomes inferior turbinate
-inferior turbinate not related to ethmoturbinals
-chronologic sequence of development:

-maxillary (65th day) ethmoid (3rd - 4th month) frontal (4th month) sphenoid (4th month)
-maxillary and ethmoid sinuses are the only sinuses at birth which are large enough to be of
clinical significance
Maxillary sinus:
-first sinus to begin development (65th day GA)
-not evident on x-ray until 4-5 months of age fluid filled
-biphasic growth:
-first 3 years of life
-second growth acceleration between 7-12 ya pneumatization laterally
-slow expansion until 18 years
-adult dimensions: 34x33x23 mm; 15 ml
Ethmoid air cells:

-begin development in 3rd fetal month
-anterior cells as evaginations in middle meatus, then posterior cells in superior meatus
-3-4 cells at birth (most developed paranasal sinus at birth)
-not evident on x-ray until 1 ya
-reach adult dimension by 12 ya
-dimensions: 20x20x10 mm; 15 ml
Frontal sinus:
-begins development during 4th month
-visible usually after 2nd year on radiographs
-sinus invades frontal bone by 5 ya, reaching adult size in late adolescence
-dimensions: 17x28x27; 6-7ml
-4-15% of population: developmental failure of one frontal sinuses present
F.Ling - Sinus Anatomy and Function (1)
218
Sphenoid sinus:
-pneumatization begins at 3 ya
-growth to sella turcica by 7 ya
-adult size by 18 ya
-dimensions: 23x20x17 mm; 7.5 ml
ANATOMY
Ethmoidal Sinus
-lateral wall: lamina papyracea
-medial wall: functions as lateral wall of nose
-midline vertical plate of ethmoid bone:
-superior portion termed crista galli
-inferior portion termed perpendicular plate of ethmoid bone
-roof of ethmoid bone = horizontal plate: separates anterior cranial fossa from nasal cavity
-thin medial portion: cribriform plate
-thick lateral portion: fovea ethmoidalis
-lateral lamella: extremely thin lateral part of cribriform plate
-Keros classification:
-Type I: cribriform plate 1-3 mm below fovea ethmoidalis
-Type II: 4-7 mm below
-Type III: 8-16 mm below
-anterior vertical attachment of middle turbinate to horizontal plate separates cribriform plate from lateral
lamella and fovea ethmoidalis
-dissecting lateral to turbinate prevents entrance into horizontal part of cribriform plate
-presence of Keros type II or III ethmoid roof risk of entering anterior cranial fossa through
lateral lamella
-dome of ethmoid bone in horizontal plate:

-area where anterior ethmoidal artery traverses ethmoid roof
-may cause orbital hematoma if injured
-anterior cells:
-drain into ethmoid infundibulum of middle meatus
-frontal recess cells:
-most anterior cells
-0-4 cells
-form frontal sinus, supraorbital air cells
-infundibular cells:
-next most anterior
-1-7 cells
-agger nasi cells extend outside ethmoid capsule
-represent superior remnant of the first ethmoturbinal
-in close proximity to frontal recess
-often opened during FESS to get better view of nasofrontal duct
-can obstruct outflow of frontal sinus
-bullar cells
-1-6 cells
-consistent location in middle meatus
219
-form bulla ethmoidalis
-may form suprabullar recess if anterosuperior wall of bulla does not reach ethmoid
roof
-uncinate process:
-thin semilunar piece of bone; part of ethmoid bone
-remnant of first ethmoturbinal
-middle turbinate:
-concha bullosa:
-pneumatization of middle turbinate; in 12% of population
-may result in nasal obstruction
-anterior end attaches to horizontal plate
-posterior end inserts laterally on lamina papyracea
-divides anterior from posterior ethmoid cells
-sinus lateralis or retrobullar recess: occurs if posterior wall of bulla ethmoidalis does not
contact third basal lamella
-posterior cells:
-drain into superior meatus
-Onodi cell:
-posterior ethmoid cell that can pneumatize an area of sphenoid bone superior and lateral
to sphenoidal sinus in 9-12% of population
-optic nerve and carotid artery can be exposed and injured during dissection in this area
-vasculature:
-anterior and posterior ethmoid arteries
-maxillary and ethmoid veins (cavernous sinus)
-innervation:
-anterior and posterior ethmoidal nerves (from nasociliary nerve, V1)
Maxillary Sinus
-supraorbital nerve dehiscent in 14% of population
-Haller cell:
-pneumatization of ethmoid complex into the roof to the maxillary sinus
-may occlude ostia
-1st and 2nd molars: two most dehiscent teeth in maxillary sinus (2.2% and 2.0% of persons, respectively)
-removal of teeth may result in oral-antral fistula
-accessory ostia present in 15-40% of cases
-Vasculature:
-maxillary and facial artery
-facial vein
-Innervation:
-infraorbital nerve (V2)
Frontal Sinus
-develops from anterosuperior ethmoidal cells
-frontal recess:
-medial wall: middle turbinate, uncinate process
-lateral wall: lamina papyracea
-posterior wall: anterior face of bulla ethmoidalis
-anterior wall: agger nasi cells
220
-drainage pattern:
-A: UP LP (80%); drainage medial to uncinate process to middle meatus
-B: UP base of skull; drainage lateral to uncinate process to infundibulum
-C: UP middle turbinate; drainage lateral to uncinate process to infundibulum
-vasculature:
-supraorbital and supratrochlear arteries
-ophthalmic (cavernous sinus) and supraorbital (anterior facial) veins
-innervation:
-supraorbital and supratrochlear nerves (V1)
-structure of sinus variable
-anterior wall is strongest, twice as thick as posterior wall
-drainage ostium in posteromedial portion of sinus floor
-Foramina of Breschet: small venules that drain the sinus mucosa into the dural veins
Sphenoidal Sinus
-anatomical relationships of sphenoid ostium:
-face of sphenoid sinus lies 7 cm from nasal sill at 30o angle with floor of nasal cavity
-empties into sphenoethmoidal recess via small ostium
-adjacent to posterior border of nasal septum
-adjacent to posterior border of nasal septum
-0.5-4 mm in diameter
-located 10-15 mm above sinus floor or 30 degree above floor of nasal cavity
-1/3 up from choana to base of skull
-Congdon classification of pneumatization:

-Conchal (5%): posterior extent of sinus well anterior to sella turcica
-Presellar (24%): posterior wall of sphenoidal sinus reaches anterior face of sella turcica
-Postsellar (67%): sinus extends past level of sella turcica to approach pons posteriorly and allows
sell to make superior indentation in the sinus
-cavernous sinus external and lateral to sinus

-bony tubercle surrounding optic nerve dehiscent in 4% of population
-dehiscent internal carotid artery in 7%
-maxillary branch of trigeminal nerve and vidian nerve produce bulges in sphenoidal sinus in 30%
population
-vasculature:
-sphenopalatine artery
221
-maxillary vein (pterygoid plexus)
-innervation:
-sphenopalatine nerve (parasympathetic fibers and V2)
Lymphatic Drainage of the nose and sinuses

-anterior 1/3 of nose submandibular nodes
-posterior 2/3 of nose and sinuses retropharyngeal nodes (Rouviere) and superior deep cervical nodes
222
PHYSIOLOGY
Functions of Sinuses (theories)

-humidification of inspired air
-lightening of skull
-aids in resonance of speech
-increased surface area for olfaction
-absorption of shock to the face or skull
-regulation of intranasal pressure
-secretion of mucous to keep nasal chambers moist
Sinus Epithelium
-pseudostratified ciliated columnar epithelium
-four basic cell types:
-ciliated columnar epithelial cell:
-50-200 cilia per cell; 9+2 microtubule doublets; 10-20 beats/s
-nonciliated columnar cells:
-contain microvilli that expand surface area to improve humidification and warming of
air
-basal cell:
-may be primitive stem cell that can differentiate into other epithelial cells
-goblet cell:
-produce thick mucous after stimulation by irritating substance
-higher amount in maxillary sinus than other sinuses
223
-submucosal glands: serous and mucinous glands penetrate lamina propria
-parasympathetics thick mucous
-sympathetics thin mucous
-density highest at ostia of maxillary, sphenoid, and anterior ethmoidal sinuses
Mucous Blanket
-two layers:
-sol layer:
-thin, periciliary fluid allowing cilia to be mobile
-produced by microvilli
-gel layer:
-upper layer of thick mucous (mucoglycoproteins) that supplies insertion point for tips of
the cilia
-produced by goblet cells and submucosal glands
-provides protection against low humidity and cold
-traps foreign particles and bacteria
-IgA inhibits adherence of bacteria to epithelial surface
-causes agglutination then clearance by phagocytosis
-IgG and interferon to provide antiviral role
-lactoferrin
-transports iron into bacteria antioxidant activity
-lysozyme
-secreted by serous cells
-mucociliary clearance:
-3-25 mm/min towards natural ostium
-maxillary sinus: star-shaped drainage pattern from sinus floor superiorly to ostium
-frontal sinus: medial wall of frontal recess roof lateral downward and medially toward
sinus ostium
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Review of Anatomy: Nose and Paranasal Sinuses Page 1 of 8
Nose and Paranasal Sinuses
A. External Nose
 anterior, caudal portion of nose is cartilaginous, while posteriorly and

superiorly it is bony
 Framework
 Cartilages: greater alar (lower lateral), septal, lateral nasal (upper
lateral), lesser alar, sesamoid.
 b. Bones: Nasal, maxillary, frontal
225
file:///C:/Users/user/Desktop/Dr%20flings%20Notes/Contents/nose.html 3/22/2013
 Musculature: Nasalis, depressor septi, procerus, dilator naris.
226
 Blood supply
 External carotid
 external maxillary: lateral nasal, angular, alar, septal, external
nasal.
 Internal carotid
 ophthalmic, which gives rise to anterior ethmoid, posterior
ethmoid, and dorsal nasal vessels
227
 Lymphatics: facial artery, submandibular, parotid nodal drainage.

 Nerve supply
 Sensory trigeminal
 Ophthalmic division: nasociliary, external nasal, infratrochlear.
 Maxillary division: infraorbital
 Motor facial: buccal, zygomatic branches
B. Internal Nose:
 Floor
 floor of nose is formed by hard palate
 nasal cavity extends as far back as soft palate, where posterior
choanae opens into nasopharynx.
 Roof
 roof of nose is adjacent to anterior cranial fossa
 cribriform plate contains numerous tiny perforations which transmit
sensory fibers to olfactory bulbs
 posteriorly, roof slants downward as anterior wall of sphenoid sinus.
 Lateral Walls
228
 turbinates, three or sometimes four bony shelves covered by erectile

mucosa, project from lateral wall of nose
 serve to increase interior surface area of nose to facilitate heat and
water exchange.
 Inferior Meatus
 inferior to inferior turbinate. Contains orifice of nasolacrimal
duct.
 Middle Meatus
 inferior to middle turbinate. Contains semilunar hiatus, with
openings of maxillary, frontal, and anterior ethmoidal sinuses
 Superior Meatus
 drains posterior ethmoid cells
 Spheno- ethmoid recess
 orifice of sphenoid sinus
 Blood Supply
 Anterior ethmoid - to roof and anterior superior portion of septum
and lateral wall.
 Sphenopalatine - to lateral wall of nose
 Nasopalatine - supplies roof, septum, and floor
 Lateral nasal - supplies lateral nasal wall anteriorly.
 Descending palatine - supplies lateral nasal wall posteriorly.
 Pharyngeal - supplies roof posteriorly
 Posterior ethmoid - supplies septum and lateral nasal wall superiorly
 Septal - supplies septum inferiorly and floor
 Nerve supply
 Medial internal nasal - to septum, anterosuperiorly
 Lateral internal nasal - to lateral wall, anterosuperiorly
 External nasal - to skin of back of nose
 Posterior superior nasal - supplies septum and lateral wall
posteroinferiorly, to middle turbinate
 Posterior inferior nasal - to floor and inferior turbinate
229
 Pharyngeal - to choana
 Anterior superior alveolar - to inferior meatus
 Infraorbital - to vestibule
 Lymphatics: drained by
 Facial venous drainage
 Retropharyngeal
 Superior deep cervical
 Submandibular
PARANASAL SINUSES
These are air- filled, mucosal- lined cavities which develop in facial and cranial
bones. spaces communicate with nasal airway. Their function is unknown but has
been subject to a great deal of speculation. They could serve to decrease weight
of skull or to function as resonators for voice. In lower animals with a more acute
sense of smell, sinuses are largely lined by olfactory epithelium. Sinuses may
have originally developed to increase available surface area for sense of smell.
Therefore, in humans, with olfaction limited to a much smaller area, sinuses may
be vestigial anachronisms.
Though their function is obscure, their medical significance is not. Sinuses

frequently become infected due to obstruction of normal drainage, and negative
pressure in a sinus can cause headache. Neoplasms which arise in sinuses can
be occult for quite a long time, so that they are usually very advanced at time of
diagnosis. There are four groups of sinuses:
A. Frontal - Paired, in frontal bone. Posterior wall is adjacent to anterior cranial

fossa. Usually asymmetrical, occasionally absent.
B. Maxillary - Paired, in maxilla. Superior wall - floor of orbit. Medial wall -

lateral wall of nose. Inferiorly related to tooth- bearing area of maxilla.
C. Ethmoid - Numerous cells in superior and lateral walls of nose, and in medial
walls of orbits.
230
D. Sphenoid - Paired, in sphenoid bone. Sella turcica projects into this space.
231
NASAL SEPTAL ABNORMALITIES
Most common deformity of nasal septum resulting form trauma:

-caudal deformity involving anterior cartilaginous septum
-septum displaced off maxillary crest
Complications from trauma of nasal septum:

-epistaxis
-hematoma
-dislocations of quadrangular septal cartilage
Causes of septal perforation:

-trauma
-digital trauma
-surgery (submucous resection)
-chrome inhalation septal perichondritis
-granulomatous/vasculitic disease
-cocaine
Nasal biopsy in Wegener’s Granulomatosis:

-granulomatous inflammation
-focal necrosis
-fibrinoid degeneration
-multinucleated giant cells
F.Ling - Nasal Septal Abnormalities (1)
232
NONALLERGIC RHINITIS
-nasal congestion, rhinnorhea, sneezing, itching and/or

Causes of Nonallergic Rhinitis
postnasal drainage
-nonallergic = not caused by IgE-mediated Infectious
immunopathologic events -viral
-bacterial
-rhinoscleroma
-rhinosporidiosis
CLASSIFICATION -rhinocerebral mucormycosis
Hormonal
Vasomotor
Infectious Rhinitis Nonallergic rhinitis with eosinophilia syndrome
-aka: coryza, common cold Occupational
-viral infection; spread via infected droplets Drug-induced (rhinitis medicamentosa)
-pathogens: rhinoviruses (most common, >100 types), Gustatory
Atrophic
respiratory syncytial virus, parainfluenza virus, influenza Anhidrotic Ectodermal dysplasia
virus, adenovirus
-SSx and stages:
-dry prodromal stage:
-nasal drying and irritation, low-grade fever, chills, general malaise, anorexia
-catarrhal stage:
-watery clear rhinorrhea, anosmia, congestion, lacrimation, worsening or constitutional
symptoms
-mucous stage:
-thickened rhinorrhea, improved constitutional symptoms
-may result in bacterial rhinosinusitis
-tx:
-usually self-limiting
-antibiotics for suspected bacterial infections only
-symptomatic therapy includes decongestants (topical and systemic), antihistamines, ipratropium
bromide sprays, hydration, humidification, nasal saline irrigations, analgesics, mucolytic agents
Bacterial Rhinitis
-common pathogens: pertussis, diphtheria, group A strep, chlamydia
-tx: antibiotic regimen, symptomatic therapy similar to viral rhinitis
Rhinoscleroma
-pathogen: Klebsiella rhinoscleromatis (Frisch’s bacillus)
-endemic to East Europe, North Africa, South Asia, Central and South America
-SSx and stages:
-catarrhal: persistent purulent rhinorrhea, nasal honey comb-colour crusting
-granulomatous: small, painless granulomatous nodules in upper respiratory tract (including glottis
and subglottis)
-sclerotic: lesion heals with extensive scarring (dense fibrotic narrowing of nasal passage)
-dx: biopsy and culture
-histopathology:
-Mikulicz’s cell: foamy histocytes continuing the bacteria, “moth eaten” cytoplasm
-Russell bodies: bloated plasma cells with bifringent inclusions
-tx: long-term antibiotics, debridement, consider laser excision or cryotherapy
F.Ling - Nonallergic Rhinitis (1)
233
Rhinosporidiosis
-pathogen: Rhinosporidium seebri
-endemic to Africa, Pakistan, India, Sri Lanka, spread from contaminated water
-SSx:
-friable, “strawberry” red polypoid nasal lesion
-epistaxis, obstruction
-dx: culture and biopsy
-histopathology:
-pseudoepitheliomatous hyperplasia, submucosal cyst, fungal sporangia with chitinous shells
-tx: surgical excision with cauterization of the base and oral antifungal angents, corticosteroid injections,
may consider dapsone
Hormonal Rhinitis
-causes:
-hypothyroidism (myxedema)
-elevated estrogen 2o pregnancy
-OCP
-menstrual cycle
- estrogen inhibits acetylcholinesterase ACh in parasympathetic ganglia edema, hypersecretion and
vascular engorgement of nasal mucosa
-manifests near end of first trimester and resolves after delivery
-tx: refractory to most regimens, conservative management (nasal saline irrigations, avoidance of allergens,
may consider nasal steroids), avoid decongestants (may place fetus at risk)
Vasomotor Rhinitis
-low nasal eosinophil counts and negative skin test results for allergy
-theory: abnormal functioning of parasympathetic input to turbinate and septal mucosa
-SSx:
-similar symptomatology to allergic rhinitis except with negative allergy evaluation, morning
rhinorrhea, alternating sides, pale nasal mucosa
-triggers:
-environmental conditions: cold air, high humidity, irritants
-medications: antihypertensives, antipsychotics, cocaine
-psychotropic: anxiety, stress, exercise
-tx:
-attempt to eliminate irritants and address causal factors if possible
-medical management:
-anticholinergic sprays
-corticosteroid sprays
-hypertonic saline sprays
-may consider short course of oral and topical decongestants or antihistamines
-surgical procedures:
-surface turbinate cautery
-septoplasty: removes mechanical points of irritation
-vidian neuronectomy (efficacy controversial)
-partial turbinectomy or turbinate ablation
-total turbinactomy risks atrophic rhinitis
Nonallergic Rhinitis with Eosinophilia Syndrome (NARES)

-lacks IgE-mediated immunopathologic events
-nasal smears contain eosinophil
234
-symptoms of perennial rhinitis
-dx: allergic symptoms with negative allergic tests
-tx: symptomatic relief similar to allergic rhinitis (nasal corticosteroids, antihistamines, decongestants)
Occupational Rhinitis
-nasal discharge or congestion due to exposure to airborne substance at work
-allergic or non-allergic
-treatment: identification and avoidance of offending irritant
Drug-induced Rhinitis
-caused by systemic drugs
-antihypertensives most often implicated
-reserpine, guanethidine, phentolamine, methyldopa, prazosin, chlorpromazine, beta-blockers,
ACEi
-Rhinitis medicamentosa:
-from prolonged used of topical vasoconstricting agents (> 7 days)
-pathophysiology:
-causes down-regulation of alpha-adrenergic receptors “rebound effect”
-refractory vasodilation of mucosal blood vessels
-increased parasympathetic activity
-increased vascular permeability
-mucosal injury can result: loss of cilia, metaplasia, fibrosis
-may be irreversible if vagale tone becomes atonic
-treatment:
-cessation of topical vasoconstrictors
-replacement with nasal saline
-acute nasal obstruction: some administer high burst of prednisone with rapid taper to
reduce mucosal edema
-may add oral antihistamines and/or steroid sprays
Gustatory Rhinitis
-food allergy possible but rare
-alcohol has direct vasodilating effect
-spicy foods watery rhinorrhea via vagally mediated mechanism
Atrophic Rhinitis (Ozena)

-SSx:
-atrophic mucosa on septum, turbinates or lateral nasal walls wide nasal cavity
-may be associated with ozena (thick, foul smelling, dry crust)
-subjective nasal congestion and constant foul-smelling odour despite lack of objective evident of
obstruction
-sensation of nasal obstruction from decreased sensation of nasal airflow or decreased
airflow from increased nasal air turbulence
-histology:
-transformation of pseudostratified columnar epithelium into islands of keratinized squamous
epithelium
-minimal or absent glandular cells; inflammatory cells and mast cells
-smears: neutrophils, bacteria and metaplastic squamous cells with few columnar and goblet cells
-causes:
-primary form:
-may be caused by infection with Klebsiella ozaenae
-seen more in developing countries; may be due to iron or vitamin A deficiency
235
-secondary causes:
-over-aggressive nasal surgery
-chronic rhinosinusitis
-granulomatous disease of the nasal cavity
-radiation
-tx:
-saline irrigations, oil based ointment impregnated nasal tampons, vitamin A and D and iron
supplements, systemic or topical antibiotics (for secondary infections), consider nasal
vestibuloplasty or periodic nostril closure for failed medical therpy
Rhinitis among Children

-common
-viral rhinitis ~6x/year in 2-6 yo
-10% of children and 20% of adolescents have allergic rhinitis
-unilateral rhinorrhea: foreign body
-caused by GERD in infants
Anhidrotic Ectodermal Dysplasia

-X-linked genetic disorder resulting in scant mucous production and atrophic rhinitis
-triad: anhidrosis, hypotrichosis, anodontia
-tx: pressure equalization tubes, saline irrigations, nasal hygiene, denture appliances
DIFFERENTIAL DIAGNOSIS
-allergic rhinitis
-rhinosinusitis
-anatomic nasal obstruction
-choanal atresia
-adenoid hypertrophy
-septal deviation, turbinate enlargement, neoplasia
-polyps (Samter syndrome: asthma, nasal polyposis, asthma)
-systemic disease:
-Wegener granulomatosis
-sarcoidosis
-relapsing polychondritis
-granulomatous obstruction: tuberculosis, leprosy, sporotrichosis, blastomycosis, histoplasmosis,
coccidiomycosis, rhinoscleroma
CLINICAL EVALUATION
History
-PMHx, medications, FHx (immunodeficiency, ciliary dyskinesia, CF)
-onset: allergic rhinitis usually before age of 20 y
-unilateral fixed obstruction: structural cause
-daytime congestion: occupational rhinitis
-cyclical: nasal cycle
-onset of symptoms with relocation: environmental factors
-hyposmia or anosmia: polyposis
-mucopurulent discharge: primary or secondary rhinosinusitis
-epistaxis: neoplasm
236
Physical Examination
-otology: SOM, TM retractions from allergy-induced ETD
-nasal exam:
-“allergic salute”: transverse crease across bridge to nose
-boggy pale mucosa typical of allergic rhinitis
-hyperaemia: infection or abuse of topical decongestants
-submucosal bumpiness and crusting suggestive of granulomatous disease
-watery secretions indicative of rhinitis
-nasal endoscopy
Other Tests:
-serum IgE and serum eosinophil levels: controversial clinical use because of unexceptional sensitivity or
specificity
-nasal cytology
-eosinophil allergic etiology
-neutrophils infectious etiology
MANAGEMENT
-avoidance: cigarette smoke

-medications:
Antihistamines
-first line therapy in children with allergic rhinitis
-reduce symptoms of allergic rhinitis
-second generation H1 antagonists:
-non-sedating
-cetirizine, fexofenadine (Allegra), loratadine (Claritin), desloratadine (Aerius)
-no efficacy in management of nonallergic rhinitis
-intranasal antihistamines to relieve nasal congestion
Decongestants
-topical:
-phenylephrine, oxymetazoline, xylometazoline
-for short term use only: infectious rhinitis, ETD and acute exacerbations of allergic
rhinitis
-oral:
-pseudoephedrine, phenylephrine, phenylpropanolamine
-used alone for vasomotor rhinitis and infectious rhinitis
-used in combination with antihistamines in allergic rhinitis
-avoid in pts with hypertension, CAD, glaucoma, diabetes, urinary retention or
hyperthyroidism
-contraindicated with MAO inhibitors or TCAs
Corticosteroids
-topical:
-control congestion, rhinorrhea, itching and sneezing
-systemic absorption is ~2% but becomes rapidly metabolized
-no suppression of HPA axis
-inhibition of inflammation through inhibition of PLP A2 and subsequent release of
arachidonic acid
237
-oral:
-high burst with rapid tapering no more than 2 weeks
-used mostly for polyposis
Intranasal Cromolyn Sodium

-inhibits degranulation of mast cells
-useful in management of seasonal allergic rhinitis
-not useful in management of nonallergic rhinitis
Intranasal Anticholinergics
-for parasympathetically mediated rhinitis: gustatory or vasomotor rhinitis
-also can be used in allergic rhinitis
-contraindicated in pts with narrow-angle glaucoma or those taking another anticholinergic agent
238
ALLERGIC RHINOSINUSITIS
THE ALLERGIC RESPONSE
-pathophysiology:
-allergens contact nasal mucosa
-early-phase response (IgE mediated)
-occurs within 5 minutes of allergen exposure with maximum effect at 15 minutes
-cross-linking of IgE receptors on mast cells causes degranulation:
-histamine
-leukotrienes (LTC4, LTD4, LTE4)
-PGD2
-PAF
-HETE5
-cytokines
-increases local vascular permeability and proteolysis
-late phase response
-starts 5-7 h and peaks at 6-8 hours after allergen challenge
-cytokines recruit eosinophil, neutrophils and basophil
DIAGNOSIS OF ALLERGY
History and Physical Exam

-nasal: sneezing, congestion, rhinorrhea
-ocular: redness, itchiness, watery, conjunctivitis, burning
-otologic: ETD, MEE
-laryngeal: scratchiness, dry, irritated, cough
-other:
-seasonal pattern
-food hypersensitivity
-fatigue
-OE:
clear rhinorrhea, congested turbinates, periorbital puffiness, “allergic salute”, open-mouthed
breathing (“adenoid facies”), prominent pharyngeal lymphoid tissue, conjunctivitis
Adjunctive Tests
-nasal smear:
-obtained from inferior turbinate mucosa
-eosinophil (>25%) allergy
-neutrophils infection
Definitive Testing for Atopy
Skin Testing:
-scratch test: not widely used
-prick test:
-series of allergens inserted by needle into skin
-positive “wheal-and-flare” reactions compared to controls
-grading is subjective
-risk of anaphylaxis
F.Ling - Allergic Rhinosinusitis (1)
239
-intradermal testing:
-similar to prick test except allergen is placed intradermally
-more sensitive than prick test
-grading is subjective and risk of anaphylaxis
-serial dilution endpoint titration:
-quantitative
-multiple solutions with differing concentrations given intradermally to titrate to a
positive response
-time consuming process
-test results obscured by histamines
In Vitro Testing:
-radioallergosorbent test (RAST)
-antigen bound to surface of paper disc
-pts serum obtained binds to antigen
-radiolabelled anti-IgE identifies specific antigen-IgE complexes
-enzyme-linked immunosorbent assay (ELISA)
-similar to RAST except fluorescing agents are used for markers of antigen-IgE
complexes
-indications:
-equivocal skin tests results
-high risk of anaphylaxis
-skin disorders
-failed immunotherapy
-uncooperative patient
-advantages:
-highly specific, no risk of anaphylaxis, no effect from skin condition or medications
-disadvantages:
-less sensitive, requires up to 1-2 weeks for results, more expensive
MANAGEMENT OF ALLERGIC RHINITIS
Anaphylaxis
-ABCs: airway, oxygenation, IV access
-inject up to 0.3 ml of epinephrine intramuscularly
-consider dopamine for hypotension
-add diphenhydramine (Benadryl) 50 mg, dexamethasone 4 mg, and cimetidine 300 mg through IV
Level I: Avoidance, Symptomatic Relief
Prevention of Symptoms by Avoidance
Environmental Control
-pets out of primary living and sleeping areas
-clean for dust
-avoidance of smoke
-nasal saline to cleanse mucous membranes
First-line Pharmacotherapy
-OTC medications: antihistamines, decongestants, cromolyn
240
Second-generation and Third-generation Antihistamines
-lipid insoluble: do not cross BBB
-loratadine
-cetirizine
-fexofenadine
Topical Glucocorticoids
-reduce local inflammation
Cromolyn:
-stabilizes mast cells preventing release of mediators in acute and late phase reactions
-effective only for prophylaxis
Level II: Management of Complicating factors

-evaluate and treat potential concurrent disorders which may mimic allergy including vasomotor rhinitis,
sinusitis, and rhinitis medicamentosa
Level III: Chronic Symptoms (Corticosteroids)

-decreasing capillary permeability
-stabilizing lysosomal membranes
-blocking migratory inhibitory factor
-inhibits arachidonic acid metabolism
-adverse local effects:
-candidiasis
-nasal irritation
-dryness
-bleeding and crusting
-septal perforation (rare)
-adverse systemic effects:
-increased gastric acid production
-hypertension
-masks signs of infection
-sodium retention
-hypokalemia
-posterior subcapsular cataracts
-psychosis, seizures, insomnia
-menstrual irregularities
-aseptic necrosis of femoral head
-intraturbinal glucocorticoid injection:
-has been associated with blindness: reflexive vasospasms or retrograde embolization into retinal
arteries
Level IV: Immunotherapy

-last resort treatment
-criteria:
-pts with symptoms not easily controlled with pharmacotherapy
-sensitive to allergens that cannot be avoided
-symptoms that span two or more allergy seasons or are severe
-are willing to cooperate in program of immunotherapy
-disadvantages:
-patient must be reliable for multiple injections
241
-requires a chronic regimen (3 years)
-risk of worsening symptoms and anaphylactic shock
-contraindications:
-pregnancy
-autoimmune disorders
-immunological compromised patients
-B-blockers (increases sensitivity to allergens)
-easily avoidable allergens
-noncompliant patients
-involves parenteral administration of antigens to stimulate formation of allergen-specific IgG-blocking
antibodies, which eventually compete with IgE antibodies for target sites on mast cells of basophil
DISORDERS ASSOCIATED WITH ALLERGIC RHINOSINUSITIS
-polyps
-sinusitis
-asthma
-otitis media
-allergic fungal sinusitis
-fungal immunotherapy has been shown to prevent recurrence and minimize dependence on
systemic glucocorticoids
242
NASAL OBSTRUCTION
ANATOMY AND PHYSIOLOGY
-functions of the nose:

-airway: -conduction of environmental air into and out of respiratory system
-filtration: -mucus, vibrissa and cilia trap and remove airborne viral, bacterial and
particulate matter (usually >30 um)
-heating: -provides radiant heating of inspired air to 31-37oC
-humidification: -increases relative humidity to 95% before reaching nasopharynx
-chemosensation: -detects irritants, chemicals and temperature abnormalities
-nasal reflex: -nasal sensation may be linked to lower respiratory and vascular reflexes
-olfaction, endocrine, pheromone detection
-respiratory epithelium:
-goblet cells: -produce protective mucous layer containing salts, glycoprotein,
polysaccharides, and lysozymes
-ciliated cells: -removes wastes for digestion and excretion
-others: -stromal cells, inflammatory cells, nerves, blood vessels, arteriovenous
anastomoses, venous sinusoids
Innervation of Nasal Mucosa

-sensory:
-olfactory nerve/neuroepithelium
-at roof of nasal vault at cribriform plate, superolateral aspects of septum and medial
surfaces of superior turbinates
-trigeminal nerve
-pain, temperature and touch
-internal nasal branch of anterior ethmoid (CN V1): anterosuperior nasal cavity
-posterior ethmoid nerve (CN V1): posterior nasal cavity
-sphenopalatine nerve (CN V2): posterior and inferior nasal cavity
-superior alveolar nerves (CN V2)
-autonomic:
-regulates vascular tone, turbinate congestion and nasal secretion
-parasympathetic:
-superior salivatory nucleus nervus intermedius presynaptic fibers travel along facial
nerve GSPN deep petrosal nerve join vidian nerve sphenopalatine ganglion
-postsynaptic fibers in sphenopalatine ganglion innervate nasal mucosa
-increased vasodilator or secretomotor activity obstruction
-sympathetic:
-vasoconstrictive decongestion
Mathematical Aspects of Nasal Obstruction

-nasal airflow directly proportional to r4
-feeling of obstruction can be due to decreased air flow secondary to increased intranasal turbulence
Nasal Valve Obstruction

-medial boundary: septum
-lateral boundary: junction of distal section of upper lateral cartilage and proximal section of lateral crura
of greater alar cartilage
-inferolateral boundary: anterior head of inferior turbinate and inferior rim of piriform aperture
-valve maintains median airflow through flow resistance
F.Ling - Nasal Obstruction (1)
243
EVALUATION AND ASSESSMENT
History
-onset, duration, unilateral vs bilateral, duration, contributing factors
-rhinorrhea/epistaxis
-nasal or orbital pain
-history of middle ear disease, respiratory illness
-drug/smoke
-nasal surgery/trauma
-Cottle manoeuver: widening alae with index finger and thumb restoration of nasal patency
-obstruction that resolves with decongestion caused by mucosal abnormality
Differential Diagnosis
Congenital Tumour
-neurogenic tumours -papilloma
-glioma -polyps
-encephalocele -hemangiomas
-meningocele -pyogenic granulomas
-dermoid -JNA
-choanal atresia -malignancy
-congenital cysts
-Tornwaldt cyst Endocrine
-nasolacrimal duct cyst -hypothyroidism
-teratoma -pregnancy
-diabetes
Infectious/Idiopathic
-infectious rhinitis Neurologic
-chronic sinusitis -vasomotor rhinitis
-rhinoscleroma Systemic
-tuberculosis -Wegener’s
-syphilis
Toxin/Trauma -sarcoidosis
-septal hematoma -tuberculosis
-septal deviation -fungal infection
-septal perforation -allergy
-medication side effects -cystic fibrosis
-rhinitis medicamentosa -relapsing polychondritis
-synechia
-environmental irritants
-foreign bodies
-valvular collapse
244
SPECIFIC ETIOLOGIES OF NASAL OBSTRUCTION
Anatomic Abnormalities
Deviated Nasal Septum

-most common cause of nasal obstruction
-pts with unilateral septal deviation most often have nasal obstruction of contralateral side
-compensatory turbinate hypertrophy
-+/- sinusitis secondary to hypertrophic mucosa
-impingement reduces nasal airflow through turbulent resistance and can induce thickening, atrophic
mucosal changes, or crusting of the nasal mucosa
Turbinate Hypertrophy
-bony and/or mucosal
-bony hypertrophy may be long term result of prolonged hypertrophy of mucosal tissue or result of
traumatic injury to septum with associated enlargement of nasal turbinates
-50% of inspired air flows along inferior extent of inferior turbinate or between middle and inferior
turbinates
-morbidity associated with radical inferior turbinate resection: haemorrhage, ozena, atrophic rhinitis
-inferior turbinoplasty:
-conservative submucous turbinate resection
-provides 3-5 years of relief without previously mentioned sequelae
-does not address mucosal hypertrophy
-performed when inferior turbinate projects medially and obstructs nasal cavity or when
hypertrophic turbinate mucosa remains unresponsive to vigorous medical management
-chronic hyperplastic mucosal disorders (eg. vasomotor rhinitis)
-available therapy: intraturbinal injection, cryotherapy, electrocautery, laser ablation
Septal Perforation
-causes:
-septoplasty (most common cause, > 50%)
-infections (tertiary syphilis)
-trauma (nose picking)
-neoplasms
-granulomatous disease, vasculitis
-cocaine abuse
-chrome inhalation septal perichondritis
-dx: consider biopsy of granulation tissue or abnormal mucosa to evaluate for malignancy, sarcoidosis,
tuberculosis and other granulomatous diseases
-tx:
-saline irrigation
-antibiotic ointment can be used to control crusting and bleeding around perforation
-polymeric silicone button used to stop whistling
-surgical repair:
-contraindications:
-cocaine abusers
-malignancy
-granulomatous or vascular diseases
-rotation flaps from septal cartilage or bone, nasal floor and lateral nasal wall
-transposition of inferior turbinate flap
245
Valvular Collapse
-nasal valve is narrowest portion of nose
-insufficient cartilage support negative pressure will cause collapse
-surgical reconstruction via open approach, can include
-internal spreader cartilage grafts
-suture repair of drooping upper lateral cartilage
-autogenous cartilage grafts to support columella
-spanning grafts or simple lateral crus onlay grafts to support lateral crura (alar batten grafts)
Choanal Atresia
-see Congenital Anomalies of the Nose
Growths and Neoplasms
Adenoidal Hypertrophy
-“adenoid facies”
-associated with improper orofacial development: dry, thin upper lip, retrognathic mandible,
narrowed maxilla, broad nasal arch, upturned nose
Nasal Polyposis
-associated with:
-Samter triad: ASA sensitivity, asthma, nasal polyposis
-cystic fibrosis (strongly suggested if polyps seen in children)
-medialization of medial maxillary sinus wall by polyps
-fungal sinus infection
-pathogenesis:
-characterized by chronic eosinophilic inflammation
-inflammatory cytokines and mediators increase polyp water retention by increasing
sodium ion uptake
-ASA believed to block COX metabolism of arachidonic acid while stimulating 5-lipooxygenase
overproduction of leukotrienes increase vascular permeability, increase mucous secretion and
bronchoconstriction
-treatment:
-topical corticosteroids
-decrease capillary permeability
-decrease excretion in response to cholinergic stimulation
-suppress cytokine synthesis in eosinophil, basophil and lymphocytes
-inhibit influx of eosinophil and basophil into nasal epithelium and decrease
production of inflammatory mediators arachidonic acid production
-oral corticosteroids
-used for recurrent conditions
-short high burst with rapid taper
-surgical management:
-FESS with polypectomy
Mucosal Disease
-allergic and nonallergic rhinitis
246
Miscellaneous Causes of Nasal Obstruction
Septal Hematoma
-risk of vascular septal cartilage necrosis saddle nose deformity
-treatment: I+D via Killian incision through perichondrium, nasal packing, prophylactic antibiotics
Septal Abscess
-from untreated haematoma
-complications:
-septal perforation
-cavernous sinus thrombosis
-intracranial infection
-saddle nose deformity
-most common pathogen: Staphylococcus aureus
Foreign Bodies
-nasal obstruction secondary to loss of cartilaginous support in the nasal septum
Granulomatous Disease
-polymorphic reticulosis, nonhealing lethal midline granuloma, Wegener granulomatosis, rhinoscleroma,
sarcoidosis, tuberculosis
-infections: blastomycosis, coccidioidomycosis, histoplasmosis, leprosy, sporotrichosis, syphilis
Rhinoslceroma
-granulomatous stage: antibiotics (eg. streptomycin, tetracycline)
-fibrotic stage: surgical treatment: resection of fibrotic tissue and intranasal stent placement
Sarcoidosis
Tuberculosis
-intranasal infection usually involves anterior portions of turbinate and septum
-histopathology:
-caseating necrosis in center of granuloma containing epithelioid cells and multi nucleated giant
cells
247
SINUS SURGERY
CALDWELL-LUC OPERATION
Indications:
-mycotic maxillary sinusitis
-multiseptate maxillary sinus mucocele
-antrochoanal polyp
-oroantral fistula closure
-revision procedures
-preparation for transantral sphenoethmoidectomy, orbital decompression, exploration of pterygomaxillary
fossa
Technique:
-nasal mucosa decongested
-superior buccogingival sulcus and lateral wall of interior meatus infiltrated with 1% lidocaine with
1:100,000 epi
-incision made from canine to second molar
-canine fossa exposed, infraorbital nerve protected
-antrum entered through canine fossa
-nasoantral window can be made in central third of inferior meatus
Complications:
-edema and ecchymosis of cheek
-infraorbital nerve dysesthesia
-oroantral fistula
-epiphora
-antral contracture due to fibrosis and bony thickening of antral walls can make revision surgery difficult
INTRANASAL ETHMOIDECTOMY WITHOUT AN ENDOSCOPE
Indications:
-nasal polyposis with hyperplastic pansinusitis
-recurrent and chronic suppurative sinusitis
-uncomplicated frontoethmoid mucopyocele
-access for intranasal sphenoethmoidectomy
Technique:
-standard nasal decongestion; eyes and medial canthal regions observed throughout procedure
-uncinectomy followed by dissection proceeding posteriorly into ethmoidal bulla
-anterior ethmoidal artery against fovea ethmoidalis and lamina papyracea are key preserved landmarks
-anterior attachment of middle turbinate is not to be disrupted to preserve the frontal recess
-middle turbinate preserved: pain and crusting appear to be more common among patients with total
resection of middle turbinate
Complications:
-retrobulbar hemorrhage
-optic nerve injury
-CSF leak
-intracranial hemorrhage
-horizontal gaze diplopia: trauma to medial rectus with subsequent fibrosis
F.Ling - Sinus Surgery (1)
248
EXTERNAL ETHMOIDECTOMY
Indications:
-frontoethmoid mucopyocele or sinusitis with orbital involvement
-revision surgery with absent or distorted landmarks - distortion can increase risk of intranasal procedure
-CSF leak repair
-anterior skull base lesion
Technique:
-Lynch incision:
-incision beginning at inferior margin of medial aspect of eyebrow, curves down toward medial
canthus, angles acutely back on to side of dorsum of nose
-incision carried to periostium
-angular vessels secured and supraorbital bundle preserved
-periosteal elevation medially and laterally - periosteal elevation ensures integrity of medial canthal
ligament and trochlea
-anterior ethmoidal artery encountered in frontoethmoidal suture line ~24 mm posterior to anterior lacrimal
crest clipped and divided
-posterior ethmoidal artery encountered ~10 mm posterior to anterior artery and ~ 5 mm anterior to optic
foramen
-exposes: lacrimal bone, frontal process of maxilla, lamina papyracea, orbital process of frontal bone
-ethmoid entered through lacrimal fossa
-frontoethmoid suture identifies level of anterior cranial fossa
-lamina papyracea taken down to allow complete exenteration of ethmoidal cells
Complications:
-same as for intranasal ethmoidectomy
-risk of orbital injury and intracranial penetration lower with external approach
-hypertrophic scar formation, medial canthal scarring, rounding of medial canthus
-injury to lacrimal apparatus uncommon
TRANSANTRAL ETHMOIDECTOMY
Indications:
-orbital decompression
Technique:
-exposure of floor of orbit via Caldwell-Luc operation
-delicate bone at junction of posterior orbital floor and medial antral wall gently perforated with
Wilhemlminski punch, and entrance into ethmoidal sinuses carefully enlarged with fine biting forceps
-exposure of ethmoid sinus is limited to anterior cells
FRONTAL SINUS SURGERY
Frontal Sinus Trephination

-useful to relieve pain and obtain cultures for acute frontal sinusitis
-may be used as an adjunctive procedure with endoscopic sinus surgery
Lynch Procedure (frontoethmoidectomy)

-consists of removal of the frontal sinus floor, middle turbinate, and anterior ethmoids
249
-risk of recurrent mucocele formation from stenosis of nasofrontal duct
Riedel Method
-removal of frontal sinus floor and anterior wall (disfiguring)
-allows for complete obliteration
Killian Method
-modification of Riedel by preserving a bridge at the supraorbital rim to reduce deformity
Lothrop Method
-creates a large drainage opening into the nasal cavity be removing bilateral anterior ethmoids, middle
turbinates and frontal septum
Osteoplastic Flap with Frontal Sinus Obliteration

-indications:
-chronic or recurrent sinusitis
-mucoceles
-frontal bone osteomyelitis
-benign tumours
-frontal sinus fractures
-orbital or intracranial complications
-technique:
-bicoronal flap for exposure
-trapdoor access to frontal sinus via periosteal and bone flap
-obtain template from a 6' Caldwell view plain film
-remove mucosa
-obliterate cavity and occlude frontonasal recess
-fat, muscle or bone
250
MIDLINE NASAL MASSES
NASAL ANATOMY
-two important embryologic defects can occur in nasopharynx:

-Rathke pouch:
-remnant of invagination of ectoderm that forms anterior pituitary gland
-cysts are located high in nasopharynx near sphenovomer junction
-tumours are called craniopharyngioma
-composed of well-differentiated epithelial elements
-tx: antibiotics with marsupialization or excision for infected lesions
-nasopharyngeal bursa of Tornwaldt:
-remnant of caudal notochord
-can become infected
-tx:
-no treatment required if asymptomatic
-if infected, consider marsupialization
CONGENITAL MIDLINE MASSES
Neurogenic Tumours
Congenital Masses of Neuroectodermal Origin

Lesion Dural Trans- Furstenberg Meningitis Histologic Findings
Connection illumination Test
Glioma None No Negative No Solid mass of glial tissue with a fibrous stalk
Encephalocele Always Yes Positive Yes Ependyma-lined space that communicates with
ventricles
Dermoid Rare Rarely Negative Rare Fluctuating cyst with sinus track leading to skin
-fonticulus frontalis: unfused space between frontal bones

-prenasal space exists between nasal bones anteriorly and cartilage posteriorly
-any defect in obliteration of dural canal leaves pathway for neural tissue to extend to prenasal space
-Nasal Glioma
-60% extranasal; 30% intranasal; 15% connect to dura by fibrous stalk
-pathophysiology:
-sequestered glial tissue or “pinched-off encephaloceles” results in unencapsulated
collection of heterotrophic glial cells
-SSx:
-intranasal or extranasal firm mass
-does not become larger with crying or straining (negative Furstenburg)
-CT/MRI scan mandatory for preoperative evaluation to r/o intracranial extension
-small tumours:
-transnasal endoscopic resection with immediate repair of skull-base defect with
free mucosal graft, pedicled mucosal flap or conchal cartilage with fibrin glue
and nasal packing for 3 weeks
-large tumours:
F.Ling - Midline Nasal Masses (1)
251
-extranasal approach
-may require neurosurgical consultation for intracranial involvement
-Encephalocele
-contains ependyma-lined space with CSF
-communicates directly with ventricles
-meningocele contains meninges
-meningoencephalocele contains meninges and brain
-meningoencephalocytocele contains meninges, brain and part of ventricular system
-clinical features:
-positive Furstenberg test: compression of jugular veins increase size of mass
-transillumination of mass
-types by location:
-occipital:
-most common
-defect occurs over occiput
-sincipital:
-defect occurs between frontal and ethmoid bones at foramen cecum
-involves frontoethmoid area and is external
-defect is anterior to crista galli in region of foramen cecum
-subtypes:
-nasofrontal (glabellar lesion)
-nasoethmoid (lateral nose)
-nasoorbital (medial orbital wall)
-basal:
-lesions are internal
-defect in floor of anterior cranial fossa between cribriform plate and clinid
process or through superior orbital fissure
-subtypes:
-transethmoidal
-transsphenoidal
-sphenoethmoidal
-sphenomaxillary
Neurofibroma
-usually associated with generalized neurofibromatosis
-excision only when tumours large enough to produce facial asymmetry, visual disturbances or severe pain
Dermoid Cyst
-entrapment of epithelial elements as dural tract resorbs
-cysts can occur anywhere from nasal tip to foramen cecum
-simple cysts: involve only skin and nasal bones
-complex cysts: extend through cribriform plate to the dura
-SSx:
-presents at birth
-forms a fistulous tract, pit or cyst on midline or off-midline of nasal dorsum or septum
-tuft of hair may protrude from pit
-dx: CT/MRI to evaluate for intracranial extension
-tx:
-meticulous excision, must excise complete tract
-craniotomy for known dural connections
252
Hemangioma
-sclerosing therapy has been a mainstay of treatment
NASOPHARYNGEAL MASSES
Nasopharyngeal Cysts
-three types described:
-intra-adenoidal
-extra-adenoidal - located deep in the pharyngobasilar fascia
-branchial cleft cysts from 1st and 2nd pharyngeal pouches
-treatment: excision if infected
Nasopharyngeal Teratoma
-50% of H+N teratomas occur in the nose
-F>M ~ 6x
-hair, skin, bone, cartilage and teeth can be found in teratomas
ACQUIRED MIDLINE NASAL MASSES
Infection
Furuncle
-most common infectious lesions of nasal vestibule
-Staph aureus
-complications: septal abscess, septal chondritis, saddle-nose deformity, cavernous sinus
thrombosis
-tx: I+D; antistaphylococcal antibiotics
Septal Abscess
-caused by furuncle or trauma with resultant septal haematoma
-tx: surgical drainage; Abx
-complication: saddle nose deformity, cavernous sinus thrombosis, meningitis, septal perforation
Rhinoscleroma
-stages:
-catarrhal: purulent rhinorrhea lasting weeks to months
-granulomatous: formation of soft nodules in the nose, pharynx, larynx and
tracheobronchial tree
-may cause progressive airway obstruction
-histology:
-Mikulicz cells: foamy histiocytes containing intracellular Klebsiella
organisms
-sclerotic: dense fibrotic narrowing of nasal passages
-treatment:
-tetracycline for 4 weeks (effective in 70% of patients)
Rhinosporidiosis
-Rhinosporidium seeberi
-public bathing inoculates nasal epithelium with colonizing fungi
253
-small tumour-like masses in nose, nasopharynx and eye
-tx: surgical extirpation with cautery at base
Other Infectious Granulomatous Diseases

-leprosy
-histoplasmosis
-coccidioidomycosis
-blastomycosis
-tuberculosis
Infectious Nasal Disorders Manifesting as Midline Nasal Masses

Lesion Cause Treatment Features
Furuncle S. aureus I+D, oral antibiotics may form abscess
Septal abscess S. aureus I+D, IV antibiotics saddle-nose deformity
Rhinoscleroma Klebsiella rhinoscleromatis tetracycline -three stages

-mistaken for ozena
-rubbery granulation tissue - Hebra nose
Rhinosporidiosis Rhinosporidium seeberi amphotericin polyploid tumours causing obstruction
Leprosy Mycobacterium leprae dapsone, rifampin congestion followed by atrophy of the mucosa,
confused with atrophic rhinitis
Coccidioidomycosis Coccidioides immitis amphotericin pulmonary involvement common
Blastomycosis Blastomyces dermatitidis ketoconazole confused with squamous cell carcinoma
Tuberculosis Mycobacterium rifampin, isoniazid, ethambutol nonspecific sinusitis, ulcers, and polyps
tuberculosis common
Inflammatory
Rhinophyma
-massive hypertrophy of sebaceous glands (form of acne roascea
-associated with Demodex folliculorum
-SSx:
-begins with coarsening of nasal skin over cartilaginous portion of nose
-develops into large protuberant lobular swelling of nasal tip
-nasal obstruction
-tx:
-surgical full thickness excision (laser, cold scalpel, or dermabrasion) until normal nasal
contour
-may require STSG
Benign Lesions
Benign Tumours of Ectodermal Origin
Papilloma
-verrucous lesions cause by HPV (types 6 and 11)
-managed by surgical excision or laser ablation
-for septal keratotic papilloma, a cuff of normal mucoperichondrium should be taken with lesion
254
to avoid recurrence
Inverting Papilloma
-M>F ~ 3x
-arise from lateral nasal wall
-malignant growth occurs in as many as 15% of cases
-SSx:
-unilateral obstruction, sinusitis, epistaxis, rhinorrhea, diplopia, typically presents on
lateral nasal wall (rarely on nasal septum), may be associated with a benign nasal polyp
-histopathology:
-cristae-laden senescent mitochondria
-inflammatory cells throughout epithelium
-endophytic growth of epithelium
-complications:
-malignant degeneration
-extension into sinuses, orbit, or intracranial and skull base
-treatment:
-surgical removal by medial maxillectomy via lateral rhinotomy or endoscopically
-recurrence rate of 44%, therefore multiple procedures might be required
-radiation therapy ineffective
Benign Salivary Gland Tumours

-relatively rare
-most common is pleomorphic adenoma
-tx: surgery
Benign Tumours of Neuroectodermal Origin

-schwannoma, neurofibroma, traumatic neuroma, paraganglioma
Benign Connective Tissue Tumours
Lobular Capillary Hemangioma

-granuloma gravidarum: involutes spontaneously after parturition
-often located on anterior nasal septum in area of Kiesselbach plexus
-tx: surgical excision with good prognosis for cure
Angiofibroma
-occurs exclusively among boys and men
-non-metastasizing tumour that is locally aggressive
-high risk of uncontrollable haemorrhage with biopsy
-tx:
-preoperative embolization
-surgical removal: open or endoscopic
Benign Tumours of Mesenchymal Origin

-chondroma, osteoma, bone cyst
-fibrous dysplasia:
-three forms:
-monostotic
-polyostotic
-McCune-Albright syndrome: precocious puberty, hyperpigmentation, hyperthyroidism
-conservative treatment; surgery for deforming lesions
255
Benign Neoplastic Lesions Manifesting as Midline Nasal Masses
Lesion Characteristics Treatment Complications
Papilloma probable viral origin, HPV excision recurrence, septal perforation
Inverting papilloma unilateral nasal mass, confused wide excision recurrence, SCC
with simple polyp
Salivary tumour relatively rare, pleomorphic type wide excision minor gland tumours have high rate of
most common malignancy
Hemangioma congenital or acquired steroids, excision, laser therapy scarring, haemorrhage
Angiofibroma juvenile males, obstruction plus embolization, wide excision recurrence, haemorrhage, especially with
epistaxis biopsy
Malignant Lesions
Malignant Tumours of Epithelial Origin
Squamous Cell Carcinoma

-most common malignant neoplasm of sinonasal tract
-more aggressive behaviour:
-less squamoid differentiation
-higher rate of metastasis
-nasal septum and turbinate most frequent intranasal tumour sites
-exposure risk factors: nickel, chromate, flour dust, isopropyl alcohol
-tx: surgery or radiation therapy
Basal Cell Carcinoma

-most common malignant tumour of external nose and vestibule
-ulcerated nodules with raised, smooth borders
Intranasal Verrucous carcinoma

-rare
-HPV proposed etiologic factor
-tx: wide local excision
Malignant Salivary Gland Tumours
Adenoid Cystic Carcinoma

-most common
-“cylindroma”
-painful: neural invasion
-10-year survival rate < 10%
-tx: surgery
Mucoepidermoid Carcinoma
-rare
-manage like SCCa
256
Neuroectodermal Lesions
Olfactory Neuroblastoma
-arise for olfactory tissue, possibly bipolar neurons
-lobular pattern of uniform cells surrounded by vascular stroma
-aggressive local growth with occasional metastasis to regional lymph nodes
-tx: radical surgery with chemotherapy and radiation therapy
Malignant Melanoma
-second only to SCCa
-primary endonasal site of origin is nasal septum pigmented masses
-50% recurrence rate with poor prognosis
-median survival 2 years; 5-yr survival 25%
-tx: wide local excision; lymph node dissection not usually used for N0 disease b/c low incidence
of nodal metastasis
Malignant Mesenchymal Tumours
Hemangiopericytoma
-arises from pericytes of Zimmermann (small cells external to capillary endothelial cells)
-tx: preoperative embolization and en bloc resection of tumour
Kaposi Sarcoma
-dark-brown nodules appear on skin or mucosa
-histology: capsule surrounding spindle cells with prominent nuclei
-tx: excision
Lymphoreticular Tumour
-lymphoma
-Hodgkin disease
-extramedullary plasmacytoma
Malignant Lesions Manifesting as Nasal Masses

Tissue Origin Lesion Characteristic Management
Epithelial SCC ulcerating lesion aggressive treatment
BCC ulcerated nodule, raised borders wide excision
Salivary Adenoid cystic carcinoma pain common, hematogenous metastasis poor prognosis, aggressive treatment
Mucoepidermoid carcinoma rare lesion low grade has good prognosis; high
grade has poor prognosis
Neuroectodermal Olfactory neuroblastoma pink or brown friable lesion aggressive radical surgery
Malignant melanoma nasal septum pain and swelling 50% recurrence rate
Mesenchymal Hemangiopericytoma lobulated mass, Zimmermann cells, epistaxis embolization, en block resection
Kaposi sarcoma Dark brown nodule HIV-associated Laser excision or surgery
257
SINUS IMAGING
INFLAMMATORY DISEASE AND POLYPOSIS
Acute Sinusitis
-thickening of sinus mucosa alone is specific for neither
acute nor chronic inflammatory change
-presence of an air-fluid level if there has been no
recent antral lavage suggests acute inflammation
Chronic Sinusitis
-long-standing chronic inflammatory disease can
produce osteitic changes of sinus walls that result in
bony thickening
-bone erosion can occur with chronic inflammatory
disease and often is associated with polyposis
-erosion into retromaxillary space is extremely unusual
and suggests presence of neoplasia or a mucocele
Clinical Significance of Mucosal Thickening

-presence of incidental abnormalities of the ethmoidal sinuses when there is no history of allergic or
inflammatory sinusitis is significant
-if pt does not have symptoms, such findings have no adverse consequences
-when sphenoidal sinusitis is identified on an imaging study, risk of optic complications should be
considered
CONSIDERATIONS FOR ENDOSCOPIC SINUS SURGERY
-osteomeatal complex, sphenoethmoidal recess, and frontal recess become prime areas of interest
-complete or partial obstruction of these outlets causes inflammatory changes in associated sinus
cavities
-anatomic variations that can contribute to disease:
-concha bullosa cell
-septal deviation and spur
-lateral convexity of middle turbinate (paradoxical turbinate)
-pneumatization and inversion of uncinate plate
-prominent agger nasi cell
-prominent ethmoidal bulla and Haller cell
GRANULOMATOUS SINUSITIS
-infectious: actinomycosis, nocardiosis, blastomycosis, tuberculosis, syphilis, rhinoscleroma, and

leprosy
-noninfectious: Wegener granulomatosis, sarcoidosis, foreign-body reactions from beryllium, chromate
salts and cocaine
-potentially destructive and can erode both cartilage and bone
-perforation of cartilaginous nasal septum is the hallmark of this group of disorders
-destruction of bony septum and sinus walls occurs later as disease progresses
F.Ling - Sinus Imaging (1)
258
FUNGAL SINUSITIS
-entities:
-invasive fungal sinusitis in immunosuppressed pt
-associated with mucormycosis or aspergillosis
-acute, fulminant destructive disease marked by vascular invasion and necrosis
-chronic indolent sinusitis
-in pt with normal immune function
-tissue-invasive infection, typically unilateral and not responsive to antibiotics
-mycetoma
-noninvasive fungal ball that causes complete or near-complete opacification of a sinus
cavity
-organisms: Aspergillus fumigatus, Pseudallescheria boydii, Alternaria
-CT:
-can be associated with thickening of sinus walls
-usually hyperdense and contains calcifications in 25% of cases
-MRI:
-hypointense on MRI (T1and T2)
-allergic fungal sinusitis
-pt with heightened immune function or atopy
-hypersensitivity reaction to fungal antigens
-CT:
-involved sinus contains peripheral
rim of low density
-edematous mucosa and complete
opacification of central cavity by
homogeneous high-attenuation
material corresponding to thick
allergic mucin
-often scattered flecks of calcific
material
-sinus walls can be surprisingly
expanded and destroyed
-MRI T2:
-mucin is extremely hypointense,
mimicking an aerated sinus cavity
RETENTION CYSTS
-common and occur with chronic inflammatory sinus disease

-mucous cysts from as result of mucous gland obstruction
-incidental finding in 10% of instances
POLYPOSIS
-smoothly rounded or pedunculated soft-tissue masses

-multiple, packed polyps can exert pressure on adjacent bony structures and enlarge involved cavity
-intersinus septation fairly well preserved
-polyps: low density on CT scans, hypointense on T1 and hyperintense on T2
-secretions: hyperdense on CT, hyperintense on T1, hypointense on T2
259
MUCOCELE
-occur as obstructive complications of chronic sinus inflammation, polyposis, trauma, surgery, or tumour
-CT: mucocele contents have low density and do not enhance
-MRI: intensity characteristics vary with protein content of mucocele and degree of hydration
NEOPLASTIC DISEASE
-malignant disease of nose and paranasal sinuses account for less than 1% of all malignant lesions in the
body and 3% of all H+N tumours
-MRI particularly useful, because nearly 95% of all sinonasal tumours are low to intermediate in signal
intensity during T2-weighted sequence
Benign tumours of soft-tissue origin

-inverted papilloma arises from lateral nasal wall near middle turbinate
-most common radiologic appearance is a nasal mass that erodes lateral nasal wall and extends
into maxillary antrum
-actual tumour invasion of bone occurs only with malignant transformation and occurs in about
13% of cases
-juvenile nasopharyngeal angiofibroma
-originates near sphenopalatine foramen
-exhibits marked enhancement on both CT and MRI
-flow voids seen on MRI
-neurogenic tumours (schwannoma, neurofibroma)
-well circumscribed, slowly growing lesions associated with bone expansion and remodelling
Malignant tumours of soft-tissue origin

-epithelial tumours:
-SCC (most common, 80%), glandular tumours, melanoma, and esthesioneuroblastoma
-nonepithelial tumours:
-lymphoma and various sarcomas
Benign tumours of bony origin

-fibroosseous or of giant cell origin
-fibroosseous lesions:
-osteoma
-seen particularly in frontal and ethmoidal sinuses
-multiple osteomas of face and skull seen in Gardner syndrome
-osteochondroma
-ossifying fibroma
-fibrous dysplasia
-hazy ground-glass appearance
-TI: signal intensity ranges from mildly hyperintense to hypointense
-T2: marked homogeneous hypointensity
-giant cell lesions:
-giant cell granuloma
-brown tumour of hyperparathyroidism
-most common giant cell lesion of facial bones
-unilocular or multilocular cystic, expansile masses with well-defined margins
260
Malignant tumours of bony origin
-most common malignant bone tumours of paranasal sinuses are multiple myeloma, osteogenic sarcoma,
and chondrosarcoma
261
RHINOSINUSITIS: CURRENT CONCEPTS AND MANAGEMENT
ANATOMY AND PHYSIOLOGY OF THE SINUSES
-function of sinuses:
-dampening of sudden increased intranasal pressure
-voice resonance
-possible participation in olfaction
-humidification of inspired air
-decreasing weight of skull
-frontal sinus:
-varies greatly in size and shape
-nasofrontal duct drains into frontoethmoidal recess of middle meatus
-10-12% of adults have rudimentary frontal sinus or lack pneumatization of frontal bone
-ethmoid sinus:
-most developed at birth
-anterior and middle ethmoidal cells drain to middle meatus
-posterior cells drain to superior meatus
-maxillary sinus:
-present at birth
-drains into middle meatus
-sphenoid sinus:
-begins developing in 2nd or 3rd year of life
-completely pneumatized by 17th or 18th year
-drains into sphenoethmoidal recess
-maxillary sinusitis is caused by disease in the ostiomeatal complex:

-frontal recess
-ethmoid bulla
-infundibulum
-maxillary sinus ostium
-middle turbinate
-middle meatus
-semilunar hiatus
-uncinate process
PATHOPHYSIOLOGY
Pathophysiologic Characteristics of Sinus Disease

Ostial patency Ciliary Function Mucous
-Edema -Decreased ciliary beat frequency -Changes in quantity

-allergens -ciliotoxins -allergens
-infection -cold air -airway irritants/pollutants
-Polyps -Loss of metachronous coordination -goblet cell metaplasia
-atopy -scarring, synechiae -Changes in quality
-CF -Loss of ciliated cells -abnormal water-electrolyte
-chronic infection -airway irritants/pollutants transport
-Structural factors -increased intranasal airflow -dehydration
-septal deviation -inflammatory mediators -CF
-Haller’s cells -viral/bacterial-mediated cell
-concha bullosa death
-instrumentation -surgical
F.Ling - Rhinosinusitis (1)
262
-osteal patency:
-hypo-oxygenation and osteal obstruction accumulation of secretions in sinus ideal culture
medium for bacteria
-mucociliary layer:
-double layer:
-superficial viscid gel layer
-underlying serous sol layer
-nasal mucous produced by:
-goblet cells
-submucosal mucous-producing glands
LOCAL, REGIONAL, AND SYSTEMIC CAUSES OF SINUSITIS
Local
-impairment of mucociliary transport function
-cold/dry air
-medications
Regional
-suppurative sinusitis: apical dental infection (main predisposing factor)
-nasal/midface trauma (alters anatomic configuration of OMU)
-septal pathology mechanical obstruction
-choanal atresia interferes with drainage of nose
-edema 2o to URTI
-barotrauma produces edema of sinus ostium
-swimming in contaminated water
-nasal polyps, FB, nasal packing, nasal tumours
-immotile cilia syndrome
-congenital: disorientation of cilia and abnormalities of dynein arms
-sinusitis and bronchitis
Systemic
-general debilitation:
-malnutrition, long-term steroid therapy, uncontrolled diabetes, blood dyscrasia, chemotherapy
-critically ill patients:
-regional obstruction from NG tubes
-colonization of UGI and URT by gram negative bacilli
-immune deficiencies (eg. IgG deficiency, AIDS)
-pseudomonas in HIV patients; microsporidium, CMV, Aspergillus (invasive), histoplasma,
Cryptococcus, atypical mycobacteria
-non-Hodgkin lymphoma in HIV patients
CLASSIFICATION OF SINUSITIS
Five axes:
a) clinical presentation (acute, subacute, chronic)
b) anatomic sites of involvement (ethmoid, maxillary, frontal, sphenoid)
c) responsible organism (viral, bacterial, fungal)
d) presence of extrasinus involvement (complicated, uncomplicated)
e) modifying or aggravating factors
263
-Acute sinusitis: 1 day to 4 weeks
-management is medical, rarely surgical
-drainage if orbital or intracranial complications threaten
-Subacute sinusitis: 4 weeks to 3 months
-medical management indicated
-Chronic sinusitis: > 3 months
-sinusitis that is uncontrolled or inadequately managed
-process irreversible without surgical intervention
-osteal patency must be restored surgically to allow clearance of mucopus from sinus
CLINICAL EVALUATION
History
-Acute sinusitis:
-pain: nasal, facial, headache
-ethmoidal pain: medial portion of nose or retro-orbital area
-sphenoidal pain: vertex or bitemporal headaches
-nasal obstruction/discharge
-fever, malaise, lethargy
-diagnosis depends on presence of > 2 major factors or 1 major and 2 minor factors:
Major factors:
-facial pain or pressure
-facial congestion or fullness
-nasal obstruction
-nasal purulence or discoloured PND
-hyposmia or anosmia
-fever
Minor factors:
-headache
-halitosis
-fatigue
-dental pain
-cough
-ear pain, pressure, or fullness
-fever
-Chronic sinusitis:
-mucopurulent discharge and symptoms of mild nasal obstruction
-pain and systemic symptoms are conspicuously absent
-mucosal edema and erythema
-+/- mucopurulent discharge
-facial pain/tenderness over affected sinuses
-look for periorbital edema, malodorous breath
-nasopharynx: adenoidal obstruction, tumours, choanal atresia, PND
-look for otitis media or serous otitis media
-transillumination not reliable
-nasal endoscopy: pus in middle meatus
264
-periorbital edema; blindness can be a complications of sinusitis
-children much less likely to report classic sinus headaches
-“cold” lasting more than 7-10 days, daytime cough with nocturnal exacerbation, mucopurulent
nasal discharge, fetid breath, low grade fever
Investigations
-plain radiography:
-indications: screening study for acute sinusitis
-evaluates presence of air-fluid levels, opacification, and bone destruction
-high rate of false positives and false negatives to evaluate for chronic sinusitis
-CT of paranasal sinuses:
-indications:
-complications of severe acute sinusitis
-medical failure of chronic sinusitis
-diagnosis of epistaxis, nasal or sinus tumours, nasal polyps
-CSF leaks
-trauma
-preoperative films
-MRI of paranasal sinuses:
-improved soft tissue detail, poor bone resolution
-indications:
-complicated sinusitis (intracranial and intraorbital extension)
-evaluation of soft tissue masses
-fungal sinusitis (hypodensity in T2-weighted sequences form the presence of metallic
proteinaceous material, magnesium, iron, and calcium)
Ancillary studies
-sinus cultures:
-obtained through an anterior maxillary puncture or from an endoscope
-indications:
-failed medical management
-complicated sinusitis (sepsis, orbital infection, intracranial extension)
-immunocompromised patients
-immunological profile:
-qualitative immunoglobulins including IgG subclasses
-ciliary biopsy
-allergy testing
MICROBIOLOGY OF SINUSITIS
-little correlation between culture results with specimens from nose or nasopharynx and those from sinus
aspiration
-antibiotic management of acute sinusitis usually empiric
-Acute (community acquired):

-viral: rhinovirus (most common)
-bacterial:
-Streptococcus pneumoniae (most common - 30%), Haemophilus influenzae (20%),
Moraxella catarrhalis (20%)
-other streptococci (S. pyogenes)
-anaerobes: Peptostreptococcus, Fusobacterium, Bacteroides (6-10%)
265
-Acute (nosocomial):
-Pseudomonas aeruginosa, enteric gram-negative bacilli (KEEPS), Staph. aureus, Candida,
streptococci
-anaerobes
-Chronic sinusitis:
-anaerobes (Bacteroides, anaerobic cocci), fungus (1-2%)
-alpha streptococci, H. influenze, S.aureus, S. pneumoniae, M. catarrhalis
-Immunosuppression:
-usual organisms plus: Pseudomonas, S. aureus, Listeria monocytogenes, Leigionella
-CMV
-Fungi (fulminant): Aspergillus, Candida, Mucor, Phaehyphomycosis, Rhizopus
-Atypical mycobacteria
-Microsporidia, Cryptococcus
-Cystic Fibrosis:
-P. aeruginosa, S. aureus
Viral sinusitis
-often follows viral rhinitis
-rarely requires treatment except in immunosuppressed (eg. with CMV infection)
Fungal sinusitis
-types:
-noninvasive: (1) mycetoma and (2) allergic fungal sinusitis
-invasive: (3) fulminant (immunosuppressed); (4) indolent (immunocompetent)
-modifying factors can predispose a patient to sinus infection or can prevent complete resolution of
infection:
-eg. atopy, immunosuppression, ciliary dyskinesia, mechanical obstruction
Mycetoma:
-pathogens: Aspergillus fumigatus (most common), Pseudallescheria boydii, Alternaria
-SSx: unilateral chronic or recurrent sinusitis, unilateral proptosis, facial hypesthesia
-dx: CT/MRI, biopsy with culture
-aspergillosis histology:
-septated 45 degree, Y-shaped (Sabouraud’s agar stain)
-tx: adequate surgical debridement, consider adjuvant less toxic antifungal medications
Allergic Fungal Sinusitis

-chronic sinusitis: nasal obstruction, sinus pain, rhinorrhea, frequent orbital symptoms (proptosis)
-characteristics:
-thick, viscid, brown-green mucus with peanut butter-like consistency
-histology:
-sheets of eosinophil
-Charcot-Leyden crystals
-breakdown products of eosinophils
-fungal hyphae (non-invasive: not in tissues)
-most commonly aspergillus sp
-demitaceous molds: Alternaria, Bipolaris, Curvularia, Exophilia
-caused by allergic reaction to a fungus colonizing sinus cavities (Gell and Coombs type I and
type III hypersensitivity)
-eosinophil secrete mediators that damage cilia
266
-promotes polyp growth
-sinus imaging:
-often unilateral involvement of one or two sinuses
-CT: areas of hyperdensity in opacified sinus cavities
-MRI: hypointensity on T1 and signal void on T2
-erosion of bony sinus wall frequently encountered:
-osteolytic factors secreted by fungi
-cytokine-mediated osteoclast activation
-long-standing pressure on sinus walls
Diagnostic criteria (Bent and Kuhn - 1994)
Major Criteria:
1. testing or history positive for fungal atopy (RAST, skin testing)
2. nasal polyposis
3. CT showing hyperdense material in sinus cavity and possible sinus wall erosion
4. allergic mucus with eosinophilic preponderance
5. identification of fungus
6. no histologic evidence of tissue invasion
Minor Criteria:
1. chronic rhinosinusitis
2. CT scan demonstrating serpiginous areas of high attenuation especially in
ethmoidal and maxillary sinuses, with bone thinning and erosions with
dislocation of adjacent structures
3. MRI showing decreased signal intensity leading to hypointense T1-weighted
and markedly hypointense T2-weighted images with typical void signal
Treatment
-ethmoidectomy
-middle meatal antrostomy with extirpation of allergic mucous and polypectomy
-post-op steroid sprays and saline irrigations
-systemic anti-fungals are of no use because fungi are not invasive
-consider immunotherapy for refractory cases
Chronic Invasive (Indolent) Fungal Sinusitis:

-pathogen invades soft tissue
-pathogens:
-Aspergillosis
-saprophytic: Mucor, Rhizopus, Absidia
-SSx:
-chronic sinusitis with or without symptoms of local invasion
-tx:
-surgical debridement and long-term amphotericin B and itraconazole (1 year)
Fulminant Fungal Sinusitis and Mucormycosis

-pathogen invades soft tissue
-in mucormycosis, pathogen invades vessel walls causing local vascular occlusion,
thrombosis, infarction and tissue necrosis
-pathogens:
-Aspergillosis
-saprophytic: Mucor, Rhizopus, Absidia
267
-risk factors: immunocompromised host (diabetic ketoacidosis, chemotherapy, HIV, bone marrow
transplant)
-SSx:
-necrotic black turbinates and soft palate, epistaxis, cranial nerve involvement, progresses
rapidly into obtundation and death
-mucormycosis histology:
-non-septated, 90 degree broad branching hyphae
-tx:
-correct metabolic abnormality if present
-urgent surgical debridement
-IV amphotericin B
MANAGEMENT
Acute rhinosinusitis:
-First-line empiric therapy:
-Amoxicillin:
-covers H. influenzae, M. catarrhalis, S. pneumoniae
-does not cover strains that have beta-lactamase enzyme
-Erythromycin and a sulfonamide
-cephalexin and a sulfonamide
-Amoxicillin-clavulanate
-for beta-latamase producing strains of H. influenzae and M. catarrhalis, but not
effective against penicillin-resistant pneumococci
-second-generation cephalosporins: cover beta-lactamase producing organisms
-Second-line therapy:
-amoxicillin-clavlanate
-clarithromycin and second-generation cephalosporin
-respiratory quinolones (levofloxacin, gatifloxacin, moxifloxacin), ciprofloxacin
-contraindicated in children and pregnant women - interference with cartilage
development
-Orbital or intracranial complications:
-IV Ceftriaxone: excellent penetration of BBB
-IV Flagyl: better CSF penetration than clindamycin
-Nosocomial sinusitis:
-cover gram-positive, gram-negative (eg. Pseudomonas), and anaerobic bacteria
-IV Flagyl + ampicillin + ceftazidime, cefotaxime, or ciprofloxacin
-imipenem
-piperacillin-tazobactam
-clinical improvement usually occurs within 48 to 72 hours of initiation of therapy

-most important management measure is antibiotic therapy for a minimum of 7 days after all
symptoms have disappeared (although trends are changing toward shorter treatment times ~5
days)
-treatment usually for 10 days to 3 weeks
-treatment for shorter periods can allow relapse, or the disease can progress to chronic sinusitis
-topical decongestants
-advocated and are beneficial, provided not used for more than 3 days
-antihistamines not recommended:
-can produce further inspissation of secretions and cause substantial side effects
268
-analgesics for pain
-humidification, mucolytics and expectorants, saline nasal irrigation to help clear secretions
Chronic sinusitis
-Antibiotics for 3-6 weeks:
-clavulin
-clindamycin
-cephalexin and metronidazole
-ciprofloxacin
-itraconazole
-cefuroxime
-clarithromycin
-nasal corticosteroid sprays
-nasal hypertonic saline irrigations
-oral decongestants and mucolytic agents
-allergy management
-surgical management frequently required
Cystic Fibrosis and Sinusitis

-patients at higher risk for pseudomonal and MRSA infections
-tx:
-attempt initial conservative medical management with mucolytics, topical steroids, hypertonic
saline irrigations
-avoid antibiotics (may develop resistant pathogens)
-avoid surgical management (high recurrence rate, increases nasal scarring, patients do not tolerate
long-term general anaesthesia d/t retained pulmonary secretions)
-surgery may be considered for uncontrolled pain, nasal obstruction, mucocele, unresolved fevers,
and fungal infections
Kartagener’s disease
-aggressive antibiotic therapy
-avoid functional antrostomies (no mucociliary clearance)
-consider “gravity dependent” inferior antostomies for refractory disease
SURGICAL MANAGEMENT
-main indication for maxillary sinus irrigation is the presence of mucopurulent material in an
immunosuppressed patient or a patient with suspected subacute or chronic maxillary sinusitis or acute
sinusitis that has not responded to antibiotic therapy
-surgery for acute maxillary sinusitis is indicated if the pain persists for more than 24-48h despite
appropriate antibiotic therapy or if ophthalmic and neurologic complications occur
COMPLICATIONS
Ophthalmologic (most common)

-intraorbital pathways:
-direct extension (especially through thin walled lamina papyracea)
-thrombophlebitis (valveless veins)
-congenital dehiscence
-trauma
269
-direct lymphatics
-orbital cellulitis, abscess, proptosis
-subperiosteal and orbital abscess
-blindness, loss of ROM, increased IOP
-osteomyelitis
-mucoceles
Stages of Orbital Complications (Chandler Classification)
1. Periorbital/Preseptal Cellulitis:
-eyelid edema, erythema, tenderness
-no vision changes, chemosis, proptosis, or restriction of ocular muscles
-tx: IV ABx and concurrent aggressive sinusitis regimen
2. Orbital Cellulitis:
-proptosis, chemosis
-may cause vision changes (anterior pupillary defect)
-may limit extraocular muscles
-tx: IV ABx and concurrent aggressive sinusitis regimen +/- FESS
3. Subperiosteal Abscess:
-collection of pus between bone and periosteum
-chemosis, proptosis
-restricted extraocular motion
-decreased vision
-tx: urgent surgical decompression
4. Orbital Abscess:
-collection of pus in orbital soft tissue
-proptosis, chemosis, restricted extraocular motion
-decreased vision
-tx: urgent surgical decompression
5. Cavernous Sinus Thrombosis:
-pathogens:
-S. aureus (most common), hemolytic Streptococcus and type III Pneumococcus
-SSx:
-spiking fevers, toxaemia
-proptosis, facial edema, ophthalmoplegia
-tx:
-IV ABx
-may require ligation of IJV if septic emboli
-anticoagulants (controversial)
-sinus surgery
Neurologic (rare)
-intracranial pathways
-congenital dehiscence
-trauma
-direct extension
-lymphatics
-olfactory nerve sheath
-venous system
-foramina of Breschet
-meningitis (most common intracranial complication)
-epidural or subdural abscesses
270
-brain abscess, cavernous sinus thrombosis
-venous sinus thrombosis
Pott’s puffy tumour:

-osteomyelitis of anterior wall of frontal sinus
-infection via direct extension or by thrombophlebitis of diploic veins
-most often seen in adolescents and young adults d/t more extensive system of diploic veins
-most common offending organism: S. aureus
-tx: IV Abx, trephination, may require surgical debridement
Superior Orbital Fissure syndrome:

-fixed globe, dilated pupil, ptosis (CN III, IV, VI)
-hypesthesia of upper eyelid (CN V1)
Orbital Apex Syndrome:

-superior orbital fissure syndrome with added involvement of optic nerve
EMERGENCIES
Ophthalmologic:
-orbital cellulitis/abscess
-ethmoid sinus most common sinus contributing to orbital complications
-third nerve palsies may be result of sphenoid sinusitis
-IV Abx, surgical drainage, early consultation if any present:
-visual changes
-change in ocular mobility
-change in ocular pressure
-proptosis
-acute ethmoidal sinusitis with orbital complications probably best managed through external
ethmoidectomy approach; if no complications then endoscopically and intranasally is reasonable
Neurologic:
-abscess (epidural/subdural/intraparenchymal), meningitis, cavernous sinus thrombosis
-IV Abx, surgical drainage, early consultation if any present:
-CN involvement (II, III, IV, VI)
-papilledema
-altered mental status/LOC
-nuchal rigidity
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ENDOSCOPIC SINUS SURGERY
ANATOMY OF THE LATERAL NASAL WALL
-agger nasi:
-ascending (frontal) process of maxilla forming a thick bony ridge inside the nose
-agger nasi cells: cells anterior to opening of frontal sinus
-ostiomeatal unit:
-medial border: anterior middle turbinate
-lateral border: lateral nasal wall
-uncinate process bisects region
-anteriorly joined to posteromedial portion of lacrimal bone by membranous attachment
-may attach anterosuperiorly to LP or to skull base
-inferolaterally fused with medial wall of maxillary sinus
-ethmoidal infundibulum:
-lateral wall is medial wall of orbit and antrum
-posterior aspect empties into inferior hiatus semilunaris
-ethmoid bulla:
-constitutes posterior boundary of inferior hiatus semilunaris
-bony medial wall of maxillary sinus:
-natural ostium of maxillary sinus
-anterior (inferior to inferior limb of uncinate process) and posterior (superior to inferior limb of
uncinate) fontanelles
-usually covered by mucosa
-perforated in 10-28% of patients accessory ostium
-frontal recess:
-typically drains medially to uncinate process and laterally to middle turbinate
-occasionally drains into inferior hiatus semilunaris
-sinus lateralis = retrobullar recess
-most posterior aspect of anterior ethmoidal cells
-basal lamella:
-lateral, sigmoid, bony attachment of middle turbinate to medial orbital wall
-separates anterior and posterior ethmoidal air cells
-ethmoidal roof classification (Keros)
-type 1: cribriform plate is 1-3 mm
-type II: 4-7 mm deep
-type III: 8-16 mm deep
-Onodi cell = sphenoethmoidal cell
-pneumatization of sphenoid bone by an ethmoidal air cell
-clinical bony dehiscence of cavernous portion of carotid canal occurs among 22% of patients
PREOPERATIVE EVALUATION
Comprehensive Nasal Endoscopy

-first pass:
-along floor of nose
-visualize inferior turbinate, inferior meatus, nasopharynx, eustachian tube
-drainage under torus tubaris suggests disease with anterior ethmoidal, maxillary, or frontal
sinuses
-drainage over torus emanates from sphenoethmoidal recess and signifies posterior ethmoidal or
sphenoidal sinus disease
F.Ling - Endoscopic Sinus Surgery (1)
272
-second pass:
-between middle turbinate and inferior turbinate
-visualize anterior and inferior portions of middle turbinate and meatus
-natural opening to sphenoidal sinus viewed
-third pass performed during withdrawal of scope
-visualize ethmoidal bulla, inferior hiatus semilunaris and uncinate process
-natural ostium of maxillary sinus usually hidden behind uncinate process
Radiographic Evaluation
-optimal time to perform CT is during
Preoperative Radiographic Checklist
quiescent phase of disease
-pts should undergo comprehensive medical 1. Shape of skull base and orbit
therapy before CT scan -medially down-sloping versus flat, particularly in region of
lateral lamella of cribriform plate
-fungal disease suspected if:
-metal-like or diffusely increased 2. Relative thickness of skull base and orbit in different areas
densities within soft tissues of along roof of ethmoid bone and presence of medial orbital or
involved sinuses bone dehiscence along skull base
-reduced signal intensity of a T2- 3. Position of anterior ethmoidal neurovascular bundles
weighted image -look just behind globe on true coronal CT scans
4. Vertical height of posterior ethmoid labyrinth relative to

posteromedial roof of maxillary sinus
SURGICAL INDICATIONS AND
CONTRAINDICATIONS 5. Presence and development of sphenoethmoid cells (Onodi
cells)
Advantages of Endoscopic Approach to Chronic
6. Relation of septa within sphenoid sinus to carotid artery and
Rhinosinusitis optic nerve and degree of protrusion of these structures into
-no surgical trauma to external skin and the sinus cavity
intervening bone and ability to minimize
intranasal and intrasinus trauma 7. Atelectasis of ethmoidal infundibulum with lateralization of
the uncinate process
-preservation of bony framework within
critical area of frontal recess 8. Maxillary sinus hypoplasia
-unparalleled visualization of nasal anatomy -associated with congenital underdevelopment of the uncinate
-preservation of mucous membranes for process
restoration of normal mucociliary clearance
Relative Indications for Endoscopic Surgery

-unresponsive, recurrent acute rhinosinusitis
-unresponsive, obstructive nasal polyposis
-extramucosal fungal rhinosinusitis
-closure of CSF rhinorrhea
-removal of foreign body
-antrochoanal polyp
-chronic rhinosinusitis
-mucocele
-periorbital cellulitis
-epiphora related to lacrimal duct obstruction
-excision of selected tumours
-epistaxis control
-nasal septal obstruction
-dysthyroid orbitopathy
273
Relative Contraindications to Endoscopic Surgery
-absence of defined ostiomeatal abnormality
-osteomyelitis
-inaccessible lateral frontal sinus disease
-frontal sinus disease accompanied by stenosed internal ostium
-threatened intracranial or intraorbital disease
ANAESTHESIA
Local Anaesthesia with Sedation

-oxymetazoline used before application of cocaine to slow absorption and diminish cardiovascular effect
-anaesthetize branches of ethmoidal and sphenopalatine vessels and nerves
-sphenopalatine block:
-intraoral through greater palatine foramen
-do not advance needle tip more than 2.5 cm into foramen reduces risk of trauma to contents of
posterior orbit and blindness
-risks temporary diplopia and visual loss
-lateral wall injections:
-ascending process of maxilla (agger nasi)
-medial surface of middle turbinate
-portions of nasal septum
Rationale for Local Anaesthesia

-surgeon-patient communication possible
-improved visualization d/t decreased blood loss
-surgeon may be alerted when pain sensitive areas along base of skull and medial orbital wall are reached
-if orbital hematoma arises, can do vision checks to assess status and severity of injury
SURGICAL PROCEDURES
Complete Sphenoethmoidectomy
-indicated for extensive disease
Concurrent Septoplasty
-usually begun after endoscopic procedure is completed on side away from septal deflection
-hemitransfixion incision made on side contralateral to deflection
Functional Endoscopic Sinus Surgery

-philosophy: removal of disease from a target area such as OMU, normal mucociliary flow is restored and
disease in dependent sinuses resolves
-transition space surgery or small hole surgery (Messerklinger approach)
-theory: disease of secondarily involved sinuses resolves once obstructed area is adequately
ventilated
-CF pts are candidates for large middle meatal antrostomy that extends from natural ostium to floor of nose
-will never have normal mucociliary clearance
-four bony landmarks followed while medial orbital wall is skeletonized in an anteroposterior direction
-uncinate process
-ethmoid bulla
-basal lamella of middle turbinate, roof of maxillary sinus, superior turbinate
-anterior face of sphenoidal sinus
274
-anterior ethmoidal artery typically just anterior to vertical portion of basal lamella, immediately below
base of skull and posterior to frontal recess
-tight nasal packing should be avoided when integrity of orbital wall is in question: blood can dissect into
orbit and cause delayed haematoma and vision loss
-base of skull usually thinnest where anterior ethmoidal artery crosses from medial orbital wall to
cribriform plate
275
APPROACHES TO THE SPHENOIDAL SINUS
ANATOMY
-classification: three types of pneumatization; incidence
varies depending on series
-Harnberger:
-sellar (86%)
-presellar (11%)
-concha (3%)
-Congdon:
-postsellar (67%)
-presellar (24%)
-conchal (5%)
-conchal pneumatization not a contraindication to sphenoid
surgery
-dehiscent carotid artery in 4%
-dehiscent optic nerve in 4%
-Cavernous Sinus:
-contents:
-internal carotid artery
-indents posterior inferior surface of sphenoid sinus
-abducens nerve travels in close association with lateral wall of artery
-oculomotor nerve
-trochlear nerve
-abducens nerve
-ophthalmic division of trigeminal
-maxillary division of trigeminal
-active sinus infection if the main contraindication to a transnasal intracranial procedure
OVERVIEW OF APPROACHES
-transseptal:
-sublabial
-intranasal
-external rhinoplasty
-transantral
-transethmoidal
-external
-intranasal
-endoscopic:
-intranasal sphenoethmoidectomy
-transantral sphenoehtmoidectomy
-transpalatal
F.Ling - Approaches to the Sphenoid (1)
276
TRANSSPHENOIDAL HYPOPHYSECTOMY
Transseptal Approaches
-indications:
-large pituitary neoplasms with extensive suprasellar involvement
-total removal impossible, but tissue diagnosis and decompression of optic chiasm can be
obtained
-pituitary microadenoma
-Sublabial Transseptal Approach

-Intranasal Transseptal Approach
-External Rhinoplasty Transseptal Approach
-columellar flap raised
-medial crura are separated to expose caudal edge of quadrilateral cartilage
-traditional transeptal approach is then continued
Columellar Flap Modification

-complete transfixion incision made caudad to quadrilateral cartilage through membranous septum
-incision extends from domes superiorly to nasal spine inferiorly
-transverse incision carried posteriorly around feet of mesial crura on both sides to join transfixion
incision
277
Previous Septal Surgery
-strategies to avoid septal perforation:
-avoidance of problem area using traditional septoplasty techniques to go around scar tissue
-careful dissection through adherent mucosal areas; usually feasible when reoperation needed
soon after initial procedure
-lateral displacement of septum
Transantral Approach
-not commonly used at present
-allows widest exposure and is 1-2 cm closer to sphenoidal sinus than transeptal approach
-increased risk of damage to cavernous sinus, optic nerve and anterior cranial fossa
Transethmoidal Approach
-external and intranasal
-only external route appropriate for hypophysectomy (not popular)
-same disadvantages as transantroethmoidal route
-intranasal approach used for extensive nasal polyposis
SPHENOID INFLAMMATORY DISEASE
-acute and chronic sinusitis

-intranasal and transantral sphenoethmoidectomies are classic approaches
278
Endoscopic Approaches to the Sphenoid Sinus
-sphenoidal sinus lies at medial inferior portion of posterior ethmoid cell
-anterior wall ~7 cm posterior to anterior nasal spine
-posterior wall ~9 cm
-approach transethmoidal or direct
Intranasal Sphenoethmoidectomy
-middle turbinate infractured
-Glasgow forceps used to enter middle ethmoid cells
-dissection continued medial to turbinate
-ostium is enlarged toward midline with Kerrison forceps
Transantral Sphenoethmoidectomy
-used by some to manage chronic hyperplastic disease, especially if extensive benign maxillary disease
encroaches on ethmoidal and sphenoidal sinuses
-antral cavity entered through sublabial canine fossa approach
-removal of nasoantral wall
-anterior sphenoid wall is opened to expose the sinus
SPHENOID TUMOURS
-transseptal, transethmoidal or endoscopic approach

can be used
Transpalatal Approach
-for neoplasms of nasopharynx, posterior
pharyngeal wall, and choanae
-tumours isolated to sphenoidal sinus and
sella are better resected with alternative
methods
-Dibble and King:
-midline palatal split; hard palate,
posterior vomer removed as
necessary
-palate closed in two layers, muscle
and nasal mucosa first, followed by
oral mucosa
-Mullan:
-U-shaped incision at junction of
soft and hard palate
-hard palate resected
-incision closed in two layers
-preserves palatal motor function
best, but exposure is limited
inferiorly
-Kennedy:
-S-shaped incision originating along
lingual alveolus and curing back
across palatal aponeurosis to dive
soft palate off midline
279
Sphenoidal Mucocele
-transsphenoidal endoscopic approach successful in management of sphenoidal and ethmoidal mucoceles
with orbital and intracranial extension and with cholesterol granuloma of petrous apex
COMPLICATIONS
Nasal
-poor appearance (saddle and tip deformities)
-septal perforation
-infection
-epistaxis
Neurologic
-injury to optic nerve and cranial nerves III, IV, V1, V2
-trauma to optic chiasm
-late prolapse of chiasm into sella
-trauma to hypothalamus
-CSF leak
Vascular
-haemorrhage from internal carotid artery
-haemorrhage from cavernous sinus
EMERGENCIES
Preoperative:
-acute sinusitis with meningitis or other neurologic signs surgical drainage
-developing visual loss in sellar or parasellar tumour surgical decompression, radiation therapy
Intraoperative:
-retrobulbar haemorrhage with proptosis and visual compromise lateral canthotomy, ophthalmologic
consultation
-persistent haemorrhage from sphenoid or cavernous sinus region interventional arteriography
280
SPHENOID SINUS DISEASE
DEVELOPMENT
-begins early in third month of fetal development and continues throughout first decade of life
-progressive pneumatization after age 3
ANATOMY
-neighbouring structures of the sphenoid sinus
-dura
-pituitary
-optic nerve and chiasm
-rests against superolateral wall
-bone overlying optic canals becomes increasingly dehiscent with increasing age
-cavernous sinus
-located within medial aspect of cavernous sinus
-passes directly across lateral wall and produces a medial deflection of the lateral wall
into the lumen of the sinus (carotid sulcus)
-abducens nerve
-oculomotor nerve
-trochlear nerve
-ophthalmic nerve
-maxillary nerve
-sphenopalatine ganglion
-pterygoid canal and vidian nerve
-sphenoid ostium:
-1.5 cm above sinus floor on anterior wall
-drainage dependent on mucociliary flow
INFLAMMATORY DISEASE
Acute Bacterial Sphenoiditis

-risk factors:
-diving in contaminated waters
-cocaine or steroid use
-diabetes
-nasal fractures
-treatment often by broad-spectrum antibiotics; mucolytics, decongestants, saline irrigations
-indications for surgery:
-failure of medical management
-complication resulting from spread of infection to neighboring structures
-complications:
-orbital cellulitis
-hypopituitarism
-sepsis
-subdural and epidural abscess
-meningitis
-intracranial abscess
F.Ling - Sphenoid Sinus Disease (1)
281
-cerebral infarction
-blindness
Invasive Fungal Sinusitis

-immunocompromised pts
-Mucor, Rhizopus, Absidia favour high glucose acidic environment
-Aspergillus in neutropenic pts
-tx geared toward reversing underlying immunologic insult, excision of all necrotic tissues and treatment
with appropriate antifungal medications
Allergic Fungal Sinusitis

-typically presents with polyposis and pansinusitis
-sinuses filled with allergic mucin:
-eosinophil-laden mucin mixed with Charcot-Leyden crystals and noninvasive fungal forms
-vascular compromise and frank necrosis not observed
-capable of significant bony erosion and sinus expansion
-organisms:
-Aspergillus, Bipolaris, Curvularia, Alternaria, Cladosporium
-pathophysiologic mechanism believed to be allergic rather than infectious
-treatment:
-exposure to fungal antigen reduced by surgical removal of allergic mucin
-perioperative use of systemic corticosteroids, nasal saline irrigations and debridement of nasal
crusts
-immunotherapy with fungal antigens initiated
Mycetomas
-fungal balls
-occur despite adequate host immunity and are noninvasive
Chronic Sphenoiditis
-from obstructive polyposis
-obstruction, mucin stasis, chronic bacterial infection
-tx: removal of obstructing polyps, regular saline irrigations, use of nasal steroids, extended course of
antibiotics
Mucoceles
-treatment requires creation of wide sphenoidotomy with decompression of the mucocele
NEOPLASTIC DISEASE
Fibrous Dysplasia
-bony encroachment on optic nerve and ocular muscles
Chordoma
-typically arise from clivus and extend by direct expansion
-derived from notochordal remnants
-treatment involves surgical removal and XRT
Malignant Tumours of the Sphenoid

-primary malignancies rare
-most common tumours: adenocarcinomas, chondrosarcomas, lymphoepitheliomas
282
OPERATIVE TECHNIQUES
Open Approaches
-transseptal approach
-columellar incision or sublabial incision
-via ethmoid air cells:
-transmaxillary approach
-transorbital approach
-transpalatal approach
Endoscopic Approaches
-minimally invasive
-Bolger technique:
-relies on entering superior meatus through basal lamella, allowing identification of anteroinferior
aspect of superior turbinate
-dissection proceeds laterally to define posterior limit of lamina papyracea
-Bolger’s parallelogram:
-medial limit: lateral aspect of superior turbinate
-lateral limit: lamina papyracea
-superior limit: skull base
-inferior limit: horizontal portion of superior turbinate (attaching to lateral nasal wall)
-anterior face of sphenoid sinus is posterior wall of this box
-natural ostium located by gently removing inferior portion of superior turbinate
-safe area of entry: medial-inferior portion of parallelogram
283
COMPLICATIONS OF SINUS SURGERY
RELEVANT ANATOMY
-lamina papyracea is superior to and just lateral to the natural ostia

-operate laterally to middle turbinate, never medially and superiorly
-antrostomy :
-placed just above inferior turbinate
-should not be more anterior than anterior end of middle turbinate
-is at the level of the inferior orbital rim
-in adults, distance from nasal spine:
-5 cm: -bulla ethmoidalis
-6cm: -frontal recess
-basal lamella of middle turbinate
-nasofrontal duct ostia (6-6.5 cm)
-7 cm: -anterior ethmoidal artery
-base of skull
-sphenoidal sinus anterior wall
-choanal bridge
-nasopharyngeal wall approximates posterior sphenoid wall to within 1 cm
-ostium of sphenoidal sinus:
-adjacent to septum ~1.5 cm above choanal bridge, or ~1/3 up from choana to base of skull
-approaches:
-medially: medial to middle turbinate
-laterally: plane between superior inferior turbinate and just above attachment of middle
turbinate to choanal bridge
-if middle turbinate must be removed, remove only inferior or anterior part of the turbinate and preserve the
superior part as an anatomic landmark
COMPLICATIONS OF SPECIFIC PROCEDURES
Inferior Meatal Antrostomy

-bleeding (greater palatine artery), synechiae, osteomyelitis, tooth numbness, pain, injury (children:
proximity of developing canines)
Middle Meatal Antrostomy

-bleeding, blindness, facial pain, numbness, nasolacrimal duct injury, synechiae
-relatively complication-free procedure with sporadic reports of numbness and pain
Frontal Sinus Surgery with Osteoplastic Flap

-postoperative headache, incomplete obliteration, recurrent disease
-hypesthesia in distribution of supraorbital nerve
-early complications: hematoma, seroma, abscess, dural injuries intraoperatively
-other: necrosis of skin dorsum of nose, anosmia, temporary ptosis, temporary dysfunction of frontalis
muscle
-CSF leak, meningitis, brain injury unusual
Intranasal Ethmoidectomy
-blindness, permanent diplopia, CSF fistula with meningitis, brain injury, major vessel injuries
-synechiae, orbital hematoma, subcutaneous emphysema, loss of smell, hemorrhage
-contributing factors: repeated procedures, extensive disease, loss of landmarks
F.Ling - Complications of Sinus Surgery (1)
284
Transantral Ethmoidectomy (TE) and External Ethmoidectomy (EE)
-fewer major complications because of direct vision
-distance to ethmoidal and sphenoidal sinuses through transantral approach is half that of an intranasal
approach
-EE: orbital edema, supraorbital anesthesia, hemorrhage, wound infection
-TE: intracerebral hemorrhage, pneumocephalus, CSF fistula
Sphenoidotomy
-injuries to carotid artery, cavernous sinus, optic nerve, and brain can be catastrophic but they are rare
-CSF fistula, blindness, carotid artery injury, carotid cavernous fistula, meningitis
Caldwell-Luc Procedure
-most common immediate: facial swelling, cheek discomfort
-most common long-term: recurrent sinusitis, recurrent polyps, facial paresthesia, dacryocystitis,
-other: fever, hemorrhage, facial asymmetry, oroantral fistula, gingivolabial fistula, devitalized teeth,
recurrent polyps, blindness
ORBITAL COMPLICATIONS
Orbital Hematoma
-risk of hematoma with retention in retrobulbar space increases greatly with penetration of the periorbita
-most frequently caused by trauma to orbital veins lining lamina papyracea
-rarely by injury to anterior and posterior ethmoidal arteries (quick hematoma formation)
-orbital septum:
-fibrous membrane dividing eyelid into anterior and posterior chambers
-preseptal hematoma: darker and more diffuse and produces more lid edema
-postseptal hematoma: proptosis, conjunctival changes such as chemosis, pupillary changes,
mydriasis, and a dilated pupil
-most cases of orbital hematoma do not have associated proptosis and pupillary changes - these findings
signal increased orbital pressure and potential damage to the optic nerve
-ecchymosis usually resolves in ~ 7-10 days
Blindness
-direct (optic nerve injury) or indirect (orbital hematoma)
-temporary or permanent
-from increased orbital pressure compromised vascular supply to optic nerve
-retinal tolerance:
-venous hematoma: 60-90 minutes
-arterial hematoma: 15-30 minutes
-neural tissue vulnerable to ischemic injury
-intranasal procedures:
-right-handed surgeon more prone to cause injury on right side
-left ethmoidal sinuses are actually more medial than appreciated by a right-handed surgeon
-do not over pack nose if dehiscence present may press into periorbita and posterior chamber
-treatment: fast arterial hematoma:
-Medical treatment:
-eye consultation
-mannitol 1-2 g/kg in 20% infusion
-orbital massage: redistributes orbital blood
-remove nasal
-high dose steroids (controversial): dexamethasone 1-1.5 mg/kg/24h
285
-Surgical treatment:
-lateral canthotomy
-medial external (lynch) decompression
-endoscopic decompression
-control bleeding artery (anterior ethmoidal artery)
Diplopia
-injury to ocular muscles: medial rectus and superior oblique
-direct muscle injury or injury to nervous or vascular supply to muscle
-persistent diplopia rare complication with poor prognosis
Nasolacrimal Duct Injury

-agger nasi cells adjacent to lacrimal sac
-ethmoidal sinus and natural antrostomy associated with lacrimal duct
-avoid operating anterior to attachement of uncinate:
-as a rule, ethmoidal sinuses or natural antrostomy should not be opened anterior to the anterior
end of the middle turbinate or into the hardened bone separating the antrostomy from the
nasolacrimal duct
-inferior antrostomy is 1 cm or more behind the anterior inferior turbinate in the inferior meatus
-most cases of epiphora resolve
-early epiphora is associated with permanent injury to the nasolacrimal system
-tx: dacryocystorhinostomy if necessary
Subcutaneous Emphysema
-from resultant fracture or perforation of lamina papyracea
-observe for orbital hematoma
-treatment in most cases is simple observation and reassurance
-emphysema resorbs within 7-10 days
Intraoperative Orbital Fat Penetration

-increases risk of retrobulbar hematoma
-tx: avoid further trauma; avoid tight nasal packing; observe for vision changes, proptosis or restricted
ocular gaze
INTRACRANIAL COMPLICATIONS
Cerebrospinal Fluid Fistula

-areas of potential injury:
-cribriform plate (most common)
-thinnest bone
-dura more adherent
-near frontal recess
-anterior ethmoid artery
-posterior ethmoid sinus
-almost any type of living tissue membrane can be used to patch a fistula:
-eg. fascia temporalis, septal or turbinate mucosa, fascia lata
-local flaps of septal mucosa or middle turbinate
-delayed fistula identification
-CT with contrast agents helps localize active leak
-diluted fluorescein injected intrathecally located with endoscope after 20-30 minutes
-endoscopic examination
286
-treatment for persistent leaks: bedrest +/- lumbar drain
-use of antibiotics is controversial and should be used with caution so as not to select out resistant
organisms
-conservative management often allows CSF fistula to heal without surgery
-if persists for 2-3 weeks should be closed surgically
Intracranial Infections
-meningitis
-brain abscess
Brain injury and Major Vessel Injury

-anterior communicating artery can be injured through cribriform plate
-can go into spasm stroke
-frontal lobe syndrome from entrance through roof of nose into brain
-carotid artery and cavernous sinus injury from sphenoidal surgery
-slight injury to the brain can be managed quickly and with minimal deficit
-serious injury always life-threatening
NEURAL AND VASCULAR INJURY
Anosmia
-three types of causes:
-interference with access of odorant to olfactory nerve
-damage to olfactory nerve
-damage to central olfactory pathway
Paresthesia and Hypesthesia

-most common complications of Caldwell-Luc, external ethmoidectomy, and frontal sinus surgery
-usually temporary, resolved in 3-6 months
Hemorrhage
-one of the most common complications during or after sinus surgery
-preoperative sedation and vasoconstriction with a topical spray improves blood pressure control and
decongestion and diminish any systematic reaction to topical cocaine
-only diseased tissue should be removed
-areas of injury:
-sphenopalatine
-carotid
-ethmoid
-carotid-cavernous fistulas
-posterior septal artery:
-runs below sphenoid bone and feeding into posterior middle turbinate can cause marked
intraoperative and postoperative hemorrhage
-tx:
-if bleeding is too great then operation is terminated and nasal packing instituted
-electrocautery
-consider embolization for carotid injuries
287
SYNECHIA
-most common complication of FESS

-amputation of anterior end of middle turbinate may avoid synechiae
-any reduction of middle turbinate can predispose it to weakness, giving it a natural tendency to lateralize,
blocking the anterior or posterior ethmoidal sinus, frontal recess, or antrostomy
-removal of agger nasi cells often opens the meatus, dramatically reducing the chances of middle turbinate
lateralization
ABNORMALITY OF FACIAL GROWTH AND SINUS DEVELOPMENT
-although growth disturbance and retarded sinus development have occurred in animals, no clinical study
has shown growth problems
OTHER COMPLICATIONS
-residual disease
-facial edema
-aspiration of packing material
-toxic shock syndrome
-osteomyelitis
-tooth numbness and pain (Caldwell-Luc)
-embossment (frontal sinus obliteration)
288
EPISTAXIS
ANATOMY
a) Internal Carotid
-internal carotid a. opthalmic a.
-branches (within orbit):
posterior ethmoidal a. (absent in 31%)
anterior ethmoidal a. (absent in 7-14%)
-posterior ethmoid artery enters posterior ethmoidal foramen within 4-7 mm of the optic nerve > 80% of
the time
-anterior ethmoid artery enters anterior ethmoidal foramen 14-22 mm posterior to maxillo-lacrimal suture >
80% of the time
-ethmoidal arteries branch into medial and lateral branches in ethmoidal cells
-medial branches: supply superior septum and Little’s area
-lateral branches: supply superior and middle turbinates
b) External Carotid
- facial artery superior labial artery
nasal arterial branches
medially to septum
laterally to ala
- maxillary artery
sphenopalatine a.: supplies septal mucosa
posterior nasal a.: supplies lateral nasal wall and turbinates
anastomosis superiorly with ethmoid arteries
anastomosis inferiorly with pharyngeal branches of maxillary artery
(Woodruff naso-nasopharyngeal plexus)
pharyngeal artery
descending palatine a. (greater palatine canal and foramen) greater palatine a.
(supplies septum and floor of nose) incisive foramen
Little’s area
F.Ling - Epistaxis (1)
289
-Kiesselbach’s plexus (Little’s area) anastomosis of:
-greater palatine artery
-anterior ethmoid artery
-nasal branches of facial artery
PHYSIOLOGY AND PATHOPHYSIOLOGY
-turbinate arterioles pass within conchal bone and are

surrounded by a venous plexus
-dilatation of arterioles blocks venous outflow
mucosal congestion
-cavernous nasal plexus - venules > arterioles
-septal cartilage depended on overlying
mucoperichondrium for blood supply
ETIOLOGY
-anterior epistaxis 90-95% of the time

-severe or recurring epistaxis should prompt further
etiologies
Local Factors
-trauma
-digital manipulation
-septal perforation turbulence and impaired
laminar airflow drying, scab formation
epistaxis
-nasal fracture
-probably posttraumatic pseudoaneurysm of internal carotid artery triad of prior
monocular blindness, ipsilateral orbital fractures, delayed epistaxis
-local inflammation
-decongestants and nasal steroids
-foreign bodies
-tumours: eg. juvenile angiofibroma, nasopharyngeal carcinoma
290
-chemical inhalants
-nasal prong O2, CPAP
-surgery: septoplasty and FESS
Systemic Factors
-vascular disorders:
-Osler-Weber-Rendu:
-autosomal dominant: mucocutaneous telangiectasias and epistaxis
-thin vessel walls without smooth muscle, increased angiogenesis resulting in vascular
proliferation, arteriovenous fistulae, mucosal fragility
-most common disease of vascular structures leading to recurrent epistaxis
-aging:
-fibrosis of muscular tunica media of arteries
-atherosclerosis NOT a risk factor
-hypertension NOT a significant risk factor for anterior epistaxis
-some possible association of increased risk for posterior epistaxis
-blood dyscrasias:
-VonWillebrand disease
-most common hereditary bleeding disorder associated with epistaxis
-AD
-epistaxis in 60%
-recommended presurgical prophylaxis: desmopressin
-Hemophilia A and B
-hematologic malignancies: leukemia, multiple myeloma, thrombocytopenia
-malnutrition
-alcohol
-drugs: ASA, NSAIDS, anticoagulants, chloramphenicol, carbenicillin, dipyrimdamole
-infectious/inflammatory:
-TB
-syphilis
-Wegener’s
-periarteritis nodosa
-SLE
MANAGEMENT
Exsanguinating Epistaxis
-due to severe midfacial trauma with maxillary artery laceration
-ABCs
-anterior nasal packs followed by oro- and nasopharyngeal pack (after airway has been secured)
-radiographic embolization
Determination of Epistaxis Bleeding Source

-anterior epistaxis: Little’s area (venous)
-posterior epistaxis: (arterial)
-posterior septum (60-65%)
-posterior lateral nasal wall (Woodruff’s plexus)
Silver Nitrate Cauterization

-for cauterization of anterior septum
-can be neutralized with application of sodium chloride
291
Electric Cauterization
-induces a deeper penetration and more tissue destruction than silver nitrate
-repetitive cauterization increases likelihood of septal perforations
Laser Photocoagulation
-argon and neodymium:yttrium aluminum garnet laser
-multiple treatments required
-photocoagulates abnormal subepithelial arteriovenous reticulum, preserving the overlying mucosa and
underlying cartilage
Nasal Packing
-Anterior
-local anesthesia may decrease the risk of apnea, bradycardia, and hypotension by blocking the nasal-vagal
reflex
-patients with chronic mucosal pathology from HHT, coagulation d/o, or leukemia should be managed
without packing in anticipation of future multiple treatments
-use Surgicel, Oxycel or Avitene
-Posterior
-patients who fail anterior packs
-main purpose is to stabilize the anterior packing
-complications/pitfalls of nasal packing:
-hypoxia; aspiration of packs
-toxic shock syndrome
-sinusitis
-alar necrosis
-septal perforation
-synechiae
-cerebral ischemic
-cardiovascular complications
-failure to control bleeding
-vasovagal syncope
-septal hematoma
-eustachian tube dysfunction; otitis media
Balloon Packs
Greater Palatine Canal Injection

-dental anesthetic injection technique of the greater palatine foramen/canal
-used to control posterior nasal hemorrhage involving sphenopalatine artery
-high pressures used in canal to tamponade the bleeding can potentially injury the greater palatine nerve as
well
Endoscopic Management
-endoscopic control under local anaesthesia for posterior epistaxis
-preliminary studies show effective control of bleeding
-benefits:
-precise localization of bleeding site and direct visualization of the injection, cauterization,
lasering, or packing
-treatment localized to smaller area
-disadvantages:
-expertise required
-expense and limited availability of instrumentation
292
Maxillary Artery Ligation
-causes decrease in intravascular pressure gradient, resulting in hemostasis of posterior nasal cavity unless
anastomoses exist with continued high pressures
-ligation of maxillary artery and distal branches:
-descending palatine, sphenopalatine, posterior nasal arteries
-note: sphenopalatine and posterior nasal arteries may bifurcate at sphenopalatine foramen or earlier
-procedure:
-Caldwell-Luc approach
-removal of posterior maxillary wall area enlarged with mastoid curettes
-identify and clip vessels within pterygopalatine fossa
-overall average success rate of 87%
-indications:
-failed medical management after 72 hours
-pts requiring more than three units of blood transfusion
-nasal anomaly that precludes nasal packing
-continued bleeding despite nasal packing
Intraoral Ligation of the Maxillary Artery

-useful in children as an alternative to embolization and external carotid artery ligation for removal of
vascular tumours
-involves exposing the posterior portion of maxilla through posterior gingivobuccal incision
Transantral Sphenopalatine Artery Ligation (Simpson)

-medial posterior inferior maxillary wall removed
-sphenopalatine artery and vidian nerve exposed
-vidian nerve dissected free, vessel ligated
-advantage: diminished risk of failure due to collateral circulation
Endoscopic Ligation of Sphenopalatine Artery

-modification of Simpson’s technique
-via meatal antrostomy and canine fossa sinuscopy
-may replace transantral approaches a surgical treatment of choice
Ligation of Anterior and Posterior Ethmoidal Artery

-generally performed in conjunction with ligation of maxillary artery or external carotid artery
-procedure:
-Lynch incision made
-periosteum elevated
-frontoethmoidal suture line followed in posterior direction ~14-22 mm to the anterior ethmoid
artery and its foramen artery is clipped or cauterized
-posterior ethmoid artery further posterior at a highly variable distance (~12 mm)
-optic nerve lies 4-7 mm more posterior to posterior ethmoidal foramen
-important because no other procedure can access these branches of the ophthalmic artery
External Carotid Artery Ligation

-advantage: rapid, local anaesthesia
-disadvantage: lack of control of potential collateral circulation
-exposure of common carotid artery along anterior border of SCM
-failure rate 7-45%
293
Septodermoplasty
-grafting technique
-telangiectatic mucosal surfaces removed with preservation of perichondrial and periosteal vascular bed
-STSG then grafted
-used mainly for patients with Osler-Weber-Rendu disease
Surgical Reconstruction/Local and Microvascular Flaps

-for those with severe, recalcitrant HHT
-resurfacing the nasal cavity after it was denuded of mucosal lining
-median forehead flaps and nasolabial flaps used to resurface the interior lining of the nasal cavity
-RFFF
-disadvantage: need for lateral rhinotomy and intranasal chronic desquamation, nasal airflow limited
Selective Angiography and Embolization

-success ranges from 87-96%
-effective only when bleeding > 0.5 ml/min
-only able to cauterize external carotid and its branches
-short-term failure due to:
-internal carotid branches attributed to dominant anterior and/or posterior ethmoid arteries
-external carotid artery branches attributed to dominant ipsilateral facial arteries or contralateral
collateral maxillary artery branches
-complications:
-skin necrosis, blindness, ophthalmoplegia, facial pain or edema, paresthesia or paralysis, and
cerebral embolization with hemiplegia
-groin hematoma most common complication
294
MANIFESTATION OF SYSTEMIC DISEASES OF THE NOSE
(Cumming’s Ch 44)
GRANULOMATOUS DISEASES
Wegener’s granulomatosis
-necrotizing granulomas and vasculitis of the upper and lower respiratory tract
-three main forms:
-Type 1: limited form of WG.
-URTI persisting for several weeks, unresponsive to antibiotics
-associated serosanguineous nasal drainage and pain
-expression of very large nasal crusts in both sides of nose
-no disease other than WG with such severe crusting
-when crusts are removed mucosa is very friable
-Type 2: sicker patient with more systemic symptoms
-nasal involvement similar as type 1 but other organs are involved
-hemoptysis and cavitating lesions
-Type 3: widely disseminated
-involvement of multiple organs including airway, pulmonary, renal, and sometimes
cutaneous lesions
Wegener’s granulomatosis involvement of other head and neck sites

-Orbital:
-nasolacrimal duct obstruction, ethmoid and nasal disease, nonspecific episcleritis
bilaterally, and bilateral or unilateral proptosis due to extension of disease into the orbit
or pseudotumor of the orbit itself
-Otologic:
-unilateral or bilateral serous otitis media, with or without mastoiditis
-Oropharyngeal:
-not common
-diffuse upper and lower gingival lesions and diffuse minor salivary gland; ulcerations
throughout oral cavity
-Subglottic involvement with or without nasal involvement:
-very common
-finding of a very short segment of upper tracheal stenosis on endoscopy may suggest
diagnosis of WG
Diagnosis of Wegener’s granulomatosis

-careful biopsy
-nasal crusts are removed and up to seven or eight pieces of tissue removed from all
turbinates
-tissue is sent for stains and culture including AFB
-antineutrophilic cytoplasmic antibody (ANCA)
-high specificity of c-ANCA for WG has been confirmed in large studies
-it is so specific that it may in some cases preclude the need for biopsy
-negative c-ANCA test does not exclude diagnosis of WG - sensitivity is limited and
depends on extent and activity at time study is done
Disorders mimicking Wegener’s granulomatosis

-previous or ongoing nasal substance abuse
F.Ling - Systemic Diseases of the Nose (1)
295
Histopathology of Wegener’s granulomatosis
-vasculitis necrosis with an inflammatory background
-typically involves medium and small vessels
-necrosis is granulomatous in nature
-small microabscesses that enlarge and coalesce until typical necrosis has developed
-necrotic center surrounded by palisading histiocytes and scattered giant cells
Treatment of Wegener’s granulomatosis

-oral cyclophosphamide (2 mg/kg/day) for 6 months to 1 year
-prednisone (1mg/kg/day) for 1 month then tapered throughout the following 2 months and then
discontinued once a complete response is determined
-other:
-TMP-SMX may prevent remission
-Plasma exchange and intravenous immunoglobulin
-methotrexate
-azathioprine
-surgical reconstruction: when in remission
Sarcoidosis
-chronic systemic granulomatous disease
-capable of involving almost any organ in the body:
-eye (episcleritis, uveitic)
-various neuropathies (sudden deafness, unilateral or bilateral facial palsy)
-salivary glands (parotid swelling)
-oropharynx (tonsillar hypertrophy)
-larynx (epiglottic swelling and subglottic stenosis)
Nasal involvement
-external
-raised, papular lesion on the nose; firm and elastic
-lupus pernio
-chronic, violaceous cutaneous lesions with a predilection for cold-sensitive
areas such as nose, cheeks, ears, and fingers
-internal
-diffuse nasal crusting or a vasomotor-like appearance to the nasal mucosa
Diagnosis
-pt’s clinical and radiographic presentation compatible with sarcoidosis
-nasal biopsy material noncaseating granuloma
-other causes for granulomatous changes need to be excluded
-bronchoalveolar lavage (BAL)
-pts with > 28% T lymphocytes in BAL fluid: high-intensity alveolitis
-pts with < 28% T lymphocytes have low-intensity alveolitis
-ACE:
-seems to correlate with the clinical activity of sarcoidosis in some patients
-not diagnostic
-other studies:
-increased ESR
-hypercalcemia and hypercalcuria may occur (10% of cases)
-hypergammaglobulinemia noted in 20-25%
-ECG abnormalities: prolonged P-R interval, bundle-branch block, arrhythmias, and
296
nonspecific sinus tachycardia (ST)-segment changes
Management
-involvement of the intranasal mucosa, epiglottis, and subglottis responds to aerosols containing
cortisone
-corticosteroids
-low dose MTX
Churg-Strauss Syndrome
-granulomatous vasculitis
-eosinophil-rich, granulomatous inflammation and necrotizing vasculitis of the upper respiratory tract
affecting small to medium vessels associated with asthma and eosinophilia
-three phases:
-prodromal phase that may persist for years
- allergic disease (e.g., allergic rhinitis and nasal polyposis, frequently followed by
asthma)
-peripheral blood and tissue eosinophilia, chronic eosinophilic pneumonia, or eosinophilic
gastroenteritis
-life-threatening systemic vasculitis
-c-ANCA and p-ANCA tests always negative
-Histopathology:
-prominent eosinophilia of vessels and perivascular tissue
-vasculitis of the small arteries and veins
-fibrinoid, necrotizing epitheloid eosinophilic granuloma
-tx:
-responds well to corticosteroids; not cyclophosphamide
INFECTIOUS SYSTEMIC DISEASES
Rhinoscleroma
-chronic granulomatous disease of the respiratory tract
-also involves larynx, trachea, and bronchi
Nasal involvement
-1. catarrhal stage:
-foul-smelling, purulent rhinorrhea for weeks or months
-2. atrophic stage:
-large nasal plaques or crusts that simulate the lesions in atrophic rhinitis
-3. granulomatous stage:
-multiple granulomatous nodules are found throughout the nose, pharynx, larynx,
trachea, or bronchi. These nodules can enlarge and coalesce
-4. fibrosis and stenosis
-often complete stenosis of the nostrils
Diagnosis
-high index of suspicion and the finding of coalescent, enlarged granulomatous nodules at or near
the nasal vestibule
-cultures of infected tissue yield K. rhinoscleromatis in 98% of cases; this is diagnostic
-identification of Mikulicz’s cell in biopsy specimens is not definitely pathognomonic because
this cell can be found (though rarely) in other disorders.
297
Histopathology
-characteristic fibrosis and eosin-staining Russell bodies
-vacuolated Mikulicz’s cell: a large, foamy histiocyte that stains well with hematoxylin and eosin.
-easiest to identify during granulomatous stage
Treatment
-Streptomycin (1 g/day for 4 weeks) plus tetracycline (2 g/day)
-Corticosteroids and radiotherapy are not effective.
Tuberculosis
Nontuberculous mycobacteria
-less virulent
-more likely to infect individuals who have altered host defences
-less susceptible to standard antituberculosis drugs
-most common infections:
(1) corneal ulcers caused by Mycobacterium fortuitum
(2) cervical lymph nodes infected by nontuberculous mycobacteria (Mycobacterium
scrofulaceum, Mycobacterium szulgai, and Mycobacterium xenopi)
Nasal involvement
-usually affects anterior septum or anterior part of turbinates
-perforations of cartilaginous portion of septum
-lupus vulgaris (an indolent and chronic form of tuberculosis of the nose) scarring is more severe
Management
-2-month course of therapy with three drugs: isoniazid, rifampin, and either streptomycin or
ethambutol
Histoplasmosis
-primarily involves larynx and tongue; can involve any part of head and neck
Nasal involvement
-accompanied by pulmonary involvement characterized by cough, chest pain, and hoarseness
-CXR: diffuse miliary or a localized type of infiltrate
-nasal involvement consists of either nodules or ulcers composed of masses of organisms in
macrophages
Histopathologic features
-lesion is an epithelioid or histiocytic granuloma
-periodic acid–Schiff, Gridley, or Grocott-Gomori methenamine-silver nitrate stain to identify
organism
Treatment
-amphotericin B, in a dose of 1 mg to 10 mg per day and progressing to 1 mg/kg for a total dose of
2 g administered during a 2- to 3-month period
Rhinosporidiosis
-caused by Rhinosporidium seeberi
-contracted by immersion in contaminated waters in Asia and Africa
-nasal mucosal lesion is flat and sessile, then enlarges painless polypoid growth that fills nasal cavities
-mx: complete surgical excision; no medical management effective
298
-microscopically: pseudoepitheliomatous squamous cell metaplasia overlies numerous multisized,
microscopic globular cysts called sporangia
Mucormycosis
-caused primarily by fungi of the order Mucorales and of the genera Mucor, Rhizopus, and Absidia
-occur in diabetics and immunosuppressed patients
-broad, nonseptic hyphae (typical of Mucorales) on tissue sections stained with periodic acid–Schiff or
Grocott-Gomori methenamine-silver nitrate stain confirms the diagnosis
-prognosis is poor, with a reported death rate as high as 50%.
-amphotericin B only effective antifungal drug treatment
-aggressive surgical debridement mandatory
PERIPHERAL T-CELL NEOPLASMS

-T-cell lymphoma replaces previously used terms such as midline malignant or polymorphic reticulosis.
Clinical diagnosis
-lymphoma lesions more likely to be unilateral, with extension into soft tissue of nose, upper lip,
oral cavity, and maxillary sinus, with or without orbital involvement
-lesions are ‘‘explosive,’’ rapidly progressive
-in T-cell lymphoma otologic, tracheal, and renal involvement is extremely uncommon
-histology: polymorphic lymphoid infiltrate with angiocentric and angioinvasive features
Treatment
-XRT for localized lesions
-multiorgan involvement best treated standard leukemia protocol
299
CEREBROSPINAL FLUID LEAKS
CLASSIFICATION
Cerebrospinal fluid rhinorrhea

-traumatic or nontraumatic in origin
-traumatic fistulas: 96%
-iatrogenic: 16% of pts with CSF
rhinorrhea
-accidental: 80% of pts with CSF
rhinorrhea
-incidence of CSF rhinorrhea
in patients who suffer serious
head trauma is only 2% to 3%
-nontraumatic: 4%
-high-pressure leaks are more common: from tumours or hydrocephalus
-normal-pressure CSF leaks: from congenital anomalies or osteomyelitis
Cerebrospinal fluid otorrhea

-traumatic or nontraumatic in origin
-most common cause of CSF otorrhea is accidental
trauma
-CSF leaks in ~0.4% to 6.7% of patients
with demonstrable skull fractures
-longitudinal temporal bone fractures
result in CSF otorrhea more frequently
than transverse fractures
-surgery for chronic suppurative ear disease or malignancy is the second-most common cause of CSF
otorrhea
PATHOPHYSIOLOGY
-CSF rhinorrhea is more common than CSF otorrhea in most reported series
Traumatic cerebrospinal fluid rhinorrhea

-most frequent sites: roof of ethmoid and cribriform plate (d/t thin bone and tight adherence of
dura)
-trauma causes dural tearing
-immediate or delayed leak may occur
-reason for delayed leak:
-delayed increase of intracranial pressure after trauma
-lysis of a clot in an area of bone and dural dehiscence
-resolution of soft-tissue edema
-maturation and contraction of wound edges
-loss of vascularity and necrosis of soft tissue and bone around wound
Nontraumatic cerebrospinal fluid rhinorrhea

-increased intracranial pressure continued erosion and weakening of bone fracture CSF
fistula
F.Ling - CSF Leaks (1)
300
-most frequent sites: cribriform plate and roof of ethmoid
-tumours may cause CSF rhinorrhea through direct erosion of bone

-escape of CSF through external auditory canal
-requires an abnormal communication between subarachnoid space and pneumatized areas of temporal
bone and TM perforation or defect in EAC
Traumatic cerebrospinal fluid otorrhea

-pathophysiology of CSF otorrhea resulting from trauma is similar to that of CSF rhinorrhea
-fractures and penetrating injuries pass through bony labyrinth of inner ear, internal auditory
canal, or tegmen (roof) of middle ear or mastoid
Nontraumatic cerebrospinal fluid otorrhea

-increased ICP probably does not play a major role because cribriform plate is weakest point of
skull base, and rhinorrhea is more likely to result
-most commonly associated with congenital anomaly:
-Mondini inner ear dysplasia (most common)
-as a result of a widely patent cochlear aqueduct or a defect in cribrose plate of
internal auditory canal or fallopian canal
-congenital dehiscence of tegmen with no inner ear malformation
-physiologic CSF pressure changes or sudden increases in ICP may play an
important role in herniation of dura through tegmen defect and eventual CSF
leakage
DIAGNOSIS
Symptoms

-major presenting symptom: fluid draining from nose
-in trauma patients:
-develops within 48 hours in approximately 55% of all patients who ultimately develop CSF
rhinorrhea as a result of trauma
-increases to 70% by end of first week as edema resolves
-hyposmia or anosmia 60% to 80%
-headaches caused by intracranial air in ~20%
-20% develop meningitis as their initial manifestation
-mostly in delayed posttraumatic group
-risk of developing meningitis in first 3 weeks after head trauma and before correction of a CSF
leak ~ 3% to 11%
-postoperative CSF rhinorrhea:
-most often from transphenoidal removal of pituitary tumours
-3% to 6% of patients
-nontraumatic
-CSF rhinorrhea is insidious at onset and may remain undiagnosed for years
-aeroceles are rarely present intracranially, and anosmia and meningitis also are rare
-headaches are common in these patients
301
-traumatic:
-94% of those who ultimately developed CSF otorrhea after trauma had an immediate onset
-symptoms may consist of hearing loss, pressure sensation in ear, or dizziness
-postop CSF otorrhea:
-leakage from incision site, a fluctuant mass at surgical site, or meningitis
-CSF otorhinorrhea after surgery for acoustic neuroma occurs in approximately 10% to 20%
-nontraumatic:
-congenital CSF otorrhea
1. petromastoid canal
2. wide cochlear aqueduct
3. Hyrtl’s fissure
4. facial canal
-children who have congenital CSF otorrhea frequently have a form of Mondini inner ear malformation and
a history of recurring episodes of meningitis
-may have a congenital dehiscence of fallopian canal or Hyrtl’s fissure
-tympanomeningeal fissure
-a congenital cleft that runs between hypotympanum and posterior cranial fossa passing
in proximity to jugular bulb
-adults who have normal inner ear function, have a CSF fistula as a result of ruptured
meningoencephaloceles that present through congenital defects in tegmen of temporal bone
Diagnostic studies
Demonstrating extracranial cerebrospinal fluid

-persistence of a clear, nonsticky, nasal discharge should arouse suspicion of a CSF leak.
1. ‘‘Halo sign’’:
-classic sign of CSF leakage:
-clear fluid area surrounds a blood stain when CSF mixed with blood is absorbed onto
paper
2. Biochemical studies on fluid:
-testing for glucose content in suspicious fluid: >30 mg/ml confirmatory for CSF
-collecting adequate amounts of fluid to analyze for chemical content difficult
-glucose content of tears may be a confounding factor
3. B2 transferring identification:
-immunoelectrophoretic identification of B2 transferrin in fluid suspected to be CSF
confirms diagnosis of a CSF leak
-other tissue fluids that contain B2 transferrin:
-aqueous and vitreous humor in eye
-perilymph in cochlea
4. CT cisternography with nonionic contrast
-radiologic diagnosis of extracranial CSF
5. Radionuclide cisternography
-injection of radioactive isotopes (radioactive sodium, 111In-DTPA [diethylenetriamine
pentaacetic acid] 99mTc-DTPA) into subarachnoid space
-combined with scintigraphy of pledgets placed intranasally
-overall success rate of 25% to 65% and has been useful in patients with intermittent
rhinorrhea not diagnosable by other means
302
Localizing site of leakage
-leak occurring in only one side of nose generally correlates with side of defect
-leakage from nose when head is upright or tilted backward suggests that leak is through cribriform plate,
ethmoid roof, or frontal sinus
-leakage only on tilting head forward suggests that leakage is coming from sphenoid sinus or through
middle ear
-use of radioactive isotopes injected into subarachnoid space is not very accurate in localizing site of
leakage
-false-positive result is common because of absorption of radioactivity within bloodstream and
redistribution of this activity through nasal mucosa to pledgets
1. Nasal endoscopic examination

-can diagnose and localize site of CFS leak in patients with CFS rhinorrhea
2. NCTC useful for localizing site
3. Injection of fluorescein into subarachnoid space
-has been used to localize site of CSF leakage
-commonly used intraoperatively
-after injection of 0.5 ml of 5% fluorescein diluted by 9.5 ml of CSF
4. MRI
-techniques of MRI have enhanced ability of MRI to localize site of CSF leakage
-advantages of MRI (over NCTC) are that MRI is noninvasive (no radiopaque dye is
injected), does not involve radiation exposure, and has multiplaner images
MANAGEMENT
Traumatic
-majority of traumatic CSF fistulas heal without surgical intervention
-if no evidence of resolution of CSF leakage by end of 1 week, probably will require surgical
exploration and closure of leak
-pts who develop CSF rhinorrhea days or weeks after trauma generally do not heal without
surgical intervention
-adjacent facial fractures should be reduced early, and reduction may result in cessation of CSF
leakage without further therapy
-indications for repair:
-failed conservative management > 2 weeks
-recurrent meningitis
-gunshot wounds
-large defects in skull base with herniation of brain and evidence of a spicule of bone penetrating
brain
-early onset that is associated with meningitis or a pneumocele (controversial)
-pts in whom injury to dura is not suspected until postoperatively when CSF rhinorrhea occurs,
conservative therapy is indicated because majority of these leaks will close
-prophylactic antibiotics have not been shown to be effective in prevention of meningitis and are not
recommended in posttraumatic patients
-conservative management of CSF rhinorrhea:

-keeping patient at bed rest in an upright position that minimizes leak
-avoid coughing, sneezing, nose blowing, and straining
-laxatives are prescribed to reduce straining with bowel movements
-if no resolution of rhinorrhea occurs in 72 hours, repeated or continuous lumbar drainage of CSF
may be tried for next 4 days with removal of 150 ml/day
303
Nontraumatic
-conservative therapy rarely helpful in nontraumatic or delayed CSF rhinorrhea
-high-pressure CSF rhinorrhea:
-decrease high intracranial pressure rhinorrhea resolves in most patients
-surgical exploration if no resolution
-normal-pressure CSF rhinorrhea:
-leaks rarely close with conservative therapy and almost always require surgical exploration and
closure
Operative approaches
-intracranial and extracranial approaches
-Intracranial approaches (“repair from above”)

-require a craniotomy with its attendant morbidity, mortality, and prolonged hospitalization
-anosmia frequent complication of craniotomy
-advantages:
-ability to achieve a fluid-tight dural closure
-ability to repair multiple areas of leakage
-Extracranial approach (“repair from below”)

-advantages:
-minimal morbidity and mortality while still achieving excellent visualization of dural
defect
-requires precise, preoperative localization of leakage site
Repair of specific sites
Ethmoid roof–cribriform plate

-done through an external approach or through an intranasal approach using an endoscope or a microscope
for visualization
-external approach:
-via orbito-nasal incision and ethmoidectomy
-dural defect sealed with temporalis fascia grafts, fascia lata, or pericranium used alone or
bolstered with fat or with mucoperiosteal flaps from lateral nasal wall or septum
-supported by absorbable surgical sponge placed against graft or flap followed by an intranasally
placed antibiotic-impregnated gauze strip
-intranasal approach
-lifting of mucosa around defect
-large bony defect reconstructed with septal cartilage or bone followed by placement of temporalis
fascia graft coated with fibrin glue
-edges of graft are subsequently tucked under mucosal edges
-graft held in place with a muscle or fat graft coated with fibrin glue and supported by gelfoam
-success rate ~ 76% to 100%
-intracranial approach if site of leakage cannot be delineated clearly or if multiple leaks exist
Frontal sinus
-best repaired through an extracranial approach using an osteoplastic flap
Sphenoid sinus
-best approached through an endoscopic approach
-anterior wall of sphenoid sinus is exposed and resected, and site of CFS leak is delineated
-site of leakage then is grafted with fascia and coated with fibrin glue
304
Ear
-defects in tegmen can be exposed by a mastoidectomy or atticotomy
-leaks from posterior fossa dura into mastoid are approached through a mastoidectomy
-craniotomy usually is reserved for those with failures of various extracranial operations and for patients
with large or multiple defects
-material for dural repair:
-temporalis fascia, fascia lata, periosteum, perichondrium, homograft dura, and methyl
methacrylate
-most frequent locations for middle ear CSF leaks are

- (1) oval window, (2) round window, and (3) Hyrtl’s fissure, in that order
305
PEDIATRIC RHINOSINUSITIS
SIGNS AND SYMPTOMS
-usually symptoms longer than 10 days

-nonsevere acute rhinosinusitis
-rhinorrhea of any quality
-nasal congestion
-cough
-headache, facial pain, and irritability
-low-grade or no fever
-severe acute rhinosinusitis
-purulent (thick, coloured, opaque) rhinorrhea
-nasal congestion
-facial pain or headache
-periorbital edema (variable)
-high fever
-in children, symptoms are non-specific
-look for purulent discharge at middle meatus
-polyps are unusual except in CF or allergic fungal sinusitis
Diagnostic Aids
-plain films are unreliable: both under- and overestimate amount of sinus disease noted on CT scans
-imaging not necessary to confirm diagnosis of RS in children
-indications for CT scan:
-severe illness or toxic condition in a child
-acute RS that does not improve with medical therapy in 48-72 hours
-immunocompromised host
-presence of suppurative complication other than orbital cellulitis
ETIOLOGY
-begin as viral URTI

-rhinovirus, parainfluenza, influenza, adenovirus
-obstruction of OMC
-anatomic variations (eg. septal deviations, paradoxical turbinates, concha bulbosa) not necessarily
associated with high incidence of chronic RS
-ciliary dysfunction
-GERD may play a role
-allergy is a risk factor
BACTERIOLOGY
-Acute RS:
-Streptococcus pneumoniae (30%)
-Moraxella catarrhalis
-Haemophilus influenzae
F.Ling - Pediatric Rhinosinusitis (1)
306
-Chronic RS:
-Aerobic bacteria
-Streptococcus pneumoniae
-Moraxella catarrhalis
-Haemophilus influenzae
-Staphylococcus aureus
-a-hemolytic Streptococcus
-Pseudomonas aeruginosa
-Anaerobic bacteria (~50%)
-Peptococcus
-Peptostreptococcus
-Bacteroides
MEDICAL MANAGEMENT
-saline irrigation
-treatment of allergy, immunodeficiency
-antibiotic treatment toward S. pneumoniae, M. catarrhalis, H. influenzae (70% of responsible organisms)
-nonsevere acute RS:
-no abx in previous 4-6 weeks: amoxicillin (45-90 mg/kg/d), cefpodoxime proxetil,
cefuroxime axetil
-previous abx: Clavulin, amoxicillin (80-90 mg/kg/d), cefpodoxime proxetil, cefuroxime
axetil
-if condition not improved in 72 hours, change to antibiotics effective against resistant
organisms
-severe acute RS:
-agent towards B-lactamase enzymes (eg. Clavulin, second-generation cephalosporin)
-severe or toxic condition with suppurative complications
-IV antibiotics against penicillin-resistant Streptococcus pneumoniae, B-lactamase-
producing H. influenzae and M. catarrhalis
-anaerobic infections generally susceptible to amoxicillin/clavulanate
-note: spontaneous resolution rate of acute bacterial RS is 49.6%
SURGICAL MANAGEMENT
-questionable efficacy
-tonsillectomy
-few advocate this procedure for RS
-adenoidectomy (unless there is hypertrophy causing obstruction)
-antral lavage
-rarely successful with one intervention
-inferior meatal antrostomy
-poor long-term patency and low likelihood of controlling sinus symptoms
-probable efficacy
-middle meatal antrostomy
-most physiologic method to ventilate maxillary sinus
-creating an accessory ostium can contribute to a recirculation phenomenon
-anterior or anterior and posterior ethmoidectomy
307
COMPLICATIONS AND EMERGENCIES
-orbital:
-orbital inflammation (preseptal)
-orbital cellulitis
-subperiosteal abscess
-orbital abscess
-blindness
-intracranial:
-meningitis
-epidural abscess
-subdural abscess
-acute, chronic brain abscess
Orbital complications
-young children frequently respond to medical treatment; older children often require surgery
-potential routes for expansion of infection from ethmoid to orbit:
-arterial
-direct expansion
-venous
-lymphatic seeding
-Chandler et al Classification:
-Group 1: Inflammatory (preseptal) edema

-edema of eyelids without tenderness, obstruction of venous drainage, no associated
visual loss or limitation of ocular movements
-Group 2: Orbital cellulitis

-with diffuse edema of adipose tissue in orbital contents, no abscess formation
-Group 3: Subperiosteal abscess

-abscess formation b/n orbital periosteum and bony orbital wall
-displacement of globe causing proptosis with decreased ocular mobility and visual
acuity
-Group 4: Orbital abscess

-discrete abscess within orbit
-severe proptosis but symmetric
-complete ophthalmoplegia and visual loss in 13%
-Group 5: Cavernous sinus thrombosis

-bilateral symptoms
-mid-facial edema
-complete ophthalmoplegia
-proptosis
-axial CT scan best to diagnose subperiosteal and orbital abscesses

-most likely pathologic organisms: S. pneumoniae, H. influenzae, M. catarrhalis, S. pyogenes
-surgical drainage required for abscesses
308
Intracranial Complications
-meningitis, epidureal, subdural (most common), and acute or chronic brain abscess
-symptoms:
-fever, headache, behavioural changes, seizures, nuchal rigidity, focal neurologic signs,
photophobia
309
CONGENITAL MALFORMATIONS OF THE NOSE
NASAL EMBRYOLOGY
-3rd week GA: nasal placodes: ectodermal origin

-5th week GA: nasal pits extend posteriorly to form nasal cavity; separated from oral cavity by nasobuccal
membrane
-6th week GA: nasobuccal membrane ruptures to form posterior choanal
-nasal septum and premaxilla formed from frontonasal process
-nostrils occluded with epithelial plug until 24 weeks GA
CHOANAL ATRESIA
-1/5000-8000 births
-50% have other associated congenital anomalies
-F:M = 2:1
-65-75% unilateral, the rest bilateral
-up to 75% of bilateral cases associated with CHARGE
-other anomalies associated with atresia:
-polydactyls, nasal-auricular and palatal deformities, Crouzon’s syndrome,
craniosynostosis, microencephaly, meningocele, meningoencephalocele, facial
asymmetry, hypoplasia of orbit and midface, cleft palate, hypertelorism
-30% pure bony; 70% mixed bony-membranous
-classically: 90% bony, 10% only membranous
-anatomic deformity:
-narrow nasal cavity
-lateral bony obstruction by lateral pterygoid plate
-medial obstruction caused by thickening of vomer
-membranous obstruction
-theories of choanal atresia:

1. Persistence of buccopharyngeal membrane from foregut
-always membranous
-nasopharyngeal atresia rather than actual choanal atresia
2. Persistence of nasobuccal membrane of Hochstetter
-failure to rupture at 6 weeks
3. Abnormal persistence or location of mesoderm forming adhesions in nasal choanal region
4. Misdirection of mesodermal flow, secondary to local factors
-in normal nasal development, migration of neural crest cells occurs from dorsal neural
folds laterally around eye and traversing the frontonasal process
-eventually, neural crest cells differentiate into a matrix of mesenchymal tissue which
will eventually mature into human facial configuration
-if flow of these cells is altered in their position or total numbers, the burrowing of nasal
pits may not create the same rotation from ventral dorsal to cephalic caudal plane alters
thinning that permits breakthrough of the anterior primary choana
-presentation:
-unilateral:
-may be asymptomatic; involved side has tenacious secretions
-bilateral:
-cyclic cyanosis relieved by crying
F.Ling - Congenital Malformations of the Nose (1)
310
-if later in life: mouth breathing, bilateral thick nasal discharge, absence of taste or
smell, undernourishment, defective speech, chronic sinusitis, conductive hearing loss
-diagnosis:
-unable to pass small catheter (6 French) through nose into nasopharynx
-other: no fogging of mirror, no movement of cotton wisp when breathing
-endoscopy
-CT scanning (procedure of choice)
-repair:
-unilateral repair usually delayed for at least 1 year; reduced risk of postoperative stenosis
-bilateral:
-oropharyngeal airway or McGovern nipple used as temporizing measures
-transnasal:
-advantages:
-can be performed quickly with minimal blood loss
-no possible risk of palatal growth or occlusal abnormalities later in life
-disadvantages:
-limited by access to the posterior nasal cavity (eg. size, septal
deviations)
-associated with higher rate of restenosis and need for serial dilations
-transpalatal:
-advantages:
-superior visualization and access to bony regions involved in atresia
(ie. posterior vomer, posterior lateral wall)
-shorter stenting period
-higher success rate
-disadvantages:
-orthodontic growth and development may be interrupted d/t
interruption of palatal growth centers
-palatal wound breakdown
-potential injury to greater palatine vessels
-transantral:
-opening posterior choana into a common cavity with a maxillary sinus to
prevent restenosis in cases of recurrent stenosis
-transeptal: older pts with unilateral atresia
-endoscopic approaches
-post-op management:
-antibiotics
-anti-reflux medications: reduce incidence of granulations and restenosis
PIRIFORM APERTURE STENOSIS
-due to bony overgrowth of nasal process of maxilla

-presents in first few months of life
-pyriform aperture is narrowest portion of nasal cavity
-anterior rhinoscopy reveals bony obstruction at nasal vestibule that will not allow passage of flexible
endoscope
-single central incisor
311
-CT:
-narrowed bony pyriform aperture
-may show nasolacrimal ducts encased in narrow pyriform aperture
-surgical correction in severe cases:
-transnasal or sublabial approach
-abnormal bone removed with drills and microscopic visualization
-stents placed for no longer than 1 week
CONGENITAL MIDLINE MASSES
-embryology:
-prenasal space lies between nasal and frontal bones and cartilaginous skeleton
-extends from nasal tip to brain
-fonticulus frontalis:
-space b/n frontal and nasal bones completely fuses in area of future cribriform plate with
foramen cecum, separating intracranial contents from extracranial structures and nose
-failure of closure herniation of intracranial contents
-more common in Asian populations

-M:F = 3:1
-three major groups:
-neurogenic tumours:
-glioma
-encephalocele
-neurofibroma
-dermoids cysts: -from ectoderm and mesodermal tissue
-haemangiomas: arise from mesoderm
Encephalocele and Gliomas

-herniation of cranial contents through defect in skull
-typically bluish and compressible
-meningocele: meninges only
-memingoencephalocele: brain and meninges
-glioma:
-thought to have developed from extracranial rests of CNS tissue
-encephalocele that has lost the intracranial connection; 15% attached via fibrous stalk
-composed of glial cells and fibrous and vascular connective tissue
-typically reddish, firm and noncompressible; do not transilluminate
-classification:
-occipital (75%)
-sincipital:
-external lesions that are apparent at birth as subcutaneous masses over the nose,
glabella, medial canthus, or lower forehead
-basal (10%)
-intranasal lesions not discovered until later in life when child complains of nasal
obstruction and discharge
-Furstenberg test: IJV compressed encephalocele enlarges but not glioma

-unilateral polyposis in children rare: avoid biopsy do sweat chloride test first
-encephaloceles managed in first few months of life
312
-neurosurgical consult mandatory
-lateral rhinotomy, transnasal approach, coronal flap approach for glabellar lesions
Nasal dermoids
-may contain skin, hair follicles, sebaceous glands and sweat glands
-contain only ectoderm and mesoderm
-most common midline nasal mass
-1-3% of all dermoids; 10% of dermoids in H+N region
-most often asymptomatic until later in life when they begin to drain
-pathogenesis:
-faulty closure of fonticulus frontalis invagination of dermal elements
-prenasal space theory:
-space b/n nasal bone and deeper cartilage - extends from dura, along midline and to tip
of nose
-during development, dura normally retracts up through foramen cecum which closes; a
dermoid may be present anywhere along prenasal space
-dura that remains in contact with skin as it retracts will result in a sinus or pit
-may present as midline pit or deformity anywhere along midline from nasal tip to glabella
-dermoids should not be manipulated or biopsied until attachment to CNS has been ruled out by radiologic
study
-CT or MRI needed in pre-op workup
-surgical excision:
-neurosurgical consultation for CNS connections
-elliptical incision made around fistula tract
-approaches:
-lateral rhinotomy
-open rhinoplasty
-inverted-U incision
-midline nasal dorsum incision
ARHINIA, POLYRHINIA, AND PROBOSCIS LATERALIS

-rare congenital anomalies
NASOLACRIMAL DUCT CYSTS

-duct begins to canalize from superior to inferior
-at birth, inferior aspect of duct has commonly not opened to communicate with the nasal passage
-about 30% of full-term infants are born with nasolacrimal duct obstruction
-when proximal and distal aspects of system are occluded, fluid accumulates and a cyst is formed
-presentation includes epiphora, nasal obstruction and respiratory distress
-obstruction resolves spontaneous ly by 9 months in 85% of infants
-cysts that cause respiratory distress require intervention
-anterior rhinoscopy: cystic mass in inferior meatus
-CT findings:
-dilated nasal lacrimal duct
-intranasal cyst
-cystic dilation of lacrimal sac
-infection
-feeding difficulties
-respiratory obstruction
-treatment:
-transnasal marsupialization; nasolacrimal stents
313
JUVENILE NASOPHARYNGEAL ANGIOFIBROMA
-Juvenile angiofibroma (JNA) is a benign tumour that tends to bleed and occurs in the nasopharynx of prepubertal
and adolescent males
Epidemiology:
-accounts for 0.05% of all head and neck tumours
-1:5,000-1:60,000 in otolaryngology patients has been reported
-occurs exclusively in males; females diagnosed with JNA should undergo genetic testing
-onset most commonly is in second decade; range is 7-19 years
-rare in patients older than 25 years
Etiology:
-originates in close proximity to posterior attachment of middle turbinate, near superior border of
sphenopalatine foramen
-hormonal theory suggested
-other theories:
-desmoplastic response of nasopharyngeal periosteum or embryonic fibrocartilage between
basiocciput and basisphenoid
-etiology from nonchromaffin paraganglionic cells of terminal branches of maxillary artery
Pathophysiology:
-tumour starts adjacent to sphenopalatine foramen
-bilobed or dumbbell-shaped, with one portion of tumour filling nasopharynx and other portion extending
to pterygopalatine fossa
-fills nasal cavity; septum deviates to other side
-superior growth is directed toward sphenoid sinus, which also may be eroded
-lateral spread directed toward pterygopalatine fossa, bowing posterior wall of maxillary sinus
-proptosis and optic nerve atrophy results if orbital fissures are encroached
Clinical:
-Symptoms:
-nasal obstruction (80-90%)
-epistaxis (45-60%)
-headache (25%)
-facial swelling (10-18%)
-other: unilateral rhinorrhea, anosmia, hyposmia, rhinolalia, deafness, otalgia, swelling of palate,
and deformity of cheek
-Signs:
-nasal mass (80%)
-orbital mass (15%)
-proptosis (10-15%)
-serous otitis due to eustachian tube blockage
-zygomatic swelling and trismus denote spread of tumour to infratemporal fossa
Differentials:
-nasal polyps, antrochoanal polyp, teratoma, encephalocele, dermoids, inverting papilloma,
rhabdomyosarcoma, squamous cell carcinoma
F.Ling - Juvenile Angiofibroma (1)
314
Imaging Studies:
-Plain x-ray
-view of sinuses may demonstrate nasopharyngeal polyp
-bowing of posterior wall of maxillary sinus and maxillary sinus opacification
-CT scan
-extension to sphenoid sinus, erosion of greater sphenoidal wing
-invasion of pterygomaxillary and infratemporal fossae (widening of pterygopalatine fissure)
-MRI is indicated to delineate and define extent of tumor
-angiography
-branches of external carotid system are primary feeders (94%)
-main supply comes from internal maxillary artery, but ascending pharyngeal or vidian arteries
may contribute
Histologic Findings:
-tumor usually sessile, lobulated, rubbery, and red-pink to tan-gray in
appearance
-encapsulated and composed of vascular tissue and fibrous stroma
with coarse or fine collagen fibers
-vessels are thin-walled, lack elastic fibers, have absent or incomplete
smooth muscle, and vary in appearance from stellate or staghorn to
barely conspicuous due to stromal compression
-immunostaining for vimentin
Staging:
Classification According to Sessions

Stage IA - Tumor limited to posterior nares and/or nasopharyngeal vault
Stage IB - Tumor involving posterior nares and/or nasopharyngeal vault with involvement of at least
1 paranasal sinus
Stage IIA - Minimal lateral extension into pterygomaxillary fossa
Stage IIB - Full occupation of pterygomaxillary fossa with or without superior erosion of orbital
bones
Stage IIIA - Erosion of skull base (ie, middle cranial fossa/pterygoid base); minimal intracranial
extension
Stage IIIB - Extensive intracranial extension with or without extension into cavernous sinus
Classification According to Fisch

Stage I - Tumours limited to nasal cavity, nasopharynx with no bony destruction
Stage II - Tumours invading pterygomaxillary fossa, paranasal sinuses with bony destruction
Stage III - Tumours invading infratemporal fossa, orbit and/or parasellar region remaining lateral to
cavernous sinus
Stage IV - Tumours invading cavernous sinus, optic chiasmal region, and/or pituitary fossa
Therapy:
-hormonal therapy
-testosterone receptor blocker flutamide was reported to reduce stage I and II tumours to 44%
-despite tumour reduction with hormones, this approach is not used routinely
-radiotherapy
-some centers have 80% cure rates with XRT
-adverse effects of XRT make this modality not very useful
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-stereotactic radiotherapy (ie, Gamma knife)
-delivers a lower dose of radiation to surrounding tissues
-most authorities reserve XRT for intracranial disease or recurrent cases
-surgical therapy:
-lateral rhinotomy, transpalatal, transmaxillary, or sphenoethmoidal route is used for small
tumours (Fisch stage I or II)
-infratemporal fossa approach used when tumour has a large lateral extension
-midfacial degloving approach, with or without a LeFort osteotomy, improves posterior access to
tumour.
-facial translocation approach is combined with Weber-Ferguson incision and coronal extension
for a frontotemporal craniotomy with midface osteotomies for access
-extended anterior subcranial approach facilitates en bloc tumour removal, optic nerve
decompression, and exposure of cavernous sinus
-intranasal endoscopic surgery is reserved for tumours limited to nasal cavity and paranasal
sinuses
Preoperative details:
-preoperative embolization used to limit blood loss during surgery
Complications:
-excessive bleeding
-malignant transformation has been reported in 6 cases
-transient blindness has been reported as a result of embolization, but it is a rare occurrence
-osteoradionecrosis and/or blindness due to optic nerve damage may occur due to radiotherapy
-fistula of palate at junction of soft and hard palate may occur with transpalatal
-anaesthesia of cheek is a frequent occurrence with Weber-Ferguson incision
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LEMIERRE SYNDROME
Definition
-an acute medical condition characterized by anaerobic oropharyngeal infection leading to septic
thrombophlebitis of the internal jugular vein
-often complicated by septic pulmonary emboli and distant metastatic infections
-since the advent of antibiotics, this syndrome has become rare and is likely frequently overlooked
-pts typically have a sore throat initially

-infection of the deep pharyngeal tissue allows anaerobic organisms to drain into the lateral pharyngeal
space, which contains the internal jugular vein
-anaerobic organisms cause septic thrombophlebitis of the internal jugular vein
Clinical Presentation
-swelling in the upper neck, with tenderness of the lateral aspect of the neck, parallel to the
sternocleidomastoid muscle
-trismus or pain when turning the head away from the side of the thrombus
-pleural effusions and occasionally thoracic empyemas, with symptoms of dyspnea and pleuritic pain
-diagnosis of Lemierre syndrome can be made if symptoms and signs of oropharyngeal infection are
followed by those of internal jugular vein thrombophlebitis
Microbiology
-Fusobacterium necrophorum most common bacteria
-others:
-Bacteroides melaninogenicus, Eikenella corrodens, and non-group A streptococcus
-Fusobacteria are gram-negative obligate anaerobes that can be found in the upper respiratory tract
and occasionally in the gastrointestinal tract and genitourinary tract
Treatment
-consists of IV antibiotic therapy and surgical drainage of purulent collections
-ligation and resection of the internal jugular vein thrombosis is usually unnecessary and should be
considered only in patients with refractory sepsis or severe respiratory compromise from repeated
pulmonary emboli
-initial antibiotic therapy should include antibiotics with good antianaerobic activity
-fusobacteria are typically sensitive to penicillins, clindamycin, metronidazole, and
chloramphenicol
-use of anticoagulation in Lemierre syndrome is controversial
-anticoagulation may expedite clinical improvement and should be considered in when
there are no contraindications
F.Ling - Lemierre Syndrome (1)
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Medical Management of Acute Bacterial Sinusitis
(Ann Otol Rhinol Laryngol 109:2000)
DEFINITION AND PATHOPHYSIOLOGY

-spectrum of acute and chronic, neutrophilic and eosinophilic, nonallergic and allergic inflammatory
processes
-obstruction of ostia > 7-10 days –> secondary infection likely
-single bacterial species in acute sinusitis
-multiple isolates in 26-30% isolates
-chronic sinusitis characterized by eosinophilia
-viral rhinosinusitis - more likely cause of nasal symptoms than any bacterial origin
-approx. 5-10% viral URTIs complicated by acute bacterial sinusitis
-superinfection in day-care centres
CLASSIFICATION
-Acute: < 4 wks
-Subacute: 4 - 12 wks
-Chronic: > 12 wks
-Recurrent: 4 or more episodes in 1 year > 7 days
EMBRYOLOGY OF SINUSES
Ethmoid -> Maxillary -> Sphenoid -> Frontal
PREDISPOSING FACTORS
-prior URTI
-concurrent Group A strep infection
-allergic rhinitis
-environmental pollutants
-dental infections
-hormonal changes
-iatrogenic: mechanical ventilation, NG tubes, nasal packing
-anatomic variations: tonsillar/adenoid hypertrophy, deviated septum, nasal polyps, cleft palate
-swimming
-immunodeficiency
-secretory disturbances (CF)
-immotile cilia syndrome
-Kartagener’s syndrome
-bronchiectasis
-asthma/ASA/polyps
-immature immune system
PATHOGENS
-Streptococcus pneumonia (30-40%)
-Haemophilus influenzae (20-30%)
-Moraxella catarrhalis (12-20%)
-Streptococcus pyogenes (up to 3%)
-Others: streptococcus sp., staph. aureus, neisseria
-fungi: diabetic/immunocompromised
-anaerobes: chronic sinusitis, dental infections
ANTIBIOTIC RESISTANCE
-d/t overuse of antibiotics
-mostly d/t B-lactamase production
-penicillin-resistant pneumococci (33-55% isolates)
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-ampicillin-resistant H.flu (~30-40% isolates)
-high rate (>75%) Moraxella resistance
DIAGNOSIS
-symptoms worsen after 5 days, persist for at least 10 days, are more severe than viral dz
-depends on presence of > 2 major factors or 1 major and 2 minor factors:
Major factors:
-facial pain or pressure
-facial congestion or fullness
-nasal obstruction
-nasal purulence or discoloured PND
-hyposmia or anosmia
-fever
Minor factors:
-headache
-halitosis
-fatigue
-dental pain
-couch
-ear pain, pressure, or fullness
-fever
Imaging (CT) used if:

-inadequate response to medical therapy
-numerous bacterial infections throughout the year
-hx of polyposis
ANTIMICROBIAL THERAPY
-40% of sinusitis patients will recover spontaneously

-sinusitis is treated empirically
-goal of treatment to prevent serious consequences:
-facial osteomyelitis
-meningitis
-orbital cellulitis
-brain abscess
-First line agents:

-amoxicillin 250-500 mg tid
-TMP-SMX 160 mg/800 mg bid
-Second line agents:
-cefpodoxime 200-400 mg bid
-cefprozil (Cefzil) 250-500 mg bid
-cefuroxime axetil (Ceftin) 250-500 mg bid
-cefdinir 300 mg bid
-amoxicillin-clavulanate 250-500 mg tid
-Third line agents:
-azithromycin 250 mg qd
-clarithromycin 500 mg bid
-cipro 500-700 mg qd
-levofloxacin 500 mg qd
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-gatifloxacin (Tequin) 400 mg qd
-moxifloxacin (Avelox) 400 mg qd
-clindamycin 140-450 mg tid/qid
DURATION OF THERAPY
-10 to 14 days
Risk factors for recurrence:

-younger than 6 months
-attend day care
-live with smoker
-history of multiple URTIs
ADJUNCTIVE TREATMENTS
-promote ciliary function and decrease edema
-saline nasal sprays, humidifiers, warm aerosols, steam, aromatic vapours, hot soups etc..
Topical decongestants:
-phenylephrine HCL, oxymetazoline HCL
-stimulate mucosal alpha-adrenergic receptors
-shrinking edematous mucosa
-limit to 3 days to avoid rhinitis medicamentosa
-use of systemic decongestants not recommended in children
WHEN TO REFER - complicated sinusitis

-deteriorating patient condition
-treatment failure
-immunocompromise
-nosocomial infection
In children: ethmoid infundibulum and anterior ethmoid most common affected sites
Surgery considered when all medical options exhausted

-reserved for pts with refractory disease or anatomic abnormalities
CONCLUSION
-diagnosis largely made clinically
-lab tests rarely require
-treatment focussing on relieving obstruction, treating infection, thinning the mucous, opening the sinus
ostia
-antibiotic selected according to resistance patterns found in community
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Overview
• Anatomy and Development
Mucoceles of the • Physiology and Pathophysiology
Paranasal Sinuses •
•
Epidemiology
Clinical Features
Francis T.K. Ling, MD BSc • Treatment
Department of Otolaryngology – Grand Rounds • Case Presentations
University of Ottawa
Wednesday, January 28th 2004
Introduction Introduction
• Definition: • Mucoceles known for > 100 years
• Epithelial lined mucous-containing sac completely filling a • 1725: Dezeimeris first described frontal mucoceles
paranasal sinus • 1818: Langenbeck commented on clinical complaints and
• Capable of expansion by virtue of bone resorption and new bone symptoms
formation • “hydatids”
• 1890: Rollett introduced the term “mucocele”
• Most common lesion causing expansion of paranasal
sinuses
Anatomy and Development Anatomy and Development

• Maxillary sinuses • Maxillary Sinuses
• Ethmoid sinuses • Occupies body of maxilla
• First to develop in the
• Sphenoid sinus
human fetus
• Frontal sinuses • Biphasic growth:
• 3 years
• 7 years to adolescence
• Average volume 14.75 ml
• Drains into middle meatus
via maxillary ostium
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1
• Ethmoid Sinuses • Sphenoid sinus
• Located in superior half of • In body of sphenoid bone
lateral nasal wall
• No significant sinus at birth
• Development begins during 3rd-
4th month of fetal development • Development begins at 5 years
• Continue to grow through • Final volume attained by 12-15
childhood until age 12 years
• Average volume 15 ml • Average volume: 7.5 ml
• Drainage: • Drainage:
• Anterior: infundibulum or • Sphenoethmoidal recess
ethmoid bulla
• Posterior: superior meatus

• Frontal Sinuses • Frontal recess
• Frontal bone • Marked variation in configuration and attachment of uncinate
• Begins as evagination of frontal process
recess • Variable drainage patterns of frontal recess
• Development begins at 2 ya and
reaches adult size at 15-20 ya
• Variable development:
• 10% unilateral
• 5% rudimentary
• 4% absent
• Drainage into frontal recess
• 2-20 mm in length
Physiology Physiology
• Sinus lining: • Pattern of clearance:
• Ciliated, pseudostratified, • Maxillary: floor
columnar epithelium stellate pattern along walls
• Mucous glands and goblet to natural ostium
cells mucous blanket • Frontal: inward flow
• “sol-gel” phase medially superior
lateral floor frontal
recess
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2
Pathophysiology Pathophysiology
• Obstruction of sinus ostium or outflow tract • Bone resorption:
• Inflammation (ie. Chronic sinusitis) • Epithelium continues to secrete
causing expansion of the mucocele
• Trauma
• Increased pressure
• Iatrogenic (eg. FESS) devascularization of bone and
• Mass/Tumour (eg. Polyps, ostioma, malignancy, ostioma) osteolysis
• Obstruction of minor salivary gland located within lining • Local inflammation secretion of
cytokines
of paranasal sinus
• Fibroblasts PGE2 + IL-1
• Eg. Mucous retention cyst of maxillary sinus • Epithelial cells TNF alpha
• Cause osteoclastic bone
resorption
Epidemiology Epidemiology
• 3rd or 4th decade • Rombaux et al (Belgium, 2000):
• M:F ~ 7:1 • 178 mucoceles
• Primitive mucoceles: 35%
• 10-15 years to develop
• Post-traumatic: 2.1%
• Frontal > ethmoid > maxillary > sphenoid
• Post-operative: 62.9%
• Fronto-ethmoidal ~65%
• Incidence after FESS not known
• Maxillary ~ 20%
• Sphenoid ~1-8%
• Posterior ethmoid ~1-6%
• Uncommon locations: middle turbinate, pterygomaxillary space
Clinical Presentation Fronto-

Fronto-ethmoidal Mucocele
• Slow expansion • Most common clinically significant mucocele
• Patients asymptomatic for many years • Classification (Har-El, 2001)
• May take 10 years or more to become symptomatic • Type 1: Limited to frontal sinus (+/- orbital extension)
• Symptoms depend on location/type of mucocele and extent • Type 2: Frontoethmoid mucocele (+/- orbital extension)
of bony erosion • Type 3: Erosion of posterior wall
• In general: • A. Minimal or no intracranial extension
• Headache and facial pressure common • B. Major intracranial extension
• Facial swelling with tenderness to palpation • Type 4 Erosion of anterior wall
• Ocular and neurological problems • Type 5 Erosion of both posterior and anterior wall
• A. Minimal or no intracranial extension
• B. Major intracranial extension
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Fronto-
Fronto-ethmoidal Mucocele Fronto-
Fronto-ethmoidal Mucocele
• General: • Ocular:
• Frontal headache (common) and/or deep nasal pain • Proptosis (common)
• Frontal swelling +/- infection/draining fistula • Periorbital pain
• Nasal obstruction and rhinorrea unusual • Displacement of globe
downward and outward
direction
• Reduced ocular mobility
• Diplopia
Fronto-
Fronto-ethmoidal Mucocele Maxillary Mucocele
• Neurologic: • “mucous-retention” cyst
• Destruction of posterior frontal sinus wall • Incidental finding
• Decreased LOC • Rarely achieve sufficient size to cause bony erosion
• Confusion
• Rarely require specific therapy if asymptomatic
• Meningitis
• Spontaneous regression without therapy
• CSF leak
Sphenoid Mucocele Sphenoid Mucocele

• Rare lesion • General:
• Headache with occipital, vertex or deep nasal pain
• Extension:
• Ocular:
• Superiorly into pituitary fossa intracranial
• Diplopia
• Posteriorly towards clivus
• Visual field disturbance
• Anteriorly into posterior ethmoids • Vision loss
• Laterally into orbits • Retro-orbital pain
• Compression: • Neurologic:
• Pituitary gland, optic chiasm, carotid artery, cavernous sinus, CN • Decreased LOC
III-VI, brain • Confusion
• Meningitis
• CSF leak
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Investigations Investigations
• CT scan provides excellent anatomical information • MRI scan:
• Findings: • Allows differentiation of mucoceles from solid component of
neoplasms or meningoencephalocele
• Completely opacified sinus cavity
• Demarcates mucocels and soft-tissue structures in the event of
• Thinned and expanded sinus walls
intracranial or intraorbital growth
• Loss of normal scalloped margin
• Depression or erosion of supra-orbital ridge and extension of soft
• Findings:
frontal tissue mass across midline • Signal intensity vary depending on state of hydration and age
• Majority show hyperintense T2 and hypointense T1
• Increased dehydration T2 become hypointense and T1 become
hyperintense
Treatment External Approaches

• Surgery is required • Traditionally preferable when there are intraorbital or
• Operate on non-infected mucocele unless acute intracranial manifestations
symptomatic mucopyocele • Typically for fronto-ethmoidal mucoceles
• Goals • Techniques:
• Reintegration of affected sinus into nasal circuit
• External frontoethmoidectomy
• Sinus exclusion with obliteration and respect of posterior wall
• Lynch
• Cranialization
• Killian
• Approaches
• Reidel
• External
• Endoscopic • Lothrop
• Combined • Osteoplastic flap
External Frontoethmoidectomy External Frontoethmoidectomy

• Indications: • Technique (Lynch)
• Acute infectious of frontal and ethmoid sinuses with orbital • Incision made near medial
extension orbital rim; avoid damage to
• Mucoceles, pyoceles, cutaneous fistulae and CSF leaks, or medial canthal ligament and
intracranial complications from fronto-ethmoidal sinuses trochlea
• Exposure for benign tumours of fronto-ethmoidal sinuses, anterior
skull base, or superior nasal cavity
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5
• Technique (Cont’d) • Killian procedure
• Periosteum elevated to fronto-ethmoid • For tall sinuses in which
suture
disease cannot be removed
• Anterior ethmoid artery divided through floor alone
• Lamina papyracea removed and
• Floor and anterior wall
ethmoidectomy performed
removed
• Frontal sinus opened in medial part of
floor • Supraorbital bony strut (10
• Diseased tissue within sinus is removed mm)
• Large chute from frontal sinus through
ethmoid cavity into the nose
• +/- stent placement

• Reidel procedure: • Lothrop procedure:
• Entire anterior wall and floor • Unilateral or bilateral anterior ehtmoidectomy
of frontal sinus removed • Interfrontal septum and superior nasal septum and frontal recesses
• Mucosa removed connected
• Sinus obliteration • High risk of cribriform plate damage:
forehead soft tissue laid • Anosmia
against posterior table • CSF leak
• Significant deformity • Meningitis
• Rarely if ever used
Osteoplastic Flap Osteoplastic Flap

• 1894: described by Brieger • Incisions:
• Fat obliteration: • Coronal approach
• First described in 1950 by Bergara • Midline forehead approach
• Prevent recurrence • Brow incision
• Associated with varying degree of
necrosis and resorption
• Indications:
• Neoplasms
• Fractures
• Chronic frontal sinusitis associated
with orbital or intracranial
complications
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6
• Technique: • Technique:
• Skin-tissue flap raised, • Periosteum incised and lifted
preserving periosteum and off bone
supraorbital nerves • Bone cuts made to create
• Perimeter of frontal sinus osteoplastic flap
marked with template from
Caldwell-view radiograph

• Bone flap removed • Mucosa lining stripped and
• Disease in frontal sinus drilling of cortical bone
removed performed
• Mucosa lining stripped and • Minimum 2 mm
drilling of cortical bone required to eliminate all
performed mucosal elements
• Minimum 2 mm
required to eliminate all
mucosal elements

• Once frontal recess reached, • Bone flap replaced and fixed
mucosa is inverted down • Periosteum closed
toward nasal cavity • Skin closure
• Fat harvested from lower left
quadrant of the abdomen
over rectus muscle used to
obliterate sinus cavity
• Frontal recess is plugged
with fascia, muscle or bone
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7
• Cranialization • Complications:
• Indications: • Fat donor site:
• Large portions of posterior frontal sinus destroyed with • Seroma
substantial epidural spread of mucocele • Hematoma
• Intracranial complications present • Abscess
• Frontal craniotomy usually required • Cellulitis
• Intracranial:
• Extradural dead space remains for extensive mucoceles
• Dural tears
• Dead space obliterates by frontal brain over several weeks
• Frontal lobe injury
• Oblteration of dead space by abdominal fat used to achieve • CSF leaks
immediate closure and to avoid scarred adhesions
• Meningitis
• Brain abscess

• Complications (Cont’d): • Complications (Cont’d):
• Ocular: • Nerve injury:
• Extraocular muscle injury • Supraorbital nerves forehead paresthesia, hypoesthesia or
• Globe injury anaesthesia
• Hemorrhage retrobulbar hematoma diplopia/blindness • Facial nerve loss of frontalis function
• Infection: • Olfactory nerve anosmia
• Fat graft • Cosmesis:
• Osteomyelitis of bone flap • Scar
• Depression or embossment
• Recurrence
External Approaches Endoscopic Approach

• Recurrence: • Introduced in 1980 by D.W. Kennedy
• Lund (1998): • “marsupialization”:
• 28 patients with combined approach (Lynch) • Opening enlarged without complete removal of mucosal lining
• Recurrence rate: 11% • Lund (1991):
• Weber (2000): • Sinus lining returns to normal with re-establishment of
• Osteoplastic flaps for various reasons mucociliary activity
• 59 patients • Advantages:
• Mucoceles after procedure: 9.8% (5 patients) • Short hospital stay
• Conboy and Jones (2003) • No facial scarring
• 23 patients with external (Lynch) or combined approach
• 26% recurrence
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Endoscopic Approach Endoscopic Approach
• Contraindications (Rombaux et al, 2000) • Technique:
• Absolute: • Polyps or polypoid
• Mucocele not accessible to endoscope mucosa cleared
• Mucocele located in external part of frontal or maxillary sinus from frontal recess
• Cutaneous fistula
• Relative:
• Loss of anatomical landmarks
• Revision surgery for recurrence lateral to frontal recess after
previous external approach
• Frontal recess stenosis with hypertrophic bone occluding area
• Associated disease (ie. Malignancy, large benign tumour)

• Identification of anterior • Agger nasi
ethmoid artery cells removed
• Posterior reference
• Frontal opening located
2-4 mm anterior

• Enlargement • Mucosa covering
anteriorly and posterior aspect of
anteriormedially to frontal sinus
avoid accidental preserved
intracranial entry • Provides source of
epithelialization
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• Technique (Cont’d) • Postoperative Care:
• Floor of frontal sinus anterior to outflow tract removed • Antibiotics and saline spray
• Mucocele identified, opened and drained • Irrigation of stent
• Lining not curetted or removed • Removal of stent 6-12 weeks after surgery
• +/- stent insertion

• Results: • Results (Cont’d):
• Many studies show recurrence rates at or close to 0% • Har-El; Laryngoscope 111:2131-2134, 2001
• Rombaux et al;Acta Oto-Rhino-Laryngologica Belg. 54:115-122, • 108 sinus mucoceles
2000 • 66 frontal and frontoethmoidal, 17 ethmoid, 7 sphenoethmoid,
• 178 patients with 3 recurrences 12 sphenoid, 6 maxillary mucoceles
• 97.9% successful • 83% intraorbital extension
• Lund et al; J. Laryngol. Otol. 112(1): 36-40, 1998 • 55% erosion of skull base with varying degrees of intracranial
• No recurrences in 20 patients extension; 31% major intracranial extension (intracranial
• Mean follow-up 34 months extent larger than sinus
• Follow-up: 1-13.5 years; median 4.5 years
• Recurrence of frontal mucocele in 1 patient (0.9%)
Endoscopic Approach External vs. Endoscopic Approaches

• Results (Cont’d): • Traditional teaching:
• Conboy and Jones; Clin. Otolaryngol. 28:207-210, 2003 • Complete removal of mucocele lining
• 68 mucoceles • Required external techniques
• 66% endoscopic, 22% external, 12% combined • Recent trend favouring endoscopic approach
• Mean follow-up 6 years
• Marsupialization for large mucoceles controversial
• Recurrences:
• Long-term follow-up required
• 9% endoscopic group
• Results of studies may not be final
• 26% external or combined group
• Follow-up in many series is short
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External vs. Endoscopic Approaches Follow-
Follow-up
• “small, well-positioned mucoceles may be attempted first • Mucoceles may recur many years after surgery
endoscopically, but in the setting of massive mucoceles • Recurrences may be as long as 49 years after initial surgery
with risk of imminent complications and instability of the (Moriyama)
facial skeleton, the more conservative approach may be the • Recurrences should be treated as early as possible
more aggressive open techniques”
• “endoscopic transnasal approach best choice for
intracranially extended mucoceles because it is the least
invasive and can provide an adequate surgical view for
wide marsupialization”
Case Presentation #1 Case Presentation #1

• 69 yo M
• Pituitary tumour removed 25 years ago
• Follow-up MRI incidental left frontal mucocele
• No orbital or intracranial extension
• Asymptomatic with no sinus complaints

• Dx: Frontal mucocele • 72 yo F
• Treatment: • Referred from ophthalmology
• Endoscopic removal of left frontal sinus mucocele • Decreased vision of left eye
• Marsupialization and aspiration of thick fluid
• Left retro-orbital pain
• Well postoperatively • No sinus symptoms
• No complications • Rhinoscopy: normal
• No recurrence
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• Dx: sphenoethmoidal mucocele • Treatment (Cont’d):
• Treatment: • Marsupialization of
posterior ethmoid cells
• Left functional endoscopic sinus surgery
• Removal of anterior and
• Uncinectomy
inferior walls
• Anterior ethmoidectomy
• Posterior ethmoidectomy greenish fluid expelled and drained

• Well postoperatively • 73 yo M
• Reduced pain • History of chronic sinusitis
• Vision still decreased • Previous septoplasty
• No recurrence at 4 • Admitted for nausea and vomiting, dehydration, frontal
months headaches and diplopia
• Previously on antibiotics and pain medication with no
improvement in symptoms
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12

• Dx: sphenoethmoidal
mucocele
• Treatment:
• FESS
• Middle turbinate fractured to
expose large cystic formation
• Aspiration of purulent
secretions
• Marsupialized
• Dehiscence of LP

• Discharged home • Repeat CT scan
• Returned to ER with progressive headache, nausea,
vomiting and dehydration
• CT report:
• “area of calcification in planum sphenoidale. It is uncertain
whether this is related to the mucocele, or possibly represents an
underlying meningioma”
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• Repeat MRI

• Dx: Tuberculum sellae meningioma • 49 yo M
• Involving: • Progressive proptosis of
• Pituitary gland right eye
• Both cavernus sinuses
• No visual deficits
• Compression of left optic nerve
• Investigations:
• Endocrinology: no endocrinopathy
• Large right frontal sinus
• Ophthalmology: mild left visual field defect lesion
• Patient not interested in craniotomy for biopsy or • Extension into orbit and
decompression intracranial cavity
• Will be followed regularly

• Dx: Right frontal mucocele
• Treatment: • Treatment (Cont’d)
• Combined ENT, Ophthalmology and Neurosurgery removal • Osteoplastic flap:
• Osteoplastic flap • Dura dehiscent anteriorly with exposed brain dural patch
• Brow incision • Orbital roof defect reconstructed
• Supraorbital nerve cut for exposure • Frontal recess plugged, sinus obliterated with fat and Tisseel
• Template osteoplastic flap raised mucocele evacuated • Bone flap replaced
• Roof of orbit and posterior sinus wall eroded
• Mucocele lining removed, sinus walls burred
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Case Presentation #4 Summary
• Post-op • Mucoceles most common lesion causing expansion of
• Accumulation of CSF under right forehead scalp paranasal sinuses
• No rhinorrhea • Long asymptomatic progress
• Bed rest and aspiration of fluid
• When symptomatic, usually present with ocular symptoms
• Persistent leak lumbar drain
+/- neurologic symptoms depending on location of
• Resolution of CSF leak
expansion
• No infection
• Fronto-ethmoidal mucoceles most common
• Discharge home
• Follow-up • Caused by sinus obstruction secondary to chronic
infection, surgery or trauma
• Well with no recurrence
Summary
• Treatment is surgical
• Traditionally, complete removal advocated via external approach
• Trend towards endoscopic management
• External or combined approaches usually reserved for extensive
involvement or failed endoscopic attempt
• Push towards endoscopic management of large intracranial
mucoceles
• Long term follow-up required to monitor for recurrence
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15
Radiation-Induced Sarcoma
Postradiation Sarcoma (PRS):

-late effect of ionizing radiation is the development of sarcoma within the field of irradiation
-historically radiation was used to treat benign conditions, such as acne, fungal infections, eczema, and
various bone diseases
-PRS is an uncommon tumor - < 1% for patients with cancer who are treated with radiation and survive 5
years
-Cahan’s criteria in the diagnosis of PRS:

-histologic features of the original lesion and PRS are completely different
-PRS is located within the field of irradiation
-patients with cancer syndromes such as Li-Fraumeni and Rothmund-Thomson are excluded
-latent period (period between initiation of radiotherapy and histologic diagnosis of second
neoplasm) is more than 4 years
Pathophysiology:
-threshold dose for PRS is not known, although in most published series, a dosage of 40-60 Gy is reported
-development of PRS also is influenced by other factors:
-genetic tendency
-influence of chemotherapeutic agents
-unknown factors
-ionizing radiation is thought to act via genetic alterations, including mutations of p53 and retinoblastoma
(Rb) genes
Mortality/Morbidity:
-reported 5-year survival rate for PRS has been extremely poor, ranging from 8.7-22%
-poor survival rate is thought to be due to a number of interrelated factors, as follows:
-Significant delay in diagnosis
-Large unresectable lesions
-Elderly patients
-Anaplastic nature of lesions
-Lack of effective adjuvant treatment
History:
-pain is the most common complaint and is abrupt and rapid in onset, relentless and progressive, constant,
and worse at night
-mass (soft tissue or bone), bleeding, and pathologic fracture also are reported
Diagnosis:
-MRI
-biopsy
Histologic Findings:
-usually is a high-grade lesion
-bone:
-osteosarcoma was the most common type, comprising 61.5% of all cases
-fibrosarcoma (23.7%), malignant fibrous histiocytoma (MFH, 9.6%), chondrosarcoma (3.7%),
and rare cases of angiosarcoma and Ewing sarcoma
-soft tissue:
-most common histological type is MFH (70%), followed by osteosarcoma, fibrosarcoma,
malignant peripheral nerve sheath tumor (MPNST), chondrosarcoma, and angiosarcoma
336
Treatment:
Medical Care:
-PRS is high grade and advanced stage or metastatic at the time of diagnosis, patients commonly are not
eligible for curative surgery, and the prognosis for these patients generally is poor
-chemotherapy is the most common treatment modality and typically is associated with poor response rates
Surgical Care:
-wide or radical resection
Consultations:
-multidisciplinary approach
337
ANATOMY AND PHYSIOLOGY OF THE NOSE
(ENT Secrets)
Five areas susceptible to nasal airflow obstruction:

-anterior naris
-nasal valve
-upper internal nasal vestibule
-lower internal nasal vestibule
-posterior choanae
Arterial supply to the nose:

-posterior inferior part of internal nose: external carotid artery and terminal branches of internal maxillary
artery (eg. sphenopalatine, greater palatine artery)
-anterior inferior nasal cavity: branches of facial artery
-superior nasal cavity: branches of ophthalmic artery from internal carotid
“Danger Triangle”
-from nasion to lateral corners of mouth
-venous supply of nose drains intracranially
-angular vein inferior ophthalmic vein cavernous sinus
-provides cutaneous nasal infections with a potential rout to spread intracranially
Nasal innervation:
-muscles: CN VII
-skin: CN V1 and V2 - touch and chemosensation
-olfaction: CN I
-sympathetic: via superior cervical ganglion sphenopalatine ganglion
-parasympathetic: superior salivatory nucleus CN VII sphenopalatine ganglion posterior nasal nerve
Nasal Reflex:
-strong nasal stimuli cardiopulmonary responses (breathing cessation and bradycardia)
-mild stimuli sneezing
Nasal lymphatics:
-nose and paranasal sinuses retropharyngeal nodes
-anteriorly submandibular or upper deep cervical nodes
Kartagener syndrome:
-immotile cilia syndrome due to absence of dynein arm on peripheral ciliary microtubules
-chronic sinusitis, bronchiectasis and situs inversus
Factors inhibiting normal ciliary activity:

-drying
-drugs (eg. cocain, adrenaline)
-excessive heat or cold
-hypertonic or hypotonic solutions
-smoking
-infections
-noxious fumes
F.Ling - Anatomy and Physiology of the Nose (1)
338
RHINITIS
(Supplements from ENT Secrets)
Rhinitis:
-nasal hyperfunction and tissue inflammation which leads to nasal congestion, rhinorrhea, nasal
obstruction, pruritus and sneezing
Classification:
-allergic
-seasonal
-perennial
-non-allergic
Most common causes of rhinitis:

-chronic rhinitis: allergy
-acute rhinitis: infection
Allergic rhinitis most often mediated by Gell and Coombs Type I hypersensitivity
Types of antigens causing allergic rhinitis:

-inhalants
-chemicals
-foods:
-fixed food allergy: causes symptoms each time food is ingested
-cyclic food allergy: causes symptoms based on amount an frequency allergen consumed
Structural abnormalities that can cause rhinitis:

-deviated nasal septum
-nasal valve collapse
-neoplasms
-polyps
-intranasal and extranasal deformities
F.Ling - Rhinitis (1)
339
Dr. F. Ling's
Otolaryngology - Head and Neck Surgery Notes
Cervical Fascia and Spaces
340
file:///C:/Users/user/Desktop/Dr%20flings%20Notes/Contents/Cervical_Fascia.htm 3/22/2013
341
ANATOM Y OF DEEP NECK SPACES
Spaces I nvolving Entire Length of Neck
 Retropharyngeal Space
 Boundaries:
 anterior: visceral division of middle layer of deep cervical fascia
 posterior: alar division of deep layer of deep cervical fascia
 superior: skull base
 inferior: level of T1 or T2
 Contents:
 retropharyngeal nodes separated by midline raphe
342
 Danger Space
 Boundaries:
 anterior: alar division of deep layer of deep cervical fascia
 posterior: prevertbral division of deep layer of deep cervical fascia
 inferior: diaphragm
 Contents:
 none
 Prevertebral Space
 Boundaries:
 anterior: prevertebral division of deep layer of deep cervical fascia
 posterior: vertebral bodies
 inferior: coccyx
 Contents:
 none
 Visceral Vascular Space (Carotid Space)

 Contents:
 carotid artery
 internal jugular vein
 vagus nerve
Spaces Limited to Above the Hyoid Bone
 Pharyngomaxillary Space (lateral pharyngeal, parapharyngeal, peripharyngeal space)

 Boundaries:
 anterior: pterygomandibular raphe
 posterior: prevertebral fascia
 inferior: hyoid bone
 medial: lateral pharyngeal wall
 lateral: superficial layer of deep cervical fascia over mandible, internal pterygoid, and parotid
gland
 Submandibular Space (= sublingual space + submaxillary space)
343
 Boundaries:
 anterior: mandible
 posterior: intrinsic muscles of base of tongue
 superior: floor of mouth
 inferior: superficial layer of deep cervical fascia; hyoid bone
 lateral: mandible
 Contents: (sublingual space)
 sublingual gland
 hypoglossal nerve
 Wharton duct
 Parotid Space
 Boundaries:
 invested by superficial layer of deep cervical fascia
 Contents:
 parotid gland
 external carotid artery
 posterior facial vein
 facial nerve
 M asticator Space
 Boundaries:
 posterior: pterygomaxillary space
 superior: temporal space
 Contents:
 masseter
 pterygoid
 ramus and body of mandible
 temporalis tendon
 inferior alveolar vessels and nerves
Space Limited to Below the Hyoid Bone:
 Anterior Visceral Space (pretracheal space)

 Boundaries:
 anterior: strap muscles
 posterior: anterior wall of esophagus
344
 superior: thyroid cartilage

 inferior: T4
 Contents:
 trachea
 thyroid gland
345
ANATOMY AND PHYSIOLOGY OF THE SALIVARY GLANDS
DEVELOPMENTAL ANATOMY
-derived from first pharyngeal pouch

-major salivary glands develop in 6th-8th weeks as outpouchings of oral ectoderm into surrounding
mesenchymal
-parotid anlage grows posteriorly and eventually surrounds facial nerve which advances anteriorly
-as mesenchymal capsule surrounds the gland, it entraps lymph nodes and sends projections into the gland
itself
-minor salivary glands develop in 6th-8th week from oral ectoderm and nasopharyngeal ectoderm
ANATOMY OF THE SALIVARY GLANDS
Parotid Gland
-acinar cells mainly serous (basophilic)
-Stensen duct arises from anterior border, 1.5 cm below zygoma
-follows along plane from external auditory canal to columella
-opens intraorally just opposite second upper molar
-deep layer of parotid fascia extends from fascia of posterior portion of digastric muscle and forms
stylomandibular membrane
-parotid tissue can herniate through a weakness in the stylomandibular membrane and lie in the
lateral pharyngeal wall
Facial Nerve
-three motor branches at stylomastoid foramen:
-stylohyoid muscle
-postauricular muscle
-posterior belly of digastric muscle
-location:
-6-8 mm anteroinferior to tympanomastoid suture
-10 mm anteroinferior and deep to tragal pointer
-branches at pes anserinus: upper temporofacial and lower cervicofacial division
-pes ~ 1.3 cm from stylomastoid foramen
-constant relationships:
-buccal branch follows course of parotid duct and lies either superior or inferior to duct
-temporal branch crosses zygomatic arch parallel with superficial temporal vessels
-marginal mandibular branch is superficial to posterior facial vein (retromandibular vein)
Great Auricular Nerve

-sensation to posterior pinna and ear lobule
-can be harvested for facial nerve grafting
Auriculotemporal Nerve
-branch of V3
-innervate scalp
-also carries postganglionic parasympathetic fibers from otic ganglion to parotid gland
-aberrant innervation to skin can result in Frey syndrome
346
Arterial Supply
-external carotid artery superficial temporal artery transverse facial artery parotid gland,
Stensen duct, masseter muscle
Venous Drainage
-posterior facial vein (deep to facial nerve)
-eventually drains into internal jugular system
Lymphatic Drainage
-two layers of nodes
-superficial layer lies between gland and capsule
-drains parotid gland, EAC, pinna, scalp, eyelids, lacrimal glands
-deep layer
-drains parotid gland, EAC, middle ear, nasopharynx and soft palate
Submandibular Gland
-comprises both mucous and serous cells
-submandibular duct (Wharton) lies inferior to lingual nerve and superior to hypoglossal nerve
-parasympathetic supply from chorda tympani
-sympathetic fibers originate from superior cervical ganglion and travel with lingual artery
-blood supply: facial artery
Sublingual Gland
-primarily mucous-secreting acinar cells
HISTOLOGY
Parotid gland Submandibular gland Sublingual gland
PHYSIOLOGY OF THE SALIVARY GLANDS
-functions of saliva:
-lubricates and moistens foods to facilitate mastication
-cools hot foods
-buffers chemicals
-lavages oral cavity (antibacterial)
-lysozyme, secretory IgA
-aids in digestion
-dental protection
-modulation of taste
347
-composition of saliva:
-water (99%)
-salts: (CaPO4, CaCO3)
-amylase
-albumin
-lysozyme
-IgA
-ptyalin
Production of Saliva
Secretory Unit:
-acinus, secretory tubules (intercalated duct, striated duct, excretory duct), collecting duct
-myoepithelial cells contract to expel preformed secretions
Secretory Process:
-serous acinar cells produce secretory granules with amylase
-mucous cell granules contain mucin
-as fluid moves distally, ducts alter its composition by secretion of electrolytes, water and organic
solutes and by resorption of water and electrolytes
-net effect: decrease in sodium and increase in potassium concentrations
-abundant mitochondria in striated duct for metabolic demands of transport of ions and water
Autonomic Innervation
Parasympathetic Nervous System:

-parotid gland:
-inferior salivatory nucleus glossopharyngeal nerve tympanic plexus (Jacobson’s
nerve) lesser superficial petrosal nerve (otic ganglion ) postganglionic fibers via
348
auriculotemporal nerve parotid gland
-submandibular/sublingual glands:
-superior salivatory nucleus nervus intermedius chorda tympani lingual nerve
(submandibular ganglion) postganglionic fibers to submandibular and sublingual
glands
-acetylcholine is the primary neurotransmitter
Sympathetic Nervous System:

-superior thoracic nerves superior cervical ganglion postganglionic fibers via arterial plexus
submandibular and cutaneous vessels
-travel with arteries that supply salivary glands
-norepinephrine is the primary neurotransmitter
-stimulation of the gland produces a scant viscous saliva rich in organic and inorganic solutes
Salivary Flow Rates

-24-h volume ~ 1-1.5 L (~1 ml/min)
-unstimulated: submandibular glands provide 69%, parotid 26% and sublingual 5% of salivary flow
-stimulated: parotid gland 66% of total flow
-hypersecretion:
-bilateral tympanic neurectomies for patients with excess drooling
-bilateral parotid duct rerouting +/- submandibular gland excision
-active role in enamel formation of maturing teeth
349
SALIVARY GLAND IMAGING
DIAGNOSTIC IMAGING TECHNIQUES
Plain-film radiography
-to evaluate calculi or detecting calcification in hemangiomas, lymph nodes or pleomorphic adenoma
Sialography
-CT and MRI have replaced sialography in evaluation of salivary gland or adjacent tumour masses
-still most useful modality to evaluate intrinsic structure of salivary ducts
-indications:
-chronic, recurrent and nonspecific sialoadenitis
-Sjogren syndrome, Mikulicz syndrome
-submandibular or parotid gland sialolithiasis
-posttraumatic or postoperative fistula, stricture or cyst
-contraindications:
-acute infections
Computed Tomography
-Hounsfield units:
-a unit of x-ray attenuation used for CTs
-air: -1000 HU
-water: 0
-bone: +1000 HU
-fat: -20 HU
-muscle: +20 HU
-enhanced parotid: +35 HU
-submandibular glands: +40 HU
Magnetic Resonance Imaging

-T2 weighted images superior to T1-weighted images for differentiating tumour from normal salivary tissue
-tumours have high signal intensity on T2
Diagnostic Ultrasound
-differentiates solid vs cystic masses
-for U/S guided FNA
Nuclear Scintigraphy
-sodium pertechnetate Tc 99m
-most commonly used radioactive pharmaceutical
-uptake by normal salivary gland tissue
-tumours usually have no uptake filling defect
-Warthin’s tumour and oncocytoma readily take up pertechnetate “hot spot”
-gallium 67 citrate:
-used for studying inflammatory or neoplastic disease
-taken up by dividing cells - excessive accumulation observed in inflammatory or neoplastic
processes:
-sarcoidosis, melanoma, lymphoma
-anticarcinoembryonic antigen imaging has high negative predictive value (100%) in malignancy of the
salivary glands
F.Ling - Salivary Gland Imaging (1)
350
INFLAMMATORY DISEASE OF THE SALIVARY GLANDS
Sjogren Syndrome
-sialography:
-gland involvement tends to be bilateral
-parotid gland mild to markedly enlarged
-multiple punctate contrast collections
throughout gland can progress to become
larger collections that are more globular
-may have areas of tubular sialectasia or
strictures
-retention of contrast material
-CT:
-bilateral parotid enlargement with multiple
areas of low attenuation
-may have cyst formation with lymphoid
infiltration (pseudolymphoma)
-high incidence of non-Hodgkin lymphoma -
presents as intraglandular mass
Chronic Inflammatory Conditions

-sialography or CT may demonstrate inflammatory masses or more specific infections of salivary glands,
such as TB, symphilis, actinomycosis or animal-scratch fever
-abnormalities:
-sialectasia of main or intraglandular ducts
-stricture and filling defects within ducts related to debris
-fibrosis
-inflammatory infiltrate
-sialography contraindicated in acute sialadenitis; may amplify disease
-CT/MRI:
-fluctuant, enlarged, variably enhancing salivary gland and extraparotid inflammation involving
masseter muscle, subcutaneous soft tissues and masticator or parapharyngeal spaces
-may demonstrate abscess formation:
-CT: hypointense central region surrounded by variably enhancing rim
-MRI: T1 dark; T2 bright
-ultrasound: locate fluid collections for aspiration
Sialolithiasis
-can be diagnosed with plain-film radiography
-20% of calculi in submandibular and 20-40% in parotid gland are not visible on plain-film
-sialography: intraductal filling defects
Lesions of the Parapharyngeal and Masticator Space

-demonstration of a fat plane separating normal parotid gland from mass indicates parapharyngeal location
-lack of fat plane implies deep lobe parotid tumour
-poststyloid lesions
-displaces parapharyngeal fat anteriolaterally
-usually schwannoma or paraganglioma
-also: retropharyngeal lymphadenopathy, meningioma, hemangioma, chondrosarcoma,
rhabdomyosarcoma, perineural metastasis
-prestyloid lesion
-pushes fat medially
351
-usually salivary gland neoplasm
-masticator space lesions:
-can be meningioma, neurolemma, sarcoma, SCC, dentigerous cyst or masseteric hypertrophy
-no salivary gland lesions
-four findings that indicate masticator space origin:
-location anterior and lateral to parapharyngeal fat
-limitation of tumour by boundaries of masticator space (ie, sphenoid bone, posterior
aspect of mandible, and zygomatic arch)
-obliteration of fat planes within masticator space
-tendency to spread through foramen ovale
-MRI:
-primary salivary gland tumours and minor salivary gland neoplasms displace internal carotid
artery
-schwannomas (vagus nerve) and paragangliomas arise posterior to ICA and displace it anteriorly
-similar signal characteristics:
-well-circumscribed lesion with intermediate signal on T1 and increasing signal on T2
-paragangliomas may have salt and pepper appearance d/t flow voids
Salivary Gland Cysts

-congenital
-first branchial cleft (type 2)
-dermoids
-epidermoid
-acquired
-posttraumatic (eg. sialocele)
-from blunt trauma, faulty dentures, buccal mucosal ulcerations, surgical sutures or
calculus removal
-lymphoepithelial
-pt may or may not have clinical signs of AIDS
-usually associated with cervical adenopathy
-retention cysts (mucocele, ranula)
-obstruction of sublingual or minor salivary gland duct
-CT: well-circumscribed low-density mass (0-20 HU)
-MRI: low intensity T1 and high intensity T2
SALIVARY GLAND NEOPLASMS
Benign Neoplasms
Pleomorphic Adenoma
-CT:
-well-circumscribed mass with homogeneous or heterogeneous density
-contrast enhancement varies but tends to be mild
-calcifications may be evident
-MRI:
-predominantly heterogeneous well-circumscribed mass
-T1 intermediate to low signal intensity
-T2 increased signal
352
Warthin Tumour and Oncocytoma
-CT:
-homogeneous well-circumscribed mass
-hypodense or cystic areas
-calcification does not occur
-MRI:
-T1 intermediate to low signal intensity
-T2 increased signal
-both Warthin and oncocytoma are unique in that they accumulate technetium-99m pertechnetate
Hemangioma and Lymphangioma

-plain film: may demonstrate calcification of multiple phleboliths within tumour
-CT: well-defined heterogeneous mass
-MRI: heterogeneous signal on T1 and T2
Lipoma
-may be intraparotid or paraparotid
-CT: low attenuation (-50 to -150 HU)
-MRI: high signal T1; intermediate signal T2
Malignant Neoplasms
-low-grade MEC has CT and MRI characteristics resembling benign lesions
-well circumscribed and regularly marinated without infiltration into adjacent soft tissues
-low to intermediate signal intensity on T1 with increasing intensity on T2
-high-grade MEC:
-more irregular appearance with irregular margination and infiltration into soft tissues
-signal intensity intermediate on T1 and T2

-perineural infiltration common
-CT signs of perineural involvement:
-obliteration of normal fat plane beneath stylomastoid foramen
-tumour enhancement along course of facial nerve
-vascular enhancement with variable infiltration into adjacent soft tissues
-recurrent disease demonstrates CT enhancement and increased signal on T2 weighted images

-usually from metastasis
-loss of margination, irregularity and soft-tissue infiltration may be identified in aggressive tumours
Malignant Variations of Pleomorphic Adenoma

-indistinguishable from other neoplasms of parotid gland
Lymphoma
-multiple, well-circumscribed, homogeneous masses withing parotid gland and in paraparotid region that
may enhance slightly with contrast
353
IMAGING PROCEDURES
Imaging Study Indications Comments
Plain films Calculus disease Limited value; may differentiate salivary gland disease from bony
abnormality
Sialography Sjogren syndrome, chronic Best means of imaging ductal system; of limited value other than in
inflammatory conditions evaluating the ductal system
CT Chronic inflammatory Excellent anatomic detail for intrinsic and extrinsic salivary gland
conditions and complications, tumours; best means of identifying calculi or calcification
intrinsic and extrinsic masses,
calculus disease
MRI Chronic inflammatory Excellent anatomic detail in tumour evaluation; may be better than CT
conditions and complications, for parapharyngeal space and intracranial extensions
intrinsic and extrinsic masses
US Abscess, cyst, intrinsic salivary Best means of determining solid vs cystic lesions, but limited
neoplasm (?) nasopharyngeal detail
Radionuclide imaging Warthin Tumour Sodium pertechnetate Tc 99m taken up by benign neoplasms; gallium
67 citrate and bone-scanning agents occasionally useful for
malignancies
354
NON-NEOPLASTIC DISEASES OF THE SALIVARY GLANDS
ACUTE INFLAMMATORY LESIONS
Mumps
-most common viral disorder involving salivary gland
-peak incidence: 4-6 ya
-pathogen: paramyxoviruses
-pain, swelling, generalized symptoms
-dx: antibodies to mumps S and V antigens and to hemagglutination antigen
-complications: sudden deafness, pancreatitis, meningitis, orchitis
-tx: self limiting; requires only supportive care, audiological evaluation, vaccine is available
Other Viral Diseases

-CMV -involves newborns and may lead to mental and physical retardation and HSM, jaundice, and
thrombocytopenic purpura
-coxsackievirus A
-echoviruses
-influenza A
-lymphocytic choriomeningitis virus
Acute Suppurative Sialadenitis

-most cases involve parotid (less bacteriostatic activity)
-usually post-operative, elderly patients
-secondary to salivary stasis; in outpts calculi or duct stricture
-20% bilateral
-organisms:
-S. aureus (most common), S.. pneumoniae, E. coli, H. influenzae, Bacteroides melaninogenicus,
Streptococcus micros
-tx:
-hydration, improved oral hygiene, repeated massage of gland, IV antibiotics
-I+D if no improvement with medical management
-elevate parotidectomy flap and make multiple openings into gland, spreading in general
direction of facial nerve
F.Ling - Salivary Gland Diseases (1)
355
CHRONIC INFLAMMATORY DISORDERS
-d/t lowered secretion rate with subsequent salivary stasis
-sialectasis, ductal ectasia, and progressive acinar destruction combined with a lymphocytic infiltrate
-IgG dominates in saliva rather than typical IgA
-permanent xerostomia in 80%
-tx:
-start with conservative measures
-progress to periodic ductal dilatation, ligation of duct, total gland irradiation, tympanic
neurectomy, and excision of gland
-recurrent parotitis of childhood:
-M>F
-sudden onset with no obvious underlying cause
-no xerostomia; child not generally ill
-disease may disappear at puberty or continue into adulthood
GRANULOMATOUS DISEASE
Primary Tuberculosis of the Salivary Glands

-common
-arises from focus of infection in tonsils or teeth
-acute form may mimic acute sialadenitis
-PPD test may be unreliable atypical mycobacteria may be involved
-dx: via FNA or excision - note: incisional biopsy should be avoided as it will cause chronic fistulous
drainage
-tx: anti-tuberculous meds
Animal-Scratch Disease
-does not involve salivary glands directly; may involve parotid by contiguous spread
-gram-negative bacillus sensitive to gentamicin
-disease is self-limiting; treatment is symptomatic
-Cat-scratch Disease:
-Bartonella henselae
-Medical Care:
-appropriate therapy in persons with CSD has not been well studied
-in most patients who are immunocompetent, CSD is self-limited
-Effective antibiotics include rifampin, ciprofloxacin, trimethoprim-sulfamethoxazole
(TMP-SMX), and gentamicin
-tx for 10-14 days. No specific dose recommendations are available
Sarcoidosis
-unknown etiology
-uveoparotid fever (Heerfordt syndrome): uveitis, parotid enlargement and facial paralysis
-involvement of minor salivary glands may occur labial or palate biopsy may establish dx
-tx: corticosteroids in acute phase
SJOGREN SYNDROME
-lymphocyte-mediated destruction of exocrine glands leading to xerostomia and keratoconjunctivitis
-second most common autoimmune disease after rheumatoid arthritis
-average age of onset: 50y
356
-associated with Non-Hodgkin’s lymphoma
-two forms:
-Primary Sjogren:
-involves exocrine glands only
-may involve up to 3% of population
-80%: unilateral or bilateral salivary gland swelling occurs
-Secondary Sjogren:
-associated with definable autoimmune disease, most commonly RA
-30-40% salivary gland swelling
-laboratory:
-B-cell hyperactivity polyclonal hypergammaglobulinemia
-70-90% have rheumatoid factor
-55-70% have ANA
-specific autoantibodies:
-anti-Ro (SSA) and anti-La (SSB)
-detected in 40-60% of pts with primary Sjogren
-dx: -requires biopsy of labial mucosal glands or parotids
-aggregates of 50 or more lymphocytes and plasma cells
-tx: -artificial saliva, frequent small drinks, artificial tears, consider pilocarpine hydrochlorate drops
and oral corticosteroids for severe acute exacerbation
SIALOLITHIASIS
-calculi: 80% submandibular gland; <20% parotid; 1% sublingual
-calcium phosphate
-commonly occur in pts with chronic sialadenitis
-gout: only systemic disease causing salivary gland calculi (uric acid)
-x-rays:
-90% submandibular calculi are radiopaque; 90% parotid calculi are radiolucent
-all detectable by CT
-submandibular calculi within duct; parotid are at hilum or within parenchyma
-tx:
-gland massage, bimanual expression
-transoral excision if calculi near duct orifice
-complete gland excision if calculi near hilum
-complications:
-fistulas, acute suppurative sialadenitis, ductal strictures
CYSTIC LESIONS
-dermoid cyst
-congenital ductal cyst
-dx by sialography
-no treatment unless repeated infections
-first arch branchial cleft cysts
-tract intimately associated with facial nerve
-acquired cysts:
-benign lymphoepithelial lesion, trauma, parotitis, calculi, duct obstruction, mucus extravasation,
HIV infection
-mucoceles and mucous cysts:
-minor salivary glands, most commonly on the lips, buccal mucosa and ventral portion of tongue
357
RADIATION INJURY
-often permanent if exposed to > 40-50 Gy
-serous cells exhibit marked degranulation and disruption
-continued irradiation leads to complete destruction of serous acini and subsequent atrophy in gland
-interstitial fibrosis seen on histology
-tx: symptomatic (pilocarpine drops, artificial saliva, frequent drinks), dental care
TRAUMA
-ductal injury:
-suspected if any penetrating injury posterior to anterior border of masseter muscle
-tx: end-to-end anastomosis over polyurethane catheter with 9-0 sutures
-if not possible, duct ligated or new duct created from buccal mucosa
-facial nerve injury:
-if wound anterior to vertical line from lateral canthus to mental foramen repair is probably
unnecessary (even with clear dysfunction) b/c recovery is likely
-injuries posterior to this line are repaired immediately
-no real advantages with delayed repair
SIALADENOSIS (Mikulicz Syndrome)

-non-inflammatory nonneoplastic enlargement of salivary gland
-mechanism unknown
-generally asymptomatic
-causes:
-obesity fatty hypertrophy
-malnutrition:
-pellagra, cirrhosis, diabetes mellitus, beriberi, anorexia nervosa, bulimia
-alcoholic cirrhosis - based on protein deficiency
-malabsorption syndromes:
-celiac disease, bacillary dysentery, carcinoma of esophagus, Chagas disease,
ankylostomiasis
-uraemia, hypothyroidism, myxedema, testicular or ovarian atrophy, pregnancy, lactation, and
chronic relapsing pancreatitis
OTHER DISORDERS
-pneumoparotitis glass blowers
-chelitis glandularis
-enlargement of labial salivary glands
-medications:
-isoproterernol, ethambutol, phenobutazone,
phenothiazine, iodine compounds and heavy
metals
-necrotizing sialometaplasia
-commonly on hard palate
-mucosal ulceration with
pseudoepitheliomatous hyperplasia, ischemic
lobular necrosis, and dissolution of acinar
walls with release of mucous
-self-healing and requires no treatment
358
CONTROVERSIES IN SALIVARY GLAND DISEASE
GUSTATORY SWEATING
-recent study showed that after 1 year, 43% of pts were symptomatic and 96% had a positive starch iodide
test
-only 5-10% had severe symptoms
Diagnosis
-Minor’s starch iodide method
-infrared thermography
-mainly used for research purposes
Prevention
-temporoparietal flap transposed immediately after parotidectomy
-sternocleidomastoid flap
-flaps have decreased rates of GS - but may interfere with postoperative tumour surveillance
Treatment
-antiperspirants and scopolamine - only provide temporary effects
-botulinum toxin:
-binds presynaptic cholinergic terminals and prevents release of ACh
-tympanic neurectomy
PAROTID CYSTS
-may be true cysts, lymphoepithelial cysts, mucoceles, keratomas, or branchial cysts
-asymptomatic masses observed
-surgical resection effective, although cysts may recur in residual tissue
-tetracycline sclerosis by direct injection
-botulinum toxin A injection subcutaneously near mass after diagnostic aspiration
XEROSTOMIA
-mostly after XRT
-pilocarpine:
-muscarinic receptor agonist
-used to ameliorate xerostomia
-stimulates undamaged cells
PAROTID SURGERY
Preoperative Evaluation
-EnoG use in parotid surgery is uncommon
-studies found that significant decrease in preoperative EnoG response correlated with postoperative facial
dysfunction
-when reduced by more than 80%, all pts were found to have facial nerve involvement
-EnoG did not correlate with facial nerve function for benign tumours
Intraoperative Facial Nerve Monitoring

-no study indicating the monitor has significant utility in protecting the facial nerve
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Benign Mixed Tumours
Extent of Resection
-arguments in favour of a limited resection include:
-potentially smaller incision
-less postoperative facial distortion
-shorter operative time
-lower incidence of Frey syndrome because less parotid is removed
-for malignant tumours, usually a total parotidectomy is performed, because of possibility of direct
extension or even intraparotid nodal metastases
Other Facts
-accuracy of FNAB in determining malignant versus benign tumours:

90%
-percentage of salivary gland tumours diagnosed as malignant on frozen section but are found to be benign
on permanent sections:
0-2%
-percentage of salivary gland tumours diagnosed as benign on frozen section but are found to be malignant
on permanent sections:
0-2%
-test with highest predictive value for recurrence in patients with adenoid cystic ca:
Ag NOR (nucleoar organizer count)
-incidence of cervical metastasis d/t oral or major salivary gland adenoid cystic carcinoma:
0-10%
-10 year survival rate for patients with adenoid cystic carcinoma who have cervical metastasis:
0-10%
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TASTE
Definitions
-hypogeusia: partial loss of taste
-ageusia: total loss of taste
-dysgeusia: abnormal taste in absence of obvious stimulus
-flavour: combined sensation of taste, smell, temperature, texture and pungency
ANATOMY OF THE TASTE SYSTEM
Tongue
Taste Buds, Receptor Sites and Taste Stimuli, Taste Quality Coding
-globular cluster of cells arranged like segments of an orange
-tips taper to thin microvilli that project above into the taste pore
-taste receptor cells have limited lifespan measured in days
-salts and acids interact with ion channel on taste pore membrane
-more than one receptor type for sweetness and bitterness
-neural fiber types specific to each of four basic tastes
Taste Papillae
-filiform:
-most numerous
-no role in taste - helps sustain tastants on tongue
-in cats are shaped like rasps for licking
-located all over tongue
-fungiform:
-distributed on tip and edge of anterior 2/3 of tongue and lateral edge
-functions in taste
-foliate:
-located between adjacent folds on edges of base of tongue; posterior lateral edge
-circumvallate:
-raised circular structures on the rear of the tongue
-forms an inverted V
Tongue Map
-myth that certain tastes occur only on one area of the tongue
-four taste qualities can be perceived on all loci where there are taste buds
Peripheral Nerves
-glossopharyngeal nerve (IX):
-taste and sensation to posterior 1/3 of tongue
-lingual branches
-taste sensations from circumvallate papillae and foliate papillae from rear edge of tongue
-afferent neurons to mucous membrane of base of tongue
-terminate in nucleus solitarius (the gustatory nucleus)
-facial nerve (VII) - chorda tympani:
-taste information from fungiform papillae on anterior 2/3 of tongue
-may also receive information from foliate papillae as well
-terminates in tractus solitarius
-facial nerve (VII) - greater superficial petrosal nerve
-taste sensation through innervation of palate; buds located on margin b/n hard and soft palates
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-vagus nerve (X) - superior laryngeal nerve
-innervates taste buds on laryngeal surface of epiglottis
-role in everyday taste is unknown
Central Connections
-taste fibers from CN VII, IX, X compose part of solitary fasciculus terminate on rostral half of
nucleus solitarius in medulla
-second-order gustatory neurons ventroposteromedial nucleus in thalamus
-third order neurons cortex (circular sulcus that separates frontal operculum from insula)
EVALUATION OF TASTE SENSE
-dysgeusia resulting from a genuine stimulus

-stimulus tastant can be rinsed out of mouth with water
-no cranial nerve losses
-topical anaesthesia should abolish a chronic taste
-taste phantoms
-bad taste may intensify when topical anaesthesia applied
TASTE LOSS OR ALTERATION PRODUCED AT VULNERABLE LOCI IN THE TASTE SYSTEM
Tongue
-substances that alter taste have effects on taste membrane
Venous Taste
-stimulation of receptor sites that are on the bottom of the taste cell (ie. below the microvilli)
Peripheral Nerves
-chorda tympani
-most commonly involved in taste disorders
-taste loss in anterior 2/3 of tongue
-most commonly from acute or chronic OM
-release of inhibition from chorda damage enhanced tastes from some stimuli
-other causes: Bell palsy, Ramsay Hunt syndrome
Nervus Intermedius
-neoplastic processes that cause nervus intermedius dysfunction: acoustic neuroma, meningioma,
or facial nerve neuroma
Glossopharyngeal Nerve
-trauma after tonsillectomy, UPPP or any insertion of deep mouth gag where base of tongue is
compressed and lateral pharyngeal wall is manipulated or stretched
-Vernet syndrome: jugular foramen lesions paralyse all nerves that traverse the jugular foramen
(IX, X and XI)
-Collet syndrome: extension of lesion to involve the CN XII unilateral tongue paralysis
-Villaret syndrome: sympathetic trunk compromise along with CN IX-XII involvement
CNS
-unilateral pontine haemorrhage
-unilateral damage to rostral insular cortex
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Phantoms from damage to peripheral structures
-chorda tympani: bitter and metallic phantoms
-nervus intermedius: salty phantoms
-glossopharyngeal nerve: bitter taste phantom that increases with topical anaesthesia
Capsaicin:
-stimulates oral pain
-can also desensitize pain receptors may be used as an analgesic
Effects of age on sense of taste

-taste is much less affected by age than is olfaction
Effects of cancer and cancer therapies on sense of taste

-effects of chemotherapy and radiation therapy on taste showed that some patients lost taste (often
temporarily) and other patients experienced taste phantoms
Taste changes with disease

-renal disease: may be due to uremic toxins that accumulate
-diabetes: neuropathies
-also deficit specific to glucose in addition to general taste neuropathy
-depression: evidence of associated taste function
Coping with taste disorders

-few effective therapies
-requires cognitive adaptations
DISEASES ASSOCIATED WITH TASTE DISORDERS
-acoustic neuroma
-Bell’s palsy
-Ramsay Hunt
-XRT/chemotx
-diabetes
-epilepsy
-hypothyroidism
-psychiatric disorders
-medications:
-ACE-inhibitors (captopril, enalapril)
Olfactory or Gustatory losses:

-conductive/transport
-smell: polyps, nasal obstruction etc.
-taste: xerostomia, oral inflammation etc.
-sensory loss:
-injury to receptor cells
-viral infection, drugs, radiation
-neural losses:
-damaged central and peripheral pathways
-eg. neoplasms, head trauma etc
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STOMATITIS
DDx Stomatitis
Infectious: Inflammatory:
-viral: -erythema multiforme
-herpes -pemphigus vulgaris
-varicella zoster -cicatricial pemphigoid
-bacterial: -bullous pemphigoid
-Vincent’s gingivitis -lichen planus
-actinomycosis -Behcets
-syphilis -SLE
-fungal: -Wegner’s
-candidiasis
Other:
Iatrogenic: -apthous ulcers
-radiation/chemotherapy induced
HERPES
Etiology
-HSV-I more commonly associated
-transmission through contact with infected body fluids
-incubation time 7 days (range 1-28 days)
-lies dormant in trigeminal ganglion until reactivation
Clinical Features
-primary herpetic gingivostomatitis:
-usually seen in seronegative children and
occasionally in adults
-small vesicles occur on any mucosal surface
-stomatitis and pharyngitis
-most frequent clinical manifestations
-may be accompanied by fever, arthralgia, malaise,
headache, cervical lymphadenopathy, oral ulcers,
and gingivitis
-secondary (recurrent) disease
-lesions are confined to hard palate and gingiva Herpes gingivostomatitis
-reactivation triggered by UV, stress, fever, cold,
fatigue, immunosuppression, trauma, menses, chapped lips
-lesions usually heal in 1-2 weeks without scarring
Histopathology
-vesicles located intraepidermally
-formed by ballooning degeneration of epithelial cells
-homogeneous and glassy nucleus with nuclear material pushed out to the perimeter of the cell
Differential
-minor aphthous ulcers, erythema multiforme, acute necrotizing ulcerative gingivitis
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Treatment
-immunocompetent:
-supportive care (analgesics, antipyretics, hydration)
-antibiotics for secondary bacterial infections
-antiviral agents:
-acyclovir 100-200 mg 5x/day
-famcyclovir, valacyclovir, foscarnet
-recurrent herpes labialis
-acyclovir cream 5% 5x/day
-immunocompromised:
-acyclovir 250 mg/m2 q8h or 400 mg po 5x/day
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
-Vincent infection, “Trench Mouth”

-necrosis of papillary and marginal gingiva
-caused by poor dental hygiene, malnutrition, degenerative
diseases, immunocompromised
-organisms: Borrelia vencentii, Fusiformis fusiformis
-SSx: ulcerative craters of interdental papilla, gray
pseudomembranous cover, malaise, fever, cervical adenopathy,
halitosis
-Tx: oral hygiene, antibiotics
Acute necrotizing ulcerative gingivitis
VARICELLA ZOSTER
Varicella (Chickenpox)
-inspiration of contaminated respiratory droplets
-incubation period 2 weeks
-rash develops into vesicular eruption over trunk, head and neck
-infection lasts 7-10 days
-vesicles may be present on oral mucosa, commonly buccal
-treatment: supportive
Zoster (Shingles)
-VZV reactivation along sensory nerves
-incidence increased in immunosuppresive states (eg. malignancy, trauma,
drug therapy, radiation, steroid treatment)
-pain and tenderness along course of involved nerve
-most common complication: postherpetic neuralgia
-treatment: Chickenpox soft palate
-immunocompetent: supportive
-postherpetic neuralgia:
-acyclovir 800 mg 5x/day for 7d
-famcyclovir 500-700 mg tid x 7d
-topical antivirals early in course of disease
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DESQUAMATIVE GINGIVITIS
-diffuse erythematous desquamation, ulceration and possible bullae formation affecting free and attached
gingiva
-manifestation of several diseases:
-lichen planus
-cicatricial pemphigoid
-bullous pemphigoid
-dermatitis herpetiformis
-drug reactions
-incisional biopsy usually required to make definitive diagnosis
-direct immunofluorescence used to detect antibody or complement bound to tissue samples
-pemphigus vulgaris: binding to epithelial intercellular substance
-cicatricial pemphigoid: binding to basement membrane
LUPUS ERYTHEMATOSUS
Clinical Features
-Discoid LE:
-least aggressive form of lupus
-most often affecting women in 3rd-5th decades
-usually asymptomatic without visceral organ involvement
-elevated erythematous plaques with hyperpigmented margins
-oral lesions in 25% of patients
-subepithelial clefting
-diagnosis:
-positive basement membrane with direct immunofluorescence; negative direct
immunofluorescence, negative serology
-treatment:
-topical steroids
-sunscreens
-SLE:
-multiple organ involvement
-“butterfly rash” of malar eminence and nose
-diagnosis:
-positive basement membrane with direct immunofluorescence
-positive ANA, SS-A, SS-B
-screening test is fluorescent test for ANA positive in 98% of pts
-treatment:
-anti-inflammatory medications (salicylates, NSAIDs)
-systemic steroids for severe inflammatory states (prednisone 10-200 mg/day)
-antimalarial (chloroquine 250-500 mg/day, hydroxychloroquine 200-400 mg/day)
-can cause ocular toxicity
-cytotoxic agents (azathioprine, cyclophosphamide, methotrexate)
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CICATRICIAL PEMPHIGOID
Etiology
-chronic blistering of mucous membranes
-autoimmune disease with antibodies to lamina lucida and occasionally to lamina densa of basement
membrane zone
Clinical Features
-mean age 66 years
-F:M = 2:1
-mucosal lesions with subepithelial clefting forming bullae that rupture
-leads to ulceration and scarring
-cutaneous surfaces rarely involved
-most commonly affected sites:
-attached gingiva, presenting as desquamative gingivitis with diffuse or patchy erythematous
appearance
-conjunctiva (second most common site) - 50-70% incidence
Cicatricial pemphigoid Ocular cicatricial pemphigoid
-positive Nikolsky sign:

-gentle rubbing of uninvolved mucosa denudes surface epithelium, producing a vesicle or ulcer
Histopathology
-positive direct immunofluorescence at basement membrane
-negative indirect immunofluorescence (localized involvement, antibodies not circulating in serum)
Treatment
-topical steroids
-systemic steroids (prednisone 20-60 mg/day) for severe cases
-immunosuppressant (azathioprine, cyclophosphamide, methotrexate) for advanced cases
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BULLOUS PEMPHIGOID
Etiology
-antibodies directed at basement membrane (lamina lucida)
Clinical Features
-affects those in 7th and 8th decades
-M=F
-usually a cutaneous presentation with up to 40% of pts with oral
lesions
-oral lesion very similar to cicatricial pemphigoid
Histopathology
-positive direct immunofluorescence at basement membrane
-positive indirect immunofluorescence titers do not correspond to
severity of disease
Bullous pemphigoid
Treatment
-topical steroids or intralesional steroids for localized disease
-systemic steroids (prednisone 50-100 mg/day) to suppress new blister formation
-immunosuppressive agents (azathioprine) for maintenance often with steroids
-intravenous gamma globulin for severe disease requiring high-dose steroids
PEMPHIGUS VULGARIS
Etiology
-mucocutaneous diseases characterized by intraepithelial vesicle formation
-autoimmune disease:
-antibodies against Ca++-dependent cell adhesion molecule involved in maintenance of epithelial
integrity
-autoantibodies against desmosome-monofilament complexes results in acantholysis (loss of
cellular adhesion
Clinical Features
-pts 40-50 ya
-mucocutaneous disease with equal sex distribution
-increased in Mediterranean populations (Ashkenazi Jews)
-positive Nikolsky sign
Histopathology
-intraepithelial clefting with Tzanck cells (spheric free squamous cells ) = acantholysis
-positive direct intracellular immunofluorescence strongest at parabasilar region with decreasing intensity
toward surface
-intraepithelial blistering
-positive indirect immunofluorescence with titer level corresponding to severity of disease
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Treatment
-long-term and high-dose steroids often needed
-initial control to heal 80% of lesions (60-120 mg/day)
-immunosuppressive agents (azathioprine 50 mg/kg/day, cyclophosphamide 50-150 mg/day, cyclosporine 5
mg/kg/day) plus steroids for more refractory patients
-intramuscular gold +/- steroids
-tetracycline 500 mg and niacinamide 500 mg tid
ERYTHEMA MULTIFORME
Etiology
-hypersensitivity reaction implicated antigen-antibody complex
deposits in small vessels of dermis and submucosa
-target lesions are pathognomonic
-multiple infectious triggers and medications have been implicated
Clinical Features
-rapid explosive onset of macules, papules, vesicles, bullae, or
plaques of hands, feet, arms, legs, face, neck involving skin, mucous
membranes, or both
-usually subepithelial clefting with occasional intraepithelial vesicles
-often precede by recurrent herpes labialis (HSV I and II - 50%)
Target lesion of erythema multiforme
Stevens-Johnson Syndrome
-severe form of EM
-high fever, malaise, photophobia
-most cases drug induced
Toxic Epidermal Necrolysis

-painful cutaneous and mucous membrane lesions
-widespread detachment of full thickness of epidermis with total or partial necrosis
-most cases drug induced: sulfonamides, barbiturates, phenytoin, allopurinol
Histopathology
-no specific histologic appearance
-direct and indirect immunofluorescence are non-specific
Treatment
-supportive care (fluids, analgesics) for mild cases
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-topical steroids for mild to moderate cases
-systemic steroids for severe (ie. Stevens-Johnson syndrome, toxic epidermal necrolysis)
-prednisone 40-60 mg/day
-pts with multiple recurrences often controlled with high doses of tetracycline and niacinamide or acyclovir
(600-800 mg/day)
LICHEN PLANUS
Etiology
-inflammatory disease in which basal cell layer is destroyed by activated lymphocytes
-may be familial; may be induced by medications
Clinical Features
-F > M
-cutaneous lesions:
-small violaceus, pruritic papules over flexor surfaces or extremities
-oral lesions with a variety of presentations
-reticular form:
-most common, with white interlacing striae (Wickham striae) in an annular or reticular
pattern
-plaque form:
-resembles leukoplakia, often on dorsum of tongue and buccal mucosa
-atrophic form:
-produces desquamative gingivitis with burning or pain
-erosive form:
-very painful, erythematous erosion covered by a fibrinous layer
-bullous form:
-rare bullae range from several mm to several cm, rapidly rupture leaving a raw, painful,
ulcer bed
-believed to have slightly higher risk of malignant degeneration

-rate of malignant transformation ~ 1-5%
Histopathology
-histologic presentation generally diagnostic:
-hyperkeratosis
-liquefactive degeneration of basal cell layer
-“saw-toothed” rete peg formation
-bandlike lymphocytic infiltration in lamina propria
-civatte bodies: degenerative eosinophil ovoid keratinocytes
Treatment
-often asymptomatic and does not require any treatment
-topical steroids or intralesional injections for control of more severe symptomatic lesions
-cyclosporine rise (500 mg/day) for 4-8 wk improves healing and reduces pain
-systemic steroids for painful erosive variety
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CANDIDIASIS
Etiology
-local factors:
-physical irritation, preexisting infection, nutritional deficits, poor oral hygiene, denture wearing,
smoking and individual sensitivity
-systemic factors:
-endocrine alterations, AIDS, malignancy, systemic broad-spectrum antibiotic therapy, systemic
and inhaled steroid therapy, immature immunologic states of infancy, radiation or chemotherapy,
altered phagocytosis, pregnancy, old age
-pseudomembranous candidiasis (thrush):
-classic form, adherent, white, soft plaques easily wiped off the mucosal surface, leaving raw bed
-acute atrophic candidiasis:
-erythematous patch or diffuse lesion, patches and depapillation and dekeratinization with burning
symptoms
-may be caused by broad-spectrum antibiotic use
-chronic atrophic candidiasis:
-diffuse erythema with pebbly to velvety surface limited to denture-bearing mucosa
-angular cheilitis involve oral commissure within folds
-hyperplastic candidiasis:
-resembles leukoplakia
-cannot be rubbed off
-mucocutaneous candidiasis:
-pseudomembranous variety involving skin and nails
-median rhomboid glossitis:
-lesion appears as an asymptomatic diamond-shaped area of depapillation found anterior to the
circumvallate papillae
Treatment
-nystatin
-imidazoles (ketoconazole, clotrimazole)
-fluconazole
RECURRENT APHTHOUS STOMATITIS
Etiology
-most common type of nontraumatic ulcer
-cause unknown
-several agents implicated:
-viral, bacterial (streptococcus sanguis), nutritional deficiencies (B12, folate iron), hormonal
alterations, stress, trauma, food allergies, immunologic abnormalities
Clinical Features
-white ulcers with erythematous halos
-minor aphthous ulcers:

-<1.0 cm, on keratinized freely movable gingiva
-heal in 7-10 days without scarring
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-major aphthous ulcers:
-1-3 cm, on keratinized freely movable gingiva, tongue, palate, anterior faucial pillar
-persist from 6 wk to several months
-heal by scarring
-herpetiform ulcers:
-painful crop of 20-200 small (1-3 mm) ulcers on movable and attached gingiva, tongue, palate
Histopathology
-no microscopic features specific to aphthous ulcers
Treatment
-tetracycline oral suspension (200 mg/5 ml) q6h for 5-7 days
-fluocinonide (0.05%) plus Orabase applied to lesion 6-7 times/day
-topical steroids may shorten duration of symptoms; use with antifungal to prevent candidiasis
-systemic steroids for severe aphthae
MUCOSITIS
Etiology
-chemotherapy, radiation therapy, or immunosuppression for bone marrow transplant
-radiation-induced mucositis often appears by the second week of therapy and may persist for 2-3 weeks
after completion of XRT
-treatment:
-cleansing of oral mucosa, maintenance of moisture, relief of pain and inflammation
-numerous anaesthetic or analgesic mucosal agents used for symptomatic relief
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PHARYNGITIS
DDx Pharyngitis
Infectious: Inflammatory/Autoimmune:
-bacterial -Stevens-Johnson syndrome
-streptococcus -pemphigus
-staphylococcus -cicatricial pemphigoid
-diphtheria -bullous pemphigoid
-pertussis -epidermolysis bullosa
-gonorrhea -Wegener
-syphilis
-viral Iatrogenic:
-herpes -radiation
-measles -chemotherapy
-EBV
-varicella Other:
-CMV -reflux disease
-fungal
-candidiasis
INFECTIOUS CAUSES OF PHARYNGITIS
-tissues of pharynx prone to reactive changes because of predominantly lymphoid tissue
Bacterial Infections
Streptococcal Infection
-most frequent: GABHS (Strep. pyogenes)
-in children with GABHS pharyngitis antibiotic tx to avoid serious complication of rheumatic
fever
-diagnosis:
-enzyme immunoassay rapid antigen test or optical immunoassay rapid antigen test
-if negative, then many recommend C+S
-however culture still remains the safest and most cost-effective treatment strategy
-treatment:
-penicillin
-erythromycin in pen allergic
-first-generation cephalosporins recommended for treatment failures
-complications:
-rheumatic fever, rheumatic heart disease
-acute, poststreptococcal glomerulonephritis (ie. Bright disease) (risk not reduced by antibiotics)
-Grisel syndrome
-subluxations of atlantoaxial joint d/t infectious inflammatory process of H+N
-Scarlet fever:
-acute streptococcal pharyngotonsillitis accompanied by rash and production of
erythrogenic toxin
-face, palms, soles spared by rash
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Staphylococcal Infection
-mucopurulent drainage, mucosal erythema and localized pustules
-tx: anti-staphylococcal penicillins, erythromycin or cephalosporins
Diphtheroid Infection
-C. diphtheria
-gram positive, nonfilamentous rods
-produces exotoxins that cause localized tissue necrosis and inflammation
-rarely seen d/t vaccinations
-diphtheria more common in children < 10ya
-antitoxin remains only specific method of treatment
-antibiotics useful as adjuvant therapy
Pertussis
-Bordetella pertussis
-nonmotile, pleomorphic, gram-negative coccobacillus
-highly communicable
-violent paroxysms of coughing accompanied by loud inspiratory sound (“whooping cough”)
-usually self-limiting; death rarely occurs
-antibiotics do not alter the course of disease
-eradicated by immunization
Gonorrhea
-Neisseria gonorrhea
-gram-negative diplococcus
-must be cultured on chocolate agar
-generally asymptomatic, but may present with sore throat, tonsillar hypertrophy or cervical adenopathy
-tx: penicillin, tetracycline, cephalosporins or quinolones
Syphillis
-Treponema pallidum
-primary stage:
-chancre: may affect tonsils
-histology:
-inflammatory infiltrate composed of plasma cells with scattered histiocytes, lymphocytes
and PMNs
-obliterative endarteritis
-identification: dark-field examination of smears, Warthin-Starry staining
-secondary stage:
-skin lesions and lymphadenopathy
-pharyngotonsillitis
-tertiary syphilis:
-CNS involvement
-gammas: granulomatous nonprogressive lesions
-investigations:
-VDRL (screening)
-FTA-ABS (confirmation)
-treatment: penicillin
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Viral Infections
Herpes Simplex Virus

-primary infection most frequently presents as gingivostomatitis
-may present as acute pharyngitis
-may appear as vesicular lesions that bleed easily and are covered with black crust or shallow tonsillar
ulcers covered with a gray exudate
-management essentially symptomatic
-anti-virals best reserved for immunocompromised pts
Measles
-coryza and conjunctivitis followed by typical spotty exanthematous lesions on buccal mucosa (Koplik
spots) and generalized cutaneous erythematous rash
Epstein-Barr Virus
-infectious mononucleosis
-lymphadenopathy and splenomegaly (50%)
-diagnosis:
-absolute lymphocytosis with atypical lymphocytes
-mono-spot test
-therapy is supportive, including rest and fluids
Cytomegalovirus
-most infections are asymptomatic, except in immunocompromised pts
-may present as an infectious mononucleosis-like picture
Fungal Infections
Candidal Infections
-Candida albicans
-if immune system is compromised then invasion of mucosal surfaces can occur dysphagia
-treatment with topical nystatin or oral ketoconazole or fluconazole
-amphotericin B for systemic involvement
GRANULOMATOUS DISEASES CAUSING PHARYNGITIS
-if confronted with presumed infectious process unresponsive to empirical antibiotic therapy, appropriate
cultures and biopsy sampling of affected tissues are necessary
-rare cause of pharyngitis
-caused by bacteria, mycobacteria, fungi, syphilis, parasites, sarcoid, Wegener granulomatosis, Crohn
disease and neoplasms
OTHER CAUSES OF PHARYNGITIS
Radiation Pharyngitis
-inevitable side effect of H+N XRT
-symptomatic treatment
-treatment of superinfections include topical antifungals or systemic antibiotics
375
Integumetal Disorders
Stevens-Johnson Syndrome
-cause unknown, but onset may follow URTI or use of certain drugs, esp. sulfonamides, anticonvulsants,
and barbiturates
-angiitis producing erythematous vesicular skin lesion which may become bullous
-treatment: symptomatic with maintenance of fluid and electrolyte balance during acute phase
Pemphigus
-autoimmune disorder
-pemphigus vulgaris:
-rapid appearance of various-sized vesicles and bullae, often involving large surface areas
-histology: intraepithelial vesicles or bullae that produce distinctive suprabasilar split
-treatment: steroids, immunosuppressive agents and antibiotics for secondary infections
Cicatricial Pemphigoid
-vesiculobullous, probably autoimmune disease
-lesions typically occur on conjunctiva and upper airway mucosa
Bullous Pemphigoid
-dz of the elderly
-generalized non-specific rash that persists for varying periods of time before vesculobullous lesions
appear
Epidermolysis Bullosa
-bullae or vesicles affect skin and mucous membranes with various degrees of severity
-ruptures of bullae leave raw, painful surfaces that heal by scarring
Reflux Pharyngitis
-associated with hoarseness, sore throat, chronic cough, globus pharyngeus, halitosis, cervical dysphagia,
esophageal and laryngeal carcinoma
-most accurate diagnostic test is 24h pH monitoring with both proximal and distal sensors
-empiric therapy with PPI or H2-blockers acceptable
PFAPA
-periodic fever, apthous stomatitis, pharyngitis, cervical adenitis
-children ~3ya
-glucocorticoid effectively control symptoms, tonsillectomy and cimetidine may lead to remission
Idiopathic Pharyngitis
-dietary and personal habits may play a role
-medications and commercial mouth washes can irritate throat
-thermal injury
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ODONTOGENIC INFECTIONS
-may arise from an in situ infected tooth or after extraction

-interval for development of infection may be less than 1day or as long as 1-3 weeks
LOCALIZED INFECTIONS
-percussion tenderness, increased pain to heat, diminished or absent response to electrical vitality testing
-soft tissue infection: diffuse cellulitis or walled-off abscess cavity
-may cause enlargement of lip (macrocheilia)
-maxilla: root ends are close to labial and buccal plates almost always produces extension buccally
-mandible: dental roots closer to lingual cortex however most cases spread buccally
REGIONAL (FASCIAL SPACE) INFECTIONS
Canine Space
-clinically a firm or fluctuant mass appears along the lateral border of the nose adjacent to the medial
canthus of the eye
-treatment: intraoral or percutaneous drainage
Buccal Space
-bounded by:
-buccinator muscle and buccopharyngeal fascia medially
-cheek skin laterally
-lip muscles anteriorly
-pterygomandibular raphe posteriorly
-zygomatic arch superiorly
-lower aspect of mandible inferiorly
-tender swelling of cheek, extends medially to middle of upper lip and involves one third of lower lip
-posteriorly extends over ramous of mandible to border of parotid gland
-superiorly may close eye entirely by producing circumferential eyelid edema
-orbital contents are protected
-treatment: percutaneous drainage
Sublingual Space
-communicates freely with that of the opposite side
-also communicates anteriorly with submental space through dehiscence in mylohyoid
-infections from anterior teeth as well as bicuspids and first molar tooth remain above mylohyoid shelf into
sublingual space
-treatment: intraoral drainage
Submandibular Space
-contents: submandibular gland, Wharton duct, lingual and hypoglossal nerves, facial artery and some
lymph nodes and fat
-involvement from infections of second and third mandibular molar teeth
-root apices beneath mylohyoid muscle
-treatment: external excision placed well below marginal mandibular nerve
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Submental Space
-source of infection by drainage from mandibular incisor teeth as well as their gingiva and central portion
of lower lip
-treatment: small upper cervical incision placed in the midline
Ludwig Angina
-refers to collective involvement of submandibular and sublingual spaces bilaterally and submental space
-cases of dental origin arise from infections of mandibular molar teeth
-clinically:
-brawny edema across entire upper anterolateral neck with elevation of floor of mouth
-potential for airway obstruction
-organisms: variety of aerobic and anaerobic gram-positive cocci and gram-negative rods
-management:
-elective tracheotomy under local anaesthesia
-nasotracheal fiberoptic intubation as an alternative to tracheotomy
-drainage through external cervical approach;
-intraoral drainage carries risk of aspiration in pts with severe edema of oral cavity and
oropharynx
-systemic antibiotics
Masticator Space
-infections tend to involve all muscles
-severe trismus with minimal external swelling
-source of infection from maxillary and mandibular molar teeth
-confirmation of diagnosis by CT
-treatment: intraoral drainage
Parapharyngeal Space
-prestyloid compartment:
-IMAX, inferior alveolar, lingual and auriculotemporal nerves
-poststyloid compartment:
-IJV, carotid artery, CN IX, X and XI, cervical sympathetic nerves
-clinically:
-intraoral bulge of tonsil and lateral pharyngeal wall and external swelling of soft tissues over
mandible and parotid region
-surgical exploration and drainage performed when pt does not improve within 24 hours or deteriorates
under observation
-drained by lateral cervical incision
-complications may be d/t infection within poststyoid compartment
-most dreaded complications:
-mycotic aneurysm of carotid artery from erosion of wall by purulent material within its sheath
angiography and balloon occlusion to determine risk of stroke
-eroded segment of artery requires ligation to prevent catastrophic event
Retropharyngeal Space
-extends from skull base to pretracheal space and ends in mediastinum at level of carina
-in front of danger space which extends to posterior mediastinum
-most common dental source is carious or periodontal involvement of mandibular third molar
-clinical:
-dyspnea and stridor, with a “hot potato” voice
-fullness and erythema of posterior pharyngeal wall often with central furrow produced by midline
raphe
378
-usually toxic with spiking fevers
-treatment:
-best drained from external approach; intraoral drainage carries risk of pulmonary complications
from aspiration
-intravenous antibiotics
-complications:
-spontaneous rupture aspiration or lung abscess
-descending mediastinitis:
-30-50% mortality rate; CT chest for early identification and drainage required
-tx: IV antibiotics, cervical drainage, thoracotomy
TREATMENT OF DENTAL INFECTIONS
Organisms:
-usually mixed flora:
-aerobic: Streptococcus, Staphylococcus
-anaerobic: Bacteroides, Fusobacterium, Peptostreptococcus, Prprionobacterium
Therapy:
-antibiotic therapy
-clavulin, clindamycin or ciprofloxacin
-local drainage of abscess
-radiographs of osseous strictures; possible CT of soft tissue spaces
-extraction or endodontic therapy of involved tooth
-intraoral drainage of local space (canine, buccal, sublingual)
-extraoral drainage of deep spaces (submandibular, submental, masticator, parapharyngeal,
retropharyngeal)
-drainage of paranasal sinus extension, orbital extension, and mediastinal extension
-debridement of osteomyelitis bone
-tracheotomy, when necessary
OTHER INFECTIONS
-classified into:
a) clostridia anaerobic cellulitis

-superficial necrosis and gas formation from anaerobic spore-forming organisms
b) nonclostridial anaerobic cellulitis

-superficial necrosis and gas formation from anaerobic non-spore-forming organisms
c) necrotizing fasciitis
-severe gangrene of skin and superficial and deep fascia
-caused by staphylococci, hemolytic streptococci, and gram-negative rods
-mostly arise from massive trauma associated with fracture of mandible; may arise from
isolated dental infection
d) synergistic necrotizing cellulitis

-variant of NF in which myonecrosis also develops which is produced by interaction of
anaerobic and gram-negative bacteria
379
-usually critically ill with extensive involvement of multiple spaces
-rapid progression of disease
-radiographic studies:
-subcutaneous emphysema, gas and pockets of suppuration in deep tissues and visceral spaces
-anaerobic and aerobic cultures should be taken
-anaerobes:
-Bacteriodes, Fusobacterium, Propionibacterum, Peptostreptococcus, Eubacterium
-gram negative:
-coliform bacilli: Proteus, Klebsiella, Enterobacter, Pseudomonas
-treatment:
-aggressive: fasciotomy and radical debridement
-intravenous antibiotics: eg. clindamycin and ceftazidime
-consider adjunctive HBO
DENTAL-SINUS-ORBITAL INFECTIONS
-superficial (preseptal: periorbital cellulitis) and deep (postseptal: orbital cellulitis, subperiosteal abscess,
orbital abscess, retrobulbar abscess) infections can occur from a dental focus
-access via pterygopalatine and infratemporal fossae
-anterior teeth retrograde spread through valveless anterior facial, angular and ophthalmic veins
-via orbital floor from maxillary sinus
-preseptal infections:
-periorbital edema w/o evidence of ocular involvement
-postseptal infections:
-proptosis, chemosis, ophthalmoplegia
-carries risk for blindness from IOP or optic neuritis
-surgical drainage:
-external ethmoidectomy and orbital decompression with antrostomy of involved
maxillary sinus
Osteomyelitis
-infection within medullary portion of bone
-organism most commonly isolated: Staphylococcus aureus and hemolytic streptococci
-risk factors:
-regional XRT, trauma, systemic disease (diabetes), osteodystropies (Paget disease, osteopetrosis),
endosteal lesions (cementomas), dental implants, immunocompromised state
-diagnosis:
-CT scanning bone destruction
-radionuclide studies increased activity at suspected site (high false positive)
-radiographically (chronic osteomyelitis):
-irregular lytic lesions
-occasionally in association with sequestrum of nonviable bone
-treatment:
-IV antibiotics (eg. clindamycin and ceftazidime for 3 weeks)
-oral antibiotics for 6 weeks
-debridement of foreign bodies, sequestra or necrotic tissue
-reconstruction as necessary following resolution of infection
Actinomycosis
-anaerobic branching gram-positive filamentous organism Actinomyces israelii
-entry through extraction site in host with poor hygiene
380
-painful indurated swelling with areas of suppuration with fistulous tracts through skin
-can cross fascial planes
-microscopy: sulfur granules seen in exudate
-treatment: Penicillin x 1 year or tetracycline
Complications of Odontogenic Infections:

-extension of infection from local to regional spaces
-orbital complications (blindness, ophthalmoplegia)
-jugular vein thrombosis
-septicaemia
-metastatic abscesses
-airway compromise
-aspiration
-carotid artery rupture
-mediastinitis
-osteomyelitis
-cutaneous fistula
-cranial nerve deficits
381
TEMPOROMANDIBULAR JOINT DISORDERS
ANATOMY
-vascular supply: superficial temporal artery

-sensory innervation: auriculotemporal, masseteric and deep posterior temporal nerves (V3)
-diarthrodial joint:
-true synovial joint (freely mobile) with two modes of movement (gliding and hinging)
-glenoid fossa:
-socket within temporal bone, lined with fibrocartilage
-articular eminence:
-anterior aspect of glenoid fossa which articulates to the condyle
EVALUATION
History:
-jaw pain
-may manifest as otalgia
-headaches
-toothache
-facial pain
-vertigo
-trsimus
-nocturnal bruxism
-recent trauma
Physical:
-evaluate occlusion and intra-incisor opening (normal 40-50 mm)
-palpate TMJ and jaw muscles
-examine for tenderness, warmth, crepitus, and joint clicking
F.Ling - TMJ Disorders (1)
382
Applied Neuroanatomy
Muscular Disorders TMJ disorders

-organic vs functional -arthralgia
-disc displacement
-most painful disorders of masticator muscles are functional
-disc dysfunction
-usually result of hyperactivity or hyperfunction -disc perforation
-hx of nocturnal or diurnal bruxism Myogenic disorders
-fibromyalgia: -muscle trismus or splinting
Chronic mandibular hypomobilities
-chronic, diffuse, MSK pain and sleep disorder,
-fibrosis of muscular tissue
w/o evidence of arthritis or myositis -capsular fibrosis
-malocclusion has been considered a cause for these -ankylosis
disorders, but they are now considered a peripheral issue in -adhesions
-coronoid process elongation
most MSK pain disorders
Chronic mandibular hypermobilities
-most TMJ pain is muscular rather than joint pain -subluxations
-dislocation
Temporomandibular Joint Disorders Fractures
-mandible
-internal derangements: disk displacements, osteoarthrosis,
-maxilla
inflammatory arthritides, congenital deformities, Inflammatory disorders
developmental deformities, ankylosis, fractures, neoplasms -synovitis, capsulitis
-traumatic arthritis
-degenerative arthritis
-disk displacements:
-infectious arthritis
-caused by disruption of ligamentous attachment -rheumatoid arthritis
of disk to condyle and subsequent pull of lateral -hyperuricemia
pterygoid muscle Disorders of maxillomandibular growth
-masticatory muscle hypertrophy or atrophy
-structural weakness, blunt facial trauma, -maxillomandibular or condylar hypoplasia
mandibular hyperextension or hyperplasia
-high female-to-male ratio of temporomandibular -neoplasia
joint disk derangements; hypermobilities more
common in women
-classification for anterior disk displacements:

-Ia: -non-painful click during opening or closing movements of mandible
-Ib: -painful click during opening or closing movements
-retrodiskal pad is stretched over condyle and compressed between
bony components; chronic irritation inflamed synovium and release
of noxious peptides into synovial fluid
-II -same as Ib but has a history of locking (inability to open mouth fully)
-disk becomes mechanical obstacle to normal condylar movements
-III -persistent closed lock; no translation of condyle under displaced disk
-outcome predictors correlate well with stage of derangements
-degenerative joint disease:

-loss of articular tissues from noninflammatory, mechanical process
-preauricular pain otalgia, lateral and endaural palpation tenderness, crepitans joint sounds
-radiographs confirm the diagnosis
-congenital and developmental internal derangements:

-branchial arch syndromes, hemifacial microsomia, isolated condylar aplasia or hypoplasia,
condylar hyperplasia
-correction requires repair of joint and reconstruction of teeth, jaws and face
383
-fibrous and bony ankylosis
IMAGING
-imaging is indicated for confirmation of disk pathology and bone status before surgery or to establish a
treatment baseline
-MRI: indicated if suspect disc displacement or dysmorphology
-CT: indicated if suspect degenerative joint disease, bony deformities, or ankylosis
-arthrotomogram: requires injection of contrast into joint space, can detect disc displacement
TREATMENT
Initial Management
-behaviour modification: soft diet, avoid
gum chewing
-physical therapy: repositioning, repetitive
jaw stretching, active and passive
mobilization
-analgesic and NSAIDS
-muscle relaxants
-warm compresses
-ultrasound
-may consider corticosteroid
injections
-dental management:
-consult for malocclusion, carious
teeth, poorly fitting dentures
Joint Disorders
-prolonged dental or occlusal therapy for
internal derangements are contraindicated
-non-painful clicking joints do not require
treatment
-painful early clicks can often be managed
with NSAIDs and soft diet
-painful late clicks or painful clicks with
locking are less likely to respond to nonsurgical therapy
Surgical Techniques
-controversial
-indicated for confirmed TMJ intracapsular derangements
-arthroscopy (closed )and arthrotomy (open)
-findings:
-disk is sound can be repositioned over condyle with plication of the retrodiskal tissue and
reattachments of the ligaments
-disk not salvageable excised
-articular cartilage damage reconstruction by autogenous auricular cartilage graft
-or rotation of pedicled temporalis fascia or pericranial temporalis flap into the joint
384
-total joint prosthesis
-complications: 10-20% failure rate, joint degeneration, malocclusion, osseous ankylosis, foreign-body
reaction (implants)
Risks of temporomandibular joint surgery

-facial paresis
-dysesthesias
-occlusal changes
-scars
-auditory canal stenosis
-implant failure
385
SNORING AND OBSTRUCTIVE SLEEP APNEA
EPIDEMIOLOGY
Snoring
-common problem
-prevalence increases with age
-~40% of people snore increasing to 84% (M) and 73% (F) in the seventh decade
-good objective tests for snoring exist
Obstructive Sleep Apnea

-Wisconsin Sleep Cohort Study:
-24% (M) and 9% (F) had RDI > 5
-4% (M) and 2% (F) had clinical symptoms and findings of OSA
-in certain subgroups OSA is more prevalent (eg. truck drivers)
SLEEP PHYSIOLOGY
Normal Sleep
-average duration for young adult: 7.5-8.5 hours
-two stages:
a) non-REM (~80% of sleep)
-slow HR and RR and low BP
-“quiet” stage of sleep
b) REM (~20% of sleep)
-bursts of rapid conjugate eye movement
-increased autonomic activity with large fluctuations of HR, RR and BP
-dreaming
-decreased muscular activity (paralysed)
-sleep architecture:
-stage 1 NREM
-low arousal threshold
-short duration: few minutes
-theta waves
-stage 2 NREM
-sleep spindles or K complexes on EEG
-duration: 10-25 minutes
-stage 3 NREM
-high-voltage slow-wave activity
-delta waves (deep sleep)
-short duration: few minutes
-stage 4 NREM
-delta waves (deep sleep)
-lasts 20-40 minutes
-sleep lightens stage 2 stage 1 or REM
-REM initially short but then increases as sleep progresses
-stage 4 sleep decreases as one ages: by age 60, stage 3/4 NREM may no longer be present
-most obstructive events occur during NREM III, IV and REM
F.Ling - Snoring and OSA (1)
386
SLEEP DISORDERS
-three distinct syndromes:

a) Upper airway resistance syndrome (UARS)
b) Obstructive sleep hypopnea syndrome (OSHS)
c) Obstructive sleep apnea syndrome (OSAS)
-common symptom of excessive daytime sleepiness in all three syndromes

-apnea = cessation of ventilation for 10 seconds or longer which leads to an arousal
-patterns of apnea:
-obstructive: lack of airflow despite ventilatory efforts
-central: lack of airflow resulting from absence of ventilatory efforts
-mixed: usually begins as a central event and ends as an obstructive event
-hypopneic event = decrease in airflow in association with oxyhemoglobin desaturation leading to arousal
from sleep
Snoring
-originates from collapsible portion of upper airway
-vibration of soft palate, uvula, tonsillar pillars or base of tongue
-histologically, palates of snorers and apneics had mucous gland hypertrophy, muscle bundle disruption,
atrophy of muscle fibers and edema of lamina propria with vascular dilation
-vibratory trauma to pharyngeal tissue is an etiologic factor in both apnea and snoring
Upper Airway Resistance Syndrome

-features:
-no significant decrease in airflow
->15 episodes/h
-no decrease in SaO2
-repetitive alpha EEG arousal which led to sleep fragmentation
-high negative intrathoracic pressures leading to increased work of breathing and sleep arousals
-M:F is 1:1; seen in non-obese patients and more common in young adults than in elderly patients
Obstructive Sleep Hypopnea Syndrome

-features:
-decrease of 30-50% airflow in > 10 seconds
->15 episodes/h
-may be associated with decrease of 3-4% SaO2
-increased ventilatory effort and excessive daytime sleepiness
-RDI (respiratory disturbance index) = number of apneas and hypopneas per hour sleep
Obstructive Sleep Apnea Syndrome

-features: Classification of Sleep Apnea and Hypoxemia Severity
-cessation of airflow for > 10 seconds RDI SaO2
->5 episodes/h
Mild 10-30 > 85%
-usually associated with decrease of >
4% SaO2 Moderate 30-50 65-84 %
-usually defined as apnea index (AI) of 5 or
Severe > 50 < 65 %
more or and RDI > 10
-apneic events vary with age
-desaturation is influence by patients
functional residual capacity, oxygen stores, length of sleep-disordered breathing event, and baseline awake
saturation level
387
PHYSIOLOGY OF UPPER AIRWAY OBSTRUCTION
-majority have collapse at level of nasopharynx

-majority have more than one site of obstruction in airway
-pharyngeal dilator muscles:
-medial pterygoid, tensor veli palatini, genioglossus, geniohyoid, sternohyoid muscles
-failure to dilate airway in many OSA patients during sleep leads to upper airway instability and
collapse
-anatomic narrowing airway more vulnerable to collapse
-septal deviation
-turbinate hypertrophy
-nasal polyps
-elongation of soft palate and uvula
-tonsillar hypertrophy
-macroglossia
-retrognatha
-rugae of posterior pharyngeal wall
-omega shaped epiglottis
-laryngeal-tracheal stenosis
Complications of OSA
-arrhythmia
-cor pulmonale
-congestive heart failure
-motor vehicle accidents
-nocturnal death
-growth delay, FTT
-hypertension
CLINICAL EVALUATION OF THE SUSPECTED SLEEP APNEA PATIENT
History
-nocturnal signs and symptoms:
-heroic snoring
-restless disturbed sleep
-observed apnea
-nocturnal sweating
-daytime signs and symptoms
-excessive daytime sleepiness
-cognitive impairment
-morning headaches
-impotence
-factors that exacerbate OSA:
-alcohol and sedatives
-nasal obstruction: rhinitis, URTI
-weight gain
-patient characteristics associated with OSA: male, advancing age, truncal obesity, large neck
circumference and hypertension
-spousal reports of apnea have be found to be unreliable in predicting the presence or severity of OSA
388
Physical examination
-vital signs and BMI
-complete head and neck examination
-tongue size, tonsil size and BMI have been shown to be significant predictors of OSA
-laryngeal, nasopharyngeal, and base-of-tongue tumours can present as new-onset snoring in a
petient who never snored
-fiberoptic endoscopy: Mueller maneuver
-scope at level of BOT just above velopharyngeal valve
-patient asked to inspire with nose and mouth closed
-examine level of collapse
-if hypopharynx and/or larynx collapse, then test is positive site of obstruction is below
level of soft palate and therefore patient would not benefit from UPPP
DIAGNOSTIC STUDIES
Sleep Scales:
-Epworth Sleepiness Scale
-Standford Sleepiness Scale
-do not predict apnea with great certainty
-no set group of symptoms or patient characteristics that can rule in or rule out sleep apnea with certainty
Oximetry
-has been used as screening device for OSA
-if percentage of time spent with SaO2 below 90% was < 1% of sleep time, clinically significant apnea is
practically excluded
Polysomnography
-standard overnight polysomnogram in sleep laboratory is the accepted diagnostic method for diagnosis of
OSA
-records:
a) EEG
b) electrooculogram
c) ECG
d) EMG (submental and anterior tibialis)
e) SaO2
f) nasal or oral airflow
g) thoracic/abdominal movement
h) sleep position
i) blood pressure
-report addresses:
-sleep latency
-sleep efficiency
-RDI
-types of respiratory disturbances as well as average and maximum length of each event type
-sleep architecture
-volume and presence of snoring
-effect of position on respiratory disturbances
-whether respiratory disturbances occur more often in particular sleep stages; number and severity
of oxygen desaturation events
389
-full-night vs split night studies
-sleep apnea worse during second half of the night
-but studies have shown RDI in first part of night is predictive of second half of night in most
patients
-can institute CPAP for second part of night
Multiple Sleep Latency Test (MSLT)

-used to measure daytime sleepiness objectively
-pt given four or more opportunities to nap throughout a day at 2-hour intervals and latency to sleep onset
and REM is evaluated
-an average sleep onset < 5 minutes is considered pathologic
-suggests excessive daytime sleepiness
-not necessary to diagnose OSA
PREOPERATIVE MEDICAL EVALUATION OF PATIENTS WITH OBSTRUCTIVE SLEEP APNEA

SYNDROME
Cardiopulmonary Disease
-initiation of nasal CPAP will bring improvement in hypertension control, congestive heart failure, and
pulmonary hypertension
-HTN has been found in 50% of OSA pts, pulmonary HTN found in 10-20% and cardiac arrhythmias also
are frequently noted in this population
Hypothyroidism and Acromegaly

-all newly diagnosed pts should be routinely evaluated for hypothyroidism
-thyroxine replacement in hypothyroidism reverses the apnea frequency independent of changes in weight
and pulmonary function
-routine screening for acromegaly not recommended but should have clinical suspicion
Obesity
-BMI > 27
-weight loss associated with improvement in apnea in most patients
Other Disorders Associated with OSAS

-pulmonary dysfunction
-GERD
-mucosal irritation may exacerbate apnea
-eliminate caffeine, tobacco, and alcohol: apnea should improve if these factors are controlled
APPROACH TO TREATING SNORING AND OBSTRUCTIVE SLEEP APNEA SYNDROME
Indications for Treatment

-treatment usually individualized
-AI score > 20 is associated with increased mortality
-recommended that even asymptomatic patients should be treated
-treatment of mild apnea based on effect of OSA on daytime functioning and baseline cardiopulmonary
function
-moderate or severe apnea should be treated regardless of their symptoms
390
Behavioural Treatment
-weight loss
-avoidance of alcohol and medications that cause sedation
-elimination of tobacco and caffeine
-many pts benefit from 1-3 month period of nasal CPAP therapy combined with weight loss or elimination
of exacerbating habits in preparation for a surgical procedure
Nonsurgical Treatment
-nasal CPAP
-most effective nonsurgical treatment of OSA
-long term compliance not obtained in as many as 75%
-oral appliances:
-mandibular advancement device
-tongue-retaining device
-other:
-efficacy not known
-positioning devices: T-shirt with ball
-nasal splints
Surgical Treatment for Snoring

-palatal procedures:
-LAUP
-preferred treatment by most surgeons for non-apneic snoring
-in pts with OSAS; 75% resolution of presenting complaints and 52% had no snoring
-UPPP
-short term success rates: 75-95%
-long term success rates can decrease to 46%
-nasal procedures:
-polypectomy, septoplasty, turbinate reduction
SURGICAL TREATMENT FOR OSAS
Nasal surgery
Palatal surgery with or without tonsillectomy

a) Uvulopalatoplasty (LAUP)
b) Uvulopharngopalatoplasty (UPPP)
-studies do not show reduction in mortality for UPPP alone
-significant improvement in OSA occurs in only 50% of patients
-this may only mean a reduction of RDI by 50% or more
-in patients with severe OSA, they may still have significant apnea despite UPPP
-Type I obstruction:
-retropalatal
-85% success in UPPP to decrease AI by 50%
-Type II obstruction:
-retropalatal, retrolingual
-5% success with UPPP
-Type III obstruction:
-retrolingual
-5% success with UPPP
391
-contraindications:
-velopharyngeal insufficiency
-submucous cleft palate
-patients with special voice or swallowing considerations
-complications:
-bleeding, VPI, voice change, FB sensation, nasopharyngeal stenosis, respiratory distress
-death
c) Transpalatal advancement pharygoplasty
-can be performed after UPPP failure
-advancement of soft palate at the junction of the hard and soft palates
-complications:
-oronasal fistula, flap necrosis, wound dehiscence
Tongue base reduction surgery

-lingual tonsillectomy, laser midline glossectomy, lingualplasty, radiofrequency tissue ablation of the
tongue
-may require temporary tracheotomy
-high complication rates preclude widespread application of this treatment modality
Maxillomandibular surgery
-two stage surgical protocol offering 97% success
-used after more conservative procedures have failed
-includes:
-mandibular advancement with genioglossus advancement (phase I)
-enlarge and stabilize retrolingual airway by advancing insertion of the genioglossus or
geniohyoid muscles without moving the entire mandible or teeth
-hyoid myotomy and suspension (phase I)
-advances hyoid bone anteriorly, which advances epiglottis as well as BOT
-maxillomandibular osteotomy and advancement
-bimaxillary surgery to advance maxilla and mandible as far anteriorly as possible
-phase II of protocol
Tracheotomy
-indications:
-morbid obesity
-significant cardiac arrhythmias associated with apneic events
-severe apnea with oxygen desaturation below 40-50%
-cor pulmonale
-disabling somnolence
-failure of CPAP
-reduces morbidity and mortality associated with OSA
-life-saving procedure and is necessary in certain pts with severe apnea
ANAESTHETIC MANAGEMENT OF PATIENTS WITH OSAS
-severe apneics have more airway edema, may have mild congestive heart failure with fluid retention and a
greater tendency to develop postobstructive pulmonary edema because of acute relief of obstruction
-difficult airways due to anatomy
-avoid oversedation
-post-operative monitoring for 24h
392
DEEP NECK INFECTIONS:
RECOGNITION, EVALUATION, THERAPY
OVERVIEW AND ANATOMY
Terminology
-Fascial layers:
-superficial fascial layer
-deep fascial layer
-anterior layer - superficial investing
-middle layer - pretracheal
-posterior layer - deep
-alar layer
-prevertebral layer
-visceral layer - buccopharyngeal
-Fascial spaces:
-Suprahyoid:
-divided by anterior layer of deep fascia:
-body of mandible, submaxillary gland, masticator, and parotid
-Peripharyngeal spaces:
-lie deep to anterior layer of deep cervical fascia
-lateral pharyngeal space, retropharyngeal space, submandibular space
-Other:
-danger space:
-formed by separation of alar and prevertebral layers
-allows access into mediastinum
-prevertebral space
-carotid sheath
-pretracheal space
-peritonsillar space
Cervical Fascia
-Superficial fascia:
-no fascial spaces
-subcutaneous tissue of head and neck enclosing muscles of facial expression and platysma
-Deep fascia:
-Anterior layer:
-originates from vertebral spinous processes and ligamentum nuchae
-encircles entire neck
-splits to enclose trapezius, omohyoid, SCM
-extends from hyoid superiorly to mandible splits to enclose inner and outer table of mandible
-outer table zygoma and temporalis muscle
-splits to encompass parotid, masseter and internal pterygoid muscles
-between hyoid and mandible: forms floor of submandibular space
-Middle layer:
-originates from anterior layer at lateral border of strap muscles
-travels posterior to strap muscles and anterior to trachea and thyroid
F.Ling - Deep Neck Infections (1)
393
-superior extent to hyoid
-inferior extent to fibrous pericardium
-Posterior layer:
-originates from vertebral spinous processes
-encircles the neck
-extends to base of skull superiorly, deep to trapezius; enclosing vertebral muscles
-splits at transverse processes of vertebrae:
-alar fascia (anterior)
-prevertebral fascia (posterior): covers longus colli muscle
-Visceral fascia:
-connective tissue surrounding esophagus, thyroid gland, trachea
-no spaces formed
Fascial Spaces
-Splitting of anterior layer of deep cervical fascia:

1. Space of body of mandible: potential space
2. Parotid space: parotid gland, facial nerve, lymph nodes
3. Submandibular space: submandibular gland, lymph nodes
4. Masticator space:
-ramus of mandible
-muscles: temporalis, masseter, internal pterygoid
-internal maxillary artery, mandibular nerve (V3)
-Peripharyngeal spaces:
1. Retropharyngeal space:
-from base of skull to bifurcation of trachea
-lies behind pharynx and esophagus
-contains loose connective tissue, lymph nodes
2. Lateral pharyngeal (pharyngomaxillary, parapharyngeal) space:
-from base of skull, contiguous with retropharyngeal space
-“conical”: base at petrous portion of temporal bone, apex at hyoid
-divided by styloid process and associated musculature into anterior and posterior compartments:
-anterior (prestyloid or muscular):
-fat and connective tissue
-closely related to tonsillar fossa medially and internal pterygoid muscle laterally
-internal maxillary artery
-inferior alveolar, lingual and auriculotemporal nerves
-posterior (poststyloid or neurovascular):
-CN IX, X, XII
-cervical sympathetic
-internal jugular vein
-common carotid artery
3. Submandibular space:
-superiorly: lingual mucosa
-inferiorly: anterior layer of deep fascia
-divided by mylohyoid muscle:
-sublingual: sublingual gland submandibular duct, lingual nerve and artery, hypoglossal
nerve, genioglossus and geniohyoid muscles
394
-submaxillary portion: anterior belly of digastric
-Other spaces:
1. Danger space:
-between alar and prevertebral fascia
-extends from base of skull to diaphragm
-provides route of spread for infection to mediastinum
2. Pretracheal space:
-most anterior of fascial spaces below hyoid bone
-defined anteriorly by middle layer of deep fascia, posteriorly by esophagus
-superior to hyoid; inferior to T4 along arch of aorta
3. Carotid sheath:
-contributions from all three parts of deep cervical fascia
-anteromedially: anterior layer, deep to SCM
-posteriorly: lamina from anterior layer prior to dividing to form middle layer
-sympathetic chain posteromedial to carotid sheath but superficial to posterior fascial layer
4. Prevertebral space:
-longus colli muscle
5. Peritonsillar space:
-faucial tonsils
MICROBIOLOGY
-aerobic streptococcal and nonstreptococcal anaerobes in majority of DNIs

-Streptococcus:
-hemolytic: group A
-commonly seen in pharyngeal infections
-non-hemolytic:
-alpha species: most common in odontogenic infections
-group D
-non-group D
-gamma species
-most commonly isolated anaerobes: Peptostreptococcus, Fusobacterium, Bacteroides
-increase in isolation of Eikenella corrodens: clindamycin resistance
-rarely gram-negative rods; may be found in immunocompromised, debilitated, elderly and diabetic patients
PATIENT ASSESSMENT AND TREATMENT RECOMMENDATIONS
-Key to DNI management:

-evaluation of airway: if unstable, control
-Posterior pharyngeal wall swelling
-symmetric: prevertebral
-asymmetric: retropharyngeal
-any sign of bleeding indicates possible carotid artery involvement; may represent a mycotic process
-If airway threatened, secure via intubation or tracheotomy
-Treatment includes:
-intravenous antibiotics
-empiric antibiotic choice: high-dose penicillin or third-generation cephalosporin
-surgical drainage if required
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Radiology:
-lateral neck film:
-critical to obtain during inspiration - high false positives if taken during expiration
-measure anterior aspect of vertebral column to air column of posterior pharyngeal wall
-at C-2 may be as wide as 7mm normally in children and adults
-at C-6 may normally extend to 14 mm in children and 22 mm in adults
-posterior pharyngeal swelling > 50% width of vertebral body
-ultrasound not very useful
-MRI: disadvantage is may require patient transport - potential hazard if patient quickly deteriorates
-CT: preferred
-CXR to assess complications from DNI
-mediastinal extension, lung abscess, pyopneumothorax, aspiration
SPECIFIC SPACE INFECTIONS
Submandibular Space
-most common DNIs
-prototypic infection: Ludwig’s angina
-alpha-hemolytic streptococcus most commonly isolated
-etiology:
-usually odontogenic (70-85%)
-disruption of mucosal layer by laceration or mandibular fracture and by tumour
-sialadenitis
-lymphadenitis
-presentation:
-typically 20-40y; 60% male
-oral cavity pain, anterior-neck stiffness, sialorrhea, dysphagia
-external swelling limited by anterior layer of deep fascia
-anterior or posterior tongue displacement
-swollen, indurated, erythematous FOM
-woody induration in suprahyoid region
-trismus minimal
-aphonic, “hot potato voice”
-tachypnea and stridor
-complications:
-asphyxia: posterior displacement of tongue (common cause of death in Ludwig’s angina)
-extension through buccopharyngeal gap: point at which styloglossus muscle exits submandibular
space between middle and superior constrictor muscles
-may enter into lateral pharyngeal space
-tongue necrosis
-aspiration pneumonia
-lung abscess
-treatment:
-evaluation and possible stabilization of airway
-antibiotics:
-high-dose IV penicillin +/- metronidazole or clindamycin for anaerobes
-surgery:
-if failure to respond to antibiotics or rapid progression threatening airway
-intraoral drainage:
-when infection limited to sublingual compartment and is uncomplicated
-external drainage recommended for all other cases via horizontal submental incision
-may require tracheotomy to secure airway
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Lateral Pharyngeal (Pharyngomaxillary, Parapharyngeal) Space
-etiologies:
-penetrating trauma
-extension of infection from another area:
-laterally from peritonsillar abscess (separation by superior constrictor muscle)
-posteriorly from submandibular space infection
-from masticator space (most common source of extension)
-presentation:
-anterior (prestyloid) compartment: “symptomatic”
-pain, trismus, dysphagia
-systemic signs
-typically antecedent pharyngitis or tonsillitis (~10days)
-classically: trismus, medial bulging of pharyngeal wall, swelling at angle of mandible,
systemic toxicity
-posterior (poststyloid) compartment: “asymptomatic”
-systemic signs
-difficult to see on examination
-vascular complications:
-involve carotid sheath
-suppurative IJ vein thrombosis (most common) - Lemierre Syndrome
-erosion of carotid artery:
-20-40% mortality rate
-internal > external > common
-signs of impending bleed:
-shock, prolonged course, Horner’s syndrome, hemorrhaging,
hematoma, neuropathies of CN IX-XII, persistent peritonsillar
swelling, bleeding from EAC
-treatment:
-control airway, antibiotics, surgical drainage
-airway easier to control than with submandibular space infections
-empiric Abx choice:
-penicillin and metronidazole or clidamycin (anaerobes found more frequently)
-surgery:
-discouraged in the initial cellulitic phase
-intraoral drainage avoided as carotid sheath difficult to control
-submaxillary (Batson) approach (if no vascular complications)
-anterior sternocleidomastoid (Mosher) approach if vascular complications suspected
Retropharyngeal Space
-etiologies:
-nose, adenoids, nasopharynx and paranasal sinus infections that drain to retropharyngeal nodes
-retropharyngeal lymphatic chains usually involute by age 5; infections therefore due to
suppurative lymphadenitis rare after this age
-if present in adults, then tends to be more aggressive than in children
-penetratring or blunt trauma
-instrumentation
-intubation
-passage of NG tube
-extension from other spaces
-presentation:
-difficult, especially in children
-trismus uncommon
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-“hot potato voice” if swelling in supraglottic region
-mass may be seen on posterior pharyngeal wall if below the palate
-bulging of posterior wall to one side (d/t midline raphe in retropharyngeal space)
-significant respiratory symptoms unusual unless involvement of mediastinum
-anterior mediastinum via pretracheal space; posterior mediastinum accessed to level of
tracheal bifurcation through retropharyngeal space
-pyopneumothorax, mediastinitis (50% mortality), purulent pericarditis, bronchial erosion
-radiology:
-lateral x-ray:
-reversal of normal cervical contour
-air in prevertebral soft tissues
-tuberculous erosion of cervical vertebra
-fluid collection in retropharyngeal space
-treatment:
-ensure secure airway; tracheotomy rarely needed
-transoral drainage and IV antibiotics will resolve most uncomplicated infections
-external approach if lateral space involved
Prevertebral Space Infection

-etiology:
-classically attributed to TB involving a vertebral body (Pott’s abscess)
-trauma, surgery, anterior extension of osteomyelitis, posterior extension from retropharyngeal
space infection
-presentation:
-non-specific
-usually minimal complaints
-complications:
-extension into danger or retropharyngeal space
-destruction of vertebral bodies subluxation or epidural compression
-treatment:
-coverage for Staph. aureus
-surgical drainage:
-C-1 to C-3: transoral approach
-external approach: incision anterior to SCM muscle or incision posterior to SCM muscle
COMPLICATIONS OF DEEP NECK INFECTIONS
-infectious complications:
-carotid artery erosion and haemorrhage
-internal jugular thrombosis
-Lemierre syndrome: caused by anaerobe Fusobacterium necrophorum
-spiking fevers
-tenderness of SCM
-neck stiffness
-metastatic abscess to lungs
-tx: anticoagulation, ligation or excision of vein for persistent embolization and
sepsis
-cavernous sinus thrombosis - via retrograde thrombophlebitis
-neurologic deficits:
-Horner’s syndrome
-cranial nerves IX-XII
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-osteomyelitis of the mandible
-osteomyelitis of the spine
-mediastinitis
-requires immediate surgery: cervical drainage and thoracotomy and drainage
-pulmonary edema
-pericarditis
-aspiration (spontaneous rupture)
-sepsis
-surgical complications
-damage to neurovascular structures
-wound infections
-septicaemia
-scarring
-aspiration (rupture from instrumentation)
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Review of Anatomy: The Neck Page 1 of 6
Neck
A. Skeleton
 primarily composed of vertebral column

 anteriorly, hyoid bone, and laryngeal and tracheal cartilages support
aerodigestive spaces
B. Muscles
 anteriorly, strap muscles connect respiratory skeleton and sternum

 muscular attachments from hyoid to tongue, mandible, and styloid
 digastric muscle passes forward from mastoid, attaches to hyoid, then
ascends to anterior mandible
 sternocleidomastoid (SCM) divides neck into anterior and posterior triangles
 posterior triangle is largely muscular
 anterior triangle which contains most of vital structures, can be divided into
smaller triangles by muscles
 anterior and posterior bellies of digastric form submandibular triangle
 submental triangle is in midline, between anterior bellies
 vascular or carotid triangle is inferior to digastric and hyoid
 omohyoid is a small muscle, running at roughly 90 degrees to SCM, from
hyoid to scapula.
C. Nerves
 Cranial Nerves
 Facial (VII )
 marginal mandibular branch dips down into neck in fascia
overlying submandibular gland
 also innervates platysma, stylohyoid and posterior belly of
digastric.
 Vagus (X)
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 exits jugular foramen and travels inferiorly in carotid sheath

 carries parasympathetic fibers of thoracic cavity and much of
GI tract, as well as laryngeal and pharyngeal sensory and
motor branches
 Spinal Accessory Nerve (XI)
 supplies trapezius and sternocleidomastoid musclesexits
jugular foramen, then runs posteriorly.
 Hypoglossal Nerve (XII)
 supplies muscles of tongue
 exits skull through hypoglossal canal, runs downward in carotid
sheath, then curves forward superficially to carotid at level of
occipital artery to reach tongue.
 Cervical Nerves
 Cervical plexus - anterior roots of C1- 4
 Ansa cervicalis - to strap muscles (some travel with XII)
 Branches to phrenic nerve
 Sensory
 Phrenic nerve - C3- 5
 Brachial Plexus - C5- T1
 Posterior rami - to posterior muscles and skin
 Cervical sympathetic chain - travels in carotid sheath
D. Major Vascular Structures
 Carotid Artery - bifurcates into:

 Internal (intracranial) - no branches in neck
 External (extracranial) - branches:
 Superior thyroid
 Ascending pharyngeal
 Lingual
 Facial
 Occipital
 Post- auricular
 Superficial temporal
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 Internal maxillary
 Thyrocervical trunk
 Suprascapular
 Transverse cervical
 Inferior thyroid
 Vertebral artery
 Internal jugular vein (within carotid sheath)
 External jugular vein
E. Visceral Column - pharynx, larynx, trachea, and esophagus.
F. Thyroid Gland
 Developmentally derived from pharyngeal floor

 Located anterior and lateral to trachea
 Closely related to recurrent laryngeal nerve and parathyroid glands
 Blood supply
 Arterial
 Superior thyroid artery (branch of external carotid)
 Inferior thyroid artery (branch of thyrocervical trunk)
 Thyroid "ima" artery (variable)
 Venous
 Superior thyroid vein
 Middle thyroid vein
 Inferior thyroid vein
G. Parathyroid Glands
 Four glands: two on each side

 Derived from branchial pouches III and IV:Ç
 superior parathyroid glands from pouch IVÇ
 inferior parathyroid gland from pouch III
 Glands usually related to posterior surface of thyroid gland, but may be
found as inferior as mediastinum
H. Anatomic triangles (superimposed on superficial neck anatomy):
402
 A. Anterior triangle
 bordered by anterior border of SCM, midline of neck, and mandible

 muscular triangle
 formed by midline, superior belly of omohyoid, and SCM
 carotid triangle
 formed by superior belly of omohyoid, SCM, and posterior belly
of digastric
 submental triangle
 formed by anterior belly of digastric, hyoid, and midline
 submandibular triangle
 formed by mandible, posterior belly of digastric, and anterior
belly of digastric
 B. Posterior triangle
 bordered by posterior border of SCM, trapezius, and clavicle

 supraclavicular triangle
 formed by inferior belly of omohyoid, clavicle, and SCM
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 occipital triangle-
 formed by inferior belly of omohyoid, trapezius, and SCM
I. Lymphatic drainage:
 major head and neck lymph node groups

 divided into six levels within defined anatomic triangles
 I- Submental and submandibular nodes

 II- Upper jugulodigastric group
 III- Middle jugular nodes draining naso- and oropharynx, oral cavity,
hypopharynx, larynx.
 IV- Inferior jugular nodes draining hypopharynx, subglottic larynx, thyroid,
and esophagus.
 V- Posterior triangle group
 VI- Anterior compartment group
Individual Lymph Nodes in Head and Neck:
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Review of Anatomy: Salivary Glands Page 1 of 2
Salivary Glands
A. Parotid Gland
 Located on side of face, anterior to mastoid tip and external auditory canal,
inferior to zygomatic arch, and superior to lower border of angle of
mandible. Anteriorly, it overlaps masseter muscle.
 Stenson's duct enters oral cavity through buccal mucosa opposite upper
second molar.
 Parasympathetic secretory afferents to parotid leave inferior salivary
nucleus with glossopharyngeal nerve and travel via Jacobson's plexus in
middle ear to synapse in otic ganglion. Post- synaptic fibers are distributed
to parotid by auriculotemporal nerve.
 Facial nerve passes through this gland.
B. Submandibular Gland
 Beneath floor of mouth, inferior to mylohyoid muscles and superior to

digastric muscle.
 Marginal mandibular branch of facial nerve travels in fascia on lateral
surface of this gland.
 Parasympathetic secretory afferents to submandibular gland arise from
superior salivatory nucleus, and leave brainstem in facial nerve. They exit
facial nerve at geniculate ganglion and travel via chorda tympani to lingual
nerve. Fibers synapse in submandibular ganglion, and postsynaptic fibers
then enter gland.
 lingual and hypoglossal nerves lie deep to this gland.
 Wharton's duct enters floor of mouth near lingual frenula.
C. Sublingual Glands
 located below mucous membrane of floor of mouth, adjacent to mandible

and mylohyoid muscle. Ten to twelve small caliber ducts drain gland, some
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Review of Anatomy: Salivary Glands Page 2 of 2
emptying into submandibular duct, and others draining directly into floor of
mouth.
D. Minor Salivary Glands
 small collections of salivary gland tissues are scattered throughout oral

mucosa, and can also be seen in pharynx, supraglottis, nose and sinuses.
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OTOLARYNGOLOGIC MANIFESTATIONS OF AIDS
(ENT Secrets)
Percentage of seropositive pts that will develop AIDS in 10 years: 50%
Most common index disease for diagnosis of AIDS:

-pneumocystis carinii pneumonia
CD4 count:
-represents absolute helper T-lymphocytes
-1000 cells/mm3: normal
-<200 cells/mm3: higher incidence of progression to AIDS; many prophylactic regimens initiated
Most common viral opportunistic pathogen seen with HIV infection:

-CMV: chorioretinitis, pneumonia, esophagitis, colitis, encephalitis, hepatitis
Most common bacterial pathogen causing cutaneous infections in HIV pts:

Kaposi’s sarcoma:
-most common malignant manifestation of AIDS
Most common otologic condition seen in HIV-infected pts:

-serous and acute otitis media
Most common middle ear pathogen in HIV-infected pt with otitis media:

-S. pneumoniae
-however OM d/t Staphylococcus sand Pseudomonas is seen with greater frequency than in normal
population
Indications to perform sinus lavage in HIV pt with sinusitis:

-failure to respond to initial medical therapy
-complication of sinusitis
-severe systemic toxicity from sinusitis
Most common oral manifestation of AIDS:

-oral candidiasis
Oral cavity lesion seen almost exclusively in HIV pts:

-hairy leukoplakia: reliable prognostic indicator of AIDS
Parotid enlargement:
-lymphoepithelial cysts: exhibit reactive lymphocytes which infiltrate parotid tissue
-management options (controversial):
-parotidectomy, needle aspiration, intralesional tetracycline sclerosis, low-dose radiation
-other: Kaposi’s sarcoma, NHL
Second most common AIDS-associated malignancy:

-non-Hodgkin’s lymphoma
-involves extranodal sites in 89% of cases and CNS in 42%
-most are high grade with poor prognosis
F.Ling - ENT Manifestations of AIDS (1)
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Dr. F. Ling's

Guidelines for Selection of Appropriate Bronchoscope and
Esophagoscope by Age*
Age Bronchoscope Size Bronchoscope Outer Esophagoscope Size

(Storz) Diameter (mm)
Premature
2.5 3.7 4
infant/neonate
Term newborn-3 mo 3 5.8 4-5
3-18 mo 3.5 5.7 5-6
1-3 yr 3.7 6.3 6
2-6 yr 4 6.7 6-7
5-10 yr 5 7.8 7
10-16 yr 6 8.2 8
* from Bailey's - Ch 74: Stridor, Aspiration and Cough
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UPPER DIGESTIVE TRACT ANATOMY AND PHYSIOLOGY
VALVE FUNCTION FOR DEGLUTITION
-series of valves are the first major component of deglutition

-six valves:
(1) lips
(2) tongue
(3) velum to back of tongue
(4) velopharynx
(5) larynx
(6) upper esophageal sphincter
-lips:
-provides a seal for generation of pressure in oral cavity
-reduces loss of food or saliva
-tongue:
-under volitional cortical control
-responsible for movement of food during chewing and oral preparation
-pharyngeal swallow:
-peripheral afferent input to cortex and brainstem swallowing centers (nucleus solitarius
and nucleus ambiguus)
-motor program output:
-base of tongue moves backward to contact inward moving posterior and lateral
pharyngeal walls
-soft palate contact to back of tongue:
-holds bolus before beginning oral stage of swallow
-soft palate actively pulled down by palatoglossus muscle to contact back of tongue
-prevents premature loss of food or liquid into pharynx and ensure breathing during chewing
-velopharyngeal port:
-closes during pharyngeal phase to prevent food or liquid into nasal cavity
-accomplished through:
-velar elevation (levator muscle) and retraction (palatopharyngeal muscle)
-anterior movement of posterior pharyngeal wall (superior pharyngeal constrictor -
Passavant pad)
-mesial movement of lateral pharyngeal walls (superior constrictor)
-larynx:
-true vocal cords close false vocal folds anterior tilting of arytenoid cartilage to contact base of
epiglottis epiglottis folds over top of airway
-during pharyngeal swallow, hyoid and larynx elevate and move forward epiglottis folded to
horizontal position
-cricopharyngeal valve:
-prevents air entry into esophagus during respiration
-musculoskeletal sphincter: cricopharyngeus muscle and cricoid cartilage
-UES opened by anterior movement of hyolaryngeal complex
PRESSURE GENERATION
-second major component of deglutition is generation of pressure on bolus to drive it from mouth, through
pharynx
-propulsion of food bolus by tongue and pharyngeal pressure generators
F.Ling - Upper Digestive Tract (1)
410
COORDINATION OF OROPHARYNGEAL SWALLOW EVENTS
-oral preparation:
-manipulation/mastication of food bolus cohesive bolus
-oral phase:
-tongue elevates bolus against palate, rolling and squeezing it posteriorly toward oropharynx
-pharyngeal phase:
-CN IX afferents stimulated medullary swallow center activated
-if bolus passes into valleculae and pharyngeal swallow has not been elicited delayed
pharyngeal swallow risk of aspiration
1. Velopharyngeal closure:
-levator veli palatini lifts soft palate
-palatopharyngeous tightens and raises pharynx and narrows oropharyngeal inlet
-superior pharyngeal constrictor (Passavant’s pad) contracts to meet soft palate and
posterior pharyngeal walls
2. Base of tongue propels bolus past vallecula
3. Laryngeal elevation and closure
-cessation of respiration
-larynx elevates ~2cm
-three sphincter for laryngeal closure:
-laryngeal inlet: epiglottis, aryepiglottic folds, arytenoids
-false vocal fold
-true vocal fold (most effective)
4. Pharynx shortens
-pharynx shortens by ~2cm
-pharyngeal constrictors push bolus while epiglottis directs food to piriform sinus
posterior pharyngeal wall cricopharyngeal sphincter
5. Cricopharyngeal sphincter opens
-food bolus enters cervical esophagus
-esophageal phase:
-cricopharyngeal valve opens
EFFECTS OF BOLUS CHARACTERISTICS ON OROPHARYNGEAL SWALLOW

-airway closure duration and cricopharyngeal opening duration increase systematically as bolus volume
increases and as bolus viscosity increases
-temporal relationship of oral and pharyngeal stages of swallow also changes systematically with bolus
volume
EFFECTS OF VOLUNTARY CONTROL

-voluntary control over many components of pharyngeal swallow:
-closure of airway at vocal folds or at entrance to airway
-duration of laryngeal elevation prolongs duration of cricopharyngeal opening (Mendelsohn
maneuver)
-muscle effort used during oral and pharyngeal phases (effortful swallow)
411
EFFECTS OF POSTURE
-chin tucked: anterior wall of pharynx is pushed posteriorly and airway entrance is narrowed
-head rotated: one side of pharynx is closed off from passage of bolus
-lifting chin: decreases oral transit time by using gravity to empty food from mouth
EFFECTS OF DEVELOPMENT AND AGING

-in adults > 60, there is a slight increase in time required to trigger pharyngeal phase
-slight prolongation in oral transit time
-increased frequency of penetration in older individuals
-entry of food or liquid into airway entrance during swallow with complete clearance of material
from the airway before the swallow is complete
RESPIRATORY-SWALLOW COORDINATION
-most frequent normal coordination involves interrupting exhalatory phase of respiration with the swallow
and briefly returning to exhalation after the swallow
-thought to increase safety exhalatory airflow may assist in clearing any residual food from
around the airway entrance
-older normal individuals and dysphagic patients swallow more often by interrupting the
inhalatory phase of the respiratory cycle less safe because of risk of aspiration
412
UPPER AIRWAY ANATOMY AND FUNCTION
F.Ling - Upper Airway (1)
413
Mucosal Cover of Vocal Fold
-squamous epithelium
-lamina propria:
-superficial (Reinke’s space - lowest concentration of
both elastic and collagneous fibers)
-intermediate (elastic fibers)
-deep (stiff - high concentration of collagen fibers)
-vocalis muscle (medial thyroarytenoid muscle)
414
RESPIRATORY PHYSIOLOGY
-functions:
-sphincter
-cough
-ejects mucous and foreign matter
-helps maintain patency of pulmonary alveoli
-three phases: inspiratory, compressive and expulsive (outflow ~ 6-10 L/s)
-valsalva manoeuvre
-regulation of airflow
-produces sudden alterations in resistance to airflow
-respiratory rate primarily controlled by varying rate of exhalation
-sensory input to respiratory control
-sensory organ that exert influences on breathing and cardiovascular function
-three types of receptors:
-negative pressure receptors
-maintains upper airway patency
-mediated by superior laryngeal nerve
-airflow (cold) receptors
-modulate central respiratory drive: stimulation can RR or cause
apnea
-“drive” receptors
-proprioceptors that respond to respiratory motion of larynx
-laryngospasm:
-forceful and prolonged closure of larynx
-can occur with URTI - sometimes a decreased threshold can persist for many months after
infection
CIRCULATORY REFLEXES
-stimulation of larynx can produce changes in heart rate and blood pressure
-OSA increased negative pressure can induce cardiac arrhythmia
-hypertension
-bradycardia hypotension
-pathways not clearly understood
-afferent limb: superior laryngeal nerve
SPEECH
-consists of three component processes:
-phonation: -vibration of vocal folds
-resonance: -induction of vibration of rest of vocal tract to modulate and amplify laryngeal
output
-articulation: -shaping of voice into words
Phonation
-five conditions required:
-appropriated vocal fold approximation
-adequate expiratory force
-sufficient vibratory capacity of vocal folds
-favourable vocal fold contour
-volitional control of vocal fold length and tension
415
-vocal cycle:
-vocal folds approximated exhalation rise in subglottic pressure
-separation of vocal folds rapid decrease in subglottic pressure
-vocal folds return to midline (d/t pressure, elastic forces in vocal fold, and Bernoulli effect)
-pressure builds and cycle is repeated
-forms the mucosal wave
-volume is influenced by the expiratory effort/pressure
-frequency is influenced by vocal fold length and tension
-ossification of thyroid cartilage with increasing age contributes to elevation of pitch
Resonance
-gives voice characteristic acoustic pattern
-amplifies voice
-controlled by altering shape and volume of pharynx, raising or lowering larynx, moving tongue or jaw
position, or by varying amount of sound transmission through nasopharynx and nose
Articulation
-controlled by lips, tongue, palate, and pharynx
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UPPER DIGESTIVE TRACT EVALUATION AND IMAGING
CLINICAL EXAMINATION
-mental status, body posture and voice quality noted

-drooling: labial incompetence, tongue weakness
-slurred speech: possible tongue palsy
-inspect and palpate tongue: detection of hypoglossal paresis or paralysis
-laryngeal examination: r/o GERD
-hypopharyngeal examination:
-thick mucoid secretions indicate standing accumulations, often d/t paralysis or adynamic muscle
function
-methylene blue test: staining of laryngeal vestibule, vocal folds and trachea without inducing cough
response suggests that dysfunction may be of long standing
-hypertonic cricopharyngeus may be observed in response to acid reflux
-secretions that fail to clear after swallow effort:
-thickened and mucoid: attributable to neurologic disorder
-frothy or foamy: attributable to structural disorder, stenosis or pouch
Differential Diagnosis of Dysphagia and Aspiration
Congenital Tumour Systemic

-TEF -CNS tumour -VCP
-dysphagia lusoria -esophageal tumours -GI disorders
-congenital esophageal webs -extrinsic compression of -Zenker’s
-cleft palate esophagus -GERD
-laryngeal cleft -achalasia
Endocrine -esophageal diverticulum
Infectious/Iatrogenic -hypothyroidism -cricopharyngeal spasm
-laryngitis -Plummer-Vinson
-pharyngitis Neurologic -myopathies
-esophagitis -altered mental status -muscular dystrophy
-Chagas disease -degenerative diseases -metabolic myopathies
-tracheotomy (Parkinson’s, MS, ALS) -polymyositis
-post-surgical head and neck -motor neuron disease -connective tissue disorders
resection -stroke -progressive systemic
-encephalopathies sclerosis
Toxins/Trauma -Guillain-Barre -globus hystericus
-caustic ingestion -myasthenia gravis
-FB ingestion -bulbar and pseudobulbar
-Mallory-Weiss syndrome palsy
-dementia
COMMON DISEASES
-reflux esophagitis - common cause of dysphagia

-may result in delayed transit of food
-symptoms of delayed passage of food through throat may actually be holdup of material in lower
esophagus
-hypertrophy of cricopharygneal muscle
F.Ling - Upper Digestive Tract Evaluation (1)
417
-causes solid food dysphagia
-may form Zenker’s diverticulum
-esophagitis:
-opportunistic infection: (eg. Candida, herpes, CMV)
-chemical injury
-strictures:
-chemical or traumatic injury
-CVA:
-common cause of dysphagia
-may need tube alimentation
-cancer:
-contrast examination documents location and size of lesion and presence of fistulae
-CT typically done to assess deep tissue invasion and to look for mediastinal adenopathy
INVESTIGATIONS
Modified Barium Swallow (MBS)

-radiographic videofluoroscopic study that visualizes oral and pharyngeal phases of swallowing
-typically reviewed with a swallowing therapist
-utilizes varying bolus amounts and consistencies
-determines oral and pharyngeal motility, laryngotracheal elevation, laryngeal penetration or aspiration, and
safety of oral feeding
MANAGEMENT
Medical Management
-address underlying disorder if possible
-consider alternative temporary route of nutrition
Swallowing Rehabilitation
-change food consistencies (pureed diet easier to tolerate initially)
-posturing techniques:
-chin tuck, head turn to poorer functioning side, palatal prosthesis, muscle strengthening exercises
-supraglottic swallow:
-patient voluntarily closes airway by holding breath before swallow
-voluntary cough after swallow
-follow with additional swallow for residual bolus in pharynx or piriform
-Mendelsohn manoeuver:
-voluntarily elevates and anteriorly displaces larynx to prolong upper esophageal sphincter
opening
F.Ling - Upper Digestive Tract Evaluation (2)
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AIRWAY EVALUATION AND IMAGING
Congenital Infectious Trauma Allergy/Autoim Neoplastic Neurologic

Anomalies mune
Above larynx -micrognathia -retropharyngeal -facial fracture -allergic rhinitis -JNA -altered mental
-macroglossia abscess -retropharyngeal -WG status
-choanal atresia haematoma
Supraglottic -laryngomalacia -epiglottitis -intubation -sarcoidosis -SCC

trauma
Glottic -web -tuberculous -laryngeal -hereditary -recurrent -vocal cord

-laryngeal laryngitis fracture angioedema respiratory paralysis
atresia papillomatosis
Subglottic -vascular ring -croup -subglottic -asthma -subglottic -paralysis of

-TEF stenosis hemangioma respiratory
muscles
PHYSIOLOGIC TESTING
Pulmonary Function Tests:

-flow-volume loops:
-variable extrathoracic obstruction
-lesion above thoracic inlet that preferentially obstructs airway during inspiration
-flattening of inspiratory curve
-eg. laryngomalacia
-variable intrathoracic obstruction
-lesion below thoracic inlet that preferentially obstructs airway during expiration
-flattening of expiratory curve
-eg. tracheomalacia, tracheal FB, intrinsic or extrinsic masses
-fixed obstruction
-limitation of flow rates during both inspiration and expiration
-eg. malignant neoplasms, sarcoidosis, tracheal stenosis
IMAGING
Plain-Film Radiography
-lateral films taken both inspiration and expiration
-“vallecular sign” - SENS and SPEC for epiglottitis
-to detect infection, foreign bodies etc..
Fluoroscopy
-dynamic study
-ball-valve effects of a bronchial foreign body can be demonstrated
-laryngomalacia can be revealed
-motion defects of each hemidiaphragm
F.Ling - Airway Evaluation and Imaging (1)
419
Contrast Radiography
-barium swallow historically used to help localize extrinsic or intrinsic mass
-now used to demonstrate GERD, aspiration and TEF
Ultrasonography
-evaluation of solid or cystic nature of extrinsic cervical airway masses
-eg. thyroid masses, TGDC, branchial cysts, hemangioma, lymphangioma, laryngocele
Arteriography
-for JNA, glomus tumours
-+/- embolization
CT
-superior bony definition
-disadvantages:
-greater cost, higher radiation exposure, limitation to axial scans
MRI
-does not rely on ionizing radiation
-can demonstrate anatomic site in multiple planes
-excellent tissue differentiation
ENDOSCOPIC ASSESSMENT
Diagnostic Endoscopy
-flexible scopes offer greater diagnostic capabilities; can be used to visualize subsegmental bronchi and
upper lobe bronchi
-rigid scopes superior for biopsies, obtaining cultures, retrieval of foreign bodies and surgical intervention
Rigid Laryngoscopy
-Jackson laryngoscope: can be used as an aid in intubation
-anterior commissure scope
-operating laryngoscopes: Jako or Dedo
COMPLICATIONS
-damage to teeth
-perforation
-pneumothorax
-from perforation by bronchoscope
-from jet ventilation at high pressures
-laryngospasm negative pressure pulmonary edema
F.Ling - Airway Evaluation and Imaging (2)
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ESOPHAGEAL DISORDERS
ESOPHAGEAL FORM AND FUNCTION
Embryology
-epithelial proliferation obliterates the lumen
-recanalization occurs by 8th week (abnormal recanalization results in congenital stenosis)
Anatomy
-three regions of natural constriction:
-cricopharyngeus: narrowest point in entire GI tract (15 cm from incisors)
-point at which aorta and left mainstem bronchus cross anteriorly (20-25cm from incisors)
-lower esophageal sphincter (40-45cm from incisors)
-esophageal layers:
-outer muscular layer
-longitudinal muscle
-no serosa layer, therefore minimal barrier to infection and tumour infiltration
-middle submucosa
-inner circular muscle
-inner mucosal layer: epithelium, lamina propria, muscularis mucosa
-upper 1/3: striated muscle; lower 2/3: smooth muscle
-blood supply:
-segmented from inferior thyroid artery (upper 1/3)
-thoracic aorta (middle 1/3)
-left gastric and inferior phrenic arteries (lower 1/3)
-histology:
-stratified squamous epithelium except distal 1-3 cm which is columnar epithelium
-innervation:
-mixed somatic innervation from CN IX and CN X
-left vagus nerve passes anteriorly and right vagus nerve passes posteriorly to form
esophageal plexus
-Auerbach’s plexus: myenteric plexus between muscle layers, parasympathetic
-Meissner’s plexus: submucosal plexus
Physiology
-primary peristalsis:
-initial peristaltic wave as food is passed into esophagus
-secondary peristalsis:
-contractions that clears any remaining food and is initiated by esophageal distention or by GER
-tertiary contractions:
-non-peristaltic and occur spontaneously or after swallowing
-may propel bolus in a retrograde direction to proximal esophagus
Upper Esophageal Sphincter

-maintained in a constant state of contraction
-prevented air influx during normal respiratory cycle
-UES pressure increases significantly if body of esophagus is exposed to acid or if volume changes occur
Lower Esophageal Sphincter

-LES is a zone of increased pressure that is 2-4 cm long
-incompetency of LES reflux; failure to relax dysphagia
F.Ling - Esophageal Disorders (1)
421
-up to 80% with symptomatic reflux have hiatal hernia
-normal tone: 10-40 mmHg (achalasia: > 40; scleroderma < 10)
-increase LES pressure
-alpha-adrenergic neurotransmitters
-beta-adrenergic blockers
-protein meals
-acid
-gastrin
-vasopressin
-decrease LES pressure
-beta-adrenergic stimulation
-alpha-adrenergic blockers
-fatty meals, chocolate, ethanol, smoking, caffeine
-secretin, nitrates, calcium channel blockers, glucagon
EVALUATION AND DIAGNOSIS
Symptoms
-dysphagia and heartburn most common
-odynophagia: inflammatory changes of esophageal mucosa
-vocal cord paralysis: compression or invasion of recurrent laryngeal nerves
-obstructive esophageal lesions may manifest as pooling of secretions in hypopharynx
Radiologic Studies
-barium swallow; videofluoroscopy; CT/MRI
Esophageal Manometry
-for esophageal motility disorders
pH Monitoring
-24h pH monitoring
-electrode placed exactly 5 cm above LES
-reflux = lowering the pH to 4.1 at a level 5 cm above LES
-normal total reflux time is less than 1 hour during a 24 hour period
Endoscopic Examination
-rigid:
-better visualization of pharynx and upper sphincter
-larger deeper biopsies
-easier removal of foreign bodies
-direct visualization during dilation permitted
-ability to use endoscopic laser techniques
-flexible:
-general anesthetic not needed
-allows concurrent examination of stomach, duodenum
-closer examination of mucosal lesions
-endoscopic photography and videotaping permitted
-more flexibility in difficult anatomic conditions
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GASTROESOPHAGEAL REFLUX DISEASE
Evaluation
-GERD common: 1/3 with occasional sxs; 10% with daily sxs
-most common ENT manifestations:
-hoarseness (71%)
-cough (51%)
-globus pharyngeus (47%)
-throat clearing (42%)
-difficulty swallowing (35%)
-heartburn, dysphagia
-slowly progressive dysphagia for solids suggests development of peptic stricture
-dysphagia for both liquids and solids suggests GERD-related motility disorder
-smoking and high-fat meals delay gastric emptying and increase potential for reflux
-diagnostic tests should be limited to patients with atypical or recurrent symptoms (indications)
-uncertain diagnosis
-recurrent symptoms
-inadequate response to therapy
-atypical symptoms (chest pain, hoarseness, cough, asthma)
-symptoms associated with complications (GI hemorrhage, unexplained weight loss, dysphagia,
odynophagia)
Treatment
-lifestyle modifications:
-avoid lying down soon after meals
-HOB elevated
-weight reduction; avoidance of fatty foods; smaller meals
-decrease intake of chocolate, peppermint, cigarettes, caffeine (decrease LES pressure)
-avoid NSAIDs which may induce mucosal injury
-medical treatment: H2 antagonists and PPI
-PPI: 95% healing of esophagitis; H2 antagonists: 35-65%
-both increased and divided doses of PPIs commonly used to treat extraesophageal manifestations
of GERD
-surgery:
-Nissen fundoplication
Complications of Reflux
-esophageal stricture
-esophageal ulceration
-aspiration chronic cough, bronchitis, aspiration pneumonia, bronchiectasis, nocturnal dyspnea, asthma
-Barrett’s esophagus adenocarcinoma in 10%
-hoarseness, frequent throat clearing, cough
-early: posterior laryngeal edema/erythema
-late: ulceration and hyperkeratosis in interarytenoid area
-contact ulcers, Reinke edema, and laryngeal granulomas all associated with GERD
423
ESOPHAGEAL MOTILITY DISORDERS
Achalasia
-neuromuscular disorder: degeneration of ganglion cells of Auerbach plexus
-features:
-peristalsis
-esophageal dilatation
-failure of LES to relax
-increased LES pressure (> 40 mmHg)
-progressive intermittent dysphagia with epigastric pain
-men > women; 30-70 years of age
-failure of LES to relax retention esophagitis
-“bird’s beak” sign on barium swallow
-esophagoscopy to r/o masses and esophagitis
-treatment:
-encourage small meals, liberal use of liquids to wash down food
-decreasing LES pressure: calcium channel blockers and long-acting
nitrates (eg. isosorbide)
-dilatations of LES: 50% recurrence of symptoms; risk of perforation
-surgery:
-repeated failed dilatations
-Heller myotomy
Diffuse Esophageal Spasm

-nonperistaltic contraction in esophageal smooth muscle
-dysphagia and pain - intermittent and vary in severity
-solids = liquids
-exacerbation by emotional stress common
-barium swallow: corkscrew-type pattern
-diverticula formation possible
-manometry: repetitive, synchronous contractions of relatively high amplitude
-treatment:
-nitroglycerin, calcium channel blockers, diazepam
-surgery for those with severe, recurrent chest pain, disabling dysphagia
or secondary pulsion diverticula
-transthoracic myotomy is procedure of choice
Scleroderma (Progressive Systemic Sclerosis)

-generalized collagen vascular disease
-small vessel arteritis and collagen deposition in region of esophageal smooth muscle
-80% eventually develop esophageal symptoms
-progressive dysphagia to solids
-atrophy of GI smooth muscle LES is attenuated GERD symptoms reflux esophagitis
-barium swallow: dilated esophagus with decreased motility; persistently patent GE junction
-no effective treatments; treat GERD
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CRICOPHARYNGEAL DYSFUNCTION
-three categories of incoordination problems:

-idiopathic
-neurologic: d/t stroke, cranial nerve palsy, parkinsonism or other neurologic disease
-reflux-induced
-symptoms:
-dysphagia localized to lower neck region
-intermittent symptoms of choking
-diagnosis:
-barium swallow:
-classic cricopharyngeal bar with transient
partial obstruction
-demonstrates lack of coordination between
pharyngeal contraction and cricopharyngeal
relaxation
-manometric pressure recordings preferred method of
diagnosis:
-high resting pressure of cricopharyngeus
-delay in sphincter relaxation
-incomplete relaxation of cricopharyngeus
-premature cricopharyngeal contraction
-treatment:
-cricopharyngeal myotomy:
-reserved for patients with severe or disabling dysphagia, aspiration and associated
pulmonary problems
-botox injection of cricopharyngeus muscle
-under investigation
-improvement of swallowing lasting 2-14 months
ESOPHAGEAL WEBS AND RINGS
-webs: thin membranes consisting of mucosa and submucosa

-rings: thicker - composed of mucosa, submucosa, and muscularis
-Plummer-Vinson syndrome:
-predominantly in Scandinavian women
-features:
-dysphagia, hiatal hernia, atrophic gastritis, achlorhydria
-cervical esophageal webs
-iron deficiency anemia (microcystic hypochromatic anemia)
-glossitis
-cheilosis, koilonychia, splenomegaly
-increased incidence of carcinoma in postcricoid and upper esophageal region
-treatment of webs: endoscopic rupture of web and iron replacement
-Schatzki’s Ring:
-occurs at squamocolumnar junction
-asymptomatic rings identified in 6%-14% of barium studies
-cause unclear
-asymptomatic: no treatment; severe: treated with dilatation
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DIVERTICULA
-true diverticula: all layers of esophageal wall represented

-pseudodiverticulum: consists only of mucosa and submucosa
-pulsion: associated with elevated intraluminal pressure
-traction: arise from extraluminal tugging by adjacent sites of inflammation and fibrosis
-hypopharyngeal areas of weakness:

-Killian’s triangle:
-superior to posterior
cricopharygneal muscle,
superior to cricothyroid muscles
-below raphae of inferior
constrictors
-Killian-Jamieson space:
-laterally, between
cricopharyngeal and esophagus
muscle
-Laimer-Haeckermann space:
-between cricopharyngeus
superiorly and circular fibers of
esophagus inferiorly
-Zenker diverticulum
-pharyngoesophageal pseudodiverticulum of the pulsion type
-herniation between inferior pharyngeal constrictor and cricopharyngeus muscle (Killian’s
Triangle)
-6th-9th decade; M:F = 3:1
-dysphagia, regurgitation of undigested foodstuffs
-diagnosis by barium swallow; pouch usually on the left (80-90%)
-treatment:
-observation for asymptomatic diverticula
-endoscopic management:
-Dohlman procedure: diathermy and a bivalved esophageal speculum
-one blade in esophagus and the other in the pouch, the common wall
was removed sequentially with diathermy instruments
-open approach:
-most popular
-options:
-cricopharyngeal myotomy alone sufficient for small pouches (< 2 cm)
-diverticulectomy with myotomy for larger pouches
-diverticulopexy
INFECTIOUS AND INFLAMMATORY CONDITIONS
-esophagitis
-most common cause = GERD
-immunocompromised patients:
-Candida albicans most common organism infecting the esophagus
-herpes esophagitis:
-cytologic examination demonstrates multinucleated cells containing intranuclear
426
inclusion bodies
-radiation esophagitis occurs rarely
-scarring and stenosis may occur from 6-18 months after radiation therapy
-drug-induced esophagitis:
-typically punctate ulcerations
-tetracycline, doxycycline, quinidine, potassium
-prevent by taking meds with sufficient fluid
-bullous dermatoses:
-pemphigoid, epidermolysis bullosa, toxic epidermal necrolysis, Stevens-Johnson syndrome
-pemphigoid:
-subepithelial clefting and linear pattern of direct immunoglobulin G
immunofluorescence at the basement membrane
-chronic blistering
-epidermolysis bullosa:
-hereditary skin disorder
-loss of cohesion between epidermis and dermis blister formation
BENIGN NEOPLASMS AND CYSTS
-relatively rare, occurring less frequently than malignant tumours

-leiomyoma most common benign tumour of the esophagus
-occurs in middle or lower third of esophagus
-require excision if symptomatic
-others:
-myomas, fibromas, lipomas, neurofibromas, granular cell tumours
-polyps
-papillomas, adenomas, hemangiomas
ESOPHAGEAL CARCINOMA
-~1% of all new cancers

-overall 3 year survival rate only 11% due to late presentation
-risks:
-elderly black males
-tobaccos and alcohol abuse
-regional (China, Iran, Russia)
-caustic burns
-radiation, petroleum, nitrates
-Plummer-Vinson disease
-achalasia, pernicious anemia, nutritional deficiencies, esophagitis
-ttylosis
-GERD
-types:
-squamous cell carcinoma:
-most common malignancy in the esophagus
-upper 1/3: 17%; middle third: 47%; lower third: 36%
-adenocarcinoma:
-less frequent than SCC, primarily in distal esophagus
-Barrett’s esophagus is primary recognized risk factor
-regular endoscopic surveillance recommended
427
-low grade lesions antireflux therapy
-high grade lesions resection of affected portion
-others:
-adenoid cystic carcinoma, mucoepidermoid carcinoma, small-cell carcinoma, sarcoma
-tumours limited to epithelium and lamina propria have not been associated with lymph node metastasis
-spread to regional lymph nodes seen in 50% of pts with infiltration of submucosa
-surgery remains treatment of choice
-tumours limited to epithelium and lamina propria: endoscopic resection, endoscopic laser
photocoagulation or thoracoscopic resection
-advanced disease: transthoracic esophagectomy with gastric pull-up or esophagogastrectomy
Perforation and Rupture

-causes: iatrogenic effects (most common 0.1-1.5%), diverticulitis, neoplasm, Boerhaave syndrome
-may lead to rapid development of mediastinitis and sepsis
-symptoms and signs:
-chest pain, dysphagia, odynophagia, SOB
-subcutaneous emphysema
-fever, tachypnea, tachycardia
-pneumomediastinum or pneumothorax
-Boerhaave syndrome:
-spontaneous rupture of esophagus
-precipitated by vigorous coughing, weight lifting, straining
-usually associated with a left-sided, transmural rupture of distal esophagus
-thoracotomy or transcervical exploration may be indicated for adequate surgical drainage
Hemorrhage
-causes: esophageal varices, neoplasm, esophagitis with erosion, Mallory-Weiss syndrome, endoscopic
surgery
-treat hypovolemia, conservative measures; if refractory endoscopic laser treatment, angiographic
embolization, surgery
Mediastinitis
-causes: perforation with leakage or abscess formation, tumour erosion
-treatment: IV Abx; exploration and drainage
Obstruction
-causes: tumour, foreign body, stricture, achalasia
-treatment: removal of FB, dilatation, surgery, esophageal replacement, gastrostomy
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TRACHEOTOMY AND INTUBATION
Indications for Tracheotomy

-bypass upper airway obstruction
-assist respiration over prolonged periods
-assist with clearance of lower respiratory tract secretions
-prevent aspiration of oral or gastric secretions
Techniques of Tracheotomy
Elective Tracheotomy
-in OR under controlled conditions
-Bjork flap:
-suturing an inferiorly based flap consisting of anterior portion of a single tracheal ring
-reduces incidence of accidental decannulation and eased reinsertion
-contraindicated in operations on children:
-can cause unacceptable rate of tracheal stenosis and persistent tracheocutaneous fistulae
Timely Tracheotomy
-must be performed in 5-10 minutes
-vertical incision that extends from cricoid cartilage to about 3.75 cm inferiorly
Emergency Tracheotomy
-anoxia causes death in about 4-5minutes; tracheotomy must be performed within 2-3 minutes
-better to perform elective tracheotomy under local anaesthesia
-best performed through vertical incision beginning at level of cricoid and extends inferiorly 1-1.5 inches
-avoids injury adjacent neck structures
Cricothyrotomy
-cricothyroid membrane near skin surface
F.Ling - Tracheotomy (1)
429
-risk of damage to subglottic larynx
-relatively contraindicated in children < 12 years, patients with infection in the larynx and pts with
laryngeal trauma
Maneuvers to Buy Time

-transcricothyroid puncture with 14-gauge catheter
-pressure driven oxygen required for ventilation
-risk of pneumothorax
-more useful in children where cricothyroidotomy is best avoided
Tracheotomy in the Pediatric Patient

-prolonged intubation generally preferred over tracheotomy in neonates up to 6 months (high risk of
subglottic stenosis)
-Vertical Incision:
-incision made in second and third tracheal rings
-excision of any anterior tracheal wall should be avoided
-Guide sutures:
-two sutures placed on either side of the vertical incision
-guides in case of accidental decannulation
-removed at first tracheotomy tube change 3-4 days after tracheotomy
-consider endoscopy every 3 months to evaluate for stenosis
Percutaneous Dilational Tracheotomy

-has never been safer or more effective than conventional tracheotomy
-advantages: shorter operating time, ease of performance ability to perform at bedside, lower expense
Complications of Tracheotomy
-Intraoperative:
-damage to great vessels (most common intraoperative complication)
-damage to tracheoesophageal common wall
-pneumothorax
-pneumomediastinum
-Early postoperative
-tracheotomy tube obstruction (most common early postop complication)
-tracheotomy tube displacement
-pulmonary edema
-infection
-respiratory arrest from loss of hypoxic drive (in pts with long standing obstruction)
-Late
-tracheal stenosis (most common late postop complication)
-granulation tissue
-trachea-innominate artery fistula
-60% of cases of fistula occur within 2 weeks of tracheotomy
-73% mortality
-mx: overinflate tracheotomy cuff
-insert ETT below level of bleeding while attempting to compress innominate
artery anteriorly against sternum
-cuff pressure kept less than 25 cmH2O - pressure at which submucosal capillaries are occluded
430
Complications of Percutaneous Dilational Tracheotomy
-misplacement of dilator in a paratracheal position
-haemorrhage
-damage to posterior tracheal wall
-death
ENDOTRACHEAL INTUBATION
Indications for Intubation

-assist ventilation
-relieve obstruction
-improve respiratory toilet
-prevent aspiration
Techniques
Intubation in Head Trauma

-issues:
-exacerbating cervical spinal trauma intubate with inline traction of cervical spine
-midfacial trauma possible fracture through cribriform plate or fovea ethmoidalis
contraindications to nasotracheal intubation
Difficult Intubation with Large-bore Laryngoscope

-allows operator to fix the larynx and expose the glottis
Use of Bronchoscope for Intubation

-rigid bronchoscope can secure the airway when most methods have failed
-can be forced into partially obstructed glottis
Complications of Intubation
-acute pulmonary edema
-caused by sudden loss of highly negative intrathoracic pressure during inspiration and positive
pressure during expiration
-rapid increase in systemic venous return
-most commonly occurs in recovery room after extubation
-mx: mechanical ventilation and diuretics
-improper tube placement
-long-term intubation
-Laryngeal Stenosis: occurs at narrowest part of airway:
-children: subglottis
-adults: glottis
-Tracheoesophageal Fistula:
-rare complication
-Recurrent laryngeal Nerve Injury:
-nerve can be pinched by an ETT
-Sinusitis: nasotracheal intubation
431
432
CONTROVERSIES IN UPPER AIRWAY OBSTRUCTION
EVALUATION OF UPPER AIRWAY OBSTRUCTION
Signs and Symptoms

-obstruction below thoracic inlet does not cause suprasternal retraction
-stridor:
-inspiratory: obstruction at larynx or above
-expiratory: distal obstruction
-biphasic: subglottic midtracheal obstruction
Causes of Airway Obstruction
Child Adult
Acute Chronic Acute Chronic
Inflammatory Supraglottic Inflammatory Tumour

-croup -choanal atresia -croup -congenital
-epiglottitis -stenosis -supraglottitis -posttraumatic
Foreign Body -mass, cyst -Ludwig angina -inflammatory (Wegener
Trauma -hypertrophied adenoids and tonsils Trauma granulomatosis, relapsing
Glottic Foreign body polychondritis, sarcoid)
-laryngomalacia idiopathic
-foreign body
-vocal cord paralysis
-papillomatosis
Subglottic
-stenosis, web
-mass
-foreign body
-haemangioma
Tracheal
-foreign body
-stenosis
-mass
-tracheomalacia
-vascular compression
MANAGEMENT OF AIRWAY OBSTRUCTION
Nonsurgical Management
-oxygen
-heliox - can improve ventilation temporarily until definitive control of airway can be obtained
-epinephrine aerosols to decrease soft tissue edema
-short duration
-can have a rebound effect
-steroids
-large doses of dexamethasone (1mg/kg)
Surgical Management
-direct neck trauma with progressive breathing difficulty
-intubation contraindicated because of possibility of laryngotracheal separation
-temporary tracheotomy if separation suspected
-postglottic stenosis: open repair
F.Ling - Upper Airway Obstruction (1)
433
-bilateral vocal cord paralysis: consider tracheotomy, arytenoidectomy
-laryngeal papilloma: CO2 laser therapy
-foreign body: rigid bronchoscopy
-indications for surgical exploration in laryngotracheal trauma

-upper airway obstruction
-haemorrhage
-evidence of cartilage exposure
-increasing subcutaneous emphysema
-palpable fracture of larynx
-internal derangement
-adenotonsillectomy:
-does not increase the likelihood of overwhelming infection
F.Ling - Upper Airway Obstruction (2)
434
MANAGEMENT OF INTRACTABLE ASPIRATION
PHYSIOLOGY OF SWALLOWING
Oral Preparatory Phase

-food placed in oral cavity, masticated and mixed with saliva
-voluntary control
Oral Phase
-tongue and bolus pressed against faucial arches and palate
triggers reflex-driven, central programmed pharyngeal swallow
-defects in pharyngeal sensation, central neurologic disease or postsurgical changes in tongue or
palate can cause inability to initiate a reflexive pharyngeal swallow
Pharyngeal Swallow
-cessation of respiration
-palate elevation and closure of nasopharyngeal isthmus
-glottic closure
-laryngeal elevation
-pharyngeal peristalsis
-cricopharyngeal relaxation
-dilation of pharyngoesophageal segment
Esophageal Phase
-involuntary peristalsis
ETIOLOGY OF ASPIRATION
-most common cause: neuromuscular dysfunction

-eg. MLS, MS, stroke, Parkinson’s disease
-eg. deficits of CN IX and X
-loss of central processing, loss of pharyngeal muscle strength, loss of pharyngeal sensation
-surgical procedures that remove, modify or denervate structures within oral cavity, oropharynx,
hypopharynx or larynx
Tracheostomy and aspiration

-presence of tracheostomy long been associated with aspiration
-for some patients, removal, plugging, or valving a tracheostomy tube can have a dramatic effect on
swallowing
-effects of tracheotomy tube:
-interferes with anterior displacement and elevation of larynx during swallowing
-FB that promotes crust formation and pooling of secretions
-compromises normal cough mechanisms (inability to produce adequate subglottic pressure)
-disrupts normal laryngeal reflexes, such as vocal cord adduction during swallowing
-cuff may compress esophagus, hindering bolus transport
-interferes with ciliary motion
-tracheotomy however facilitates pulmonary toilet
F.Ling - Intractable Aspiration (1)
435
Glottic Closure
-aspiration often associated with vocal cord paralysis or inadequate glottic closure
-other abnormalities often occur before a patient with aspiration due to incompetence of the glottis has
substantial morbidity
Sensory Loss
-sensory loss correlates with risk of aspiration pneumonia among patients who have had a stroke
EVALUATION OF A PATIENT EXPERIENCING ASPIRATION
Identification of aspiration
-aspiration pneumonia
-recurrent pneumonia of unknown causation
-“bronchorrhea” after tracheotomy
-coughing, choking with eating
-dysphagia and prolonged time for eating
-weight loss
Clinical Evaluation
-history and physical
-endoscopic laryngeal evaluation:
-hypopharynx and larynx examined for anatomic and physiologic abnormalities
-pharynx can be rapidly assessed during swallowing to ascertain aspiration risk and alternative
feeding strategies
-dye test (for patients with tracheostomy)
-modified barium swallow
-swallowing scintigraphy
Modified Barium Swallow Examination

-small amounts of barium-coated foods of varying consistency are administered
-swallow is videotaped
-aspiration identified and quantified
-definitions:
-aspiration: food materials penetrate laryngeal inlet and enter trachea
-penetration: food materials penetrate laryngeal inlet but do not enter trachea
THERAPEUTIC OPTIONS
Initial Interactions
-nonsurgical:
-NPO, NG feeds, mx of respiratory failure, control of GER
-risk of aspiration pneumonia not eliminated with nonoral feeding
-tracheostomy tube may facilitate pulmonary toilet
Valving of a Tracheostomy Tube

-Passey-Muir valve
-used if decannulation is impossible; may have dramatic beneficial effect for some pts and facilitates oral
feeding for a pt otherwise dependent on tracheostomy
436
Other Nonsurgical Options
-through speech pathologist
-dietary modifications
-thickened feeds reduce aspiration for pts with inappropriate delay in initiation of swallow
-compensation techniques
-supraglottic swallow:
-for residue on glottis
-patient voluntarily closes airway by holding breath before swallow
-cough and second swallow before next inspiration
-turning head to side of unilateral pharyngeal weakness compresses piriform sinus to prevent
accumulation of residue
-chin tuck: flexing neck compresses vallecula
-Mendelsohn manoeuver:
-voluntary elevation and anterior displacement of larynx to prolong upper esophageal
sphincter opening
Surgical Options
Adjunctive:
-G-tube
-cuffed tracheotomy tube
-reduce saliva production
-bilateral chorda tympani section
-ligation of submandibular or parotid duct
Procedures to Enhance Glottic Closure:

-vocal cord augmentation
-vocal cord medialization:
-thyroplasty
-rotation of arytenoid cartilage (arytenoid adduction)
-combination
-medialization valuable in the management of aspiration when patient has unilateral vocal cord paralysis
and neurologic function is otherwise intact
-severe neurologic impairment: bilateral medialization and tracheotomy
Cricopharyngeal Myotomy:
-reduce obstruction at pharyngoesophageal segment
-considered when radiographic evidence of restriction at cricopharyngeus muscle is found
-Laryngeal stenting:
-aspiration likely for a finite period and recovery is expected
-stent for 2-3 months
-Montgomery glottic closure procedure:

-vocal cords sutured together via laryngofissure
-will require tracheotomy
-Laryngeal Suspension:
-indicated for severe aspiration from supraglottic and pharyngeal dysfunction
-suspends larynx anteriorly by positioning thyroid cartilage under mandible
-may improve voicing and swallowing
437
-Tracheoesophageal Diversion (Lindemann Procedure) and Laryngotracheal Separation:
-Lindemann procedure:
-trachea divided and proximal end anastomosed to anterior esophagus
-distal end of trachea brought to skin as it is in total laryngectomy
-Laryngotracheal separation:
-proximal tracheal stump closed in a pouch: theoretically reversible procedure
-standard procedure in most institutions for mx of intractable aspiration unresponsive to more conservative
measure or adjunctive surgical procedures
-Total Laryngectomy:
-gold standard
-intractable aspiration after partial laryngectomy or total glossectomy
-indicated for life-threatening complications
-unacceptable to pts with neurologic disease: risk of pharyngeal closure higher in debilitated pts
CONCLUSIONS
-if function is not likely to return proceed immediately to laryngotracheal separation

-most cases, alternative strategies are attempted first then laryngotracheal separation
-decannulation or valving of tracheostomy tube can be valuable
-medialization thyroplasty can be valuable
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EVALUATION OF THE DYSPHONIC PATIENT
History
-character of dysphonia:
-onset and duration
-time course
-periodicity
-recent URTI, fever, sore throat, cough, congestion, history of voice, tobacco, alcohol abuse
-PMHx:
-peripheral nerve diseases and other neurological disorders, GERD, hypothyroidism,
psychological stressors
-previous laryngeal trauma, surgery or airway manipulation
-associated symptoms:
-odynophagia, dysphagia, aspiration, weight loss, hearing loss, heartburn
DDx
Congenital Infectious/Idiopa Trauma/Toxic Tumour Endocrine Neurologic Systemic
thic
-laryngeal web -vocal cord -laryngeal -papilloma -hypothyroidism -CP -GERD

-underdeveloped paralysis trauma -polyp -MS -psychogenic
larynx -laryngitis -iatrogenic VCP -vocal cord cyst -MG
-adductor -caustic -cancer -GBS
spasmodic ingestion -Parkinson’s
dysphonia -vocal abuse -stroke
-muscle tension -Reinke’s edema -ALS
disorders -vocal fold
granuloma
Perceptual Voice Abnormalities
-abnormally high fundamental frequency:

-tension producing vocal fold masses, muscle tension phenomenon, protracted pubescence
-abnormally low fundamental frequency:
-load producing vocal fold masses (Reinke’s edema, growths), hypothyroidism (myxedema)
-abnormally loud voice:
-hyperfunction (muscle tension dysphonia), excessive respiratory efforts, psychogenic
-abnormally soft voice:
-reduced respiratory efforts, glottic incompetence, vocal fold paralysis, bowing defect,
psychogenic
-hoarseness:
-vocal fold mass, VCP, bowing defect, muscle-tension abnormalities, vocal fold swelling,
psychogenic
-diplophonia:
-two simultaneous pitches
-recruitment of false vocal cords, presence of asymmetric mass
-harshness:
-strained or strangled
-UMN dysarthria (spastic), adductor spasmodic dysphonia, psychogenic, muscle-tension
abnormalities, or a compensatory result from an underlying vocal fold mass
-tremorous:
-suggests organic vocal tremor (extrapyramidal system), spasmodic dysphonia, or psychogenic
-breathy:
439
-excessive airflow from a longer “open phase” or incomplete adduction
-glottal chink, bowed deformity secondary to vocal fold paralysis, presbylarynx, glottic lesions,
muscle-tension dysfunction, abductor spasmodic dysphonia, psychogenic
-arrest of phonation:
-sudden stops
-spasmodic dysphonia, load bearing vocal fold mass, muscle-tension disorders, psychogenic
-aphonia:
-often functional disorder
-stridorous:
-hypernasality or hyponasality
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Review of Anatomy: Oral Cavity and Pharynx Page 1 of 2
Oral Cavity and Pharynx
ORAL CAVITY
A. Boundaries
 Anterior - lips
 Posterior - anterior tonsillar pillars
 Roof - hard and soft palate
 Floor - mucosa overlying sublingual and submandibular glands.
 Walls - buccal mucosa
B. Contents
 Alveolar processes and teeth

 Anterior tongue to circumvallate papilla
 Orifice of parotid gland (Stenson's duct) in buccal mucosa opposite upper
second molars
 Orifice of submandibular duct (Wharton's duct) in anterior floor of mouth
 Orifices of sublingual glands
PHARYNX
A. Nasopharynx
 extends from posterior choanae of nose to soft palate

 related posteriorly to base of skull
 contains adenoid tissue and orifices of eustachian tubes
B. Oropharynx
 extends from soft palate superiorly to vallecula inferiorly

 posterior and lateral walls are formed by superior and middle pharyngeal
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Review of Anatomy: Oral Cavity and Pharynx Page 2 of 2
constrictors
C. Palatine Tonsils
 lymphoid aggregates between mucosal folds created by palatoglossus and

palatopharyngeus muscles
 covered by stratified squamous epithelium, which continues down into deep
crypts
 vary widely in size and may be sessile or pedunculated
D. Hypopharynx
 lies inferior to tip of epiglottis

 posterior and lateral walls are formed by middle and inferior pharyngeal
constrictors
 extends inferiorly to cricopharyngeus, where pharynx empties into cervical
esophagus
 inferior limit is the pharyngoepiglottic fold
 anteriorly, it extends from valleculae and contains epiglottis and larynx
 lateral to larynx are piriform sinuses, two mucosal pouches whose medial
borders are lateral walls of larynx. posterior aspect of hypopharynx contains
posterior pharyngeal wall and post cricoid mucosa
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Alaryngeal Speech
Type of Speech Advantages Disadvantages

Pneumatic speech aid -“natural” non-electronic sound -bulky
-easy to learn -requires access to stoma
-intelligible speech -difficult to maintain seal at stoma
-inexpensive
Electronic speech aid (Neck Type) -easy to learn to use -noisy electronic sound
-fits in pocket or purse -cannot be used with heavily scarred or
-volume and pitch controls erythematous neck
-adequate volume to be heard in noisy -moderate initial cost; occasional repair cost
places -requires clear articular skills
-intelligible speech
Electronic speech aid (Oral Type) -as for Neck Type -electronic sound
-less noisy than neck types -“clumsy” feeling initially to talk with tube
-can be used soon after surgery even in in mouth
presence of much scar tissue -moderate initial purchase cost; occasional
repair cost
-requires excellent articulation skill for easy
intelligibility
Esophageal speech -“natural” non-electronic sound -period of therapy required

-no dependence on mechanical instrument -may be difficult for 1/3 or more to learn
or device well enough for intelligible speech
-sound of the voice does not call attention to -difficult to hear in noisy environments
itself -requires excellent articulation skills
-may be able to vary pitch and volume -may exacerbate symptoms of GER
control -may be difficult to hear in a noisy
-frees up hands during speech background
Tracheoesophageal speech -“natural” non-electronic sound -if not done as primary procedure, requires
-requires short learning period another surgical procedure
-smooth, fluent speech using long sentences -requires manual dexterity, visual acuity,
because of availability of pulmonary air and level of alertness to care for
-flexibility of loudness and pitch variations -requires use of finger to occlude stoma or
-sound of voice does not call attention to daily affixing of valve to peristomal area
itself -buildup of candida deposits requiring
-extended wear prosthesis types obviate frequent cleaning
need for frequent removal -puncture may stenose
-slight risk of aspiration if prosthesis
dislodged
PNEUMATIC DEVICES
Types
-DSP8 Speech Aid
-Tokyo Speech Aid
-ToneAire Artificial Larynx
ELECTRONIC DEVICES
Description:
-vibrator provides sound source
443
Specific Types:
1. Cooper-Rand Electronic Speech Aid
2. Servox Inton
3. Romet Speech-Aid
4. SPKR
5. Denrick Speech Aid
6. TruTone Electonic Speech Aid
7. Nu-Vois Artificial Larynx
8. P.O. Vox (no longer available)
9. UltraVoice
10. SolaTone
11. Optivox Electrolarynx
Indications for Use:

-oral type can be used effectively soon after surgery
-adjunct for those learning esophageal speech
-may be preferred primary means of communication
-person who is eager to speak
-person who cannot master esophageal speech
-back-up for emergencies
ESOPHAGEAL SPEECH
Description:
-production of voice source within esophagus
-uses cricopharyngeal muscle
-air expelled through the narrowed segment (pharyngoesophageal or PE segment) vibrates and
produces sound
Anatomy of Esophageal Speech:

-PE segment: portion of the pharynx and esophagus where muscle fibers from inferior constrictor,
cricopharyngeus, and esophagus blend together
-shape or size of PE segment appear to be factors in predicting successful acquisition of
esophageal speech
-air flow rates are variable and depend on volume of air in esophagus, pressure, and resistance of
the PE segment
Techniques for Obtaining an Air Supply:
1. Injection method
-air injected from mouth into esophagus via tongue and pharynx
-“glossal press”; “glossopharyngeal press”
2. Inhalation method
-relax PE segment
-lower pressure within esophageal segment relative to atmospheric pressure
3. Swallowing
-not advantageous for creating an air supply for esophageal speech
-requires a trigger to initiate a swallow
-not possible to “dry swallow” quickly and repetitively as required for speech
-voluntary control of the air supply from the stomach may be impossible to achieve
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Indications for Use of Esophageal Speech:
-exceptions: extensive pharyngeal, esophageal, lingual, and/or mandibular resection; patients with
compromised medical status; significant hearing loss; no desire to learn esophageal speech
TRACHEOESOPHAGEAL PUNCTURE (TEP)
Description:
-surgical, endoscopic voice restoration preocedure
-small puncture made through tracheoesophageal wall into esophagus
-pulmonary air drives vibration of PE segment
-oral cavity articulates sound
-prosthesis with one way valve prevents aspiration, maintain patency of puncture, and allow flow
of air into esophagus for voice production
Surgical Procedure:
-primary of secondary puncture
-primary puncture for uncomplicated cases of total laryngectomy
-secondary usually delayed a minimum of 6 weeks after completion of post-op radiation therapy
445
LARYNGITIS
DDx: Laryngitis
Infectious: Inflammatory/Autoimmune:
-viral: -Wegener’s
-croup (parainfluenza) -relapsing polychondritis
-rhinovirus, RSV, adenovirus -SLE
-bacterial: -epidermolysis bullosa
-H. influenzae, -cicatricial pemphigoid
pneumococcus, hemolytic
strep Iatrogenic/Trauma:
-epiglottitis -radiation laryngitis
-diphtheria -thermal injury
-tuberculosis -laryngopharyngeal reflux
-syphilis
-leprosy Idiopathic/Infiltrative:
-scleroma (Klebsiella) -amyloidosis
-fungal: -sarcoidosis
-histoplasmosis
-blastomycosis Allergic:
-candidiasis -angioedema
-aspergillosis
-coccidiomycosis
CHILDHOOD LARYNGITIS
Viral Laryngitis
-most common cause of laryngitis
-associated with URI
-rhinovirus, parainfluenza, RSV and adenovirus implicated
-self-limited
Acute Laryngotracheitis (Croup)

-generally affects those < 5ya
-typically lasts 3-7 days
-Parainfluenza I
-febrile URI followed by classic “barky” or croupy cough; stridor may ensue
-“steeple sign” on AP x-ray from sub-glottic narrowing
-conus elasticus is the most common site involved
-treatment:
-humidification and hydration
-aerosolized epinephrine and high-dose corticosteroids often used
-tracheotomy if impending airway obstruction
Secondary Bacterial Laryngitis

-various degrees of airway obstruction
-high fever and purulent drainage
F.Ling - Laryngitis (1)
446
-organisms usually responsible:
-Haemophilus influenzae, pneumococcus and hemolytic streptococci
Acute Supraglottitis (Epiglottitis)

-often caused by H. influenzae type B; may also be caused by B-hemolytic streptococci and staphylococcus
-2-4 ya most often affected
-airway emergency
-rapid onset of fever, sore throat and inspiratory stridor
-muffled voice; “sitting upright in “sniffing” position; drooling
-“thumb” sign on lateral x-rays
-should be taken to OR immediately to establish diagnosis and control the airway
-epiglottis usually appears swollen and cherry red; also aryepiglottic folds and false vocal cords
-antimicrobial therapy initiated against H. influenzae
-eg. ampicillin/sulbactam, cefuroxime, ceftriaxone
-extubation usually possible after 48-72 hours
-immunization dramatic decrease in incidence of supraglottitis
Laryngeal Diphtheria
-uncommon
-Corynebacterium diphtheria
-exudative inflammatory response of mucous membranes thick, gray-green plaquelike membranous
exudate over tonsils, pharynx and larynx
-complications:
-nephritis, airway obstruction, death (secondary to neurological toxin)
-tx: diphtheria antitoxin, erythromycin or penicillin
Laryngopharyngeal Reflux
-associated with laryngomalacia, vocal nodules, polyps, granulomas, laryngeal and tracheal stenosis and
laryngospasm
Spasmodic Croup
-noninfectious form of laryngeal inflammation, possible related to allergy or LPR
-affects children 1-3 ya
-usually at night with nocturnal stridor and respiratory distress - asymptomatic during day
-humidification is all that is need to alleviate symptoms
ADULT LARYNGITIS
Viral Laryngitis
-viral URI - rhinoviruses most common agent
-voice breaks, episodic aphonia, hoarse cough, lowering of vocal pitch
-self-limited; humidification, voice rest, hydration, smoking cessation, cough suppressants, expectorants
Bacterial Laryngitis
-supraglottitis
-fever, sore throat, muffled voice, odynophagia and dyspnea
-Haemophilus influenzae most common organism; Streptococcus pneumoniae, Staphylococcus aureus, and
B-hemolytic streptococci also found
-tx: humidification, hydration, corticosteroids, IV antibiotics
-ampicillin, cefuroxime, ceftriaxone, aztreonam, chloramphenicol
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NON-INFECTIOUS LARYNGITIS IN ADULTS
-implicated in development of granulomas, stenosis, recurrent laryngospasm, globus pharyngeus, cervical
dysphagia, asthma, laryngeal carcinoma, chronic cough
-pts often deny heartburn
-possible findings:
-red arytenoids with interarytenoid mucosal hypertrophy
-subglottic edema forming “pseudosulcus vocalis”
-diffuse edema, Reinke edema, or mucosal thickening w/o significant erythema
-gold standard for diagnosis: 24H pH double probe monitoring
Traumatic Laryngitis
-vocal abuse
-persistent coughing, muscle tension dysphonia, direct endolaryngeal injury
-treatment: voice conservation and humidification
Thermal Injury
-exposure of larynx to steam, smoke or very hot liquids or food supraglottic edema and erythema
Angioedema
-vascular dilation and increased vascular permeability
-cause:
-medications: ACE inhibitors
-foods, insect bites, transfusions and infections
-hereditary angioedema:
-AD deficiency of C1 esterases inhibitor recurrent attacks of mucocutaneous edema
-aggressive treatment:
-O2, epinephrine, corticosteroids, antihistamines, aminophylline
Allergic Laryngitis
-controversial
-inflammation and fibrosis with destruction of cartilage of ears, nose, larynx, tracheobronchial tree
-airway involvement leads to high mortality seen with this disease
-treatment: dapsone, corticosteroids, immunosuppresive drugs; tracheotomy
Systemic Lupus Erythematosis

-laryngeal inflammation in up to a third of patients
-most patients respond to systemic corticosteroid therapy
Epidermolysis Bullosa and Cicatrical Pemphigoid

-mucosal blister formation
-involvement of larynx uncommon
Amyloidosis
-diffuse mucosal thickening, submucosal nodules or polyploid lesions
-usually involves supraglottis
-biopsy amorphous Congo red-staining material
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CHRONIC GRANULOMATOUS LARYNGITIS
Tuberculosis
-most common granulomatous disease of larynx
-may resemble carcinoma
-areas of involvement:
-interarytenoid space (most common)
-false and true vocal cords
-epiglottis
Syphilis
-second stage: diffuse erythematous papules, edema and ulcers (painless) that mimic carcinoma along with
cervical lymphadenopathy
-tertiary stage: gumma formation
Leprosy
-rare
-commonly involves supraglottic larynx
Histoplasmosis
-systemic mycotic disease
-Histoplasma capsulatum
-nodular superficial granulomas that can ulcerate and become painful
-amphotericin B is treatment of choice
Blastomycosis
-Blastomyces dermatitidis
-usually have multiorgan involvement
-histology: caseous necrosis with acute inflammatory infiltrate, microabscesses, pseudoepitheliomatous
hyperplasia, giant cells
-treatment: long-term amphotericin B, ketoconazole, itraconazole
-may develop pharyngocutaneous fistula if left untreated
Scleroma
-primarily involves nasal cavity but may involve larynx
-subglottis most commonly involved
-histology:
-foamy vacuolated histiocytes (Mikulixz cells)
-degenerated plasma cells (Russell bodies)
-tx: tetracycline, fluroquinolones, clofazimine
Sarcoidosis
-multisystem granulomatous disease
-noncaseating granulomas and pale diffuse edema of supraglottis
-treatment: steroids
-necrotizing granulomas with vasculitis involving respiratory tract and kidneys
-treatment: cyclophosphamide, corticosteroids, and optional TMP-SMX
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Immunocompromised Host
-at risk for developing laryngeal opportunistic infections and malignancies (Kaposi sarcoma, non-Hodgkin
lymphoma, SCCa)
Radiation Laryngitis
-erythematous, swollen larynx with exudate and crusting
-treatment: hydration, humidification and acid suppression with steroids and antibiotics occasionally
-ddx: recurrent cancer, LPR, radionecrosis, hypothyoidism
DDx Pseudoepithelial hyperplasia

-granular cell tumour
-blastomycosis
-histoplasmosis
-tuberculosis
-syphilis
-pachyderma laryngitis
-radiation
-papillary keratosis
-rhinoscleroma
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HOARSENESS AND VOCAL CORD PARALYSIS
ANATOMY OF VOCAL CORD
-mucosal layer: pseudostratified squamous epithelium

-medial cord borders: nonkeratinizing squamous epithelium
-subepithelial tissues (3 layers):
-lamina propria (Reinke space) - allows vibration of overlying mucosal cover layer
-intermediate layer - elastic fibers and moderate number of fibroblasts
-deep layer - collagenous fibers
-muscles:
-adductors:
-thyroarytenoid, lateral
cricoarytenoid,
interarytenoid muscles
-supplied by adductor
branch of recurrent nerve
-tensor:
-cricothyroid muscle
-supplied by external
branch of superior
laryngeal nerve
-abductor:
-posterior cricoarytenoid
-supplied by abductor
branch of recurrent nerve
-motor nucleus of vagus: nucleus ambiguus
-posterior commissure defects causing aspiration, air leakage, and hoarseness are commonly seen after
prolonged intubation
VOICE GENERATION
-folds vibrate at fundamental frequency (lowest frequency, highest amplitude)

-folds vibrate in horizontal plane with vertical undulation of mucosa as air passes through glottis
-change in vibratory quality of glottic mucosa or inadequate apposition of true vocal cords interferes with
generation of proper glottic mucosal waves hoarseness
EVALUATION AND INITIAL ASSESSMENT
Patient History
-SSx:
-hoarse-breathy dysphonia, aspiration, stridor, dysphagia, limited phonation time, vocal fatigue
-inspiratory or biphasic stridor, weak cry, aspiration, hoarseness
-URTI, fever, cough, postnasal drip
-alcohol/tobacco
-voice abuse
-GERD
F.Ling - Hoarseness and Vocal Cord Paralysis (1)
451
-previous neck trauma, toxin exposure
-previous surgery (cardiothoracic, thyroid)
-previous history of cancer, cardiopulmonary disease
-hypothyroidism, diabetes, neurological disorders
-medications: ACEi chronic cough induced changes
Physical Examination - flexible or rigid laryngoscopy
Ancillary Tests
-videostroboscopy
-demonstrates subtle mucosal motion abnormalities
-electromyography
-laryngeal EMG used to differentiate between vocal cord fixation d/t cricoarytenoid joint
disorders vs neuromuscular disease
-studies primarily thyroarytenoid and cricoarytenoid muscles
-loss of muscle function: normal frequency of firing but decrease in amplitude
-loss of nerve function: normal amplitude but decreased frequency
-provides most accurate diagnosis of SLN paralysis
-CXR
-CT scan: head, neck, thorax
-modified barium swallow test
-labs: CBC, FTZ-Abs, lyme titers, thyroid function, toxin screen (lead+arsenic levels)
VOCAL CORD POSITION AND SYNKINESIS
-note:
- below are “classic findings” however position of vocal cord paralysis is not very predictive of
site of nerve involvement and vice versa
-superior and recurrent laryngeal nerve paralysis:

-produce a lateral position (intermediate or cadaveric position)
-RLN paralysis:
-paramedian cord position airway obstruction if bilateral
-preserves partial adduction from action of cricothyroid muscle
-SLN paralysis:
-asymmetric vocal cord tension
-produces diplophonia
-loss of vocal fold tension (lowers pitch of voice)
-inaccurate vocal cord apposition
-paralysed side slightly shortened and bowed
-may be depressed below level of normal side
-rotation of AP axis of vocal cords
-posterior commissure points to side of paralysis
-loss of laryngeal sensation increased risk of aspiration
-synkinetic reinnervation antagonistic muscles also activated produce non-purposeful movements
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VOCAL CORD PARALYSIS IN CHILDREN
-differentiate from laryngomalacia - most common cause of stridor in children

-VCP second most common cause of stridor in children
-when diagnosed - laryngoscopy and bronchoscopy (r/o subglottic stenosis)
-MRI of CNS and CT neck and chest
-serologic studies to investigate for systemic diseases - eg. syphillis
Etiology
-neurologic disorders: DDx Vocal Cord Paralysis (Children
-Arnold-Chiari malformation: traction on vagal
rootlets producing neuropraxia or axonotemesis Congenital
-paralysis often temporary, but tracheotomy -idiopathic
needed for bilateral VCP Infectious
-earlier decompress may lead to faster -syphilis (rare)
recovery time of paralysis and may avoid
tracheotomy Iatrogenic/Trauma
-surgery
-congenital idiopathic VCP -patent ductus arteriosus repair
-usually unilateral -TEF repair
-recovery in 20% -mediastinal and neck surgeries
-birth trauma -birth trauma
-traction and stretching of laryngeal nerves Neurologic
-surgical trauma -Arnold-Chiari malformation
-patent ductus arteriosus repair, TEF repair,
mediastinal and neck surgeries
-congenital infections
-rare
-syphilis
Management
-establish secure airway
-unilateral paralysis
-rarely requires tracheotomy
-usually observation
-bilateral paralysis
-may require tracheotomy
-arytenoidectomy and lateralization procedures postponed a minimum of 6 months to await
functional recovery
-lateralization good airway at expense of voice and airway protection
-arytenoidectomy or arytenoidopexy are irreversible - may offer decannulation of pt
VOCAL CORD PARALYSIS IN ADULTS
-left side paralysed more frequently because of longer and intrathoracic course
Etiology
-surgical trauma - most common cause of unilateral and bilateral VCP
-neoplastic causes - bronchogenic carcinoma, thyroid carcinoma, upper esophageal and laryngeal ca
-neurologic conditions - poliomyelitis, pseudobulbar palsy, ALS
-idiopathic
-other causes: infection (eg. TB), drugs (eg. cisplatin), NG tube, ETT
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DDx Vocal Cord Paralysis (Adults)
Idiopathic -skull base lesions: -myasthenia gravis

-paraganglioma -multiple sclerosis
Infectious (glomus vagale, glomus -stroke
-syphilis jugulare) -Wallenberg syndrome
-Lyme disease
-TB Iatrogenic/Trauma Toxins/Medications
-EBV -thyroid surgery -cisplatin
-cardiothoracic surgery -vincristine
Neoplastic -laryngeal trauma -lead, arsenic, quinine,
-bronchogenic carcinoma -post-intubation neuropraxia streptomycin
-thyroid carcinoma
-cupper esophageal and Neurological Systemic
laryngeal carcinoma -poliomyelitis -sarcoidosis
-mediastinal disease (eg. -pseudobulbar palsy -diabetes
lymphoma) -cardiomgaly
Evaluation and Diagnostic Tests

-cortical lesions - difficult to identify; may result in spasticity or aphonia
-LMN lesions - processes affecting vagal nuclei; other symptoms of brainstem injury often found
(aspiration, dysarthria, dysphagia)
-peripheral nerve lesions
-above or at nodose ganglion: affect both SLN and RLN aspiration and VCP
-below nodose ganglion: RLN injury only
-most pts compensate over time - no treatment required
-isolated SLN injury: rare
-results in change or decreased range of pitch
-laryngoscopy: tilting of larynx with rotation of posterior glottis toward paralysed side
-dx with EMG of cricothyroid
-dx: usually obvious from history
-CT scans of base of skull, neck and upper chest
-+/- MRI for central causes
-laryngeal EMG, panendoscopy, and palpation of arytenoids indicated if preliminary tests fail to
elucidate cause
Management
Medical Management:
-treat underlying cause if possible
-voice therapy:
-for unilateral paralysis
-isometric manoeuvers to improve glottal competence
Surgical Management:
Unilateral Vocal Cord Paralysis

-if cord paramedian, likely no treatment required - compensation occurs
-avoid definitive treatment for 6-12 months
-medialization for widely abducted paralysed cord causing hoarseness or aspiration
1. Injection Thyroplasty:
-can be done external or internal (indirect or endoscopic)
454
-advantages:
-easy, immediate improvement, may be complete in office
-disadvantages:
-irreversible if Teflon used
-changes mucosal wave
-does not correct large posterior defects
-materials used:
-Gelfoam:
-augmentation for pts in whom recovery is expected but who require immediate
improvement
-resorption occurs in 6-8 weeks
-Teflon:
-permanent injectable material
-irreversible complications: interference with vocal cord vibration and
destructive Teflon granuloma
-risk of migration
-supplanted by safer, more efficacious treatments
-Collagen:
-autologous or bovine collagen (risk of host reaction
-effective for up to 3 years
-collagen eventually resorbed and replaced with host tissue
-Fat:
-autologous
-does not last long
-complications
-over or underinjection
-acute hypersensitivity
2. Thyroplasty Type I:
-placement of silicone block to push inward against
paraglottic tissues, medializing membranous true
vocal cord
-cartilage window dimensions:
-upper: ½ distance from thyroid notch to
insertion of cricothyroid
-lower: ½ distance from upper rectangle to
insertion of cricothyroid
-posterior: 1/3-1/2 distance from midline of
thyroid cartilage
Typical dimensions of silastic wedge for thyroplasty
-anterior: within 5-7 mm lateral to midline
of thyroid cartilage
-advantages:
-reversible
-preserves mucosal wave
-immediate results
-may be done under local anaesthesia
-disadvanges:
-requires neck incision
-possible extrusion of implant
-not adequate for posterior defects
-risk of airway compromise
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3. Arytenoid Adduction:
-permanent sutures to anchor muscular process of arytenoid in adducted position to medialize VC
and close posterior commissure
-may be used in conjunction with type I thyroplasty
4. Laryngeal Reinnervation:
-types:
-ansa hypoglossi to recurrent nerve anastomosis
-end-to-end anastomosis of RLN
-ansa cervicalis to neuromuscular pedicle (omohyoid) to thyroarytenoid muscle
-vagus, ansa, phrenic nerve fibers or motor endplate insertion into thyroarytenoid
-no laryngeal motion appreciated due to synkinesis of reinnervation, but excellent voice quality
was achieved
Bilateral Paralysis
-treatment directed toward lateralizing one or both cords to improve airway at expense of aspiration and
voice quality
1. Tracheotomy
2. Laser Cordectomy:
-endoscopic removal of one vocal cords to open a/w
-scarring may narrow airway
3. Laser Cordotomy:
-posterior gap created as posterior portion of VC is released from vocal process and resected with
laser
-risk of aspiration
4. Arytenoidectomy:
-Woodman: -arytenoid excised with exception of vocal process; suture passed through vocal
process and thyroid ala and tightened to proved adequate airway and usable
voice
-endoscopic laser or microlaryngeal removal of arytenoid opens posterior glottis
5. Arytenoidopexy:
-suture passed around vocal process of arytenoid cartilage and positioned laterally without
removing arytenoid cartilage
-for pts where bilateral VCP may not be permanent
6. Electrical Pacing:
-pacing posterior cricoarytenoid muscle to coincide with inspiration
-long term efficacy and reliability remains to be proven
456
DDx Immobile Cord
Infectious Inflammatory/Autoimmune
-syphilis -Wegener’s
-tuberculosis -relapsing polychondritis
-scleroma -rheumatoid arthritis (joint
-fungal infections involvement)
Neoplastic Idiopathic/Infiltrative
-laryngeal carcinoma -idiopathic
-amyloid
Iatrogenic/Trauma -sarcoid
-dislocation of arytenoid
-laryngeal trauma Neurogenic:
-vocal cord paralysis (see DDx for
cord paralysis above)
-central
-peripheral
457
BENIGN LESIONS OF THE LARYNX
DDx Benign Laryngeal Lesions
Congenital Iatrogenic/Traumatic
-? sulcus vocalis -vocal cord nodules
-embryonal cyst -capillary ectasia
-laryngocele -vocal fold hemorrhage
-saccular cyst -vocal fold polyp
-intracordal cyst
Infectious -contact ulcer
-tuberculosis -intubation granuloma
-syphilis -reflux disease
-fungal infections
Idiopathic/Infiltrative:
Neoplastic -sarcoidosis
-laryngeal papillomatosis -amyloidosis
-laryngeal polyps
-granular cell tumour Systemic:
-chondroma -hypothyroidism (myxedema)
-subglottic hemangiomas
-rhabdomyoma Other:
-lipoma -bilateral diffuse polyposis
-benign mixed neoplasm (Reinke’s edema)
-neurofibroma
-neurilemmoma
NODULES
-usually bilateral
-involve anterior or middle third of true VC
-edema in submucosa (Reinke space) organized fibrous tissue (hyalinization)
-tx: voice therapy (at least 6 months) and voice rest
-sx if malignancy suspected
-unilateral or asymmetric nodules usually are intracordal cysts
POLYPS
-pedunculate or sessile lesions involving middle half, anterior half or entire VC
-most common benign lesions of adult larynx
-two types:
-mucoid
-inflammatory process in subepithelial layer of loose connective tissue
-translucent
-angiomatous
-vascular
-dark red, protuberant, multinodular
-women most commonly affected with bilateral vocal fold polyps or polyploid change
-d/t heavy smoking and vocal abuse
-tx: surgical removal
-treatment of GERD important to prevent irritation, inflammatory changes and poor healing
F.Ling - Benign Larynx Lesions (1)
458
CYSTS
-most common site is supraglottic larynx
-mucous retention cysts most common
-found in valleculae, BOT, epiglottis or A/E folds
-embryonal cysts:
-congenital; arise in aryepiglottic fold or lateral pharyngeal wall
-tx:
-supraglottic cysts: excised or marsupialized
-intracordal cysts: careful dissection for complete removal while maintaining mucosal flaps
(microflap technique)
GRANULOMA
-usually arise near vocal process or body of arytenoid
-hx of GERD or previous traumatic or prolonged endotracheal intubation
-hoarseness, chronic throat clearing
-airway obstruction: “ball valving”
-tx:
-remove irritation: voice therapy, antireflux management
-surgical treatment:
-CO2 laser excision
-adjunctive steroid injection post-surgical ablation
-post-op:
-voice rest x 1wk
-modified voice use
-systemic broad-spectrum antibiotics for 3-4 weeks
-inhalational steroids not routinely recommended
-botulinum toxin type A injection: prevent forceful closure of arytenoids during phonation and
coughing
LARYNGEAL PAPILLOMATOSIS
-most common benign laryngeal tumour
-more prevalent in children and less common in individuals over 30ya
-transmission of HPV to child occurs in birth canal (1:80-1:500 risk of transmission)
-histo:
-papillary projections and hypervascular fibroconnective
tissue covered by hyperplastic squamous epithelium
-HPV-6 correlated with extent and severity of disease (ie. spread of
papillomas into trachea and lungs)
-most common sites:
-vocal folds and subglottic larynx
-avoid tracheotomy if possible
-malignant degeneration rare; associated with rad tx, tobacco abuse
-tx:
-frequent excisions to avoid tracheotomy
-laser excision:
-power setting of 2-8 W, impact spot sizes of 0.3 to 0.8 mm, intermittent mode of 0.1-0.5
second exposure
-other techniques: microlaryngeal techniques, cryosurgery, microcauterization, microdebridement
-other tried therapies:
-vaccines, chemotherapy, hormonal therapy (unsuccessful)
-interferon and photodynamic therapy
-intralesional injections of cidofovir or indole-3-carbinol
459
LYMPHATIC AND VENOUS MALFORMATIONS
-haemangiomas:
-lesions with increased mitotic activity
-rapid postnatal growth slow involution usually by age 7
-treatment may not be necessary
-associated with cutaneous haemangiomas
-other treatment options:
-systemic steroids and tracheotomy if symptomatic stridor
-CO2 laser ablation for smaller, solitary lesions
-may cause scarring and laryngeal stenosis for larger circumferential lesions
-Nd:YAG laser NOT RECOMMENDED for subglottic hemangiomas because these lesions are
not vascular high risk of stricture formation and tracheal perforation
-malformations:
-lesions that are inborn errors of vascular morphogenesis and grown proportionately with the child
-venous malformations rarely involve larynx
-Nd:YAG laser treatment highly effective
GRANULAR CELL TUMOUR

-uncommon, benign
-originate from Schwann cells
-two types:
-mucosal granular cell tumour
-congenital epulis or gingival giant cell tumour
-tongue most common site
-larynx uncommon (3% of cases)
-located most commonly on posterior 2/3 of true
VC or arytenoid
-histology:
-large polygonal cells with distinct borders
arranged in nests, strands or sheets within bands
of fibrous tissue
-hyperchromatic and bland nuclei
-abundant, eosinophilic cytoplasm filled with
granules of varying sizes
-tx: complete excision
-larger tumours may require laryngofissure
CHONDROMA
-rare
-originate from epiglottis, cricoid, arytenoid or thyroid cartilages
-composed mostly of hyaline cartilage
-tx: complete surgical excision
-thyrotomy or lateral pharyngotomy approach
-endoscopic removal only indicated for extremely small tumours
-total laryngectomy reserved for extremely large tumours or recurrent poorly defined growths
NEUROGENIC TUMOURS
-extremely rare
-schwannomas
-benign and slowly growing
-submucosal, smooth, located in aryepiglottic folds and extending into supraglottic space
-most common nerve of origin: internal branch of superior laryngeal nerve
460
AMYLOIDOSIS
-uncommon problem
-larynx most common site of localized amyloid deposition in respiratory tract
-supraglottis involved most frequently > glottis > subglottis
-laryngeal amyloid almost always localized and rarely systemic
-histology:
-extracellular, amorphous pink material
-“apple-green birefringence” seen with Congo red stain under polarized light
-EM: linear, nonbranching fibrils in B-pleated sheets
-tx: conservative removal
-steroids and antimetabolites are not helpful
-surgical removal either endoscopic or via laryngofissure
SARCOIDOSIS
-larynx involved in 1-5% of pts with sarcoidosis
-epiglottis most common site aryepiglottic folds > arytenoids > false vocal cords > subglottis
-lab studies:
- LFTs
- ACE levels, cutaneous energy, ESR, eosinophilia, hypercalcemia, hypercalciuria,
hypergammaglobulinemia
-histology:
-small noncaseating granuloma
-tx:
-endoscopic excision of obstructing lesions
-steroids
SURGICAL TECHNIQUE
-Benninger: cold vs laser excision
-no statistical difference in voice quality after surgery with either method
461
CONTROVERSIES IN LARYNGOLOGY
CONTROVERSIES IN DIAGNOSIS
Telescopic versus Fiberoptic Laryngeal Examination

-laryngeal biomechanics are dramatically altered when one pulls on the tongue and introduces a telescope
-transnasal fiberoptic laryngoscopy slow to gain popularity because images were inferior to those obtained
with rigid telescopes
-telescopic laryngoscopy is an inferior examination method for assessing many common movement
disorders such as vocal cord paresis and paralysis, spasmodic dysphonia, tremor and functional muscle
tension dysphonia
-TFL thought to be superior to telescopic laryngoscopy in evaluation and diagnosis of most functional and
neuromuscular disorders of the larynx
Stroboscopy
-stroboscopy allows evaluation of mucosal waves of vocal folds
-not useful in differentiating functional from organic voice disorders
-not useful in evaluating neoplastic lesions that involve anterior commissure, vocal processes, or
posterior larynx
-principle indications:
-differentiate intracordal cysts from vocal nodules
-evaluate for vocal fold fibrosis/scarring (adynamic segments after trauma, surgery, or
inflammatory disease)
-demonstrate recovery of vocal fold function after vocal fold surgery or laryngoplastic
phonosurgery
-determine functional significance of vocal fold vascular lesions
-evaluate thickness of some free edge neoplastic lesions
Laryngeal Electromyography
-provides essential information about neuromuscular status of larynx that no other test can provide
-cricothyroid superior laryngeal nerve
-thyroarytenoid recurrent laryngeal nerve
-parameters evaluated:
-recruitment
-waveform morphology
-presence of spontaneous activity
-indicates ongoing neural degeneration
-helpful in directing site of lesion analysis
-may indicate prognosis in paresis/paralysis
-eg. good prognosis = plentiful, low-amplitude, polyphasic motor units
-eg. poor prognosis = markedly reduced recruitment and large-amplitude motor units
-differentiates paralysis from fixation
-controversy surrounds diagnosis and treatment, and its role in causing or exacerbating laryngeal diseases
-reasons for underdiagnosis:
-most otolaryngology pts with LPR do not have esophagitis or heartburn because they have
upright (daytime) reflux with normal or near-normal esophageal acid clearance
-traditional diagnostic tests for reflux are essentially tests for esophagitis
-ambulatory double-probe pH monitoring gold standard
-therapeutic trials with low-dose PPIs often ineffective for LPR because of short treatment times
F.Ling - Controversies in Laryngology (1)
462
-most common findings of LPR are effacement of the ventricles by swollen false and true vocal cords
(ventricular obliteration) and pseudosulcus vocalis (subglottic edema)
Flexible Endoscopic Evaluation of Swallowing vs Modified Barium Swallow

-although concerns about amount of information that can be obtained from endoscopic approach - one
excellent study has confirmed its accuracy and reliability
-reproducible laryngopharyngeal sensory thresholds can be determined
-done by directing calibrated puffs of air to various locations in laryngopharynx
SURGICAL CONTROVERSIES
Vocal Process Granulomas

-causes:
-LPR
-endotracheal intubation
-hyperfunctional compensation secondary to vocal fold paresis
-vocal abuse
-underlying cause must be determined
-treatment should focus on acid suppression and voice therapy
-biopsy when possibility of carcinoma exists
-airway obstruction if granuloma are quite large
-if granuloma matures and becomes a fibroepithelial polyp
-to restore voice in selected cases
Treatment of Early Carcinoma of Vocal Fold

-CO2 laser or endoscopic excision:
-advantages:
-surgical exploration of lesion reveals true extent of disease
-simultaneous diagnosis (biopsy) and definitive treatment
-comparatively low cost
-outpatient treatment with pt usually able to return to work within days of surgery
-no side effects of radiation
-irradiation is retained as a future therapeutic option
-overall voice results were comparable to XRT
Use of Polytef (Teflon) in Laryngology

-drawbacks:
-Teflon granuloma formation
-subsequent fixation of arytenoid d/t inflammatory process
-inability to close posterior glottis
-when endoscopic removal is attempted, complete removal is not possible
-Teflon should not be injected into mobile vocal cords produce a stony hard vocal fold with gradual,
progressive worsening of voice over time
-Teflon injections usually only for pts with limited life expectancy
-laryngoplasty is considered superior treatment for vocal fold paralysis
463
Microlaryngeal Surgery
-use of lasers in phonosurgical treatment of benign lesions remains controversial
-some claim thermal damage created by laser impairs surgical result
-some suggest that differences in outcome may be related more to surgical technique and
experience than to instrumentation
Lipoinjection
-use of autologous fat for injection augmentation of vocal fold has become an accepted tool
-areas of concern: optimal technique for graft harvest and injection, relatively poor long-term yield, and
inability to control fat cell graft distribution in injected tissue
Surgery for Spasmodic Dysphonia

-selective RLN section of branches to thyroartenoid muscle results preliminary
-bilateral ML and lipoinjection used to better approximate vocal folds for abductor-type SD
-procedures are new and not widely used, in part because botox injections are so effective in treating the
majority of pts
464
LARYNX - ANATOMY
(Cummings Ch. 97)
SKELETOMEMBRANOUS FRAMEWORK OF THE LARYNX
Hyoid bone
-derived from mesodermal cells that form cartilaginous masses in the second
and third branchial arches
-lesser horn derived from second branchial arch
-body and greater horn derived from third branchial arch.
-proximal portion of second branchial arch forms stapes of middle ear, styloid
process, and stylohyoid ligament
-In adults, the styloid process, stylohyoid ligament, and lesser horn of the hyoid
bone symbolize the line of the second branchial arch cartilage.
Laryngeal cartilages
-major cartilages of the larynx:

-thyroid
-cricoid
-epiglottic
-arytenoids
Thyroid cartilage
-important landmarks: paired superior and inferior horns, lateral
plates or laminae, and thyroid notch/laryngeal prominence
-important synovial joints: cricothyroid joints
-similar to other synovial joints of the body, are subject
to arthritis
-pts with cricothyroid arthritis frequently complain of
odynophonia
-impaired mobility loss of pitch range and vocal
fatigue
-physical findings: bilateral vocal fold bowing, inability to
lengthen vocal folds with attempts to elevate pitch, and loss
of normal laryngeal crepitance during manual manipulation
of the cricoid and thyroid cartilages.
Cricoid cartilage
-only complete skeletal ring for the airway
-signet ring with a broad arch located posteriorly
-thyroid and cricoid cartilages attached anteriorly in midline by
median cricothyroid ligament
Epiglottic cartilage
-composed primarily of elastic cartilage
-mucosa covering anterior surface: stratified squamous epithelium -
posteriorly, near the inlet of the larynx, the epithelium is
pseudostratified, ciliated, and columnar.
-anterior midportion attaches to tongue by median glossoepiglottic
F.Ling - Larynx Anatomy (1)
465
fold and the paired lateral glossoepiglottic folds
Arytenoid cartilages
-landmarks: concave articular base, the apex, a muscular process
projecting laterally, and vocal process projecting anteriorly
-corniculate cartilage, usually articulates with the apex of the
arytenoid and is located within the inferomedial part of the
aryepiglottic fold
-posterior commissure, a reference landmark during laryngoscopy
-on the lateral aspect of the corniculate cartilages, within the
aryepiglottic folds, are cuneiform cartilages
-during laryngoscopy, corniculate and cuneiform cartilages appear as
small, paired swellings in the aryepiglottic folds lying on either side
of the posterior commissure
The cricoarytenoid joint (a synovial joint) may also be involved with arthritis.
This process should be considered in adult patients with idiopathic
vocal fold motion impairment and in patients with impaired motion after
prolonged endotracheal intubation.
LARYNGEAL MEMBRANES
Quadrangular membrane
-begins at lateral border of epiglottic cartilage and spans space
between epiglottic and arytenoid cartilages
-superior border of membrane is free and has oblique course from
upper part of epiglottis to corniculate cartilage
-inferior border of the quadrangular membrane extends from
inferior point of attachment of the epiglottic cartilage on the
thyroid cartilage to vocal process of the arytenoid cartilage
-anterior and posterior borders are fixed; superior and inferior
borders are free
-upper free border aryepiglottic fold
-lower free border vestibular folds
Triangular membrane
-in lateral profile, has a narrow base, the midline,
attaching to the thyroid and cricoid cartilages,
projecting to an apex, which is the vocal process of
the arytenoid cartilage
-superior border begins at the thyroid cartilage,
extending posteriorly as a concave line to the vocal
process forms vocal ligament
-inferior border attached to the cricoid cartilage
-quadrangular and triangular membranes and, in particular,

the vestibular and vocal ligaments form the structural base
for the formation of vocal folds
Laryngeal mucosa
-essentially all of mucosa from trachea to aryepiglottic fold composed of a pseudostratified, ciliated,
columnar epithelium, except for covering of true vocal folds, which is stratified squamous epithelium
466
-tubuloalveolar glands are abundant, particularly in region of ventricle
lubrication for vocal folds
-at aryepiglottic fold, mucosa becomes stratified squamous epithelium
and covers lateral surface of quadrangular membrane
-pear-shaped mucosal recess: piriform recess
Three important folds:

-aryepiglottic fold (superior border of the quadrangular membrane)
-false vocal fold (inferior border of the quadrangular membrane)
-true vocal fold (formed by the mucosal covering of the upper surface
of the triangular membrane)
Laryngocele
-laryngocele is a herniation of ventricular mucosa
-expands upward in the pathway of least resistance
-inferiorly, triangular membrane (conus elasticus) blocks the
way
LARYNGEAL MUSCULATURE
Extrinsic and accessory musculature

-extrinsic muscle: cricothyroid
-accessory muscles:
-elevators or larynx:
-digastric, geniohyoid, stylohyoid,
stylopharyngeal, and thyrohyoid muscles
-depressors of larynx:
-sternothyroid, sternohyoid, and omohyoid
muscles
Intrinsic musculature
-associated with the quadrangular membrane:
-thyroarytenoid
-thyroepiglottic
-aryepiglottic muscles
-acting on arytenoid cartilage:
-posterior cricoarytenoid
-lateral cricoarytenoid
-arytenoid muscles
-vocalis muscle: longitudinally arranged group of muscle
fibers paralleling the vocal fold
VOCAL FOLD FUNCTION
Respiration
-during maximal inspiration, larynx is drawn downward by
the effect of sternothyroid and sternohyoid muscles and by
traction on the trachea. True and false vocal folds flatten
(unfold) against the lateral wall of the larynx to maximally
open the airway
467
-cricothyroid contraction, by itself, results in elongation of the vocal fold and slight adduction
Phonation
-myoelastic-aerodynamic theory (Voice cycle):
-requires that a mass of subglottic air be compressed by thoracic respiratory muscles while the
vocal folds are adducted and tensed
-at the moment glottic resistance is overcome by the pressure of the compressed air column, the
folds open, allowing air to flow through the glottis and reduce subglottic pressure
-elastic recoil of the vocal folds reestablishes glottic resistance, and, as long as subglottic pressure
is maintained, a cyclic movement or horizontal oscillation of the vocal folds will continue
-frequency of vocal cord vibration and hence frequency of phonated tone are related
mathematically to subglottic air pressure, airflow, and glottic resistance
-neuromuscular theory:
-muscles vocal folds by adjusting their length, tension, and mass, thus regulating the glottic
resistance.
-increased glottic pressure and increased glottal resistance result in an increased fundamental frequency;
decreased cricothyroid muscle activity is probably a response to regulate the fundamental frequency
Effort closure
-important to increase intrathoracic and intraabdominal pressure
Closure during swallowing

-movement of the epiglottis is a more significant added feature compared with effort closure
MOTOR AND SENSORY INNERVATION
-recurrent laryngeal nerve axons arise from motoneuron cell bodies in the nucleus ambiguus
-axonal processes from the nucleus ambiguus contribute to the vagus nerve and the cranial portion of CN XI
-two laryngeal branches are given off:
-superior laryngeal nerve:
-external laryngeal nerve
-to cricothyroid muscle and to inferior constrictor muscle of the pharynx
-recurrent laryngeal nerve:
-enters the larynx at the cricoid cartilage between the muscle fibers of cricopharyngeus muscle
and the esophagus
-muscles innervated unilaterally from their respective vagus, with the exception of the
interarytenoid muscle, which is innervated from both vagi
-sensation of larynx:
-internal laryngeal nerve:
-laryngeal mucosa at level of false vocal cord and piriform sinus
-recurrent laryngeal nerve:
-mucosa of the true vocal fold, subglottic mucosa, and adjacent esophageal mucosa
AUTONOMIC INNERVATION
-larynx receives autonomic innervation—adrenergic and cholinergic—from superior cervical ganglia and
vagus nerve, respectively.
BLOOD SUPPLY
-superior laryngeal artery
-branch of the superior thyroid artery, derived from the external carotid artery
468
-distribution of the vessel includes the piriform sinus and the medial surface of the quadrangular
membrane as far inferiorly as the false vocal fold.
-inferior laryngeal artery
-derived from the inferior thyroid artery, which originates from the thyrocervical trunk of the
subclavian artery
-enters the larynx, along with the recurrent laryngeal nerve, at the junction of the cricopharyngeal
and esophageal muscle fibers
-supplies the muscles attaching to the arytenoid cartilages and the laryngeal mucosa adjacent to
the false vocal fold and laryngeal ventricle
VENOUS DRAINAGE
-follows the same pattern as arterial supply
-superior laryngeal vein parallels the course of the superior laryngeal artery and eventually empties into the
internal jugular vein
-inferior laryngeal vein is a tributary of the thyrocervical trunk of the subclavian vein
469
CHAPTER 98: LARYNGEAL AND PHARYNGEAL FUNCTION PART SIX:
ELECTROMYOGRAPHY OF LARYNGEAL AND PHARYNGEAL MUSCLES
ELECTROMYOGRAPHY RECORDINGS: INSTRUMENTATION AND TECHNIQUES
-an electrical potential can be picked up and displayed or recorded as EMG signals if a pair of electrodes
are placed in the muscle tissue.
Intrinsic laryngeal muscles

-percutaneous route taken for reaching cricothyroid, thyroarytenoid, and lateral cricoarytenoid
-cricothyroid:
-needle insertion: level of lower edge of cricoid cartilage and 5 mm lateral to midline
-needle directed toward inferior tuberculum of thyroid cartilage
-verification : subject raises pitch of his or her voice
-cricothyroid shows marked activity for a quick rise in voice
pitch
-thyroarytenoid:
-subject in a supine position and attempting sustained
phonation
-skin is pierced at midline at the level of cricothyroid space
-needle is advanced to pass through cricothyroid membrane,
and tip is directed submucosally laterally and upward to
reach muscle
-verification: subject asked to sustain low-frequency
phonation
-thyroarytenoid also shows marked activity during
swallowing and glottal attack
-lateral cricoarytenoid:
-point of insertion is almost same as for cricothyroid
-needle is then inserted laterally and slightly upward,
penetrating cricothyroid membrane at a point anterior to
inferior tuberculum of thyroid cartilage and deeply enough to reach lateral cricoarytenoid
-verification: patient hold his or her breath or attempt glottal stop production
-posterior cricoarytenoid and interarytenoid:

-peroral route
-indirect laryngoscopy, a curved probe bearing a needle electrode at its tip is directed to point of
insertion through mucosa covering targeted muscle
-verification is made by having subject repeat short periods of vowel phonation interspersed with
deep, quick inspiration
-posterior cricoarytenoid is active for inspiration and suppressed during phonation
-interarytenoid: general pattern of interarytenoid activity is almost reciprocal to posterior
cricoarytenoid
Pharyngeal muscles
-perioral approach is always attempted with subject in a sitting or a supine position
-levator palatini:
-insertion is made into levator ‘‘dimple’’ on soft palate, approximately 1 cm from midline and 1
cm from posterior edge of hard palate
470
-palatoglossus and palatopharyngeus:
-inserting an angulated needle into anterior and posterior pillars
NORMAL ELECTROMYOGRAPHY PATTERNS
-in general:
-complete relaxation of healthy muscles gives no EMG activity
-NMU activity is recorded as action potentials when muscles contract
-strength of contraction of abductor laryngeal muscle (posterior cricoarytenoid) increases during deep
inspiration, whereas that of adductors increases during phonation, coughing, and swallowing
-pharyngeal muscle activity also increases during swallowing
PATHOLOGIC ELECTROMYOGRAPHY PATTERNS: LARYNGEAL AND PHARYNGEAL

PARALYSES
-EMG is now widely accepted as a routine procedure for examination of facial, pharyngeal, and laryngeal
paralysis
-useful in differentiating laryngeal paralysis from mechanical fixation of CAJ and in estimating degree and
prognosis of paralysis
-usually two innervation territories (i.e., thyroarytenoid innervated by recurrent laryngeal nerve and
cricothyroid innervated by superior laryngeal nerve) are examined bilaterally
Normal laryngeal EMG pattern of TA during phonation and A. Incomplete paralysis. B. Complete paralysis.
deglutition
-in B: type of discharge is termed a fibrillation potential; prognosis for paralysis is usually poor
-synkinesis:
-misdirected regeneration of nerves to abductor and adductor muscle groups
-volitional EMG activity is recorded months to years after onset of paralysis without any sign of a
recovery of vocal cord mobility
LIMITATIONS OF ELECTROMYOGRAPHY EXAMINATION
-technical difficulty of its application

-verification of accurate placement of electrodes is notably difficult in patients with paralysis
471
LARYNGEAL AND PHARYNGEAL FUNCTION
PART ONE: BREATHING AND SPEECH
(Cummings - Chapter 98)
LARYNGEAL MOTION
-vocal folds move in three dimensions, and length and shape may be actively altered
LARYNGEAL FUNCTION IN BREATHING
Protection
-laryngeal closure reflex is sensitive in infants and may be elicited by a stimulus as weak as water
-reflex increases, then decreases, along a time course similar to that of the incidence of SIDS,
suggesting that laryngeal reflexes may play a role in its cause
Cough
-plays important role in cleaning the tracheobronchial tree and in maintaining patency of the lower
airways
-abnormal cough may be a serious clinical problem
Control of Ventilation
-larynx regulates airflow
Sensory receptors
-larynx location of variety of sensory receptors
-exert influences on breathing and cardiovascular function
-three major types of laryngeal respiratory receptors: negative pressure, airflow, and ‘‘drive”
Circulatory reflexes
-stimulation of larynx affects heart rate and blood pressure
-bradycardia and hypertension
-afferent limb: superior laryngeal nerve
PHARYNGEAL FUNCTION IN BREATHING

-most of muscles acting on pharynx show no respiratory activity during awake, tidal breathing, but they are
recruited by increased respiratory drive or upper airway obstruction
-most important pharyngeal dilator is the genioglossus (GG)
-fan-shaped muscle originating from anterior mandible and spreads out to insert into tongue
-may be responsible for pulling base of tongue forward to dilate the airway
FUNCTION IN SPEECH
-three fundamental components in the processes: phonation, resonance, and articulation
-phonation: generation of sound by vibration of the vocal folds
-resonance: induction of vibration in the rest of the vocal tract to modulate laryngeal output
-articulation: shaping of voice into words
Phonation
-requirements for phonation:
-adequate breath support
-approximation of vocal folds
-favorable vibratory properties
-favorable vocal fold shape
-control of length and tension
-voice cycle:
-exhalation causes subglottic pressure to increase until the vocal folds are displaced
laterally
F.Ling - Laryngeal and Pharyngeal Function (1)
472
-produces sudden decrease in subglottic pressure
-forces that contribute to return of vocal folds to midline:
-pressure decrease
-elastic forces in the vocal fold
-Bernoulli effect of airflow
-vocal folds return to midline, pressure in trachea builds again, and cycle is repeated
-‘‘body-cover’’ concept of phonation:

-vibration of mucosa does not correspond directly to that of rest of vocal fold
-‘body’’ of vocal fold is relatively static, whereas wave is propagated in mucosal
‘‘cover’’
-mucosal wave begins on inferomedial aspect of vocal fold and moves rostrally
Expiratory force
-breath support available for phonation becomes a clinical issue in two situations:
-functional dysphonia:
-insufficient prephonatory inspiration excessive glottic pressure required to
produce acceptable volume
-may lead to stress-induced injury of the vocal folds
-patient has an organic voice disorder and impaired pulmonary function limits capacity to
compensate for glottic defect
-eg. pt with laryngeal paralysis more symptomatic with coexisting emphysema
Vocal fold positioning

-gap too wide: breathy voice is breathy, aphonic, only turbulent airflow noise and no periodic
sound
-vocal folds are too tightly apposed: excessive pressure required, phonation sounds strained or
may not even be possible
Pitch control
-changes in vocal fold length and tension are used to control the fundamental frequency of vocal
fold vibration to produce dynamic inflections of the voice
-size and physical properties of a larynx determine the range of pitch that may be produced
-age-related loss of elasticity and increasing ossification of the thyroid lamina result in an
elevation of pitch
Resonance
-phonated sound acquires the characteristics of a human voice because of resonance of chest,
upper airway, and skull
VOICE ANALYSIS
Self-assessment
-patients subjective assessment of their own voice
Perceptual Analysis
-perceptual analysis is an important component of voice evaluation because it is the only approach that
really addresses how the voice sounds to other humans
-a systematic perceptual assessment involves ranking voice according to a standard scale
-voice may be described in terms of pitch, loudness, and vocal quality
-most commonly used scales employ ordinal severity rankings of equal-appearing intervals, usually with
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scores of one to seven in a few judgment categories, such as breathiness or roughness
-GRABAS Scale, widely used
-G: Overall grade
-R: Roughness
-B: Breathiness
-A: Asthenic quality
-S: Strain
Rating system: 0 Normal; 1 Mild abnormality; 2 Moderate dysfunction; 3 Severe impairment
-Perceptual voice abnormalities:

-abnormally high or low pitch
-abnormally loud or soft voice
-hoarseness
-diplophonia
-harshness
-tremorous
-breathy
-arrest of phonation
-aphonia
-stridorous
-hyper- or hyponasality
Performance Assessment
-graphic plot of the pitch and loudness ranges is termed the phonetogram = voice profile
-one limitation of the phonetogram is that it only measures pitch and loudness, and it is not sensitive to
changes in quality
-Maximal Phonation Time:

-maximum period for which a subject can maintain audible phonation of a vowel at comfortable
pitch and loudness
-average male: 22 to 34 seconds
-average female: 16 to 25 seconds
-prolonged MPT: excessive glottal closure (eg. adductor spasmodic dysphonia)
-low MPT: inadequate pulmonary reserve, glottal incompetence, or submaximal effort
-minimum of 5 seconds required to provide adequate phonation
-Phonation Quotient:
-MPT/vital capacity
-useful in sorting out contributions of pulmonary function and glottic competence when
equipment for aerodynamic testing is not available
Acoustic Analysis
-acoustic algorithms analyze the complex sound waves of the voice in the domains of frequency, intensity,
and time
-spectrographic analysis may be used to identify presence of noise or loss of harmonic components in a
sound and clearly documents voice or pitch breaks
-fundamental frequency:
-slowest component frequency in voice
-indicates the rate of glottal opening and closing
-one cycle of fundamental frequency corresponds to one glottal cycle
-males: ~128 Hz; females: ~256 Hz
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-harmonics to noise ratio: correlates with perception of voice roughness
-harmonics = frequencies that are integer multiples of fundamental frequency
-noise = frequencies that are not integer multiples of f0
-shimmer and jitter are referred to as perturbation measures; reflect instability of vocal fold
vibration
-shimmer = average cycle-to-cycle change in
amplitude (loudness)
-expressed as a percentage of the mean
amplitude
-normal = 0.50 dB
-jitter = average cycle-to-cycle difference
in duration of the cycle
(fundamental period)
-expressed in milliseconds or as a
percentage of cycle length
-normal = 0.40%
-perceptual correlate of increased levels of jitter and
shimmer is harshness
-Standard deviation of the fundamental frequency (SDF0)

-measured by determining f0 at several points within a sample and then statistically calculating
variability
-detects longer-term instability of vocal signal
-SDF0 is increased in those with neurologic disorders of motor control, which are characterized
by fluctuating pitch
-abnormal and correlates with hoarseness caused by local pathology
AERODYNAMIC ANALYSIS
-measurement of phonatory airflow, pressure, and volume provides information about respiratory support
and laryngeal valving
Mean phonatory flow rate

-most commonly used aerodynamic parameter
-sudden decreases in airflow result from adductor spasm, whereas abductor spasms manifest by sudden
increases in flow
-average airflow ~100-200 cc/s
-rate is lower with inadequate breath support
-increased phonatory airflow is seen in those with inadequate glottal closure caused by laryngeal paralysis,
tissues defects of the vocal fold, or mass lesions that prevent closure
Subglottic pressure
-degree of expiratory effort and tightness of glottic closure determine subglottic pressure
-subglottic pressure correlates with loudness
-techniques to measure subglottic pressure:
-include direct measurement by tracheal puncture or by suspending a miniaturized solid state
pressure transducer with its connections passing through the glottis
-esophageal pressure may be monitored as an indicator of intrathoracic pressure by using an
esophageal balloon, a fluid-filled catheter, or solid state transducer
-indirect estimation:
-intraoral pressure is monitored during repetition of the syllable /pi/ at a rate of about 1.5
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syllables per second
-when the lips are sealed and the glottis opens for production of a plosive consonant (P),
the pressure in the mouth should be same as in the subglottis, which should be the same
as that sustained during the phonation of /i/
Laryngeal resistance
-ratio of subglottic pressure to mean phonatory airflow rate
-a calculated value; only as reliable as the values measured or estimated for flow and pressure
-reflects degree of glottic closure, force of adduction, and vocal fold stiffness
-increased in patients with disorders manifesting as tight glottal closure, such as in those with spasmodic
dysphonia, plica dysphonia ventricularis, or hyperfunctional dysphonia
-low when glottal closure is inadequate, as in patients with abductor spasmodic dysphonia, hysterical
aphonia, or vocal fold tissue deficits
-vocal efficiency
-calculated by dividing sound pressure level of voice by simultaneously determined laryngeal
resistance
-reflects the amount of effort involved in phonation.
-phonation threshold pressure
-minimum subglottic pressure that can support phonation
VOCAL FOLD MOVEMENT
-videostroboscopy provides a slow motion image of vibration, but this is an average of motion over many
cycles and not a true account of motion
-glottographic techniques, including photoglottography (PGG) and electroglottography (EGG), offer
simpler alternatives
Electroglottography
-electroglottograph, also known as laryngograph, tracks changes in vocal fold contact during phonation by
measuring electrical impedance across larynx
-low-voltage, high-frequency (approximately 1 MHz) sinusoidal current is passed between two electrodes,
one over each side of the thyroid cartilage
-output is filtered to produce the ‘‘LX’’ waveform, which reflects the impedance between the two
electrodes
-current passes most easily (i.e., with lowest impedance) during the period in which there is greatest
surface area of contact between two vocal folds
-only provides information about closed phase of glottic cycle
-one useful application of EGG is to derive f0
-for this same reason, Lx is a useful signal for driving the stroboscope
Photoglottography
-makes use of light transmitted across the glottis to track vocal fold motion during phonation
-light usually is introduced above glottis via a fiberoptic scope or a flashlight in the mouth, with the
photosensor placed on the skin of neck over the upper trachea
-glottis behaves as a shutter, as the amount of light transmitted is proportional to the area of glottic
opening.
-PGG only provides information about the open phase of the glottic cycle and therefore is complimentary
to EGG
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-EGG and PGG permit calculation of:
-speed quotient = (opening time divided by the closing time)
-stiff vocal folds result in a low speed quotient because glottis opens slowly and snaps
shut quickly
-flaccid vocal folds result in a higher speed quotient because the vocal folds open easily
and quickly but drift back to midline more slowly
-open quotient = duration of opening time divided by glottal cycle
-shift quotient = time of peak opening over glottal cycle
477
NEUROLOGIC EVALUATION OF THE LARYNX AND PHARYNX
(Cummings)
IDENTIFICATION OF LESION SITE SYMPTOMS SUGGESTING

NEUROPATHOLOGY
-Cortex
-Aphasia -Speech problems
Lack of volume
-Aphonia Breathiness
-Dysarthria Instability of pitch or volume
-Dysphonia Lack of voice inflection
-Stridor Abnormal resonance
Dysarthria
-Extrapyramidal system: lesions result in abnormal motor control -Swallowing problems

-Vocal strain and pitch breaks Oral incompetence
-Tremor Velopharyngeal incompetence
Inability to initiate a swallow
-Spasmodic movements Aspiration
-Focal, regional, or generalized dystonia
-Breathing abnormalities
-Cerebellar lesions: impair coordination of motor activities Fluctuating inspiratory stridor
Weak breathy cough
-Ataxia ‘‘Gurgly’’ breathing noises
-uncontrolled loudness and pitch outbursts
-Dysmetria
-Tremor
-Incoordination
-Vocal strain similar to spasmodic dysphonia
-Brainstem lesions
-Flaccid paralysis
-Never isolated
-Peripheral nerve lesion

-Vagus nerve: flaccid, cadaveric position
-Recurrent laryngeal nerve: position variable, partial lesions, and aberrant regeneration common
-effect of an isolated superior laryngeal nerve lesion on level of vocal fold and rotation of glottis
also is controversial
-come report rotation of the glottis to the side of the lesion in patients with unilateral cricothyroid
muscle paralysis (although cricothyroid muscle does not appreciably influence the spatial
orientation of either the vocal fold or the glottis as a whole)
LARYNGOLOGIC MANIFESTATIONS OF NEUROLOGIC DISEASES
Myasthenia Gravis
-defect of the neuromuscular junction
-easy fatigue with muscle use
-symptoms:
-involvement of ocular muscles most common: ptosis, diplopia
-general fatigue
-difficulty speaking, breathing, or swallowing
-bulbar muscle weakness
-weakness of palatal muscles nasal twang to the voice and nasal regurgitation
478
-signs:
-fatigue of larynx and pharynx as a result of repetitive movements
-tests:
-EMG
-edrophonium (Tensilon) test
-treatment:
-ACh-esterase inhibitors
-thymectomy
-corticosteroids
-azathioprine, cyclophosphamide, cyclosporine
-plasma exchange: for acute worsening symptoms
-IV Ig
Amyotrophic Lateral Sclerosis

-idiopathic and progressive degeneration of upper and lower motor neurons
-results in muscle wasting, fasciculations, and weakness
-as many as 25% of these patients initially have complaints related to speech and swallowing
-death d/t respiratory insufficiency caused by weak breathing muscles and aspiration pneumonia
-voice symptoms:
-monotonous and raspy voice with abnormal hypernasal resonance
-speech is dysarthric and labored
-dysarthria is related to tongue involvement -d/t weakness and slowed tongue
-velopharyngeal incompetence
-signs:
-visible fasciculation in tongue “bag of worms”
-weakness in palate, pharynx, and larynx
-inability to make rapid muscle adjustments or repetitive motions
-pooling of secretions in the hypopharynx
-ALS vs MG: extraocular motion is preserved in ALS
-treatment:
-supportive care
-palatal-lift prosthesis may improve speech intelligibility and decrease nasal regurgitation during
speech
-NG or PEG to prevent aspiration
-tracheostomy for airway protection and assisted ventilation
Multiple Sclerosis
-diffuse demyelination process
-signs and symptoms consist of relapsing and remitting sensory and motor deficits
-visual problems, numbness, and limb weakness are common
-ENT problems include vertigo, tremor, scanning speech, and dysphagia
Bulbar Poliomyelitis
-postpolio syndrome
-syndrome may be derived from natural loss of motor neurons during the aging process
-acute bulbar polio causes pharyngeal and laryngeal paresis, but spares the cricopharyngeus
-leads to hoarseness, dysphagia, and aspiration
-cricopharyngeal myotomy often is helpful in patients with recent onset of polio
479
Palatal myoclonus
-uncommon disorder consisting of rhythmic contractions of the soft palate, pharynx, and larynx at a rate of
one to two contractions per second
-symptoms:
-unstable voice
-resulting speech sounds similar to that of spasmodic dysphonia
-caused by a specific lesion - infarction of central tegmental tract (CTT = pathway from the midbrain to the
inferior olive complex)
Parkinsonism
-hypokinetic dysarthria
-extrapyramidal syndrome caused by cell death in the substantia nigra
-symptoms: resting tremor, muscle rigidity, bradykinesia, and loss of postural reflexes, flat facial
expressions and abnormal posture
-speech:
-generalized bradykinesia sluggish articulation and monotone voice with decreased loudness
-vocal folds are adynamic and bowed
-tremor may affect voice
-less often, a predominant effect of rigidity on the larynx strained voice with frequent breaks
similar to voice of spasmodic dysphonia
Pseudobulbar Palsy
-spastic dysarthria
-bilateral lesions of corticobulbar tracts
-muscle spasticity and hyperreflexia of the pharynx, palate, lips, tongue, and larynx
-voice:
-harsh, strained, and strangled, and sounds somewhat like spasmodic dysphonia
-hypernasality and slow, labored articulation and emotional lability and subcortical cognitive
impairments
Essential Tremor
-common neurologic disorder affecting those in middle to late adulthood that causes 6 to 8 Hz shaking of
the hands, head titubation, and tremulous voice
-vocal symptoms related to tremor of muscles in the larynx, pharynx, and soft palate and, sometimes, in the
cervical strap muscles
-often responds to a local injection of botulinum toxin
Multiple System Atrophy

-commonly associated with failure of vocal-fold abduction with inspiration
-eg. Shy-Drager syndrome:
-idiopathic failure of the autonomic nervous system characterized by orthostatic hypotension,
impotence, sphincter dysfunction, and anhidrosis
-patients may require tracheotomy for airway obstruction
Dystonia
-uncontrolled contractions of any voluntary muscle or group of muscles and results in a torsional posture or
repetitive movements
-Spasmodic dysphonia appears to be an idiopathic focal dystonia of the larynx
-Meige’s syndrome is a regional dystonia of the head and neck
-may be evident in those with blepharospasm, oromandibular dystonia, torticollis, or spasmodic
dysphonia
480
-Laryngeal dystonia
-adductor dysphonia
-more common than abductor spasmodic dysphonia
-focal laryngeal dystonia, causes vocal fold hyper-adduction
-can be exacerbated by stress
-SSx:
-spasmodic closure of the vocal folds during speech strained and strangled
voice
-glottic stammering (phonation breaks)
-may be associated with other dystonia, tremors or difficulty in breathing
-tx:
-voice therapy
-botulinum toxin injections of thyroarytenoid and lateral cricoarytenoid muscles
-effective for an average of 3 months
-abductor dysphonia
-focal laryngeal dystonia(in fewer pts) intermittent or sustained opening of the larynx
during speech breathy voice breaks or a whispering voice
-tx:
-voice therapy
-botulinum toxin injections of posterior cricoarytenoid muscles
-Botox injections decrease the symptoms of patients with dystonia, particularly for patients with adductor
spasmodic
NEUROLOGIC EXAMINATION OF THE MOUTH, LARYNX, AND PHARYNX
Oral cavity
-Observe lips, palate, and tongue for abnormal spontaneous movement
-spasmodic motions are characteristic of Meige’s syndrome
-involuntary, slow, athetoid movements of the tongue tardive dyskinesia
-quivering, ‘‘bag of worms’’ characteristic sign of ALS
-test palatal movements and strength of tongue
-rapid repetition of the syllable “Pa” shows lip function, “Ta” shows tongue function
-LMN lesion decreases strength of this action
-UMN lesion decreases rate at which the patient can repeat the syllable, but regular rhythm
should be preserved
-cerebellar rhythm is erratic
-MG results in fatigue with repetitive motion
Flexible laryngoscopy
-Soft palate
-observed for any tremor or spasmodic movement at rest
-assess symmetry and competence of velopharyngeal closure
-Larynx
-repetitive phonations fatigue in patients with MG
-to assess the cricothyroid muscle (SLN), perform a pitch glide, phonating from a low pitch to a
high pitch and back down pitch should rise as the vocal folds become longer and thinner
-assess for hyperfunctional dysphonia:
-compression of the glottis in the anterior-posterior dimension
-contraction of aryepiglottic folds
481
-false vocal-fold adduction, which may be severe enough to totally obscure true vocal
folds
-pt elevate larynx and speak with a low lung volume
-amenable to voice therapy
-Stroboscopy:
-slowed motion allows the most accurate assessment of the mucosal wave, which may be impaired
by scarring, edema, or subtle defects in the mucosa
-subtle edema, vocal cord cysts, or early carcinoma adynamic segment of the vocal cord on
stroboscope.
-allows accurate evaluation of closing and opening pattern of the larynx
-vocalis muscle atrophy
-posterior laryngeal edema
-faulty vocal technique
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PHONOSURGICAL PROCEDURES
(Cumming’s)
Laryngeal framework surgery (Isshiki):

-medial displacement (type I)
-lateral displacement (type II)
-shortening or relaxation (type III)
-elongation or tensioning procedures (type IV)
MANAGEMENT OF UNILATERAL VOCAL FOLD MOTION IMPAIRMENT
Vocal fold medialization by injection
-performed using absorbable gelatin sponge or polytef

-polytef:
-used for permanent vocal cord paralysis]
-contraindicated if vocal cord function is likely to return
-gelatin sponge used as a temporizing measure
-injected percutaneously
-material injected lateral to vocalis muscle leaving the mucosa overlying vocal fold unaltered
Percutaneous injection
-through thyroid ala at level of vocal fold determined by
palpating thyroid notch and inferior border of thyroid ala
anteriorly
-an anterior approach may be used through cricothyroid
membrane, approaching the vocal folds from below
-needle angled superiorly and laterally under
direct visualization using a flexible fiberoptic
nasopharyngoscope.
Transoral injection
-indirect laryngoscopy
-injection performed using a curved laryngeal needle
Laryngoscopic injection
-usually under G/A
-arytenoid cartilages palpated to ensure mobility
-laryngeal needle inserted lateral to vocal fold 2 mm deep at the level of vocal process
-Polytef paste or absorbable gelatin sponge is injected at single click intervals
-complications:
-underinjection, requiring repeat procedures
-overinjection with airway compromise
-improper placement of polytef, causing subglottic extension and potential stenosis
-migration of polytef
-intrachordal injection of polytef, impairing vibratory capability
-granuloma formation
-management of overinjection: -incising the mucosa over the site of injection and removing
excess material by suction
-polytef granulomas also require surgical excision
F.Ling - Phonosurgery (1)
483
Medialization thyroplasty
-type I thyroplasty by Isshiki

-advantages:
-(1) it is performed with local anaesthesia
-(2) patient positioning is more anatomic, allowing better assessment of voice during the
procedure
-(3) it is potentially reversible
-(4) structural integrity of the vocal fold is preserved, allowing medialization in the presence of a
mobile vocal fold
-disadvantages:
-(1) the patient is subjected to an open procedure
-(2) procedure is technically more difficult
-(3) intubation for surgery subsequent to medialization may result in displacement of the
prosthesis or mucosal erosion secondary to endotracheal tube pressure
-indications:
-management of vocal fold paralysis
-vocal fold bowing resulting from aging or cricothyroid joint fixation
-sulcus vocalis
-soft-tissue defects resulting from excision of pathologic tissue
-paralytic dysphonia when recovery is anticipated:

-procedure considered for aspiration or severe dysphonia as an alternative to repeated
injections with absorbable gelatin sponge
Technique
-performed through window
in thyroid lamina at level of
vocal fold
-inner perichondrium remains
intact
-silactic or hydroxylapatite
implants used
-overmedialization is
supported by Isshiki and
others deterioration in
voice quality over time as
intraoperative edema resolved
in postoperative period
-complications:
-penetration of endolaryngeal
mucosa
-wound infection
-chondritis
-implant migration or
extrusion
-airway obstruction
-limitations: posterior glottic chink
484
Arytenoid adduction
-for posterior glottal chink or difference in level of two

vocal folds
-associated with high vagal nerve injuries when
denervation of ipsilateral cricothyroid muscle
and recurrent laryngeal nerve injury coexist
-arytenoid adduction procedure results in rotation of
arytenoid with downward displacement of vocal process
and closure of the posterior gap
-performed separately or in combination with type I
thyroplasty
-disadvantages:
- degree of difficulty and irreversibility
-contraindications:
-anticipated spontaneous recovery of function
Technique
-same incision used for medialization thyroplasty is extended just beyond posterior aspect of
thyroid lamina
-pharyngeal constrictor muscle is incised at its attachment to the thyroid lamina, exposing the
posterior margin
-cricothyroid joint disarticulated to allow exposure and elevation of piriform sinus mucosa
-penetration of endolaryngeal mucosa requires termination of procedure
-muscular process of arytenoid is identified by palpation beginning at the cricothyroid joint and
moving obliquely up the cricoid cartilage
-cricoarytenoid joint is opened by incising posterior cricoarytenoid muscle posterior to the
muscular process, allowing identification of the articulating surface
-adduction performed by tying two 4-0 nylon sutures around the muscular process and passing the
ends out through the thyroid lamina in directions that simulate the pull of the thyroarytenoid and
lateral cricoarytenoid muscles
-each suture is then tied over the thyroid lamina
Reinnervation procedures
-ansa hypoglossus and nerve branches to the anterior

belly of the omohyoid muscle are identified
-nerve carefully dissected to muscle insertion site a
block of muscle is removed, 2 to 3 mm per side
-inner perichondrium of thyroid ala opened and
thyroarytenoid muscle incised superficially; muscle
pedicle sutured in place
-reinnervation procedures limited to management of

abductor or adductor paralysis
-require presence of an appropriate donor nerve or
nerve-muscle pedicle
-not primary procedure for aspiration
485
BILATERAL VOCAL FOLD MOTION IMPAIRMENT
-airway management: tracheotomy

-most procedures that enlarge laryngeal airway, thus eliminating need for tracheotomy, result in poorer
quality voice and increased possibility of aspiration
-procedures:
-endoscopic arytenoidectomy
-lateralization of the vocal cord by suture placement
-laser arytenoidectomy:
-only good for removing anterior 2/3 of vocal cord; posterior 1/3 represented by
arytenoid more difficult to remove successfully laser
-partial arytenoidectomy predisposes pt to a greater incidence of postoperative chondritis
-laser cordotomy:
-transverse incision is made with laser through vocal fold immediately anterior to vocal
process wedge-shaped widening of posterior glottis
-external arytenoidectomy
-maximum success rate for any of these procedures is generally 70%
Management of bilateral vocal fold motion impairment with weak voice and aspiration
-bilateral adductor paralysis is an unusual condition characterized by weak voice and aspiration
-methods effective with unilateral adductor paralysis, specifically injection of polytef paste, surgical
medialization, or arytenoid adduction, are not effective in this setting
-narrow-field laryngectomy most effective method for prevention of aspiration; however, it results in
elimination of the larynx as an organ of communication
-Other surgical approaches:
-epiglottic sew-down procedure
-surgical approximation of vocal folds
-tracheal diversion procedures
SPECIAL CONSIDERATIONS IN PHONOSURGERY
Surgical procedures to alter vocal pitch
Lower pitch
-Type III thyroplasty
-for mutational falsetto and gender transformation
may be considered only after 3 to 6 months of voice
therapy and, when indicated, psychologic evaluation
and therapy
-dysphonia resulting from increased vocal fold
stiffness associated with laryngeal trauma,
radiotherapy, chronic laryngitis, sulcus vocalis, and
vocal fold atrophy Type III thyroplasty: A, Location of cartilaginous incisions. B,
-pts present with high vocal pitch associated with a Cartilaginous strips are removed. C, Relaxation of the vocal
narrow glottal chink and small amplitude mucosal folds decreases tension and the size of the glottic aperture.
wave
486
Elevated pitch
-lengthening the vocal folds elevating vocal pitch
-achieved by advancing anterior commissure or by cricothyroid approximation
-indications:
-vocal fold bowing resulting from aging or trauma
-postsurgical defects
-androphonia
-gender transformation
-other methods:
-decrease vocal fold mass increasing frequency of vibratory cycle
-by removing tissue with laser or by mechanically inactivating the vocalis muscl
-vocal fold stripping
-laser vaporization
-steroid injection
Lengthening procedures
-Expansion of thyroid ala

-incising thyroid lamina in vertical dimension at
junction of anterior and middle one third of thyroid
ala
-Silastic strip implant is secured between the edges
-most technically difficult lengthening procedure
-Anterior commissure advancement: LeJeune procedure

-inferiorly based flap or superiorly based flap
-use of tantalum shim
-Cricothyroid approximation
-simulates contraction of the cricothyroid muscle
-nonabsorbable mattress sutures placed, first
through cricoid cartilage and then through
thyroid cartilage
-simplest and safest lengthening procedure
-disadvantages include greater risk of reversion to lower pitch and potential narrowing of pitch range
Sulcus vocalis
-congenital soft-tissue deficit or linear furrow running longitudinally along the free edge of true vocal fold
-furrow may vary in length and depth extreme cases the sulcus divides medial edge into an upper and
lower lip double vocal fold appears
-cause unknown
-symptoms related to incomplete glottal closure:
-decrease in phonation time
-breathy high-pitched turbulent airflow
-speech therapy not been successful in managing symptomatic patients, and surgery has been directed
toward correcting the incomplete glottal closure
-management:
-intrachordal injection with cartilage paste or paraffin or collagen
-lengthening and shortening procedures
-medialization thyroplasty has been used successfully in managing patients with sulcus vocalis
487
BENIGN VOCAL FOLD MUCOSAL DISORDERS
(Cummings)
-membranous vocal fold layers (5):

-nonkeratinizing, stratified squamous epithelium
-lamina propria:
-superficial layer
-mostly amorphous material
(Reinke’s potential space)
-intermediate layer
-mostly elastic fibers
-elastin
-hyaluronic acid
-fibromodulin
-deep layer
-mostly collagenous fibers
-vocalis muscle = thyroarytenoid muscle
-“body-cover” concept:
-cover:
-epithelium and superficial layer of lamina propria
-transitional zone:
-intermediate and deep layer of lamina propria = superior free edge of conus elasticus = vocal
ligament
-vocal fold muscle = body
EVALUATION OF PATIENT
History
1. Onset and duration of vocal symptoms.

2. Patient beliefs about causes or exacerbating influences.
3. Common symptom complexes.
4. Talkativeness (vocal personality or ‘‘push from within’’).
5. Vocal commitments or activities (‘‘pull from without’’), including voice type and training if a performer.
6. Other risk factors.
7. Patient perception of severity of the disorder.
8. Vocal aspirations and consequent motivation for rehabilitation.
Other risk factors

-tobacco and alcohol use
-acid reflux
-insufficient fluid intake
-certain drying medications
-systemic illnesses
-allergies
F.Ling - Benign Vocal Fold Lesions (1)
488
GENERAL MANAGEMENT OPTIONS
-hydration
-sinonasal management
-when optimal laryngeal function is of concern, as in a vocal performer, nasal conditions should
be managed locally (topically) when possible
-management GERD
-avoiding caffeine, alcohol, and spicy foods
-eating the last meal of the day (preferably a light one) no fewer than 3 hours before retiring
-using bedblocks to place the bed on a mild head-to-foot slant
-taking at bedtime an antacid or H2 blocker, or proton pump inhibitor 1 hour before dinner
-systemic medicines that may affect the larynx
-e.g., antidepressants, decongestants, antihypertensives, diuretics may dry and thicken normal
secretions mucosa more vulnerable to the development of benign disorders
SPECIFIC BENIGN VOCAL FOLD MUCOSAL DISORDERS
Vocal nodules
-term reserved for lesions of proven chronicity
-occur most commonly in boys and women: ‘‘vocal overdoers’’
-pathophysiology:
-only anterior 2/3 of vocal folds participates in
vibration
-localized vascular congestion with edema at the
midportion of the membranous (vibratory) portion of
the vocal folds, where shearing and collisional forces
are greatest submucosal swelling
-long-term voice abuse hyalinization of Reinke’s
potential space and possibly some thickening of the
overlying epithelium
-laryngeal examination:
-nodules can vary in size, contour, symmetry, and color
-do not occur unilaterally
-management:
-medical: -good laryngeal lubrication through general hydration, managing contributions
of allergy and reflux
-behavioural: -voice therapy should play a primary role initially
-surgical: -option when nodules persist and voice remains unacceptably impaired (from
the patient’s perspective) after an adequate trial of therapy (generally a
minimum of 6 months, usually much longer)
Capillary ectasia
-occurs most often with vocal overdoers
-dilated capillaries more frequent in women speculation of estrogen effect
-pathophysiology:
-repeated vibratory microtrauma may lead to capillary angiogenesis
-capillary ectasia predisposes to mucosal swelling, a small incidence of vocal fold hemorrhage,
and hemorrhagic polyp formation
489
-diagnosis:
-most often in female singers who complain that they
become a little hoarse after relatively short periods of
singing (reduced vocal endurance)
-abnormal dilation of the long arcades of capillaries that
proceed mostly anterior to posterior
-capillary lake: confluent dilated capillaries that almost
resemble a chronic haemorrhage
-management:
-medical: -stop anticoagulant drugs; treat acid reflux
-behavioural: -usual behavioral changes, which are also appropriate for persons with nodules,
are advocated
-no sudden, explosive use of voice
-surgical: -spot-coagulation to interrupt blood flow every few millimetres
Vocal fold hemorrhage and a unilateral (hemorrhagic) vocal fold polyp

-more common in men, particularly men who engage in
intermittent severe voice abuse or who work in noisy
environments
-pathophysiology :
-shearing forces acting on capillaries within the
mucosa during extreme vocal exertion lead to
capillary rupture
-diagnosis:
-abrupt onset of hoarseness during extreme vocal
effort
-largely unilateral lesion process in the node position, a contact reaction on the fold opposite the
polyp, or a nodule if the person is a longstanding overdoer
-treatment:
-medical: -stop anticoagulant medications
-behavioural: -short course of voice therapy is appropriate, mainly to instruct the patient in
voice care
-small, early hemorrhagic polyp will resorb completely with many months of
conservative measures
-surgical: -evacuation of blood through a tiny incision in a recent large haemorrhage
-long-standing polyp trimmed away superficially
Intracordal cysts
-history of vocal overuse
-histological classification:
-epidermoid inclusion cyst (EIC)
-contain accumulated keratin
-rupture of cyst leaving opening as large as cyst glottic sulcus
490
-mucus retention cyst (MRC)
-arise when duct of a mucus gland becomes plugged and retains glandular secretions;
epidermoid cysts
-diagnosis:
-history of voice abuse factors
-MRC often cause less vocal limitation than anticipated
from laryngeal appearance; EIC often cause more
limitation than expected
-MRC mucus retention cysts often originate just below
the free margin of the fold with significant medial
projection from the fold
-EIC project less from the fold and are harder to
diagnose when small
-treatment:
-medical: -hydration, potential acid reflux management may be helpful
-behavioural: -postoperative voice therapy may facilitate healing
-not successful for treatment, requires surgical removal
-surgical: -careful dissection around the cyst free of the mucosa and vocal ligament
-postoperative recovery takes longer than for nodule or polyp surgery (many
months rather than a few weeks)
Glottic sulcus
-occurs exclusively in the vocal overdoer
-pathophysiology:
-“congenital” vs “acquired”
-an epithelium-lined pocket whose lips
parallel the free edge of folds may
represent an epidermoid cyst that has
spontaneously emptied, leaving the
collapsed pocket behind to form a sulcus
-mucosal bridge: result of two parallel
sulci arising from a single cyst
-diagnosis:
-voice overuse and complaints of chronic
hoarseness
-stroboscopic evaluation reveals a segment of reduced vibration
-microlaryngoscopy required for definitive diagnosis because the lips of the sulcus are only
occasionally faintly visible with inspiratory phonation during the office or voice laboratory
examination
-management:
-surgical: -removal is technically demanding; involves considerable disturbance of the
vocal fold mucosa
-cordal injection to make the sulcus lips spread and the sulcus more shallow and
491
to accomplish some hydrodissection
-circumcision of lips of sulcus and dissection of the invaginated mucosal pocket
from underlying fold without injuring the vocal ligament
Bilateral diffuse polyposis

-chronic Reinke’s edema or smoker’s polyps
-middle-aged women who have been long-term smokers
-pathophysiology:
-chronic smoking and voice abuse edema, vascular congestion, and venous stasis diffuse
polypoid changes
-diagnosis:
-voice examination reveals lower pitch than would be
expected, often well into the masculine range for
women
-upper voice is lost
-pale, watery bags of fluid attached to the superior
surface and margins of the folds
-management:
-medical: -stop smoking
-thyroid function tests if hypothyroidism is suspected
-behavioural: -short-term voice therapy: may reduce the polyps’ turgidity, with a
corresponding modest improvement in vocal functioning.
-surgical: -polyp reduction with mucosal sparing
Postsurgical dysphonia
-vocal fold stripping or laser vaporization of mucosa that removed underlying fibrous tissue or even muscle
-pathophysiology:
-results from scarred stiff vocal fold cover, phonatory mismatch of the vocal fold margins, or both
-videostroboscopy is essential
-allows careful analysis of mass lesions, areas of asymmetry, and the mucosa’s vibratory pattern
-management:
-behavioural: -voice therapy voice building approach
-using voice will soften scar tissue
-goals are to strengthen the laryngeal musculature to compensate for the
damaged mucosa and to encourage the mucosa to oscillate more freely because
of this sort of ‘‘phonatory massage’’of the mucosa
Contact ulcer or granuloma

-seen primarily in males—commonly in lawyers, ministers, teachers, and executives
-chronic coughing or throat clearing and reflux of acid from the stomach into the posterior larynx during
sleep also seem to cause contact ulceration
492
-pathophysiology:
-thin mucosa and perichondrium overlying the cartilaginous
glottis become inflamed
-acid reflux may also increase inflammation of the vocal
process area.
-traumatized area ulcerates or produces a heaped-up
granuloma
-depressed, ulcerated area with a whitish exudate clinging to it
or a bilobed, heaped-up lesion on the vocal process may be
noted
-management:
-empiric antireflux regimen
-maturation and resolution may occur spontaneously over 3 to 6 months
-surgery as last resort because postoperative recurrence of ulcer or granuloma is predictable
-microlaryngoscopy if after a several-month trial of management an uninflamed, pedunculated
lesion remains and is causing symptoms
-removal should be limited, leaving the base or pedicle undisturbed
Intubation granuloma
-pathophysiology:
-direct abrasion of the arytenoid perichondrium, a break in the mucosa covering it as a result of
coughing on ETT, or long-term pressure necrosis of the vocal process area
-often large and spherical with some pedunculation
-attached directly to vocal process and are frequently bilateral
-may be partial or complete fixation of one or both arytenoid cartilages
-interarytenoid synechium also may be noted on occasion
-management:
-with time intubation granulomas usually mature and ‘‘fall off’’
-persistent granuloma:
-surgery or a trial of indirect corticosteroid injection in the office may be an option
-any identifiable stalk should be left with patient to minimize size of the surgical wound
BENIGN MESENCHYMAL NEOPLASMS
-benign tumours of the larynx are rare
Epithelial tumours
Recurrent respiratory papillomatosis

-squamous papillomas most common benign neoplasms seen by laryngologists
-4.3 per 100,000 children and 1.8 per 100,000 adults
-mucosal infection by HPV
-association between maternal genital condylomata and recurrent respiratory papillomatosis is
known - only 1 in 400 children at risk relatively low infectivity
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-types:
-juvenile form:
-papillomatosis usually presents in infancy or childhood as
hoarseness and stridor
-often aggressive and rapidly recurrent, requiring frequent
laryngoscopies for management
-tracheal and brochial involvement increased with history of
tracheotomy, a high number of endoscopic procedures, and a
long duration of the disease
-adult-onset:
-occasionally solitary or at least more localized than juvenile-onset ones
-less aggressive
-treatment:
-carbon dioxide laser remains the most widely accepted management for papillomas in the larynx
-laser preferred because of precision and hemostatic properties
-other possible treatments:
-interferon: papillomas tended to regrow on cessation of interferon
-indole-3-carbinol, a natural derivative of cruciferous vegetables such as cabbage and
broccoli
-methotrexate
-cis-reninoic acid
-intralesional (S)-1-(3-hydroxy-2-phosphonylmethoxypropyl) cytosine as potential
management for many deoxyribonucleic acid (DNA) viruses, including human
papillomavirus
-some medical management modalities hold promise; all need further investigation and validation
-optimal management is careful serial laser laryngoscopies with consideration of investigational
use of interferon, indole-3-carbinol, or hydroxy phosphonyl methoxypropyl cytosine for patients
with a particularly severe form of this disease
Vascular neoplasms
Polypoid granulation tissue

-polypoid granulation tissue is the most common vascular tumour in the larynx
-consists of radially arranged capillaries
-formation attributed to several forms of trauma
-treatment:
-conservative measures, including removal of the source of any ongoing irritation, as from
inappropriate voice use or acid reflux laryngitis, and intralesional corticosteroids
-endoscopic removal for nonresponse and continuing symptoms
Laryngeal hemangiomas
-often have associated with cutaneous haemangiomas
-mucosa-covered mass with or without bluish coloration may be seen in the subglottis
-management:
-tracheotomy for airway protection
-gives hemangioma an opportunity to involute spontaneously
-carbon dioxide laser for small, symptomatic tumours
-adult hemangiomas usually found at or above the level of the vocal folds
-should be left alone if at all possible
-corticosteroid or radiotherapy used when necessary
-carbon dioxide laser is not generally advised for adult cavernous hemangioma because the
494
diameter of the vascular spaces exceeds this laser’s coagulating ability
Muscle neoplasms
Rhabdomyoma
-can be confused with a granular cell tumour or a rhabdomyosarcoma
-complete local excision is curative
Neoplasms of adipose origin
Lipoma
-most frequent site of origin: false vocal fold
-conservative excision with complete removal or enucleation because incompletely removed lipomas
regrow
Benign neoplasms of glandular origin
Benign mixed neoplasm

-pleomorphic adenomas are extremely uncommon in the larynx
-most of tumours involve the subglottic laryngeal region
Oncocytic neoplasms of larynx

-oncocytic metaplasia and hyperplasia of the ductal cell portion of glandular tissue
-simple excision is the management of choice by whatever approach necessary according to lesion size and
location.
Cartilaginous neoplasms
Chondroma
-‘‘obvious smooth rounded mass covered by mucous membrane in the subglottic region of the larynx,’’ and
in most cases this mass was situated posteriorly and laterally
-laryngofissure used most often for removal and total laryngectomy for high-grade malignant tumours
Neoplasms of neural origin
Granular cell neoplasms

-granular cell tumours originate in Schwann cells
-frequent association with overlying pseudoepitheliomatous hyperplasia of the mucosa
-insufficiently deep biopsy of this lesion may lead to an incorrect diagnosis of epidermoid
carcinoma
-middle to posterior part of the true vocal fold is the most frequent site
-conservative but complete local excision is considered definitive therapy
Neurofibroma
-most common site of origin was the arytenoid or aryepiglottic fold
Neurilemmoma
-less common than neurofibromas and usually involve the aryepiglottic fold and false vocal fold
-conservative but complete removal by an approach consistent with tumour size and location
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LASER SURGERY OF THE LARYNX
(Cummings)
-carbon dioxide, potassium-titanyl-phosphate (KTP), and neodymium:yttrium-aluminum garnet (Nd:YAG) lasers

main wavelengths used
-applications:
-removal of benign lesions
-excisional biopsy of T1 lesions
-incisional biopsy and biologic staging of T2-T3 lesions
-debulking of obstructing tumours to secure an airway and avoid tracheotomy
-palliation of poor surgical candidates or patients with terminal disease
-debulking of tumour mass before radiotherapy
BENIGN CONDITIONS
-carbon dioxide laser

-microspot delivery system (0.3 mm spot diameter)
-power settings from 1 to 3 W are sufficient
-0.1-second intermittent pulses
-usual magnification setting on the microscope is 16x
Nodules
-excision required when lesion is well organized or fibrotic or if there is suspicion about the nature of the
lesion
-careful low-power vaporization from medial to lateral is technique of choice
Polyps
-excision using carbon dioxide laser allows precise removal because of its hemostatic capability and
nontouch technique, which does not obscure the surgeon’s view
-postsurgical management includes complete voice rest for 48 hours, followed by soft vocalization for 10
days
Cysts
-managed with the carbon dioxide laser by unroofing the cyst, aspirating its content, and marsupializing it
completely
Granuloma
-best management is to remove the factor that is causing chronic inflammation
-if surgical management is required, the carbon dioxide laser is ideal for excision
-postoperative antibiotics and systemic corticosteroids for up to 1 month is usually necessary for complete
resolution and healing
Papillomatosis
-frequent excisions recommended in children to avoid a tracheotomy and to allow the child to develop
good phonation, preserving normal vocal cord anatomy as much as possible
-done at a power setting of 2 to 3 W (0.3 mm spot size), at a 0.5- to 1-second exposure
-lesions vaporized to level of mucosa; avoid entry into Reinke’s space and deeper vocal ligament
-anterior commissure should also be avoided, leaving at least 1 mm of mucosa unmanaged
F.Ling - Laser Surgery of the Larynx (1)
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Arytenoidectomy
-for management of bilateral vocal cord paralysis
-carbon dioxide laser is coupled to an operating microscope with a 400-mm objective lens
-laser settings: 0.1-second pulse duration, in repeat intermittent mode, at the power of 10 W and a
focussed spot size of 0.8 mm (20 W/cm2)
-disadvantages:
-(1) inaccuracy in final placement of the vocal cord as compared with external procedures
-(2) learning curve associated with the laser
-complications:
-granuloma formation, posterior commissure strictures, complete or partial failure with
medialization of the cord, loss of good voice production, perichondritis, and aspiration through a
largely patent posterior commissure
Infantile subglottic hemangioma

-present as a lateral subglottic submucosal bluish mass, causing respiratory symptoms
-if mildly symptomatic managed conservatively with corticosteroids and observation
-usually involute spontaneously with time
-carbon dioxide laser is used to vaporize tumour until an adequate airway is achieved
-Nd:YAG laser NOT RECOMMENDED for subglottic hemangiomas because these lesions are more
compact capillary-type vascular lesions
Laryngeal stenosis
-scar tissue is excised using a carbon dioxide laser with a spot size of 0.3 mm at 2 watts of power
(irradiance, 21.1 W/mm2) directed by a micromanipulator
-ensure mucosa over arytenoids and uninvolved interarytenoideus muscle are not injured
-surgical wound after scar excision is covered with autologous fibrin glue
-mucosal buccal graft to cover the mucosal defect
LARYNGEAL CANCER
Excision
Glottic cancer
-excision of early tumours of true vocal cords
-lesions most suitable for transoral laser excisional biopsy
-hyperkeratosis, dysplasia, carcinoma in situ, and early invasive squamous cell carcinoma (T1
tumours)
-excellent cure rate for T1 squamous cell carcinoma using this approach, which is comparable with results
achieved with radiotherapy
-criteria for endoscopic excision:
-lesion should be minimally invasive
-localized to the mid to anterior portion of true vocal cord
-should not extend to anterior commissure, the vocal process of the arytenoid cartilage, or
supraglottic or subglottic larynx
-vocal cord mobility should be normal, which indicates minimal deep invasion of the carcinoma
-if the tumour extends into anterior commissure region recurrence is likely with an endoscopic technique
-advantage of using laser is noncontact microprecision in a bloodless field
-potential disadvantage: risk of thermal damage, which for superficial lesions (e.g., keratosis, dysplasia)
puts an extra burden on the clinician in regards to the need for meticulous technique
497
-carcinoma in situ:
-deeper excision exposing the vocalis muscle is required, and a 2- to 3-mm margin around the
tumour is obtained
-if lesion is found to violate vocal ligament invasive carcinoma.
-T1 lesions:
-carbon dioxide laser offers a 90% cure rate which is comparable with that for radiotherapy
-offers one-session treatment versus the multiple treatment sessions required with radiotherapy
-associated with less morbidity, can be repeated in cases of failure, and can be done as a biopsy
procedure
-when lesion extends to anterior commissure or to arytenoid cartilage, carbon dioxide laser
excision is contraindicated.
-margin of at least 2 to 3 mm of healthy surrounding tissue
-6-8 W of energy are used in a pulsed 0.1-second exposure
Supraglottic carcinoma
-role of carbon dioxide laser excision for supraglottic carcinoma is limited
-rare situations, a small T1 epiglottic carcinoma involving the suprahyoid portion of the epiglottis, the rim
of the arytenoepiglottic fold, or both can be managed by endoscopic laser excisional techniques
-radiotherapy is management of choice for patients with these tumours because the primary cancer and
high-risk lymph nodes are managed simultaneously
-laser usually used for a patient who refuses radical management, a high-risk surgical candidate, a patient
requiring palliation of symptoms) used for staging and to secure an airway
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VOICE REHABILITATION AFTER LARYNGECTOMY
VOICE RESTORATION PROCEDURES
Artificial Larynx
-rapidly learned speech substitute
-placement on neck or tube adapter to direct sound to oral cavity
-advantages: low cost, availability, short learning time, loudness
-disadvantages: dependence on batteries, mechanical sound, conspicuous appearance, loss of hands-free
speech, hygiene of intraoral tubes or dental appliance
Esophageal Speech
-only 30% of laryngectomized population develop useful esophageal speech
-voice is low in fundamental frequency (~65 Hz)
-air trapped and stored in esophagus (80 ml) released by diaphragmatic action to produce speech
-disadvantages: low acquisition rate and prolonged learning period
Shunts and Valves

-limited use because of a series of problems:
-particularly following radiation, mucosal-lined tracts are difficult to maintain
-continued salivary flow through them causes inflammation, breakdown, and necrosis
-risk of aspiration
-radiation therapy has been a general contraindication to techniques that rely on tissue valving
-inability to place prosthetic material in contaminated airway for long-term incorporation
Tracheoesophageal Prosthesis (duckbill voice prosthesis)

-placed through tracheoesophageal puncture
-direct midline communication from posterior trachea to anterior esophagus at location inferior to
cricopharyngeus muscle and pharyngeal constrictor muscles
-provides more natural phrasing
-produces intense, continuous sound
-more acoustically similar to normal laryngeal speech and more intelligible and acceptable than standard
esophageal speech
PATIENT EVALUATION FOR SECONDARY TRACHEOESOPHAGEAL PUNCTURE CANDIDACY
-reduced success of voice restoration due to:

-pharyngeal stricture with symptomatic dysphagia
-radiation exceeding 65 Gy
-malnutrition
-diabetes, dementia, severe COPD
-contraindication to voice restoration is microstomia
-preoperative esophageal insufflation test to predict likelihood of successful secondary tracheoesophageal

speech
-estimates possibility of dysfluency from pharyngeal constrictor spasm
-subjective evaluation of esophageal distention but should not be used as sole method for
determining need for open-neck exploration and pharyngeal constrictor relaxation
-pharyngoesophageal spasm may be confirmed by anesthetic block of pharyngeal plexus
-evaluation by videofluoroscopy
F.Ling - Rehab after Laryngectomy (1)
499
-anesthetic placed at level of prevertebral fascia - skin entered at level of C2-C3
immediately parapharyngeal and medial to carotid sheath
-typical appearance shows reduction in mass of constrictor muscles, including axial
length
DIFFERENTIAL DIAGNOSIS FOR SPEECH FAILURE
-prosthesis failure: position, size, type, patency

-reflex pharyngeal constrictor spasm (most common cause for failure)
-non-vibrating pharyngoesophageal segment:
-radiation induced
-edema
-reconstructed segment
-puncture closure
-inadequate air supply
-decreased respiratory support
-improper stoma occlusion
-largest percentage are pts who reflexively elevate upper esophageal sphincter pressure during esophageal
distention above threshold for voice fluency
-using breath control and internal feedback reduce esophageal distention and resultant upper
esophageal sphincter tonicity
-open-tract test: voice prosthesis removed and patient voices
-demonstrates failure is result of mechanics of unfavourable voice prosthesis
-if voice retains strained quality after proper fit change to TEP with low-resistance
characteristics and larger diameter
MANAGEMENT
-candidiasis results in premature failure of prosthesis (usually valve degradation with aspiration of liquids
through the prosthesis)
-tx with oral Nystatin
-persistent pharyngoesophageal spasm after successful primary TEP
-pharyngeal constrictor myotomy
-pharyngeal constrictor neurectomy
-botulinum toxin A injection
VOICE RESTORATION DURING LARYNGECTOMY
-requires careful construction of tracheostoma and pharyngeal constrictor relaxation procedure

-constrictor myotomy in posterior midline raphe or pharyngeal plexus neurectomy
RESULTS
-failures ~15%; after revision failures ~9%

-speech successful 10-35 days postop
-tracheostoma stenosis in 4%
-closure of TEP in 10%
500
-complications:
-tracheoesophageal puncture dilation
-aspiration
-esophageal prolapse
-tracheostoma prolapse
-tracheal granulation tissue
-leakage at TEP
-aspiration
EMERGENCIES
-aspiration of prosthesis
-airway obstruction
-tracheoesophageal necrosis
-voice prosthesis incompetence
-dilatation must be performed with as little resistance as possible because it its possible to dissect into the
tracheoesophageal common wall and enter the anterior mediastinum
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GLOTTIC AND SUBGLOTTIC STENOSIS
ETIOLOGY AND PATHOPHYSIOLOGY
Congenital laryngeal stenosis

-secondary to inadequate recanalization of laryngeal lumen at end of 3rd month GA
Congenital subglottic stenosis

-considered to be congenital in absence of history of endotracheal intubation or other apparent acquired
causes of stenosis
-management:
-mild cases: watchful waiting; child may outgrow problem
-more severe cases: tracheal dilatation; tracheotomy and reconstructive repair
Acquired laryngeal stenosis
External laryngeal trauma

-haematoma formation deposition of fibrous tissue
Internal laryngeal trauma
-Endotracheal tube injury:

-prolonged intubation (90% most common)
-incidence ~ 0.9-8.3%
-area most commonly injured:
-children: subglottis
-adults: posterior endolarynx
-pathophysiology:
-ETT causes pressure necrosis mucosal edema and ulceration
-mucociliary stasis and infection and perichondritis
-chondritis and cartilage necrosis
-healing by secondary intention granulation tissue proliferation and deposition of fibrous tissue
in submucosa
-risks:
-prolonged intubation: greater than 7-10 days
-use of oversized ETT
-repeated intubations
-coexistence of ETT and NG tubes
-poor general condition
Other causes:
-laryngeal surgery
-emergency cricothyroidotomy
-high tracheotomy
MANAGEMENT
Tracheotomy:
-for severe cases of stenosis and airway difficulty
F.Ling - Glottic and Subglottic Stenosis (1)
502
-with normal growth and development, decannulation usually within 2 years
Endoscopic management:
-dilatation for early stenosis
-use of corticosteroids controversial
-CO2 laser - useful for early lesions
External surgical reconstruction:

-grades II and IV lesions require external methods
-Anterior cricoid split

-alternative to tracheotomy in management of acquired subglottic stenosis in premature infants
-division of cricoid and upper two tracheal rings
-ETT stent for 7 days
-corticosteroids administered before extubation and continued for 5 days
-Combined laryngofissure and posterior cricoid division

-for combined posterior glottic and subglottic stenosis, moderate subglottic and upper tracheal
stenosis with loss of cartilaginous support and for complete glottic and subglottic stenosis
-for pts of all ages
-divided halves of posterior cricoid lamina distracted laterally; ~ 1 mm per year of age up to 10
years
-cartilage graft placed
-autogenous costal cartilage
-thyroid cartilage
-auricular cartilage
-nasal cartilage
-other grafts possible (adults)
-vascularized hyoid-sternohyoid myo-osseous flaps
-Cotton-Lorenz stent placed
-Cricoid resection with thyrotracheal anastomosis

-limited to pts in whom stenosis is entirely subglottic or upper tracheal with a normal lumen of at
least 10 mm below the glottis
-suprahyoid release
-partial cricoid resection
-thyrotracheal anastomosis
-avoid extension of the neck for 10 days
-stenting not required
Decannulation in Children
-endoscopy performed to ensure airway is clear
-removal of suprastomal granulation tissue if present
-plugging of tracheotomy in hospital with oxygen monitoring
-if no desaturation then remove trach tube and occlude stoma
F.Ling - Glottic and Subglottic Stenosis (2)
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Dr. F. Ling's
Otolaryngology - Head and Neck Surgery

Notes
Laryngeal Development
Phase I (Carnegie Stage 11)
 respiratory primordium (RP) along ventral aspect of foregut

(approximately 4th pharyngeal pouch area [4PP])
 RP separated from inferior hepatic primordium by septum transversum
(ST) ==> central tendon of diaphragm
Phase I I (Carnegie Stage 12)
 early:
 RP out-pouches to develop respiratory diverticulum (RD)
 origin of RD is primitive pharyngeal floor (PPhF) ==> glottic
region
 cephalic portion of RD ==> infraglottic region
 pharyngeal floor (PF) at level of 4th pouch
 area from PF to PPhF = primitive laryngopharynx (PL) ==>
supraglottic region
 later:
 bronchopulmonary buds (BPB) from RD ==> lower
respiratory tract
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Phase I I I (Carnegie Stage 13 and 14)
 upper foregut and RD migrate superiorly, BPB drawn inferiorly

 development of:
 main bronchi
 carina
 infraglottis
 vascular compromise to developing esophagus ==> EA or TEF
 vascular compromise to developing trachea ==> genesis or stenosis
with complete rings
Phase I V (Carnegie Stage 15)
 obliteration of ventral PL gives rise to epithelial lamina (EL)

 arytenoid swellings (AS) develop from pharyngeal floor at same
anatomic level as 4PP
 hypobronchial eminence (HE) is initial epiglottic swelling
 entrance to PL seen as "T" b/n AS and central epiglottic swelling
Phase V (Carnegie Stage 16)
 EL continues to obliterate PL from a ventral to dorsal direction except

for pharyngoglottic duct (PhGD)
 laryngeal cecum (LC) develops between AS and epiglottis
505
Phase VI (Carnegie Stage 17 and 18)
 LC continues caudal descent to level of glottic region
Phase VI I (Carnegie Stage 19 to 23)
 EL begins to recanalize from dorsocephalic to ventrocaudal direction

to re-establish communication between ventral LC and dorsal PhGD
 Type 1 atresia: complete supraglottic stenosis (failure of EL to
recanalize)
 Type 2 atresia: incomplete supraglottic stenosis
 Type 3 atresia: glottic web
506
Phase (VI I I )
 lateral outgrowths of LC ==> laryngeal ventricles

 EL has completely recanalized
Overview
507
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Review of Anatomy: The Larynx Page 1 of 3
Larynx
A. Skeleton
 Hyoid Bone
 attachment to epiglottis and strap muscles.
 Thyroid Cartilage
 anterior attachment of vocal folds. Posterior articulation with cricoid
cartilage.
 Cricoid Cartilage
 complete ring. Articulates with thyroid and arytenoid cartilages.
 Arytenoids
 two cartilages which glide along posterior cricoid and attach to
posterior ends of vocal folds.
B. Divisions
 Supraglottis - usually covered with respiratory epithelium containing

mucous glands.
 Epiglottis
 leaf- shaped mucosal- covered cartilage, which projects over
larynx.
 Aryepiglottic folds
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 extend from lateral epiglottis to arytenoids.

 False vocal cords
 mucosal folds superior to true glottis
 separated from true vocal folds by ventricle
 Ventricle
 mucosal- lined sac, variable in size which separates
supraglottis from glottis
 Glottis
 true vocal folds attach to thyroid cartilage at anterior commissure
 posterior commissure is mobile, as vocal folds attach to arytenoids
 bulk of vocal fold is made up of muscle covered by mucosa
 free edge is characterized by stratified squamous epithelium
 vocal folds abduct for inspiration and adduct for phonation, cough,
and valsalva.
 Subglottis
 below vocal folds, extending to inferior border of cricoid cartilage.
510
C. Innervation - branches of vagus nerve.
 Superior Laryngeal Nerve

 internal branch:Çsensation of glottis and supraglottis
 external branch:Çmotor fibers to cricothyroid muscle, which tenses
vocal folds
 nerve leaves vagus high in neck
 Recurrent Laryngeal Nerve

 sensation of subglottis, and motor fibers to intrinsic muscles of larynx
 branches from vagus in mediastinum, then turns back up into neck
 on right, it travels inferior to subclavian artery and on left, aorta
511
AURICULAR TRAUMA AND SALVAGE
-untreated open auricular injuries invariably result in infection, ensuing deformities, and further tissue loss
Blood supply to external ear

-external carotid artery posterior auricular artery (PAA)
-superficial temporal artery (STA)
-deep auricular artery, a branch of maxillary artery coming up through auditory canal
-occipital artery supplies a minor contribution to auricular blood flow to posterior auricle
-venous drainage of posterior surface of auricle occurs principally via posterior auricular vein
Nerve supply to external ear

-main nerve supply of auricle is great auricular nerve
-anterior branch supplies lower half of lateral (anterior) surface of ear
-posterior branch supplies lower half of medial (posterior) surface
-auriculotemporal nerve branches supply upper half of anterior surface
-branches from lesser occipital nerve supply upper half of posterior surface of auricle
-exiting from external auditory canal, Arnold nerve supplies anterior skin of concha
SURGICAL THERAPY:
-defects less than 1 cm with intact cartilage and vascularized perichondrium can be left to heal by
secondary intention
-alternatively, FTSG from contralateral postauricular sulcus can be used to cover defect
Abrasions
-abraded areas must be cleaned and thoroughly irrigated
-covered with topical antibiotic impregnated gauze for 24 hours
-treated as open wounds
Blunt trauma
-commonly result in hematoma and seroma formation between cartilage and perichondrium on anterior
surface of ear
-acute treatment involves drainage of effusion via needle aspiration or incision followed by application of a
pressure dressing
Lacerations
-closed by primary closure
Avulsions and amputations
-severed yet pedicled auricular tissue:

-a partly avulsed ear portion can be attached directly to its base with a good chance of success
-composite grafts:
-reattachment of completely severed auricular portions of less than 1.5 cm in diameter as
composite grafts is successful in limited circumstances
-success rate usually has been poor
F.Ling - Auricular Trauma and Salvage (1)
512
-small or large avulsions:
-“pocket principle” is used in reattachment of small or large avulsions
-involves dermabrading avulsed ear segment, reattaching it in its correct anatomic position, and
burying it under a layer of postauricular skin in subcutaneous tissue
-additional blood supply to reattached segment while in "pocket" secondary to increased contact
surface with surrounding dermis results in improved survival of reattached tissue
-remove segment from pocket after 10-14 days with overlying skin covering
-cover postauricular defect with local tissue advancement or a skin graft
TPFF
-used to salvage a major auricle replantation by covering salvaged or harvested autologous cartilaginous
framework
-a flap up to 17 x 14 cm in area can be harvested and can be used as an ipsilateral turndown flap or as a
free flap from contralateral side
-dermabrade and inset amputated ear
-raise TPFF based on superficial temporal artery and turn it over to cover reattached cartilage
-harvest a full-thickness skin graft to cover TPFF flap
Periauricular tissue expanders

-ensures availability of sufficient color-matched skin cover that can be raised as a flap instead of as a graft
to complete repair
Microsurgical replantation
-when traumatic injury results in total or near total auricular avulsions, microsurgical replantation provides
an excellent reconstructive option
Complete reconstruction
-procedure involves up to 3 staged procedures starting with harvesting of autogenous rib cartilage from
sixth, seventh, and eighth costal cartilages
-first stage, implant sculpted framework and rotate remnant earlobe into position
-second stage involves creation of tragus and conchal cavity several months later
-final stage consists of elevation of implanted auricle with split-thickness skin graft placement
retroauricularly
Auricular prostheses
-auricular prosthetics provides a final option
-problems with prosthetics have included detachment, improper color match, patient psychologic
discomfort about having prosthetics detach at inopportune moments, and surrounding tissue irritation
secondary to adhesives
-development of osseointegrated implants, in which pure titanium implants are placed into mastoid bone
region and after a period of healing, load-bearing superstructures are connected to implants, has reduced
significance of these problems
Bites
-among most common injuries to auricle
-treatment should include debridement, copious irrigation, primary closure or split-thickness skin graft
closure, and oral antibiotics, followed by a 24-hour check
-if cartilage is involved, risk of infection is significantly greater, and intravenous antibiotics should be
instituted
F.Ling - Auricular Trauma and Salvage (2)
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FACIAL TRAUMA
GENERAL
-Reduced and stabilized within 7 to 10 days if possible

-Secondary revision delayed until scars have matured (~6-12 months)
Emergency Care:
-ABC’s
-suction + tracheostomy
-direct pressure to wounds - no clamping necessary
-fluid resuscitation
-irrigation and debridement
Soft Tissue Defects:

-facial wounds: closed up to 24h post injury if necessary
-tetanus prophylaxis prn
-awareness of injured underlying structures (eg. CN VII, parotid duct, lacrimal apparatus)
-topical Abx sufficient; systemic Abx for gross contaminations
-special care: re-approximation of vermillion border; do not shave eyebrows.
-sutures x 5-7 days
FACIAL FRACTURES
General Principles:
-nasal and zygomatic malar area most commonly involved followed by mandibular area
-O/E look for:
1. Sources of cervicofacial hemorrhage
2. Soft-tissue injury (contusions, abrasions, lacerations, haematomas, edema)
3. Ecchymosis (subconjunctival, circumoral, intraoral, or post-auricular)
4. Subcutaneous emphysema
5. Cervical spine injury
6. Intracranial injury
7. Bone deformity
8. CSF rhinorrhea
9. Cranial nerve dysfunction
10. Epistaxis
11. Patency of nasal airway
12. Trismus
13. Malocclusion of teeth
14. Point tenderness and pain at fracture site
15. Evidence of compound fracture
16. Integrity of tympanic membrane and ear canal
17. Eye injury (central and peripheral vision, ocular motility, diplopia, displacement, and
papillary function)
-Inv:
-C-spine films (seen in 15-20% with facial injuries)
-facial bone series (Water’s, AP and lateral)
-+ CT head
-panorex for mandibular fractures
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Mandibular Fractures:
-ring structure of mandible 94% have associated second fractured area:
-condyle # assoc. /w symphysis + contralateral condyle
-body # assoc. /w contralateral angle
-fractures by area:
-condylar: 36%
-body: 21%
-angle: 20%
-symphysis: 14%
-alveolus, ramus, coronoid (3%, 3%, 2%)
-Sxs: malocclusion, pain, inability to close jaw
-Treatment:
-closed reduction (jaw wiring) for minimally displacement
-intermaxillary fixation: 4-6 weeks in adults
-open reduction - plating/wiring; better approximation
-Complications:
-delayed healing, mal-union malocclusion, non-union
Mandibular condyle fractures:

-preauricular pain, deviation of mandible toward fractured side
-pain on palpation of anterior wall of EAC; occasionally hemotympanum
-treated with closed reduction
-complications:
-ankylosis, TMJ dysfunction, limited ROM, malocclusion, chorda tympani damage
Nasal Fractures:
Hx:
-anterior blow: comminuted # with flattening of bridge
-lateral blow: convex deformity on other side
Dx:
-epistaxis
-external displacement of nasal bones
-localized bone tenderness
-nasal airway obstruction
-septal edema or deformity
-septal haematoma
-Treatment:
-closed reduction in 3-4 days after edema
-drain septal haematomas
-stabilization with external splints and internal packs
-nasoethmoidal # tx with ORIF
-Complications:
-CSF rhinorrhea if roof of ethmoid sinus or cribiform plate involvement
-disruption of nasolacrimal apparatus and medial canthal tendon
”pseudohypertelorism” or traumatic telecanthus
-ethmoid sinus disruption interstitial periorbital emphysema
-septal haematoma - risk of necrosis saddle deformity; prompt drainage required.
-septal deformity nasal obstruction
-lacrimal apparatus injury
Orbital Fractures:
-Orbital floor blow out most common; may occur with midface and zygomatic fractures
-Sxs:
-exophthalmos
-diplopia ( EOM d/t muscle/nerve entrapment; muscle contusion, edema, temporary
515
neuropraxia)
-facial asymmetry
-sensory nerve injury (V2)
-ocular complication
-Inv: CT scan
-Exploration and stabilization required if:
-exophthalmos
-diplopia with EOM disturbance after resolution of edema
-facial deformity
-persistent anesthesia in V2
-Tx: orbital floor reparation with bone graft or prosthetic material
-Complications:
-retrobulbar haematoma, residual entrapment of orbital contents
-continued diplopia
-late exophthalmos 2o to atrophy of periorbital fat-Ophthalmology consult prn
Zygomatic Arch Fractures:

-Medially displaced arch contacting coronoid process and temporalis point tenderness,
trismus, pain on mandibular movement, limited mandibular excursion
-Dx: submental vertex radiograph
-Tx: simple, non-comminuted arch elevation of depressed segment
Zygomatic or Malar Bone Fractures:

-Four processes articulating with:
-frontal, maxillary, temporal, sphenoid bones
-Ssx:
-flattening of upper cheek; step-off deformity
-lowering of lateral canthal ligament attachment
-diplopia
-lateral subconjunctival hemorrhage; chemosis
-limited ocular motility
-hyperesthesia over V2
-epistaxis
-trismus
-potential laceration to maxillary sinus hematoma
-open reduction within 10 days of injury to prevent functional or cosmetic deformity
Maxillary and Midfacial Fractures:

-Classification according to LeFort system:
-LeFort I:
-d/t central midline blow
-lower midfacial fracture which runs transversely through lower maxilla and into lower nasal
cavity
-involves teeth, portion of maxillary sinus, hard palate, lower segment of pterygoid plates
-Ssx: malocclusion and mobility of maxilla
-O/E:
-buccal vestibule ecchymosis
-maxillary crepitus
-false motion of lower maxilla with stability of upper nose and orbits
-possible assoc. /w: lengthening of face, septal deformities, V2 paresthesias
-Tx:
-fix mandibular injuries first
-IMF usually gives sufficient reduction and stabilization
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-Complications:
-malocclusion
-paresthesia
-septal deformities
-facial asymmetry
LeFort II:
-aka “pyramid fracture”
-fracture lines through nasal and lacrimal bones, floor of orbit, inferior orbital rim, across
upper portion of maxillary sinus and pterygoid plates to pterygomaxillary fossa
-Ssx:
-naso-orbital flattening
-mobility of nasal bridge
-epistaxis
-malocclusion
-step deformities along orbital rims and nasofrontal areas
-CSF rhinorrhea
-V2 paresthesia
-Tx: ORIF /w plate and screw + bone graft if comminution or bone loss
-Complications as per LeFort I
-greater incidence of orbital injuries, CSF leaks, nasal deformities, lacrimal damage
-LeFort III:
-aka craniofacial dissociation
-fracture line across suture line b/n nasal and frontal bones, along ethmoid junction bone,
across superior orbital fissure, lateral wall of orbit and frontomaxillary and
zygomaticomaxillary suture lines
-Sxs similar to LeFort II + basilar skull injuries
-Battle’s sign (mastoid ecchymosis), Raccoon eyes, CSF otorrhea, hemotympanum
-Inv: CT
-Tx: as per LeFort II: ORIF
-stabilization via frontozygomatic sutures and zygomatic arches
-Complications:
-as per LeFort II + cranial base injuries/ neurological damage
-Treatment may be delayed for 7 to 10 days until pt is stable

-re-estabilishment of normal occlusion
-suspension, ORIF of fracture fragments
Frontal Bone Fractures:
Frontal Sinus and Glabellar Fractures:

-rare; 90% associated with nasal fractures
-frequently comminuted and depressed
-dura may be ruptured CSF rhinorrhea
-Dx: clinically, X-rays: Caldwell, Water’s, lateral views
-Tx: open reduction
Supraorbital Ridge Fractures:

-Signs and symptoms:
-flattening of brow
-displaced orbital contents
-anesthesia of forehead
-periorbital ecchymosis
-ptosis (injury of elevator palpebrae superioris)
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-diplopia (downward displacement of trochlear and superior oblique muscle)
-overlying facial laceration
-Dx: Water’s or Caldwell views
-Open reduction invariably required, internal fixation seldom necessary.
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AURICULAR TRAUMA
HEMATOMA
-caused by shearing forces
-blood between skin-perichondrial layer and cartilage
-“cauliflower ear”
-accumulated subperichondrial blood causes formation of neocartilage
-evacuate haematoma through incision in helical sulcus or antihelical fold
-pressure dressing applied for 7-10 days
TOTAL AND SUBTOTAL AVULSION
General Concepts
-usefulness of avulsed segment:
-avulsed segment bites should not be reused as simple composite graft
-condition of surrounding tissue can limit reconstructive possibilities
Total Avulsion
-microvascular reimplantation yields best results
-if reimplantation not possible:
-existing cartilage used as subsurface framework and covered by vascularized tissue:
-a) temporoparietal fascial flap with delayed skin grafting
-used if missing postauricular skin
-b) postauricular advancement flap
-c) posteromedial skin removed, cartilage fenestrated, segment reattached against raw
postauricular surface established by means of raising a postauricular flap
-d) pocket principle technique
Partial Avulsion
-most important contour to recreate: helical rim

-least important contour to recreate: antitragus
Helical Rim
-helical rim advancement
-for defects lest than 2 cm in area
-tube flap
-for larger defects
-made from postauricular skin and transferred to auricle in multistage procedure
Defects of Upper Third

-helical rim advancement for small defects
-composite grafting for larger defects (less than 1.5-2 cm)
-if no useable avulsed segment replaced with contralateral conchal cartilage or rib cartilage covered by
vascularized skin flap
Defects of Middle Third

-small defects closed primarily with wedge or star excision
-larger defects: cartilage grafting with vascularized skin flap methods
F.Ling - Auricular Trauma (1)
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Defects of Lower Third
-lobule involved:
-primary closure with available tissue
-Pardue’s adjacent flap technique for earring cleft injury
-total lobule reconstruction
F.Ling - Auricular Trauma (2)
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LARYNGEAL TRAUMA
PATHOPHYSIOLOGY OF LARYNGEAL INJURIES
Blunt Trauma
-endolaryngeal mucosal tears, edema, or haematoma
-fractures of laryngeal cartilages and disruption of laryngeal ligaments
-subluxation or dislocation of arytenoid cartilage fixed vocal fold
-cricoarytenoid joint injury unilateral injury to RLN
-cornus of thyroid cartilage can lacerate pharyngeal mucosa; pharyngoesophageal tears
-“clothesline” injury:
-cricotracheal separation
-bilateral RLN injury
-child (compared to adult):
-larynx situated higher in neck and protected by mandible
-less laryngeal fractures because of elasticity of cartilages
-increased likelihood of soft tissue damage
-cricothyroid membrane narrower less likely to have laryngotracheal separation
Penetrating Trauma
-damage directly proportional to velocity and mass of wounding object
DIAGNOSIS AND EVALUATION
Symptoms
-hoarseness
-pain
-dyspnea
-dysphagia
Signs
-stridor
-hemoptysis
-laryngeal tenderness
-loss of thyroid cartilage prominence
-vocal fold immobility
-laryngeal haematoma
-laryngeal edema
-laryngeal lacerations
Radiology
-CT scan
-contraindicated when airway is unstable
-not needed when:
-pts with obvious fractures,
large endolaryngeal lacerations,
or severe penetrating trauma
-pts with minimal anterior neck
trauma and normal physical
findings
F.Ling - Laryngeal Trauma (1)
521
-used to:
-detect cartilage fractures that are not clinically apparent (hyoid, thyroid, cricoid)
-assess poorly visualized areas (subglottis, anterior commissure)
-identify cervical injuries
-arteriography
-cervical spine radiography
-contrast esophagography
-start with water soluble contrast to avoid barium induced mediastinitis if tear exists
MANAGEMENT
Emergency Care
-multisystem trauma:
-establish airway
-cardiac resuscitation
-control of haemorrhage
-stabilization of spinal injuries
-adult airway
-controversy:
-establishing airway in presence of laryngeal trauma
-intubation can cause iatrogenic injury or loss of an already precarious airway
-many advocate tracheotomy under local anaesthesia or rigid bronchoscopic intubation
-alternatively, endotracheal intubation only with:
-experienced personnel
-direct visualization; no endolaryngeal lacerations; stable laryngeal framework
-small-diameter endotracheal tube
-pediatric airway
-difficult of near impossible to do tracheotomy under local anaesthesia
-inhaled anaesthesia with spontaneous respirations
-rigid bronchoscopic intubation followed by tracheotomy
Treatment Decision Making

-injuries not requiring repair:
-edema
-small haematoma with intact mucosal coverage
-small glottic or supraglottic lacerations without exposed cartilage
-single nondisplaced thyroid cartilage fractures in a stable larynx
-injuries requiring open laryngeal exploration and repair:
-lacerations involving free margin of vocal fold
-large mucosal lacerations
-exposed cartilage
-multiple and displaced cartilage fractures
-avulsed or dislocated arytenoid cartilages
-injuries requiring open exploration, repair, and endolaryngeal stenting:
-disruption of anterior commissure
-multiple and displaced cartilage fractures
-multiple and severe endolaryngeal lacerations
-avulsion of arytenoid cartilage
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Medical Treatment
-observation for 24 h
-voice rest
-systemic steroids (no evidence)
-elevate head
-humidified air
-antibiotics
-antireflux measures
Surgical Treatment
-early vs. late exploration (controversial):
-early:
-offers complete assessment of injuries, lower postoperative infection rate, quicker
healing, less granulation tissue, less scarring
-late:
-3-5 days
-allows edema to resolve
-may become infected; presence of granulation tissue
-tracheotomy under local for unstable airway
-endoscopy:
-ascertains extent of injury:
-look for haematoma, edema, lacerations, exposed cartilage and range of motion of true
vocal cords
-reduction of dislocated arytenoid
-bronch: evaluate subglottis and trachea
-esophagoscopy: r/o unsuspected perforations
-exploration:
-via laryngofissure (thyrotomy)
-exposed cartilage is a source of fibrosis and granulation tissue and must be covered primarily
-lacerations meticulously re-approximated
-fractures fixed with wire, nonabsorbable suture, or miniplates
-anterior commissure reconstructed; keel placed to prevent webbing
Grafting
-to cover exposed cartilage
-mucous membrane, dermis and STSG suitable
Stents
-indications:
-controversial
-extensive lacerations involving anterior
commissure
-multiple cartilaginous fractures that
cannot be stabilized adequately with
open reduction
-stent fixed to larynx in such a way that it moves
with larynx during swallowing
-pass suture through stent and larynx at
level of laryngeal ventricle and at
cricothyroid membrane
-usually left in place for 10-14 days
-remove early to avoid granulation tissue formation
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Cricotracheal Separation
-risks:
-precarious airway
-loss of cricoid support
-high risk of injury to RLN
-late development of subglottic stenosis
-trachea tends to retract substernally and the larynx tends to migrate superiorly
-high mortality
-tracheotomy under local anaesthesia
-intact cricoid:
-mucous membrane repaired directly with absorbable suture
-fractured cricoid:
-reconstitution +/- stenting preferable to extensive resection and thyrotracheal anastomosis
Severed Recurrent Laryngeal Nerve

-attempt primary anastomosis
-nerve regeneration may prevent muscle atrophy may provide enough bulk for a useable voice
-synkinesis can occur
COMPLICATIONS
-granulation tissue
-prevent by covering all exposed cartilage
-avoid stents when possible; leaving stents for the minimum amount of time when necessary
-careful excision
-laryngeal stenosis
-excision with mucosal coverage
-stenting selected cases
-laryngotracheoplasty
-tracheal resection with reanastomosis
-observe
-vocal fold injection
-thyroplasty-type vocal fold medialization
-arytenoidectomy and vocal fold lateralization for bilateral paralysis
-displaced stents
-may occur during coughing
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MANAGEMENT OF SOFT-TISSUE TRAUMA
ANATOMY OF SKIN
Epidermis
-stratum corneum: no nucleus, keratin in cytoplasm, loosens then
desquamates
-stratum granulosum: 3-5 layers thick, flattened, keratohyalin
granules
-stratum spinosum: basophilic cells
-stratum basale: single layer of cuboidal cells at basal lamina
Epidermal-Dermal Junction:
-rete pegs: epidermal projections into dermal layer
-papillae: dermal, vascularized projections into epidermal layer
Dermis:
-papillary dermis: collagen and elastin fibers
-reticular dermis: denser layer
Subcutaneous layer:
-contains fat and fibrous tissue
WOUND MANAGEMENT
EMERGENCIES
Specific Types of Wounds Immediate intervention needed

-major vessel haemorrhage
-airway compromise
Abrasions
-loss of eyelid tissue
-managed with ointment and dressing
Urgent intervention needed
Contusions -parotid duct injuries
-facial nerve branch injuries
-small asymptomatic hematomas may be observed
-auricular injuries with exposed cartilage
-large haematomas drained through small incisions during first 7- -injuries extending into nasal or oral
10 days after injury cavities
-aspirated successfully after 10-14 days
Lacerations
-greater blood supply in face wounds can be closed primarily up to 48 or even 72 hours after injury
-non-traumatic handling of tissue required to prevent necrosis of skin
-wound contamination most directly related to elapsed time since injury occurred
Avulsions
-full-thickness tissue loss severe cosmetic deformity
-small defects can be excised and closed primarily
-options: skin grafting vs healing by secondary intention
Scalp Wounds
-five layers: skin, subcutaneous tissue, muscle and aponeurosis, loos connective tissue, pericranium
-lacerations repaired by undermining subaponeurotic plane above pericranium and performing a layered
closure
-secondary tissue expansion and flap reconstruction can resurface as much as 50% of scalp
F.Ling - Management of Soft-Tissue Trauma (1)
525
-local flaps for defects < 5cm
Facial Nerve Injuries

-injuries posterior to vertical canthal line require exploration and repair
-excitability of facial nerve loss after 72h, therefore repair is best during this time frame
-nerve grafting:
-greater auricular nerve: provides up to 7 cm of nerve tissue
-sural nerve: up to 30 cm provided
Parotid Duct Injuries

-vertical lacerations below anterior border of masseter muscle likely to injure parotid duct
-duct usually at a line from tragus to upper lip
-buccal branch of facial nerve travels alongside duct and often is damage as well
-duct is repaired over a stent
-stent sutured to buccal mucosa for 10-14 days
-complications: sialocele and fistula
Lip Injuries
-may close primarily up to ½ the upper or lower lip
-reconstruct in 3 layers including the orbicularis oris muscle
-use absorbable suture in mucosal and muscular layers
-for larger defects consider local flaps
Eyelid and Lacrimal System Injuries

-mandatory ophthalmologist consult
-orbicularis muscle responsible for blinking and must be repaired
-full-thickness lacerations of eye margin require 3-layered closure:
-anterior aspect of tarsal plate
-posterior lid margin
-tarsal plates
-canalicular injuries repaired with silicone stents
-medial canthal injuries repaired with permanent suture to avoid traumatic telecanthus
-loss of up to 1/4 of eyelid can be repaired primarily
-greater than 1/4 defects may require skin grafts
Complications
-hypertrophic or keloidal scarring
-trapdoor deformities
-scar contracture
-step-off or distortion of anatomic landmarks
-sialoceles or salivary fistulae
-facial nerve palsy
-auricular deformities
-ectropion or other deformities of the eyelids
BURNS
Ears
-prone to suppurative chondritis
-redness swelling and deep pain
-tx: incision, drainage and debridement
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Mouth
-usually from electrical cord biting in children
-conservative treatment: can be complicated by haemorrhage form labial artery
-delayed surgical excision and grafting: allows demarcation of involved area
-long term complication: microstomia from contracture; may consider placing an oral stent
Eyes
-risks ectropion, lid contraction, keratitis, and cataracts (electrical burns)
-FTSG to lower lids and STSG to upper lids may be needed to protect the globe
Frostbite
-commonly involve ears, cheeks and nose
-local rewarming by immersing involved part in bath maintained at 37.8-42.3oC
-surgical debridement delayed until extent of injury can be assessed
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MANDIBULAR FRACTURES
-most common in young males (ages 18-30)

-after nose, mandible is second most commonly fractured facial bone
-causes: assault (most common), MVA, sports, falls, gunshot wounds
ANATOMY
-components:
-symphysis, parasymphysis, body, angle, ramus,
coronoid process, condyle, alveolus
-inherent sites of weakness:
-third molar area
-socket of canine tooth
-condylar neck
-anterior muscles
-mylohyoid, geniohyoid, genioglossus, platysma,
anterior digastric muscles
-depress and retracts mandible
-posterior muscles: (muscles of mastication_
-temporalis: raises and retracts mandible
-masseter: raises and retracts mandible
-medial pterygoid: attaches to medial ramus; raises mandible
-lateral pterygoid: attaches to condyle; protrudes and depresses mandible
Biomechanics of the Mandible

-favourable fractures:
-muscles tend to draw fragments toward each other
and reduce the fracture
-managed usually by closed reduction
-horizontally (B) and vertically (D) favourable
fractures
-unfavourable when fragments tend to be distracted
-usually managed with ORIF
-horizontally unfavourable (A):
-angle fracture
-vector force of masseter and temporalis
muscle pulls fragments apart
-vertically unfavourable (C):
-body and symphysis-parasymphysis areas
-vector force of anterior muscles
(mylohyoid, digastric) and pterygoid
muscles pulls fragments apart
-upper border of mandible muscles of mastication produce tension stress use thinner, monocortical
tension plate along superior border
-lower border of mandible muscles produce compression stress use rigid compression plates along
inferior border
F.Ling - Mandibular Fractures (1)
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Types of Fractures
-simple (closed wound, skin and mucosa intact) versus compound (open wound, exposed bone)
-fracture pattern: comminuted, oblique, transverse, spiral, greenstick
-pathologic: fractures secondary to bone disease
Dental Evaluation
-32 permanent (secondary teeth)
-8 incisors, 4 canines, 8 bicuspids or premolars, 12 molars
-20 primary deciduous teeth
-8 incisors, 4 canines, 8 molars
Angle’s Classification
-Class I: orthognathic;
-mesiobuccal cusp of maxillary first molar lines buccal groove of mandibular first molar
-Class II: retrognathic
-Class III: prognathic
History
-pain and malocclusion
-haematoma in FOM
-laceration of attached gingiva
-fragment mobility
-trismus
-deviation toward side of fractured condyle
-anterior open bite contralateral to side of fractured condyle
-possible anaesthesia or paraesthesia of lower lip and chin
-bilaterally displaced fractures of condylar neck symmetric anterior open bite deformity
Radiographic Evaluation
-panoramic view the single best radiographic evaluation
MANAGEMENT (GENERAL)
Principles
-goals:
-restore occlusion
-establish bony union
-return of function
-avoid TMJ ankylosis
-repair within first week, delayed repair increases complications
-in general favourable fractures may only need closed reduction, open fractures ten to require open
reduction
-all fractures involving tooth-bearing part of mandible considered compounded into mouth Abx
prophylaxis started
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Closed Reduction (Maxillo-Mandibular Fixation - MMF)
-indications:
-for most favourable fractures that are minimally displaced
-selected condylar fractures
-for initial stabilization of occlusion prior to exposure of the fracture
-methods:
-arch bars, interdental eyelet wires (Ivy loops), circumferential wiring of dentures or teeth
-duration of fixation:
-depends on age and type of injury:
-children: 3-4 weeks
-adults: 4-6 weeks
-elderly: > 8 weeks
-condylar fractures: 1-2 weeks
-body and angle fractures: 4-6 weeks
-complications:
-airway compromise
-dental injury
-weight loss
-loss of fixation (malunion, nonunion)
-TMJ dysfunction
-aspiration
Open Reduction
-indication for ORIF:
-anticipated fragment displacement despite closed reduction
-unfavourable and comminuted fractures
-elderly; edentulous patients
-poor pulmonary reserve (unable to endure MMF)
-noncompliant patients, alcoholics, seizure disorder, mental retardation, psychosis
-multiple fractures or injuries
-bilateral fractures
-displacement into middle cranial fossa
-seizure disorder
-relative contraindications:
-poor bone height
-pediatric mixed dentition that limits placement of fixation devices
-approaches:
-transoral
-avoids injury to marginal mandibular nerve
-no external scar
-easy access to symphyseal, parasymphyseal, and body regions
-external:
-indicated for more posterior fractures which cannot be accessed intraorally or severely
comminuted fractures
-materials:
-rigid (plates, lag screws etc..) vs. non-rigid (interosseous wires)
-sagittal and oblique fractures may be more amenable to repair with lag screw techniques
-hole drilled perpendicular to fracture line
-compression not used in cases of infection or comminution large reconstruction plates used
instead
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MANAGEMENT BY TYPE OF FRACTURE
Coronoid, Greenstick, Unilateral Nondisplaced Fractures

-observation with soft diet, analgesics, oral antibiotics
-physiotherapy exercises for 3 months
Favourable, Minimally Displaced Non-condylar Fractures

-consider closed reduction and 4-6 weeks of MMF
Displaced Fractures
General Management Options:

-compression and tension plates
-inferiorly placed compression plate and a superiorly placed monocortical tension
miniplate provides stable fixation for early removal of MMF and early oral intake
-compression bar with MMF
-eccentric dynamic compression plates
-interosseous wires with MMF
-lag screws
-bicortical screws
-drill through superficial cortex, through fracture line, and into deep cortex of opposite
bone
-overdrill proximal segment brings fracture together
Symphysis-Parasymphysis Area
-tend to be vertically unfavourable
-custom acrylic lingual splint in addition to IMF to resist scissorslike collapse of mandibular arch
-ORIF avoids use of splints
-lag screws
Body
-transoral application of compression plate
-external incision and compression plate
-multiple lag screw fixation
531
Angle
-associated with highest incidence of infection
-in general have the highest complication rate by site because of location posterior to dentition,
thin-walled bone, and vector forces from masseter muscle
Ramus
-fractures are naturally splinted by pterygomasseteric sling and are amenable to closed reduction
-early release of IMF for non-displaced fractures (3-4 weeks)
-ORIF may be considered for multiple fragments or marked displacement
Condyle and Condylar Neck

-nondiplaced fractures:
-observation with close follow-up, soft diet, analgesics, oral antibiotics, and physiotherapy
exercises for 3 months
-displaced fractures:
-may be addressed with closed reduction by pushing jaw down while rotating chin upward
-may consider MMF for severe displacement for 2 weeks followed by rubber band fixation
-*indications for open reduction of condylar fractures:
-Absolute indications:
-displacement into middle cranial fossa
-impossibility of obtaining adequate occlusion by means of closed reduction
-lateral extracapsular displacement of condyle
-invasion by foreign body (eg. Gunshot wound)
-Relative indications:
-bilateral condylar fractures in edentulous patient when splinting is impossible
-unilateral or bilateral condylar fractures when splinting is not recommended for medical
reasons or adequate postoperative physiotherapy is impossible
-bilateral condylar fractures associated with comminuted midfacial fractures
-bilateral condylar fractures associated with marked preinjury malocclusion
-exercise sessions every 2 weeks allow a brief release form IMF to avoid intra- and periarticular fibrosis
and ankylosis
SPECIAL CONSIDERATIONS
Edentulous Fractures
-closed reduction with arch bars applied to pt’s dentures
-Gunning splints secured to maxilla and mandible with wires
-rigid techniques often are used to manage edentulous fractures without advance mandibular atrophy
Treatment by Means of Observation Only

-soft diet and follow-up
-for unilateral nondisplaced fracture of condylar area in which patients can easily bite to their normal
occlusion
Pediatric Fractures
-in general prefer conservative management
-usually can tolerate some malocclusion which adjusts with growth
-rigid techniques place developing tooth buds at risk and usually are avoided
532
-most dreaded complication is development of ankylosis of TMJ can alter jaw growth and produce a
severe facial deformity
-allow weekly mobilization of jaw with rapid return to normal jaw function
Management of Teeth in the Line of Fracture

-indications to remove tooth:
-teeth with fractured roots
-tooth within fracture line that interferes with occlusion
-infected tooth within fracture line
-non-viable tooth or exposed pulp
-controversy exists regarding retention of uninjured, stable teeth in line of mandibular fracture most can
be retained
-disadvantage:
-an extracted tooth leaves a point of entry for infection and a point of weak fixation
External Fixation
-indications:
-contaminated gunshot wounds resulting in loss of part of the mandible
-osteomyelitis
-elderly
-provides the advantage of fragment stability with neither IMF nor a foreign body in the wound
Removal of Hardware
-controversial
-probably unnecessary
COMPLICATIONS
-infection
-ostoomyelitis
-malocclusion
-malunion
-caused by inadequate immobilization, inaccurate reduction, infection, gross loss of bone,
compromised blood supply, malnutrition, osteogenesis imperfecta, osteopetrosis
-nonunion
-non-osteogenic matrix produced
-may require bone grafting
-plate exposure
-TMJ ankylosis
-TMJ dysfunction
-sensory disturbances of inferior alveolar nerve
-marginal mandibular nerve injury
-necrosis of condylar head
-dental injury
EMERGENCIES
-airway obstruction (bilateral fractures of mandibular body)
-condylar displacement into middle cranial fossa
-adjacent injury to internal carotid artery
-haemorrhage
533
MAXILLARY AND PERIORBITAL FRACTURES
MAXILLARY FRACTURES
ANATOMY
Buttress System
-vertical buttresses:
-nasamaxillary
-zygomaticomaxillary
-pterygomaxillary
-horizontal buttresses:
-frontal bar: superior orbital rims and glabellar area
-inferior: inferior orbital rims, maxillary alveolus
and palate, zygomatic processes, serrated edges of
greater wings of sphenoid bone
LeFort Classification
-LeFort I
-low maxillary; transverse maxillary fracture
-upper alveolus becomes separated from upper maxillary
-typically caused by a low anterior-to-posterior force
-involves anterior lateral maxillary wall, medial maxillary wall, pterygoid plates, septum at floor
of nose
-LeFort II
-pyramidal
-caused typically from a superiorly directed force against the maxilla or an anterior to posterior
blow along the Frankfort plane
-involves nasofrontal suture; orbital foramen, rim and floor; frontal process of lacrimal bone,
zygomaxillary suture; lamina papyracea of ethmoid, pterygoid plate; and high septum
-LeFort III
-craniofacial dysjunction
-separates facial skeleton from base of skull, typically caused by high velocity impacts, moto
vehicle accidents, oblique forces
-involves nasofrontal sure; medial and lateral orbital wall and floor; zygomaticofrontal suture;
zygoma and zygomatic arch; pterygoid plates and nasal septum
LeFort I LeFort II LeFort III
F.Ling - Maxillary and Periorbital Fractures (1)
534
PATHOPHYSIOLOGY
Buttress System Loading

-disruption of a single buttress can weaken entire lattice and cause its collapse
-random collapse under anterior or lateral impact usually prevented by strength of horizontal buttresses
combined with their relation to base of skull
Anterior Impact Forces

-causes LeFort type fractures
-maxillary retrusion or rotation, midfacial elongation and malocclusion
Lateral Impact Forces

-zygomatic process of frontal bone almost always spared clean separation of zygomaticofrontal suture
-zygomatic arch sustains single fracture near its midpoint
-“tripod” fracture
PATIENT EVALUATION
Computed Tomography
-critical areas in CT evaluation:
-vertical buttresses
-zygomatic arch
-orbital walls
-bony palate
-mandibular condyles
-orbital injuries likely to produce exophthalmos are those in which disruption of orbital floor exceeds at
total area of 2 cm2, bone volume changes exceed 1.5 cm3, or considerable fat and soft tissue displacement
occur
Ophthalmologic Evaluation
-testing of visual acuity, pupillary function, ocular motility
-inspection for hyphema
-inspection of fundus for gross disruption
MANAGEMENT PHILOSOPHY
Immediate Reconstruction
-usually within 24-48 hours
-immediate reconstruction is usually less difficult and more successful than delayed reconstruction
-delayed reconstruction:
-risk of cicatricial contraction of facial soft tissues, scarring, bone resorption
-can allow up to 2 weeks for delayed repair
Extended Access Approaches

-bicoronal, sublabial and transconjunctival incisions, subciliary, brow incisions, pretragal incisions
-closed reduction and maxillomandibular fixation are adequate management of less complex, minimally
displaced maxillary fractures
-maxillary fractures found to be displaced on CT are best managed by extended access approaches that
allow direct visualization
535
Stable Internal Fixation
-rigid internal fixation devices can obviate the need for IMF used to stabilize maxillary fractures
-pts still need to be on soft diet to reduce mechanical loading of buttresses
SURGICAL TECHNIQUES
Zygoma
-four sutures involved in zygomaticomaxillary complex fractures (“tripod fracture”)
-zygomaticofrontal
-zygomaticomaxillary
-zygomaticotemporal
-zygomaticosphenoid
-stabilization requires minimum of two point fixation:
-zygomaticofrontal suture
-inferior orbital rim
-lateral antral wall
-zygomatic arch
-procedures usually delayed 5-7 days to allow resolution of edema
-closed reduction:
-used if no comminution Gilles operation +/- transzygomatic Steinmann pin fixation
-open reduction:
-used if comminution of lateral antral wall sublabial incision with plating at
zygomaticomaxillary buttress
-tripod fracture add transconjuntival incision to access medial orbital rim and lateral brow
incision for zygomaticofrontal suture
-centrally displaced zygomatic arch approached via coronal, hemicoronal, or extended pretragal
incision
536
Maxilla
-restoration requires reestablishment of proper occlusion and stabilization of midfacial buttress system
-must first ensure proper alignment of mandibular condyles
-usually IMF done first then midfacial vertical dimension stabilized by ORIF
-if condylar height cannot be maintained, then midfacial buttress system reconstructed first to
establish vertical and horizontal positioning of the occlusal plane
-restoration of zygoma required
-palatal fractures:
-parasagittal splits reduced anteriorly at inferior rim of piriform (plates) aperture and posteriorly
(interossous wire)
-maxillary reduction usually starts with reattachment of zygomaticomaxillary buttress (usually has less
severe injury) to obtain vertical height
-panfacial fractures:
-work from stable base
-begin with MMF and associated mandibular fractures
-work lateral (zygoma and ZM buttress) to establish anterior projection
-work medial to restore buttress system
537
COMPLICATIONS
-lid damage
-meticulous closure of transconjunctival incision required to prevent ectropion
-lip distortion
-caused by sublabial approach
-hollowing of soft-tissue contours over canine fossa
-superior deviation of corner of mouth and lateral aspect of upper lip
-caused by collapse and contracture of buccal soft tissues into large anterior and anterolateral
antral wall defects
-vision loss
-from trauma
-occasionally an oversized implant causes acute increase in IOP and must be removed
-implant visibility
-malocclusion
-can be caused by plates that are not correctly adapted to bone tightening of screws can produce
torque causing movement of fragments
-malunion, nonunion
-plate exposure
-forehead/cheek hypesthesia
-osteomyelitis
-dental injury
ORBITAL FRACTURES
ANATOMY
-seven orbital bones:

1. frontal
2. zygomatic
3. maxillary
4. lacrimal
5. ethmoid
6a. greater wing of sphenoid
6b. lesser wing of sphenoid
7. palatine
-optic canal contents:
-optic nerve
-ophthalmic artery
-superior orbital fissure contents:
-CN III, IV, V1 (lacrimal, frontal, nasociliary
divisions), VI
-supraorbital vein
-inferior orbital fissure contents:
-zygomaticofacial and zygomaticotemporal divisions of V2
-inferior ophthalmic vein
CLINICAL PRESENTATION
SSx: enophthalmos (? 2-3 mm pathologic), hypopthalmos, exophthalmos, proptosis, entrapment diplopia,
hypesthesia of infraorbital nerve, psedoptosis
538
Theories of Orbital Floor Injury
-Hydraulic Theory:
-force to orbital region increases intraocular pressure fractures floor
-Buckling Theory:
-force on inferior rim directly fractures floor
Traumatic Optic Neuropathy

-injury to optic canal and superior orbital fissure results in compressive injury to involved nerves
-SSx: ophthalmoplegia (optic nerve), ptosis (V1), pupillary dilation (CN III), anaesthesia of upper eyelid
and forehead (V1)
-tx: -for progressive loss consider high-dose corticosteroids and osmotic diuresis, if no improvement
may consider orbital or optic nerve decompression
-if CT reveals bony impingement may undergo decompression urgently
MANAGEMENT
-indications for surgical intervention:

-enophthalmos (>2-3 mm)
-mechanical entrapment
-diplopia
-dehiscence of intraorbital tissue
-high risk of enophthalmos and/or hypophthalmos (large floor defects)
-contraindications for surgical intervention:
-hyphema
-retinal tear
-globe perforation
-only seeing eye
-sinusitis
-frozen globe
-timing ideally should be completed 7-10 days after swelling has subsided
-delayed repair may reveal bone resorption and scar contracture
-approaches:
-subciliary incision:
-placed 2-3 mm below cilia of lower eyelid (may extend into crow’s feet for better
exposure)
-transconjunctival incision
-Lynch incision:
-allows exposre to medial wall
-brow incision:
-allows exposure to posterolateral wall
-subtarsal incision:
-incision placed 5-7 mm below cilia of lower eyelid in a crease line
-Caldwell-Luc (transantral) approach:
-indicated for severely comminuted and posterior fractures
-reconstruction of orbital floor:
-reconstruction of orbital floor positioned higher than pretrauma level to prevent inferior
displacement of orbit
-medial orbital floor (orbital plate of maxilla) reconstructed with alloplastic implant
-options:
-polyethylene (Marlex)
-gelflim
-bone
539
COMPLICATIONS
-postoperative blindness
-CSF leak
-persistent enophthalmos and diplopia
-ectropion
-ectropion
-epiphora
-cheek hypesthesia
-extrusion of grafts
-osteomyelitis
-palpable or observable plates
540
FRACTURES OF THE NASAL AND FRONTAL SINUSES
NASAL FRACTURES
Basic Anatomy
-sensory innervation:
-supratrochlear nerve
-infratrochlear nerve
-anterior ethmoidal nerve external nasal nerve
-infraorbital nerve
-most fractures occur in lower half of nasal bones (thin at inferior articulation with upper lateral cartilage)
-see Nasal Anatomy Notes
-medial canthal ligament
-extension of tarsal plates which attaches to medial orbital wall
-receives contributions from tendinous portion of preseptal and pretarsal parts of orbicularis oculi
muscle, superior suspensory ligament (Whitnall), and inferior suspensory ligament (Lockwood)
-lacrimal collecting system
-puncta: located a medial aspect of upper and lower eyelids
-canaliculi: upper and lower canaliculi form common canaliculus
-lacrimal sac: located in lacrimal fossa, insertions of MCL straddle the lacrimal sac and act as a
pump
-lacrimal duct: enters into medial maxilla and exits into inferior meatus
Pathophysiology
-factors:
-patients’ age (tissue flexibility)
-amount of force applied
-direction of force
-nature of striking object
-soft tissue injuries: lacerations, hematoma, ecchymosis
-skeletal injuries: fractures, dislocation, fracture-dislocation
-force required to produce nasal fracture: 25-75 lb/in2
-frontal force: injury varies from minor to marked flattening of external skeleton
-lateral force: depression of ipsilateral nasal bone +/- outfracture of contralateral nasal bone
-from below: septal fractures and dislocations
-can cause telescoping of fragments and shortening of nose or blockage of one side
Treatment
-goals:
-restore satisfactory appearance
-restore nasal airway patency
-replace septum in midline
-preserve nasal valve integrity
-prevent postoperative stenosis, septal perforation, columellar retraction, and saddle deformity
-avoid interference with growth
General
-best opportunity during first 3 hours after injury
-reduction usually performed within 3-7 days
-indications for closed reduction:
-unilateral or bilateral fracture of nasal bones
-fracture of nasal-septal complex with nasal deviation less than one half width of nasal bridge
F.Ling - Nasal and Frontal Sinus Fractures (1)
541
-indications for open reduction:
-extensive fracture-dislocation of nasal bones
-nasal pyramid deviation exceeding one half width of nasal bridge
-fracture-dislocation of caudal septum
-open septal fractures
-persistent deformity after closed reduction
Anesthesia
-2% lidocaine with epinephrine spray
-injection of 2% lidocaine with 1:100000 epinephrine along dorsum of nose lateral to nasal pyramid and at
base of anterior septum
-alternative: EMLA and intranasal cocaine
Delayed Management
-surgery usually delayed 6 months or more from initial closed or open fracture reduction to allow fracture
lines to stabilize and fibrosis to mature
542
Nasal Fractures in Children
-child’s nose more cartilaginous more flexible and resilient

-more associated injuries - edema obscures extent of nasal involvement
-dislocation of cartilaginous structures
-greenstick fractures of nasal and septal bones more common
-haematoma more common
-signs and symptoms:
-epistaxis
-nasal dorsum edema
-periorbital ecchymosis
-tenderness of dorsum of nose
-abnormal radiographic findings
-visible nasal deformity
-crepitus of nasal bones
-other differences:
-fractures heal within 2-4 days
-traumatic damage of growth centers can be caused by injury or surgical management
543
Nasofrontal-Ethmoidal Fractures
-force directed from inferior aspect to external nose
-associated injuries:
-injury to nasofrontal duct or cribriform plate
-detachment of medial canthal ligaments pseudohypertelorism
-CSF rhinorrhea , anosmia, ocular injury, interruption of lacrimal system, cerebral contusion
-management:
-open reduction and stabilization of bone fragments
-“open sky incision”: bilateral Lynch incision connected by transverse incision below glabella
-fragments stabilized with wiring or plates
-calvarial bone grafts for severe fractures for dorsonasal reconstruction
Nasoethmoidal Orbital Fractures

-common fracture patterns:
-nasal bones and frontal process of maxilla are telescoped behind frontal bone
-comminuted fracture with fragments into orbital space, cranial fossa, and nasal vault
-SSx:
-flattened nasal dorsum
-periorbital swelling
-epistaxis
-nasal obstruction
-medial canthal ligament injury (telecanthus, epiphora)
-CSF rhinorrhea
-bowstring sign:
-tests integrity of medial canthal ligament
-grasp medial eyelid near lash line and pull laterally, normally should snap back
-traumatic telecanthus:
-intercanthal distances:
-<22 mm in infants
-<32-35 mm in adults
-presents with rounding of medial canthus from releasing medial canthal ligament
-involve lateral aspect of nose, inferior orbital rim, medial orbital ethmoid wall, nasal maxillary buttress,
and frontal process of maxilla
-tx: ORIF +/- bone grafting
Classification and Management of MCL Injuries:

-Type I:
-MCL remains attached but bone fragment is detached or ligament has been severed completely
-tx: attempt to wire bone fragments with attached MCL to stable bone or release lateral canthal
ligament then reattach the MCL to the medial wall of the orbit posterior to the lacrimal fossa
(slight overcorrection is required)
-Type II:
-comminuted medial orbital wall fracture
-tx: attach MCL with wires transnasally to the opposite side medial orbital wall (may also consider
releasing the lateral canthal ligament to allow for some overcorrection)
-Type III:
-bilateral medial orbital wall fractures
-tx: attach MCL with wires transnasally to opposite MCL (transnasal canthoplasty), may also
consider wiring both MCLs to the opposite frontal process
544
Complications
Early
-edema
-ecchymosis
-epistaxis
-haematoma
-suspected when any patient has persistent swelling and pain
-infection
-CSF leak
Late
-airway obstruction
-fibrosis, contracture
-secondary deformity
-synechiae
-saddle nose
-septal perforation
Emergencies
-severe bleeding cauterization, packing, vessel ligation
-septal fracture-dislocation causing nasal airway obstruction in neonate closed reduction with cotton
swabs; no nasal packing
-septal haematoma in child immediate I+D; tissue destruction begins within 48h
-CSF rhinorrhea neurosurgical consultation
-visual impairment immediate ophthalmologic consultation
FRACTURES OF THE FRONTAL SINUS
Epidemiology and Etiology

-frontal and ethmoidal involvement occur among 15% of patients with head injuries
-MVA most common cause
-other causes: GSW, fights, sports, industrial accidents, falls
Anatomy
-three sides: anterior, posterior, floor (thinnest)
-drains through frontal sinus
-course of frontonasal duct is posterior and caudal
Biomechanics of Frontal Sinus Fracture

-frontal bone has highest tolerance of direct trauma
-anterior wall: 360-990kg of force
Evaluation
-ABCs
-CT scan
-coronal scans provide good definition of floor of sinus, FND, cribriform plate
-presence of fractures through floor of frontal sinus or anterior ethmoidal fractures suggests
presence of injury to FND
545
-surgical access:
-bicoronal flap or extension of laceration
-bilateral sub-brow incision
-“open sky” incision
-wound debridement
-surgical approaches:
-obliteration of FND
-obliteration of frontal sinus
-cranialization
Antibiotic Prophylaxis
-prevention of sinusitis and intracranial sepsis
-ceftriaxone or ceftazidine, and metronidazole
-for compound fractures, antibiotic therapy maintained for at least 2 weeks
-no antibiotics for closed fractures and isolated nondisplaced anterior table fractures
Treatment
-prevention of intracranial sepsis
-prevention of frontal sinus disease
-cosmetically acceptable outcome
Anterior Table Fracture

-non displaced:
-conservative management
-if persistent opacification, frontal sinus trephination and endoscopic examination may be
worthwhile
-displaced:
-bicoronal or supraorbital brow incision or extension of overlying laceration
-explore to inspect posterior wall and FND
-remove mucosa from fractured edges
-stabilization with wires or mini-plates
-if >1 cm bone loss then consider split calvarial graft or mesh
Posterior Table Fractures

-non-displaced:
-observe with prophylactic antibiotics
-trephination with endoscopic examination for persistent soft-tissue pacification to prevent
cerebral herniation
-consider exploration if sinus fluid does not clear within 6 weeks
-displaced:
-requires exploration via osteoplastic flap
-reduction of displaced fragment
-no obliteration necessary in absence of injury to FND
-posterior wall fractures heal if drainage into nose is maintained
-obliteration recommended if injury to FND
-comminuted, contaminated or through-and-through fractures require neurosurgical consult and
consideration for cranialization
-indications for exploration
-persistent CSF rhinorrhea
-posterior table fracture
-frontal nasal duct injury
-persistent unilateral opacification of frontal sinus visible on CT scan after 2 months
546
Frontonasal Drainage
-best evaluation of FND integrity and patency is made intraoperatively
-patency evaluated with fluorescin, benzylpenicillion solution or methylene blue dye
-obliterate cavity if obstruction of FND is found
-fat, fascia, muscle, pericranium, cancellous bone
Complications
-frontal sinus
-headache, fullness; sinusitis; mucocele
-intracranial
-CSF leak; meningitis; brain abscess; seizures
-cosmetic
-scar numbness; wound infection; forehead depression
-ophthalmic
-diplopia; eye pulsations
547
PENETRATING FACE AND NECK TRAUMA
Definition:
-penetrating neck/face injury = breach of platysma
-muzzle velocity:
-low velocity (<1000ft/s) tissue damage
-high velocity (>1000ft/s) tissue loss
-mechanisms of GSW injury:
-direct tissue injury
-temporary cavitation
-anatomic structures may be significantly damages without actually being penetrated by
the projectile
-transmission of shock waves
-projectile rotation
-projectile shatter and secondary projectiles
PENETRATING FACIAL INJURIES
-classification (Chen et al) based on entry zones

-division I:
-above supraorbital rim
-high risk of intracranial complications and frontal
sinus injuries
-division II:
- midface - from supraorbital rims to lateral
commissure of mouth
-division III:
-mandible - below lateral commissure of mouth
Shotgun Injuries
-I: long-range:
- >7 yards distance between weapon and victim
-subcutaneous or deep fascia injuries only
-II: medium range:
-3-7 yards
-injuries to structures deep to deep fascia
-III: close range:
-<3 yards
-massive tissue destruction
-zoning system not helpful in predicting injury pattern
-high incidence of ocular injury ophthalmology consult
Stab Wounds
-AP and lateral skull X-ray to evaluate depth of penetration if
weapon still in place
-angiography with weapon in place can control proximal
vessels with balloons if major vessel is involved
F.Ling - Penetrating Face and Neck Trauma (1)
548
Gunshot Wounds
-midface wounds:
-high prevalence of vascular injury (20%), globe injury (20%), intracranial penetration (20%) and
facial fracture (35%)
-indications for angiograms:
-proximity to major vascular structure
-penetration posterior to mandibular angle plane (imaginary vertical coronal plane at
level of angle of mandible)
-mandible wounds:
-often require emergency management of airway (50%)
-deflection of bullets by mandible into neck or intracranial cavity
Management of Specific Injuries
Facial Nerve Injury

-exploration and repair if injury is lateral to lateral canthus
Parotid Duct Injury
-wounds to cheek below zygomatic arch that injure buccal branch of facial nerve
-if injured then repair over a stent
Complications
-facial injuries:
-blindness/visual loss/diplopia
-facial nerve paresis or paralysis
-CSF leak
-soft tissue loss
-bony malunion, malocclusion, trismus
-orbital/periorbital cellulitis, sinusitis, oroantral fistula
-nasal obstruction/stenosis, choanal stenosis
-neck injuries:
-airway obstruction
-pharyngocutaneous fistula
-neck abscess
-mediastinitis
-vocal cord paresis
-cervical spine osteomyelitis
PENETRATING NECK INJURIES
-zone I: root of neck to inferior border

of cricoid cartilages
-zone II: inferior border of cricoid to
angle of mandible
-zone III: angle of mandible to skull
base
-most commonly injured structures:

-larynx and trachea (10%)
-pharynx and esophagus
(10%)
549
-most common vascular structures injured:
-internal jugular vein (9%)
-internal and common carotids (7%)
-subclavian artery (2%)
-external carotid artery (2%)
-most commonly missed injury in the neck: pharyngoesophageal injury
-most common cause of death: exsanguinating hemorrhage
Diagnosis Signs and Symptoms Tests
Vascular injury shock angiograms

haematoma neck exploration
haemorrhage
pulse deficit
neurologic deficit
bruit or thrill in neck
Laryngotracheal injury subcutaneous emphysema laryngotracheoscopy

airway obstruction, dyspnea neck exploration
sucking wound CT scan
hemoptysis
stridor, hoarseness or dysphonia
Pharynx/esophagus injury subcutaneous emphysema contrast esophogogram

hematemesis esophagoscopy
dysphagia or odynophagia neck exploration
MANAGEMENT
Zone I Injuries
-high risk injury to great vessels, trachea and lungs
-symptomatic/asymptomatic: angiography, esophageal evaluation (esophagoscopy and contrast
esophagography increases specificity and sensitivity to 100%)
-up to 1/3 patients are asymptomatic
-esophageal injury silent: risk of mediastinitis and sepsis
Zone II Injuries
-high risk injury to carotid sheath and aerodigestive system
-symptomatic neck exploration
-asymptomatic:
-controversial management:
-exploration vs directed serial examination
-exploration:
-may discharge patients home earlier if negative findings
-more accurate than diagnostic tests
-up to 50-70% of elective neck explorations are negative
-mandatory surgical exploration:
-gunshot wounds that cross midline
-obvious serious injury (stridor, active hemorrhage, absent carotid pulse)
-active bleeding, air bubbling through wound
-arteriorgraphy not available
-directed examination:
-missed injuries, serial examinations required
-arteriography, esophagogram/esophagoscopy, laryngoscopy, bronchoscopy
550
Zone III Injuries:
-high risk injury to distal carotid artery, parotid and pharynx
-potential injury to major blood vessels and cranial nerves at or near skull base
-treatment may be managed by interventional radiologist (arteriography and balloon occlusion)
Management of Specific Injuries
Pharyngeal and Esophageal Injuries

-primary closure not always necessary in penetrating injuries to upper hypopharynx
-NPO with IV Abx for 5-7 days
-primary closure needed if injury inferior to arytenoids
Vertebral Artery Injury

-embolization preferred due to difficult exposure and control
-for failed embolization may consider surgical repair
Carotid Injury
-associated with high mortality (10-20%)
-primary repair treatment of choice, otherwise may consider patch grafting, by-pass grafting or ligation
-ligation should not be considered if suspect a stroke to avoid haemorrhagic stroke with revascularizatoin
551
COMPLEX FACIAL TRAUMA WITH PLATING
Basic Principles of Rigid Fixation

-metallic plates designed to span a fracture and provide stress shielding and fracture stability
-compression or loading of bone across fracture enhances stability by increasing friction between fracture
edges
-larger plates provide greater stress shielding; large screws provide stronger fixation; bicortical screws
provide greater stability; increasing number of screws or fixation points increases stability
Fixation Device Classification and Terminology

-miniplate designed for screws 1.2-2.5 mm range
-microplate designed for screw diameters ~1mm
-plates designated for function: eg. mandibular vs maxillary miniplates
-compression plates: push fracture fragments together as screws are driven
Principles of Screw Application

-drill hole must match inner screw shaft diameter
-“gliding”: drill bit’s diameter matches screw’s outer diameter with threads and can be pushed or pulled
through the drill hole without turning the screw
-“tapping”: cutting of screw threads in drill hole
-overtightening can lead to microfracture or stripping of bone threads
Lag Screw Application

-presses two pieces of bone together by compressing first piece of bone between second piece in which the
tip of screw is engaged
-top fragment is compressed between head of screw and second fragment in which threads are engaging on
the other side of the fracture
Fracture Reduction
-re-establishment of anatomic position and continuity of bony buttresses is key to fracture reduction
-stable reference points are used for fixation
-intervening gaps in buttresses are bone grafted
-buttresses must ultimately transmit forces of mastication to skull base
-donor sites: calvaria, ilium, ribs
Occlusion
-normal molar occlusion in anterior-posterior dimension defined as intercuspation of mesial buccal cusp of
maxillary first molar with buccal groove of mandibular first molar
-normal transverse relationship: buccal cusps of mandibular molars are between buccal and palatal cusps of
maxillary molars
-normal anterior dental relationship: maxillary anterior dentition is 1-3 mm anterior to mandibular anterior
dentition with central incisa overlap of 1-3 mm
-wear facets are main occlusal guide
Incisions and Exposure

-intraoral vestibular sulcus incisions:
-exposes entire mandible except for condyles
-risk of injury to mental nerve, failure to achieve watertight closure of incision, failure to
resuspend mentalis muscle if chin is degloved
-not recommended with comminuted fractures, severe periodontal disease or hygiene problems
-difficult to contour a heavy plate to outer cortex
-high subcondylar fractures best approached through Risdon or preauricular incision
F.Ling - Complex Facial Trauma with Plating (1)
552
-superior circumvestibular incision:
-exposes inferior maxilla
-pitfalls: infraorbital nerve damage, nostril stenosis, leaving inadequate oral vestibular mucosa for
wound closure
-bicoronal incision:
-exposes upper face
-pitfalls: damage to frontalis innervation and inadequate closure of galea brow ptosis
-lower lid incision:
-exposes infraorbital rim and orbital floor
-brow incision:
-exposure of frontozygomatic region
Approach to Panfacial Fractures

-ABCDEs
-immediate repair is best approach:
-before full development of injury edema (24-48h)
-reduced bacterial contamination cf delayed repair
-less fibrosis and contraction of soft-tissue envelop around fractured skeleton
-fractures are typically repaired centripetally, working from skull base and mandible toward midface and
working from lateral midface toward medial midface
-after complete fracture reduction is achieved, soft-tissue structures that were detached traumatically or to
provide exposure must be resuspended
-medial and lateral canthi
-mentalis muscle suspended from drill holes in menton
-cannulation of lacrimal ducts
Soft Tissue Loss

-rigidly fixed bony structures will generally survive even in absence of adequate soft-tissue coverage
-restoration of skeletal framework should be done acutely; soft tissue defects can be repaired later
-free tissue transfer
Complications
-osseous:
-osteitis/osteomyelitis
-delayed union/nonunion/malunion/malocclusion
-fibrous union with poor function
-bone loss
-TMJ dysfunction
-soft tissue:
-deficiency
-scarring
-ptosis/lagophthalmos
-entropion/ectropion
-nasal obstruction
-neurosplanchnic:
-brain injury
-globe injury/malposition
-CSF leak
-meningocele/encephalocele
-CN dysfunction
-glandular dysfunction
F.Ling - Complex Facial Trauma with Plating (2)
553
-Most common cause of death for individuals between 1-44 years
-third most common caus of death for all ages
-100,000 deaths per year in US; MVA ~50%
-Primary survey : resuscitation: secondary survey: diagnostic evaluation: definitive care

-primary survey: -Airway, with c-spine protection
-Breathing
-Circulation
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-conscious pts with normal voice do not require further evaluation

-elective intubation (prevention of airway compromise) in:
-penetrating injuries to neck and an expanding haematoma
-chemical or thermal injury to nares, mouth, hypopharynx
-extensive subcutaneous air in neck
-complex maxillofacial trauma
-airway bleeding
-abnormal voice or altered mental status suction (blood, vomit, tongue, FB, soft tissue swelling)
-airway access:
-nasotracheal, orotracheal, or operative intervention
Nasotracheal intubation:
-only in patients breathing spontaneously
Orotracheal intubation:
-manual in-line cervical immobilization in patients with potential c-spine injuries
-advantages: ability to visualize cords, larger-diameter endotracheal tubes
-disadvantages: requires neuromuscular blockade or deep sedation
Cricothyroidotomy:
-failed intubation or extensive facial injuries
-disadvantage: ETT must be < 6 mm in diameter
-contraindicated in patients < 12 years damage to cricoid cartilage, risk of subglottic stenosis
Percutaneous transtracheal ventilation:

-IV catheter through cricothyroid membrane O2 source of 50 psi or more
-CO2 retention may occur
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-all should receive supplemental oxygen monitored by oximetry

-immediate life threatening conditions: (1) tension PTX; (2) open PTX; (3) flail chest/pulmonary
contusion
Tension Pneumothorax:
-respiratory distress, tracheal deviation away from affected side, lack of or decreased breath
sounds on affected side, distended neck veins or systemic hypotension, subcutaneous emphysema
554
on affected side
-treat with large gauge needle in 2nd ICS MCL followed by CT thoracostomy
Open Pneumothorax:
-full-thickness loss of chest wall with free communication b/n pleural space and atmosphere
-if diameter of injury greater than narrowest portion of upper airway, air preferentially moves
through injury site rather than the trachea
-treat with occlusive dressing over wound taped on 3 sides prevents conversion to tension PTX
-definitive treatment: wound closure and CT thoracostomy
Flail Chest:
-four or more ribs are fractured in at least two locations
-paradoxical movement of free-floating segment
) * + %,"
-check pulses, if palpable then sBP is at least: 60 mmHg (carotid); 70 mmHg (femoral); 80 mmHg (radial)
-control external haemorrhage: compression and splints
-avoid blind clamping risk to injure nerves
-two large bore IVs (16 gauge or larger) in antecubital fossa
-Saphenous vein cutdowns: 1 cm anterior and 1 cm superior to medial malleolus
-pediatric patients < 6 years:
-percutaneous femoral vein cannulation contraindicated b/c of DVT risk
-interosseous cannulation an option: proximal tibia or distal femur
- " % + + . $/ /* % %,"
-1L IV bolus of NS, LR in adult; 20cc/kg in children

-repeat once or twice before adding RBCs
(a) tachycardia: earliest sign

-watch for well-trained athletes, patients on beta-blockers, children since they may not have HR
(b) hypotension: not a reliable early sign of hypovolemia (BV must by 30-40%)
(c) altered mental status: hypoxia, hypercarbia, hypovolemia, or ICP
(d) urine output: reliable indicator of organ perfusion
-maintain > 0.5 cc/kg/h in adults; 1.0 cc/kg/h in children; 2.0 cc/kg/h in infants
Signs and Symptoms for Different Classes of Shock

Class I Class II Class III Class IV
Blood loss < 750 cc 750-1500 cc 1500-2000 cc > 2000 cc
(%BV) <15% 15-30% 30-40% > 40%
HR <100 > 100 >120 >140
BP normal normal decreased decreased
Pulse pressure normal or decreased decreased decreased
RR 14-20 20-30 30-40 >35
U/O > 30 cc/h 20-30 cc/h 5-15 cc/h negligible
CNS status sl. anxious mild anxiety anxious and confused and
confused lethargic
555
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a. Nonresponders:
-usually cardiogenic
-look at CVP and neck veins:
-flat neck veins, CVP < 5, hypovolemic ongoing haemorrhage
-distendend neck veins, CVP > 15 cardiogenic shock
-Ddx cardiogenic shock: (1) tension PTX; (2) pericardial tamponade; (3) myocardial
contusion or infarction; (4) air embolism
Tension PTX: most common cause of cardiac failure
Pericardial tamponade:
-decreased RV output and CVP
-with acute tamponade, as little as 100 cc of blood can produce life-threatening homodynamic
compromise
-Beck’s triad: hypotension, distended neck veins, muffled heart sounds
-increased pulsus paradoxus
-treat with pericardiocentesis
-done even if pt stabilizes with volume loading still risk of subclinical myocardial
ischemia sudden lethal arrhythmias
-if still hypotensive emergency thoracotomy
Myocardial contusions:
-ECG abnormalities: ventricular dysrhythmias, a-fi, sinus bardycardia, BBB
-early placement of Swan-Ganz, urgent echocardiogram (r/o septal or free wall rupture, valvular
disruption, or pericardial tamponade)
Air embolism:
-air accumulation in LV impedes diastolic filling; can disrupt coronary perfusion
-Trendelenberg position emergency thoracotomy cross-clamping of pulmonary hilum air
aspirated from LV with 18-gauge needle
b. Transient Responders:
-usually have some degree of active haemorrhage
-penetrating injuries OR for exploration
-blunt trauma: CT or angiography if hemodynamically stable
-traditional volume resuscitation of patients sustaining penetrating torso trauma (PTT) has been questioned:
-active bleeding increases as venous and arterial pressure increases
-no survival advanced in hypotensive patients sustaining PTT and required operative treatment
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-special attention to back, axillae, perineum (often overlooked)
-DRE sphincter tone, blood, perforation, high-riding prostate
-Foley catheter:
-stable pts at risk for urethral injury urethrography before catheterizaiton
-signs of urethral injury: blood at meatus, perineal or scrotal haematomas, high riding prostate
-NG tube: decrease risk of gastric aspiration
-X-rays: AP chest, pelvis, c-spine
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-penetrating trauma: damage localized to path of bullet or knife
-classified according to wounding agent: stab, gunshot, shotgun etc..
556
-high vs. low velocity; close vs. long range
-blunt trauma: associated with multiple, widely distributed injuries
-high vs. low energy transfer
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-Glasgow Coma Scale:

Eye Opening: -(4) spontaneous; (3) to voice; (2) to pain; (1) no response
Verbal: -(5) oriented; (4) confused; (3) inappropriate words; (2) sounds; (1) none
Motor: -(6) obeys commands; (5) localizes pain; (4) withdraws; (3) abnormal flexion;
(2) abnormal extension; (1) no movement
mild (13-15); moderate (9-12); severe (<9)
-lateralizing findings: eg. unilateral dilated pupil unreactive to light, asymmetric movement, unilateral
Babinski’s reflex suggest treatable intracranial mass lesion
-stroke syndromes search for carotid dissection or thrombosis with doppler or angiography
-basilar skull fractures: otorrhea, rhinorrhea, “raccoon eyes”, Battle’s sign (mastoid ecchymosis)
-risk of meningitis
-CT +/- plain films should be done
Epidural Hematoma:
-blood accumulates b/n skull and dura
-disruption of middle meningeal artery
Subdural Hematoma:
-occur b/n dura and cerebral cortex
-venous disruption or laceration of parenchyma of brain
Post-injury Hydocephalus:
-bleeding into ventricles
Diffuse Axonal Injury:
-from high-speed deceleration injury and represents direct axonal damage
-CT: blurring of grey matter with multiple, small, punctate haemorrhages
-associated with poor outcome
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-pts assumed to have c-spine injury until proven otherwise

-C-spine series: lateral (C7-T1), AP, trans oral odontoid
-CT if pain persists in spite of normal plain films identifies fractures, but can miss subluxations
-flexion/extension views for ligamentous injuries opening of intervertebral space
Spinal cord injuries:

-complete: loss of motor function and sensation two or more levels below bony injury
-incomplete:
-Central cord syndrome:
-older patients with hyperextension injuries
-motor function, pain and temperature sensation intact in lower extremities but
diminished in upper extremities
-Anterior cord syndrome:
- motor, pain and temperature below level of injury
-position, vibratory, and crude touch sensation preserved
557
-prognosis and recovery poor
-Brown-Sequard syndrome:
-penetrating injury causing hemisection of cord
-ipsilateral loss of motor function, proprioception, and vibration
-pain and temperature on contralateral side lost
Penetrating Anterior Neck Injuries:

-Classification:
-Zone I: between clavicle and cricoid cartilage
-Zone II: between cricoid and angle of mandible
-Zone III: above angle of mandible
-Management:
-Zone I:
-involvement of visceral and vascular injuries in the thoracic outlet
-angiography of great vessels, esophagram, esophagoscopy, bronchoscopy if stable
-surgical exploration if unstable
-Zone II:
-prompt exploration if airway compromise, expanding haematoma, significant external
haemorrhage
-local exploration in stable patients:
-no penetration of platysma close wound and d/c home
-penetration of platysma observation for 12 h
-Zone III:
-require carotid and vertebral angiography if evidence of arterial bleeding
1. exposure of distal internal carotid and vertebral arteries difficult
2. internal carotid my have to be ligated high risk of stroke
3. active haemorrhage can be controlled be selective embolization
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Aortic Tears:
-tear of descending thoracic aorta most threatening
-findings on CXR suggestive of aortic tear:
1. widened mediastinum
2. abnormal aortic contour
3. tracheal shift
4. NG tube shift
5. left apical cap
6. left or right paraspinal stripe thickening
7. depression of left main bronchus
8. obliteration of aorticopulmonary window
9. left pulmonary hilar hematoma
-most otfen seen in high-energy-transfer deceleration MVA with frontal or lateral impact
-tear usually distal to left subclavian artery, where aorta is tethered by ligamentum arteriosum
-CT and angiography required
- 6., $"
-presence of abdominal rigidity or gross distention in patient with truncal trauma indication for prompt
surgical exploration
Penetrating wounds:
-gunshot wounds mandatory laparotomy
-anterior and lateral stab wounds explore in ER and determine if peritoneum violated
-injuries that do not penetrate peritoneal cavity no further evaluation
558
-DPL: most sensitive test for determining presence of intraabdominal injury
-positive if:
1. More than 10 ml of free blood aspirated
2. RBC > 100,000/mm3; > 10,000/mm3 when evaluating for diaphragmatic injury
3. Detection of bile, fecal material or observation of effluent draining through CT, NG, or Foley
-diaphragm penetration laparotomy
Blunt abdominal trauma:

-ultrasound in emergency:
-specific anatomic regions:
eg. Morison’s pouch (b/n right kidney and liver), left upper quadrant, pelvis
-sensitive for detecting intraperitoneal fluid collections > 250ml
-CT scanning of abdomen:
-good for detecting solid organ damage
-limitations:
-poor sensitivity for intestinal injuries and acute pancreatic injuries
-poor correlation b/n splenic and hepatic CT images and subsequent risk of bleeding
requiring an operation
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-frequently produces complex fractures
-potential injury to bladder, rectum and vagina
7% $ %$/
Signs and Symptoms of Arterial Injury

Hard Signs (Operation Mandatory) Soft Signs (Further evaluation desirable)
Pulsatile haemorrhage Proximity

Significant haemorrhage Minor haemorrhage
Thrill or bruit Small hemat oma
Acute ischemic Associated nerve injury
-arteriography in certain cases to localize injury and limit operative dissection

-for soft signs: measure systolic pressure in both extremities using Doppler if difference greater than 10
percent arteriogram indicated
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"/3 / ,"
-restore blood volume with type O RBCs intravascular haemolysis ~ 0.05%
-hemolytic reactions due to irregular antibodies in pts plasma (eg. Kell, Duffy, Kidd etc..); usually
not as severe as ABO incompatibility
-correct any coagulopathy with FFP and platelets
& ,1( + 7 /
-all undergoing operation should receive preemptive antibiotic therapy
-first generation cephalosporins for most operations
-tetanus prophylaxis
-compressive pulsatile stockings DVT prophylaxis
-thermal protection - hypothermia impairs coagulation and myocardial contractility and increases
559
myocardial irritability
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-arteries for which repair should always be attempted:
aorta and carotid, innominate, branchial, superior mesenteric, proper hepatic, renal, iliac, femoral
and popliteal
-veins: SVC, IVC proximal to renal veins, portal vein
-options for treatment:
-pulsatile observation, ligation, lateral suture, end-to-end anastomosis, interposition grafts
(autogenous vein or artery, PTFE graft, Dacron), transpositions, extraanatomic bypass,
interventional radiology
-exogenous grafts less than 6 mm more prone to thrombosis
-ligation of SVC associated with sudden blindness from compression of optic nerve from venous
hypertension
-ligation of suprarenal IVC associated with acute renal failure from venous hypertension
- % #$. 1$ %,"/
-“Bloody Vicious Cycle”: coagulopathy, profound hypothermia, metabolic acidosis fatal arrhythmia
-heat loss appears to be the central event since neither of other components can be corrected until
core temperature is restored
-staged operations indicated when a coagulopathy develops and core temperature < 34oC
-unorthodox techniques used to expedite wound closure reoperation planned within 2-
24h allows for correction of hypothermia, coagulopathy and metabolic acidosis
-“Abdominal or Thoracic Compartment Syndrome”
-sources: blood and edema
-acute increase in intracavitary pressure
-decreased residual functional capacity hypoxia
- venous return CO
- venous resistance perfusion to intraabdominal organs acute renal failure
-life-threatening hypoxia and renal failure if IAP > 25 mmHg (measured with Foley)
-treatment: decompress abdominal cavity; volume expansion and inotropic support
< 15: normal
15-25: volume expansion, may need decompression
26-35: watch PaO2, SaO2, U/O, decompression likely
> 35: decompress in operating room
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-blunt injuries of liver, spleen and kidneys
-requires homodynamic stability
-extent of injuries delineated by CT scanning
-monitor in ICU for first 24h
-complications: continuing haemorrhage, delayed haemorrhage, necrosis of liver, spleen or kidney from
embolization, abscess, biloma, urinoma
560
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-CPP = MAP - ICP; lowest acceptable CPP is 60 mmHg

-haematoma: shift > 5mm indication for evacuation
-epidural haematoma:
-typical course (1) initial LOC; (2) awakening and lucid interval; (3) recurrent LOC with unilateral fixed,
dilated pupil; (4) cardiac arrest
-burr hole craniotomy on side of fixed pupil; transfer to facility with NSx capability
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Cervical Spine:
-axial traction to reduce subluxations external fixation with halo-vest (3-6 months)
-surgical fusion for:
-neurologic deficit
-angulation greater than 11 degrees on flexion and extension x-rays
-unstable after external fixation
Spinal Cord:
-complete injuries untreatable
-concussive injuries in 3% of pts presenting with flaccid quadriplegia recover
-significant improvement if methylprednisolone used within 8h of injury
Larynx:
-cricothyroidotomy or tracheotomy in severe fracture to protect airway
-larynx repaired with fine wires and sutures
Carotid and Vertebral Arteries:

-may cause dissection, thrombosis, or pseudoaneurysm
-mechanism: facial contact resulting in hyperextension and rotation
-dissection and thrombosis tx with anticoagulation with heparin then Coumadin (3 months)
-pseudoaneurysm stenting
Venous Injuries:
-thrombosis generally asymptomatic
-stent placement if ICP remains elevated
& $"$% %"# "4 $/
Carotid and Vertebral Arteries:

-carotid artery injuries require surgical repair
-inaccessible carotid artery injuries near base of skull stents
-if ligation necessary anticoagulation therapy x 3 months
-vertebral artery injuries ligation proximal and distal to injury; rarely indication for repair
-neurologic complications uncommon
Trachea and Esophagus:

-repair with running 3-0 absorbable monofilament suture
-avoid injury to recurrent laryngeal nerves
-viable tissue routinely interposed between adjacent suture lines to prevent post-op fistulas
561
(, * * %+$%
Great Vessels:
-angiography desirable for planning incisions
-median sternotomy: exposure of innominate, proximal right carotid and subclavian, proximal left carotid
artery
-“trapdoor” thoracotomy for good exposure of proximal left subclavian artery
Trachea and Esophagus:

-approaches in thoracic outlet:
-neck incision and high anterolateral thoracotomy
-median sternotomy
($/%
-most common life-threatening complications from blunt and penetrating thoracic injury are hemothorax,
pneumothorax or a combination of the two
-chest tubes are a definitive treatment
-sources of bleeding: intercostal vessels, internal thoracic artery, pulmonary parenchyma, heart
-Indications for Operative Treatment of Penetrating Thoracic Injuries

-caked hemothorax
-large air leak with inadequate ventilation or persistent collapse of lung
-drainage > 1500 cc blood from C/T
-continuous haemorrhage >200 cc/h for > 3 consecutive hours
-esophageal perforation
-pericardial tamponade
Thoracic Incisions:
-anterolateral thoracotomy exploratory thoracotomy for haemorrhage
-excision can be extended bilaterally
-posterolateral thoracotomies only for:
-injuries of posterior aspect of trachea
-main bronchi near carina
-tear of descending thoracic aorta
Lungs:
-pulmonary tractotomy:
-linear stapling devices inserted directly into injury tract and position to cause the least degree of
devascularization
-lobectomy or pneumonectomy rarely necessary
Descending Thoracic Aorta:

-concerned about paraplegia form ischemic injury of the spinal cord
-techniques:
1. “Clamp and sew”:
-vascular clamps proximal and distal to injury and repair or replacement of damaged
aorta
-paraplegia uncommon if clamping time < 30 min
2. Extraanatomic shunting
-Gott shunt: heparin-impregnated tube
-left heart bypass (preferred method): left superior pulmonary vein left femoral artery
562
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-exsanguinating haemorrhage: injury to liver, aorta, IVC, or iliac vessels

-blunt trauma: liver, spleen, kidneys
-penetrating trauma: small bowel, liver and colon
Vascular Injuries:
-vascular injuries in blunt trauma less common; usually involve renal artery and veins
-left medial visceral rotation expose upper abdominal aorta
-right medial visceral rotation expose infrahepatic vena cava
-injuries at bifurcation of IVC hidden by right common iliac artery; this artery is divided for exposure and
must be repaired after venous injury treated
Liver:
-manual compression, clamp hepatic pedicle (Pringle manoeuver), and perihepatic packing
-tight packing can compress IVC and reduce cardiac filling, and decrease tidal volume and FRC
-resectional debridement: remove non-viable tissue; do not remove > 75%
-complications after significant hepatic trauma:
-haemorrhage, infection, fistulas
-bilomas: loculated collections of bile (may or may not be infected)
-sterile bilomas will eventually resort
-biliary fistulas (3%): usually close without treatment
Gallbladder and Extrahepatic Bile Ducts:

-treated by lateral suture or cholecystectomy
-if significant tissue loss Roux-en-Y choledochojejunostomy
Spleen:
-splenic repair (splenorrhaphy), partial splenectomy, resection, or non-operatively
-trend toward non-operative management
-overwhelming postsplenectomy infection (OPSI):
-encapsulated bacteria: S.pneumonia, H. influenze, N. meningitidis
-resistant to treatment
-occurs in young children and immunocomporomised adults
-hilar injuries or pulverized splenic parenchyma splenectomy
-pneumococcal vaccine routinely given after splenectomy
Diaphragm:
-injured on left 75% of cases
-blunt trauma tear in central tendon that may be large
-laceration closed with 1-0 monofilament permanent suture
Duodenum:
-duodenal haematoma:
-more common in children
-blood b/n seromscular and submucosa layer obstruction
-x-rays: “coiled-spring sign of obstruction”
-most managed non-operatively with NG and parenteral nutrition
-duodenal perforations:
-caused by both blunt and penetrating trauma
-often contained by retroperitoneum
-most treated by primary repair
563
Pancreas:
-blunt pancreatic transection at neck of pancreas pseudocyst or pancreatic ascites
-dx with CT
-ductal injury require treatment
-methods of identifying ducal injuries:
-operative pancreatography
-coronary artery dilatory into main duct via papilla and observe wound
-ERCP
-injuries to head of pancreas final option is to drain pancreas; if fistula or pseudocyst develops, diagnosis
is confirmed; most fistulas close spontaneously with only supportive care
-injuries to neck, body, tail distal pancreatectomy
-pancreatic injuries should be drained when there is a possible unidentified major ductal injury
Pancreaticoduodenal Injuries:
-risk of duodenal suture line dehiscence and development of lateral duodenal fistula
-repair duodenal injury and drain pancreatic injury
-pancreatoduodenectomy:
-transection of intrapancreatic bile duct and main pancreatic duct in head of pancreas
-avulsion of papilla of Vater from duodenum
-destruction of entire second portion of duodenum
Colon:
-primary repair: definitive treatment at initial operation, but risk of leakage
-colostomy: avoids unprotected suture line in abdomen, but second operation required to close colostomy
-exteriorized repairs:
-suspending repaired perforation or anastomosis on abdominal wall with appliance after the
fashion of loop colostomy; if suture line does not leak after 10 days, it can be returned to
abdominal cavity under local anesthesia
-no longer indicated
Rectum:
-often injured by gunshot wound, rarely by stab wound, and frequently by acts of autoeroticism and sexual
misadventure
-intraperitoneal portion treated as per colonic injuries
-extraperitoneal injuries drained via retroanal incision
Stomach and Small Intestine:

-no special issues in treatment
Kidneys:
-CT, IVP, arteriography used to evaluate extent of injury
-95% of blunt injury treated non-operatively
-persistent gross hematuria embolization
-nephrectomy an option provided that opposite kidney normal
-all penetrating wounds to kidneys are explored
Ureters:
-injuries from external trauma are rare
-occur in a few patients with pelvic fracture
-can be repaired primarily
-nephrostomy for proximal urethral injuries when renal function mut be preserved and patient will not
tolerate surgery for the length of time required for ureteral repair
564
Bladder:
-diagnosed by cystography, CT or during laparotomy
-intraperitoneal injuries primary repair
-extraperitoneal injuries foley catheter; direct operative repair not necessary
Urethra:
-blunt disruption of posterior urethra managed by bridging defect with Foley catheter
-strictures repaired electively
-penetrating injuries treated by direct repair
Gynecologic Injuries:
-rare
-repair of transected fallopian tube unjustified suboptimal repair increases risk of tubal pregnancy
-blunt trauma can cause uterine rupture in pregnancy
, 1+$%," ,3%($ 1 ,%, ". ,/%,1$ %2$ ,"/ .$ %,"/8

-abdomen irrigated with warm saline
-integrity of gut pivotal role in severity and outcome of MOD and nosocomial infection
-enteric feedings initiated in ICU; advanced to full strength within 72 h
-prevents mucosa atrophy (as seen in TPN)
$+2 /
-can cause exsanguinating retroperitoneal haemorrhage
-branches of internal iliac vessels and lower lumbar arteries often responsible
-options to decrease hemorrhage:
-external fixation
-MAST
-angiography with embolization
-pelvic packing
-open pelvic fracture: risk of sepsis and osteomyelitis high
-reduce risk of infection with sigmoid colostomy
-wound manually derided and irrigated daily until granulation tissue covers the wound
7% $ %$/
Vascular Injuries with Fractures:

-rare, occurring in only 0.5-3% of patients with extremity fractures
-associated vascular injuries:
-# clavicle laceration of distal subclavian artery
-shoulder dislocations or proximal humeral fractures axillary artery injury
-supracondylar fractures of distal humerus and elbow dislocations branchial artery injuries
-dislocation of knee, supracondylar fractures of femur or tibial plateau fractures popliteal
vessels
-mechanisms of paralysis:
-ischemic
-nerve injury
-compartment syndrome
-primary amputation strongly considered when primary nerve transected in addition to fracture and arterial
injury
Compartment Syndrome:
-acute increase in pressure in a closed space that impairs blood flow to the structures within
565
-causes: arterial haemorrhage into compartment, venous ligation or thrombosis, crush injuries, infections,
crotalid envenomation, ischemia/reperfusion
-presence or absence of pulse is unreliable in diagnosis
-pressures > 45 mmHg require operative intervention
-treatment: elevation, evacuation of haematomas, fasciotomy
,#",/ / ". %*, $ 2 + %,"
-Abbreviated Injury Scale (AIS):

-1(minor injury) to 6 (always fatal)
-evaluates only solitary injuries
-Injury Severity Score (ISS):
-takes into account multiple injuries
-calculated by squaring the AIS from the worst injured of three body compartments and adding them
together
-scores range from 1-75
-characterized according to mechanism of injury and age
-does not take into account physiologic status
-Revised Trauma Score (RTS):
-calculated fomr GCS, BP, RR
-Trauma and Injury Severity Score (TRISS):
-incorporates RTS and ISS
-all scales/scores have limitations in predicting outcome and prognosis
' !
6 $/
-most domestic animal bites are provoked attacks; it this history is obtained, rabies vaccine usually can be withheld
if the animal appears healthy
-unprovoked attack by a domestic animal more likely to indicate animal is rabid
-fully vaccinated dog or cat unlikely to become infected with rabies
-animals who have bitten observed for symptoms of rabies for 10 days
-incubation period: 10 days 1 year (most w/n 20-90 days)
-post-exposure prophylaxis:
-human rabies immunoglobulin (HRIG): 20 IU/kg
-vaccine: human diploid cell rabies vaccine (HDCV) or rabies vaccine adsorbed (RVA)
-five doses of 1ml IM:
-post-exposure, then days 3, 7, 14, 28
-routine postvaccination serologic examination not necessary unless patient is known to be
immunosuppressed
-corticosteroids can interfere with development of active immunity after vaccination and may predispose
the patient to rabies
-pregnancy not a contraindication
Manifestations and Treatment of Rabies:

-2-4 day prodromal period patient reaches excited stage
-paraesthesia in region of bite
-h/a, vertigo, stiff neck, malaise, lethargy, severe pulmonary symptoms (wheezing, hyperventilation,
dyspnea)
566
-laryngospasm, dysphagia
-drooling, maniacal behaviour, convulsions death, coma, paralysis, and death
-respiratory supportive care only treatment
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Pit Vipers:
-venoms known to have neurotoxic, haemorrhagic, thrombogenic, hemolytic, cytotoxic, antifibrinolytic and
anticoagulant effects
-contain hyaluronidase
Coral Snakes:
-contributes to only 3% of all bites and 1.5% of all deaths from poisonous snakes
-blurred vision, ptosis, drowsiness, increased salivation, and sweating
-death may occur from inadequate ventilation
Management of Snake Bites:

-tourniquet, incision and suction within 1 h of time of bite
-incisions made proximal to the bite are contraindicated
-severe envenomation: surgical excision of entire area around snakebite within 1 h of time of bite
-antivenin:
-copperhead, rattlesnake, cottonmouth moccasin: antivenin crotalidae polyvalent
-coral snake antivenin
-beware of sensitivity to horse serum
-most common bacteria isolated from rattlesnake venom: Pseudomonas aeruginosa, Proteus species,
Clostridium species, Bacteroides fragilis.
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-honeybee, bumblebee, wasp, yellow and black hornet, fire ant
-venom causes more deaths in US yearly than are caused by snakebites
-fatal cases may manifest glottal and laryngeal edema, pulmonary and cerebral edema, visceral congestion,
meningeal hypermia, and intraventricular haemorrhage
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-treat with copious irrigation with water to wash out any toxin and fragments of the ray spine’s
integumetary sheath
-venom is inactive when exposed to heat place injured part in hot water
-complications: tissue necrosis with prolonged drainage and chronically infected wounds
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-application of a substance with high alcohol content, followed by drying agent (eg. flour, baking soda,
talc, or shaving cream)
-tentacles removed by shaving
-baking soda neutralizes acidic toxins
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-Black Widow Spider:
-Latrodectus mactans venom primarily neurotoxic and centers on spinal cord
-generalized muscle spasm most prominent physical finding
567
-priapism and ejaculation have been reported
-treatment:
-narcotics and muscle relaxant
-calcium gluconate relieves symptoms by depressing threshold for depolarization
-Brown Recluse Spider:
-Loxosceles recluse: body 7-12 mm
-initial bite may go unnoticed
-severe bites result in progression to necrosis and sloughing of skin with residual ulcer formation
-haemolysis and thrombocytopenia responsible for deaths
-conservative therapy usually is preferred treatment
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-bark scorpion medically significant
-venom is neurotoxic release of neurotransmitters from autonomic nervous system and adrenal glands
-tap test: hyperesthesia persists at site intense pain with light tap
-anxiety, blurred vision or temporary blindness, wandering eye movement, dyspnea, wheezing, dysphagia,
involuntary urination and defecation, opisthotonos
-somatic symptoms
-treated with cold compresses
568
AIRWAY IMAGING IN CHILDREN
UPPER AIRWAY OBSTRUCTION
-upper trachea characteristically buckles anteriorly and to

right on expiration in infants and young children
Supraglottic Obstruction
Acute epiglottitis:
-lateral neck: thickening of both epiglottis and
aryepiglottic folds
-beware of normal findings:
-“omega epiglottis”: areyepiglottic folds
will remain thin
-other causes of epiglottitic enlargement:
-angioneurotic edema, candidal infection,
burns from corrosive ingestion, laryngeal
sarcoidosis, neoplasms, lymphatic
malformation, allergic reactions,
aryepiglottic fold cysts
Laryngomalacia:
-downward and posterior bending of epiglottis and
anteroinferior buckling of aryepiglottic folds
during inspiration
-best seen with fluoroscopy or endoscopy
Glottic Obstruction
Croup:
-lateral view:
-inspiration: distension of hypopharynx and narrowing of subglottic area
-expiration: collapse of hypopharynx and re-expansion of subglottic trachea
-indistinct vocal cords
-AP view:
-steeple or funnel-shaped subglottis
Bacterial Tracheitis:
-irregularity of walls of subglottic trachea
Laryngeal papilloma:
-nodular thickening of vocal cord on lateral view
Subglottic Obstruction
Subglottic Stenosis:
-narrowing persists during both inspiration and expiration
-CT or MRI best for diagnosis
F.Ling - Airway Imaging (1)
569
Tracheomalacia:
-hypercollapsibility of trachea on expiration due to weakness of supporting cartilage
Subglottic Hemangioma:
-occur on lateral or posterior walls of subglottic trachea
-eccentric narrowing seen
-ddx: granuloma, ectopic thyroid or thymus tissue, subglottic mucoceles, post-inflammatory
histiocytoma, tracheal cysts
Foreign Body Ingestion:

-usually at cricopharyngeal muscle or aortic arch level
RETROPHARYNGEAL MASSES AND THICKENING
Retropharyngeal Abscess:
-lateral view:
-convex anterior displacement of posterior pharyngeal airway
-loss of normal step-off at origin of esophagus
-false positive if x-ray taken in expiration (clue: anterior buckling of trachea)
-straightening or hyperflexion of cervical spine 2o muscle spasm
-+/- gas in soft tissues
-CT scan:
-focal hypodensity with rim contrast enhancement
-US: to evaluate drainable fluid collection
-MRI:
-T1: dark
-T2: increased signal
NASAL AND NASOPHARYNGEAL OBSTRUCTION
Choanal Atresia:
-most common cause of nasal obstruction in neonate
-axial CT scans:
-children < 2ya: choanal orifice < 0.37 cm
-children < 8ya: vomer exceeds 0.34 cm
-medial bowing and thickening of lateral walls of nasal cavity
-fusion of lateral walls with enlarged vomer
Nasal Polyp:
-most common nasal mass seen in children
-MRI: bright T2 (fluid)
Adenoids and Tonsils:

-no reliable radiographic criteria for determining when adenoidal and palatine enlargement
becomes pathologic
Juvenile Angiofibroma:
-enhances with contrast
-MRI: bright T2, flow voids
F.Ling - Airway Imaging (2)
570
PEDIATRIC SLEEP-DISORDERED BREATHING
PATHOPHYSIOLOGY
-anatomic and neuromuscular factors:
1. Hypertrophied lymphoid tissue (adenotonsillar hypertrophy most common cause)
2. Dysmorphic constricted craniofacial development:
-retrodisplaced/hypoplastic mandible: Pierre Robin sequence
-small nasopharynx: Treacher Collin, Apert, and Crouzon syndromes
3. Macroglossia
4. Low lying hyoid bone
5. Neuromuscular hypotonia: eg. Down syndrome, cerebral palsy
-sleep fragmentation and decreased REM sleep causes daytime symptoms of the disorder
-pediatric SDB typically related to adenotonsillar hyperplasia with varying degrees of other skeletal and
soft-tissue anatomic factors playing less common or less important roles
-hypercapnia and hypoxemia and resulting arousals often result in reduction in REM sleep associated
with a reduction in growth hormones
-sequelae:
-instead of excessive daytime sleepiness
-hyperactivity, attention deficit, aggression, and other behavioural disorders may be seen
-mouthbreathing and hyponasal speech with articulatory errors
-SDB shown to affect school performance intervention resulted in improved grades
-high prevalence of allergy in snorers
-nocturnal enuresis frequently reported in children with OSAS
-failure to thrive
-poor weight gain due to:
-decreased GH production
-increased energy expenditure with nocturnal movement and calorie expenditure
-difficulty smelling and tasting food
-pulmonary hypertension, arrhythmias, cor pulmonale
EVALUATION
History
-sleep history:
-typical bedtime, number of hours of sleep, abnormal sleep positions, parasomnias (nocturnal
enuresis), character of snoring, observed pauses in respiration and signs of respiratory distress,
problems after waking up (headache/fatigue), behavioural disorders, school performance,
hypersomnolence
-look for mouth breathing
-assess dental malocclusion, pharyngeal soft tissue anatomy, lingual shape and size relative to
oropharyngeal airway, shape of hard and soft palates, size of uvula, velopharyngeal function, degree of
tonsillar enlargement
Laboratory Evaluations
-PSG remains the gold standard for diagnosis of OSAS
-criteria for abnormal study:
-apnea index > 1
-oxygen desaturation > 4% more than 3x/h or associated with > 25% change in HR
-oxygen desaturation < 92%
F.Ling - Sleep Disordered Breathing (1)
571
-elevation of end-tidal CO2 to > 50 mmHg for more than 8% total sleep time or 45 mmHg for
more than 60% of sleep time
-flexible endoscopy provides the best assessment of the nasopharynx and its soft tissues
TREATMENT
-adenotonsillectomy remains the mainstay of treatment for pediatric OSAS

-optimal age b/n 4-7 years
-outpatient treatment safe with a suitable period of post-op observation
-post-obstructive pulmonary edema occurs in less than 1%
Differences between Adult and Childhood Sleep-Disordered Breathing

Feature Adult Child
Snoring intermittent continuous
Mouthbreathing uncommon common
Obesity common uncommon
FTT uncommon common
Daytime somnolence common uncommon
Gender predilection male none
Most common obstructive event apnea hypopnea
Arousal common uncommon
Treatment Non-surgical: CPAP in most Surgery in most

Surgery only in selected cases
F.Ling - Sleep Disordered Breathing (2)
572
LARYNGEAL STENOSIS
PEDIATRIC ANATOMY
Parameter Infant Adult

laryngeal size 1/3 size of adult
vocal cord length 7-8 mm 14-23
vocal process to vocal cord ratio 1:2 1:4
level of cricoid C4 vertebra C6 vertebra
angle of thyroid cartilage 110-1200 900 (male)
pliability elastic more fibrous
-other features:
-subglottis is narrowest part of airway in children
-stenosis present if cricoid area < 4mm
-hyoid over-rides superior larynx
-superior border of infant larynx is located at C1
-epiglottis:
-overlaps dorsal surface of soft palate
-omega shaped
-more acute angle b/n glottis easily falls into laryngeal inlet
-circumferential mucosal edema of 1 mm narrows subglottic space by > 60%
LARYNGEAL STENOSIS
-signs and symptoms by region of obstruction:

-supraglottis: muffled voice, fluttering inspiratory stridor, severe feeding problems, no cough
-glottis: hoarse voice or aphonia, inspiratory (early) or biphasic (late) stridor, normal
feeding, no cough
-subglottis: hoarse or normal voice, biphasic stridor, normal feeding, barking cough
F.Ling - Laryngeal Stenosis (1)
573
Congenital Laryngeal Stenosis
Subglottic Stenosis
-cricoid lumen < 4 mm in diameter
-d/t failure of laryngeal lumen to recanalize (failure with autolysis GRADING SCALE FOR LARYNGEAL
of epithelial remnant of growing respiratory tract) STENOSIS
-varying degrees of respiratory problems Grade Laryngeal Lumen Obstruction
-types: I < 50%
-membranous stenosis II 51-70%
-circumferential, fibrous soft-tissue thickening III 71-99%
IV complete obstruction
-granulation tissue
-submucsal gland hyperplasia
-submucosal fibrosis
-cartilaginous stenosis
-cricoid cartilage deformity
-normal shape small for infant’s size
-abnormal shape
-large anterior or posterior lamina
-generalized thickening
-elliptical shape
-submucosal cleft
-trapped first tracheal ring
-combined stenosis
Atresia
-high frequency of other congenital anomalies
-high mortality
-complete failure to recanalize laryngeal lumen
-requires tracheotomy
Webs
-usually arise anteriorly; 90% located at level of glottis
-10% associated with congenital anomalies; strong association with VCFS
-represent failure to completely recanalize larynx
-thin webs easily lysed; thick webs require open reconstruction
Acquired Laryngeal Stenosis
Postintubation Stenosis
-incidence 1-8%
-more common than congenital stenosis in pediatric age group
-pathophysiology:
-pressure of tube causes ulceration and necrosis of cricoid mucosa
-infection and perichondritis/chondritis of underlying cartilage
-healing and fibrosis occurs stenosis
-risk factors:
-cricoid ring is narrowest portion or airway
-ischemic necrosis can be caused by ETT pressure
-superimposed respiratory tract infection
-length of time of intubation
-repeated intubations
574
-diagnosis:
-CT scan reconstructions: length of
stenosis Neonate
-bronchoscopy: size of stenosis -laryngomalacia
-vascular compression (eg. innominate artery, aberrant
subclavian vascular ring)
Postoperative Stenosis -vocal cord paralysis
-after high tracheotomies and -bilateral (eg. Arnold-Chiari deformity)
cricothyroidotomies -unilateral (eg. traumatic postductus ligation)
-hemangioma, subglottic
-failed laryngotracheoplasty -complete tracheal rings
-laryngeal cleft
-cri-du-chat syndrome
Infectious or Inflammatory Stenosis -laryngeal saccules, laryngoceles
Child
Granulomatous Disease -dermoids, saccular, epiglottic cysts
-tuberculosis of larynx: -lingual thyroid
-most common sites: -infections (eg. epiglottitis, croup, bacterial
laryngotracheitis)
-interarytenoid space, -foreign bodies
arytenoid cartilages, -papillomatosis
posterior surface of true
vocal cords, laryngeal Adult
surface of epiglottis -viral, granulomatous, fungal laryngitis
-nodular lesions and ulceration of -Reinke edema
epithelium perichondritis and -laryngeal trauma, potintubation
chondritis extensive scarring and -hemangioma, supraglottic
-idiopathic
stenosis -neurologic (eg. ALS, MS)
-systemic treatment leads to -caustic ingestion
complete healing of larynx -systemic disease (eg. RA, polychondritis)
-sarcoidosis, rhinoscleroma, WG (rare in -Tracheal tumours or obstruction
children)
Trauma
-d/t foreign bodies and instrumentation
-anterior blunt trauma posterior supraglottic and glottic stenosis
Systemic Diseases
-lupus, gout, rheumatoid arthritis or juvenile rheumatoid arthritis (Still disease) fixation of cricoarytenoid
joint
-dx: laryngoscopy and palpation to differentiate from vocal cord paralysis
Thermal Injuries
-steam, laser airway fires
-three factors: direct thermal injury, toxic effects of combustion products, and prolonged intubation
Caustic Ingestions
-laryngeal stenosis rare
-fibrosis of posterior cricoarytenoid muscle
-supraglottic scarring and stenosis
Gastric Acid Reflux

-exacerbating factor in subglottic stenosis
-treat with H2 blockers, PPIs or fundoplication
575
Radiation Effects
-may cause pharyngeal or laryngeal edema and stenosis
MANAGEMENT
-fewer than half of patients with congenital laryngeal stenosis require tracheotomy
Medical Therapy
-prevention
-experienced intubation personnel
-correctly sized ETT
-supportive therapy:
-humidification, antibiotics, steroid therapy
-management of GERD
-PPI
Surgical Treatment
-Preoperative workup:
-secure airway, endoscopic evaluation of
FACTORS PREDISPOSING TO FAILURE IN
airway size TREATING SUBGLOTTIC STENOSIS WITH CO2
-cardiac and pulmonary function LASER
-gastric reflux assessment
-failure of previous endoscopic procedures
-radiographic studies -significant loss of cartilaginous framework
-combined laryngotracheal stenosis
-Grade I or II stenosis, unilateral lesions -circumferential cicatrical scarring
-no treatment (majority) -fibrotic scar tissue in interarytenoid area of posterior
commissure
-dilatation, cryosurgery, division, micro- -abundant scar tissue greater than 1 cm in vertical
trapdoor flaps dimension
-endoscopic resection with laser surgery -severe bacterial infection of trachea after tracheotomy
(CO2 or KTP laser excision with dilation) -exposure of perichondrium or cartilage during CO2 laser
excision predisposing to perichondritis and chondritis
-66-80% success) -concomitant tracheal disease
-contraindications: significant
cartilage loss, concurrent
laryngotracheal stenosis, posterior
commissure involvement, circumferential cicatricial scar or thick scar (> 1cm), infected
tissue (chondritis)
-Failed extubation stenosis
-anterior cricoid split (for neonate only)
-tracheotomy
-Grades II, III, and IV stenosis; circumferential lesions, thick webs, failed endoscopic therapy, loss of
cartilaginous framework
-anterior cricoid split
-posterior cricoid split
-laryngotracheal reconstruction
-via laryngofissure:
-anterior split with lumen augmentation
-posterior split with lumen augmentation
-anterior and posterior split with lumen augmentation
-segmental resection with end-to-end anastomosis, tracheal or cricotracheal
576
Anterior Cricoid Split
-used instead of tracheotomy in neonate
-*Criteria:
-two or more extubation failures secondary to laryngeal pathologic conditions
-weight > 1500 g
-no assisted ventilation for 10 days before evaluation
-O2 requirements < 30%
-no CHF for 1 month
-no acute upper or lower respiratory tract infection
-no antihypertensive medication for 10 days
-anterior laryngofissure should only extend to lower one third of thyroid cartilage
Laryngotracheal Reconstruction
Anterior Cartilage Graft

-boat-shaped costal cartilage graft placed b/n divided anterior lamina of cricoid cartilage
Posterior Cartilage Graft

-narrow graft 6 mm adequate
-overaugmentation risks aspiration
-used for grade II or III subglottic stenosis with primarily posterior cricoid scarring
Anterior and Posterior Cartilage Graft

-for grades III and IV stenosis
Cricotracheal Resection
-reserved for severe (grade III or IV) subglottic stenosis
-technically challenging but higher chance of achieving decannulation
-contraindication: subglottic scarring within 3 mm of vocal cords
-advantages:
-glottic sparing
-avoidance of donor site morbidity
-near normal-appearing and mucosalized airway
-disadvantages:
-risk to RLN
-anastomotic dehiscence
Stenting Options
-T-tube (Montgomery or Hood)
-wired-in metal tracheotomy tube within a Teflon stent (Aboulker or Cotton Lorenz)
577
STRIDOR, ASPIRATION, AND COUGH
ANATOMY, PHYSIOLOGY AND PATHOPHYSIOLOGY
Stertor
-inspiratory low-pitched sound
-nasopharyngeal and oropharyngeal obstruction
Stridor
-inspiratory stridor with supraglottic and glottic obstructions
-expiratory stridor with intrathoracic lesions
-biphasic stridor with fixed subglottic laryngeal and cervical tracheal lesions
-infant larynx:
-vc length: 6-8 mm
-posterior glottis transverse length: 4 mm
-subglottic diameter: 5-7 mm
-tracheal length: 4 cm
Cough
-inspiratory, compressive, expiratory phases
Swallowing
-preparatory, oral, pharyngeal, esophageal phases
-anatomical differences in children:
-hard palate closer to skull base
-larynx higher in neck
-adenoid pad, tonsils, tongue relatively larger
-airway protection: 3 interlocking systems:
-first system: swallowing mechanism
-second system:
-level 1: epiglottis, aryepiglottic folds, arytenoids
-level 2: false cords
-level 3: true cords
-third system: mucociliary clearance and cough reflex
STRIDOR
Evaluation
History
-birth history
-age of onset
-severity
-progression
-posturing and position changes
-hoarseness, eating or feeding difficulties, sleep-disordered breathing
-ABCs
-H+N exam, FNL
F.Ling - Stridor, Aspiration and Cough (1)
578
Radiology and Special Studies
-CXR - in/ex views
-barium esophagram: r/o vascular rings and TEF
-CT: choanal atresia/stenosis
Airway Endoscopy
-good communication with anaesthetist
-inspection of equipment before induction of anaesthesia
-Storz bronchoscope
-Hopkins rod-lens telescope
-inhalational anaesthesia, spontaneous ventilation maintained
-steroids +/- racemic epinephrine to limit postoperative edema
Differential Diagnosis of Common Causes of Noisy Breathing in Children

Congenital Inflammatory Neoplastic Neuromuscular Traumatic
-choanal atresia or stenosis -nasal polyps -encephalocele -hypotonia, neurologic -foreign body
-piriform aperture stenosis -rhinitis -dermoids disease -haematoma
-glossoptosis / macroglossia -retropharyngeal abscess -glioma -vocal cord paralysis -laryngeal fracture
-lingual thyroid -adenoid hypertrophy -dermoids
-vallecular cyst -tonsil hypertrophy -hemangioma
-craniofacial anomalies -epiglottitis -lymphangioma
-laryngomalacia -angioneurotic edema -papilloma
-laryngocele / saccular cyst -laryngitis -granuloma
-glottic web / atresia -laryngeal spasm -mediastinal tumours
-subglottic stenosis -croup -thyroid
-subglottic cysts -bacterial tracheitis -thymus
-tracheal stenosis -bronchitis
-tracheomalacia -asthma
-vascular ring
-complete tracheal rings
-foreguts cysts
-TEF
-congenital etiology in 85% of children < 2.5 years presenting with stridor
Laryngomalacia
-most common cause of stridor in infancy
-typically resolve by 12-18 months
-low pitch stridor with fluttering quality; most prominent in supine position
-FNL: cyclical collapse of supraglottic larynx with inspiration
-Type A: inward movement of AE folds
-Type B: curling of epiglottis
-Type C: inward collapse of cuneiform cartilages
-Type D: inward collapse of arytenoid cartilages
-Type E: folding inward of epiglottis
-Type F: shortened aryepiglottic folds
-usually no surgical intervention required
-supraglottoplasty if:
-inability to feed orally
-cor pulmonale
-FTT
-life-threatening episodes of obstruction
579
-types of supraglottoplasty:
-excision of cuneiform cartilages and/or redundant mucosa
-excision of superior epiglottis
-incision/release of aryepiglottic folds
Laryngeal Stenosis
-congenital laryngotracheal stenosis second most common cause of stridor in infants
-see Ch 73
Subglottic Hemangioma
-2:1 female predominance
-1.5% of all congenital laryngeal anomalies
-50% have cutaneous hemangiomas present at time of diagnosis
-most resolve by 5 years
Laryngeal Papillomatosis
-HPV-6 and HPV-11
-squamociliary junction (vocal cords) areas of injury (tracheotomy site)
-rate of vaginal transmission low (1-3%)
-C-section not routinely recommended to patients with genital papilloma
-tx: CO2 laser or debrider debulking
-non-surgical modalities:
-interferon-a, indole compounds, antiviral therapy, phototherapy
-tracheotomy:
-50% rate of tracheal spread
Vocal Fold Paralysis

-10% of congenital laryngeal lesions
-congenital bilateral paralysis:
-high-pitched inspiratory stridor
-most commonly from central pathology: Arnold-Chiari malformation
-acquired paralysis:
-cervical or mediastinal (cardiac) surgery
-paralysis usually resolves in 6-18 months
-surgical procedures (after > 2 years of paralysis) include:
-lateralization
-excisional procedures (from posterior glottis)
-laser arytenoidectomy or posterior cordotomy
-arytenoidopexy
-laryngeal expansion with costal cartilage augmentation to posterior cricoid plate
Vascular Anomalies
-d/t tracheal compression by:
-vascular rings (double aortic arch)
-pulmonary slings
-aberrant right subclavian artery
-absolute indications for surgical repair:
-reflex apnea: reflexive respiratory arrest secondary to stimulation of vagal afferent nerve fibres
during swallowing
-failure of medical management of respiratory distress after 48h
-prolonged intubation
580
Laryngeal Dyskinesia, Exercise-induced Laryngomalacia, and Paroxysmal Vocal Fold Motion
-resulting from neuromuscular dysfunction
Gastroesophageal Reflux Disease
Laryngotracheobronchitis
-“croup”
-most common infectious cause of stridor (affecting 3-5% of children at least once)
-peak incidence 2ya
-cause: parainfluenza virus type 1
-other: parainfluenza virus types 2 and 3, RSV, and influenza virus A
-barking cough, inspiratory high pitched stridor
-CXR: “steeple sign” - symmetric narrowing of subglottic space
-treatment:
-humidified oxygen
-dexamethasone (0.6-1 mg/kg) for severe breathing difficulty
-nebulized racemic epinephrine (be wary of rebound edema)
-< 5% of hospitalized children will require intubation and ventilation
Acute Supraglottitis (Epiglottitis)

-children 1-5 ya
-cause: Haemophilus influenzae type B
-gram-positive organisms in adolescents and adults
-rapid progression, fever, sore throat and respiratory difficulties
-drooling
-unable to lie flat
-avoid manipulation/agitation
-neck XR: “thumb sign”
-treatment:
-intubation in OR
-direct laryngoscopy, blood and epiglottis cultures
-antibiotics: ceftriaxone
-admission to ICU - extubate when cuff leak
Bacterial Tracheitis (Membranous Tracheitis)

-complication of viral laryngotracheobronchitis
-agent: Staphylococcus aureus
-also: H. influenzae, Streptococcus pyogenes, Streptococcus pneumoniae, parainfluenza virus
-rapid progression of harsh, inspiratory or biphasic stridor and respiratory distress
-toxic appearing
-no drooling
-able to lie flat
-CXR: irregularities of airway
-treatment:
-bronchoscopy for removal of adherent thick secretions
-intubation to assist with aggressive pulmonary toilet
-antibiotics
581
ASPIRATION
Evaluation and Diagnosis

-aspirated organisms:
-nonhospitalized pts: Bacteroides melaninogenicus, Fusobacterium, and anaerobic gram-positive
cocci
-hospitalized pts: gram-negative organisms (Pseudomonas)
Special Diagnostic Studies
Rehabilitative Swallow Study

-modified barium swallow
-normal upright eating posture and swallows feedings of varying consistency
-liquid, paste, solids
-evaluates four phases of swallowing
Functional Endoscopic Evaluation

-FNL observation of hypopharynx and larynx
-evaluates:
-pharyngeal pooling
-premature spillage
-laryngeal penetration
-aspiration
-residue
Radionuclide Scintigraphy
-calculates percentage of aspiration
Electromyography
-permits study of individual muscles during swallowing
-pharyngeal constrictors, thyroarytenoid and cricopharyngeal muscles
-patterns: tonic, phasic, or absent
-can distinguish upper from lower motorneuron lesions
Management
-medical management of aspiration pneumonia

-SLP: altering food consistencies, adjusting posture during swallowing
-feeding gastrostomy and jejunostomy: for chronic aspiration associated with malnutrition
-fundoplication
-cricopharyngeal myotomy:
-for cricopharyngeal achalasia: failure of cricopharyngeus to relax during pharyngeal phase
-control of salivary output and sialorrhea:
-bilateral submandibular gland excision with parotid duct ligation
-laryngeal incompetence procedures:
-tracheotomy
-laryngectomy
-laryngeal suspension
-partial cricoid resection
-vocal fold medialization
-laryngeal closure
-laryngeal diversion and separation
582
COUGH
Evaluation
-chronic coughing
-productive (tracheobronchial disease) vs non-productive (upper airway lesion or asthma)
-PND, GERD, smoking
Investigations
-CBC, CXR, sputum: cytology, bacteria, TB, fungus
-+/- CT sinuses, PFTs
-+/- endoscopy
Differential Diagnosis of Cough

-pharyngeal, laryngeal, bronchial receptors:
-environmental:
-smoking, air pollution, allergens
-inflammatory:
-pharyngitis, laryngitis, rhinitis and PND, pneumonia, GERD
-neoplastic:
-pharyngeal and laryngeal neoplasms, bronchogenic carcinoma
-cough-variant asthma
-afferent neurons of cough reflex:
-vagus neurilemomas
-cervical osteophytes
-other receptor sites:
-ear, pleura, pericardium, stomach
-central:
-psychogenic cough
583
CAUSTIC INGESTION AND FOREIGN BODIES
IN THE AERODIGESTIVE TRACT
CAUSTIC ESOPHAGEAL INJURIES
-current mortality rates with severe transmural burns ~ 0-20%

-most common agents:
-caustic agents or alkali
-liquefaction necrosis (deep penetration into tissues)
-disk batteries may cause mucosal damage as early as 1 hour after ingestion
-corrosives or acids
-coagulation necrosis (coagulum limits deeper absorption until agent reaches stomach)
-can cause gastric perforation
-“chemical epiglottitis”: requires securing airway
-bleaches
-sequelae of deep burns:

-adhesive bands pseudodiverticula
-stricture formation
-pathophysiology:
-inflammatory response
-granulation tissue with fibroblasts
-contraction of collagen fibers
-pseudodiverticula and fibrous scar formation
-areas with greatest extrinsic compression most likely to burn:

-cricopharyngeus
-aortic arch
-left mainstem bronchus
-distal esophagus at GE junction
-most signs, symptoms, lab tests are not consistently predictive of gastroesophageal involvement
-presence of oral injuries cannot accurately predict presence or absence of more distal involvement
-severity of external and oropharyngeal injury does not correlate with extent of esophageal and gastric
injury
-dysphagia, retrosternal pain, or abdominal pain often indicates severe esophageal injuries
Treatment Principles (General)

-ABCs, NPO, IV fluids
-identify agent, determine pH, amount and concentration (call poison information center)
-avoid neutralizing agents and induction of vomiting
-use of diluting agents: water or milk to cleanse esophagus
-evaluate for complications:
-CXR: r/o mediastinitis
-abdominal series: r/o gastric perforation
-ABG: assess for acid/base disturbances
-endoscopy:
-if performed 12h after ingestion: underestimation of damage
-delayed examination: risk of iatrogenic injury because of structural weakness of esophageal wall
-should be performed between 24 and 48 hours to achieve highest degree of patient safety
-avoid endoscopy after 48 hours; use barium swallow to verify perforation or stricture (late)
F.Ling - Caustic and Foreign Body Ingestion (1)
584
-assess severity of injury:
-grade 1: superficial injury
-grade 2: transmucosal injury
-grade 3: circumferential transmucosal injury
-grade 4: transmural injury
ENDOSCOPIC APPEARANCE OF ESOPHAGEAL BURNS
Burn Severity Endoscopic Appearance
First Degree nonulcerative esophagitis, mild erythema, edema of mucosa
Second Degree whitish exudate, erythema, underlying ulceration that may extend into the muscularis
Third Degree dusky or blackened transmural tissue, deep ulcerations that may extend into periesophageal tissue, lumen may be
obliterated
-insertion of feeding tube (controversial) - under direct vision

-antibiotics: decreases intramural spread of infection and mediastinitis
-steroids: reduce stricture formation
-antireflux medications
-contrast esophagogram at 6 weeks to evaluate for stricture
Specific Treatments Based on Endoscopic findings

-grade 1 injuries:
-conservative management
-observation overnight
-discharge with refux regimen, follow-up after 2 weeks
-grade 2-3 injuries:
-steroid administration for decreasing stricture formation only in grade 2 injuries
-no consensus dose
-usually 1-2 mg/kg/day prednisone to max of 60 mg for 21 days
-prophylactic antibiotics controversial (treat for 14 days)
-lathyrogenic agents that reduce collagen cross-bonding used to decrease strictures:
-eg. B-aminopropionitrile, acetylcysteine, penicillamine have decreased formation of
laryngeal strictures from alkali injury
-sulcralfate: protection of injured esophageal wall from gastric acid may decrease granulation
tissue and subsequent scar formation
-treatment of strictures:
-serial esophageal dilatation
-early mechanical stenting (with NG tube) for second- and third degree injuries has been
suggested
-severe injuries (grade 4):
-early surgical resection with reconstruction
-may require esophagectomy/gastrectomy with exploratory laparotomy to remove
necrotic tissue
-steroids contraindicated
-masks infection and increases risk of perforation
Complications
-most common: stricture formation
-tracheoesophageal fistula
-gastric perforation
585
-mediastinitis, peritonitis, pneumonia
-sepsis, death
-(esophageal carcinoma)
AERODIGESTIVE FOREIGN BODIES
-most common age group 2-4 years

-M:F = 2:1
-any pt with prolonged nonspecific pulmonary complaint, even without hx of acute aspiration, should raise
the question of a retained foreign body
FB Aspirations
-types of objects:
-vegetable matter (70-80%)
-peanuts, watermelon seeds, pumpkin seeds
-plastic pieces (15%)
-SSx:
-choking, stridor, chest pain, wheezing, hoarseness, audible slap
-auscultation:
-decreased air entry to affected side
-wheezing
-CXR:
-25% may be normal
-inspiratory and expiratory films needed:
-expiratory view:
-mediastinal shift opposite side of FB
-air trapping on affected side
-left lateral decubitus film: dependent lung remains inflated if obstructed
-right mainstem bronchi most commonly involved:
-larger than left side
-steeper angle
-greater airflow
-position more towards center
-types of obstruction:
-air valve: air can pass in/out normal CXR
-check valve: air can pass out but not in atelectasis
-ball valve: air can pass in but not out hyperinflation, deviation of mediastinum
-stop valve: air cannot pass in/out
-Management:
-avoid digital manipulation, back slapping, Heimlich manoeuver (unless completely obstructed)
-obtain description of object
-anaesthesia consult
-IV corticosteroids for organic aspirations
-bronchoscopy:
-must rule out multiple foreign bodies
-patient should be spontaneously breathing (ie. no paralysis)
-organic ingestions: IV steroids to reduce inflammation
-if unable to retrieve object after 1 hour stop procedure and bring back to OR the next day
-thoracotomy for multiple failed attempts at FB retrieval
586
FB Ingestions
-may present with respiratory distress d/t extreme compliance of wall b/n esophagus and trachea and mass
effect of FB
-most common area: C6 or level of cricopharyngeal muscle
-most common objects:
-coins (75%)
-meat/vegetable, small round trinkets etc (20%)
-complications:
-mediastinitis
-pneumomediastinum
-pneumothorax
-aspiration
587
CONGENITAL NECK MASSES AND CYSTS
NECK MASSES BY LOCATION
Lateral neck masses

-branchial anomalies
-laryngocele
-pseudotumour of infancy
Midline
-thyroglossal duct cyst
-thymic cyst
-dermoids cyst
-plunging ranula
-teratoma of the neck
Entire neck
-haemangioma
-lymphatic malformation
LATERAL NECK MASSES
Branchial Anomalies
-development of branchial apparatus (BA) begins at 2 weeks GA
-4th week of embryonic development
-condensation of mesoderm
-separated by external ectodermal cleft and internal endodermal pouch
-thin epithelilial plate separates each cleft and pouch
-each arch composed of an artery, cartilaginous bar, muscles and nerve
-course of each BA is caudal to structures derived from its arch and dorsal to structures that develop from
the following arch
F.Ling - Congenital Neck Masses and Cysts (1)
588
Arch Nerve Muscle Skeletal Structure Artery Pouch # and Derivative
I Trigeminal (V) Mastication muscles, Meckel cartilage, malleus, Maxillary 1. Eustachian tube, middle
(Mandibular) mylohyoid, anterior incus, anterior ligament of ear
digastric, tensor malleus, sphenomandibular
tympani, tensor velum ligament
palatini
II (Hyoid) Facial (VII) 1. Stapedius Reichert cartilage Stapedial 2. Palatine tonsil

2. Posterior digastric 1. Stapes
3. Stylohyoid 2. Styloid process
4. Muscles of facial 3. Stylohyoid ligament
expression 4. Lesser cornu/upper
portion of body of hyoid
III Glosso- Stylopharyngeus Greater cornu hyoid, lower Common and 3. Thymus and inferior
pharyngeal (XI) body hyoid internal parathyroid
carotid
IV Superior Constrictors of the Laryngeal cartilages Subclavian 4. Superior parathyroid,

Laryngeal (X) pharynx, cricothyroid on right, arch parafollicular cells of
of aorta on thyroid
left
VI Recurrent Intrinsic laryngeal Laryngeal cartilages Pulmonary

Laryngeal (X) muscles artery on
right, ductus
arteriosus on
left
Anomalies:
-Sinus: vestigial cleft (external sinus) or pouch (internal sinus)
-Fistula: persistence of both cleft and pouch with dissolution of intervening separation plate
-Cyst: trapped portion of cleft or pouch
First Branchial Anomalies: (1%)
-usually presents as a preauricular cyst (may

also be infra- or postauricular)
-Type I
-contain only epidermoid elements
without cartilage or adnexal
structures
-duplication anomalies of EAC and
may pass close to facial nerve
-medial, inferior or posterior to
conchal cartilage and pinna
-parallels external auditory canal
-Type II
-more common
-ectodermal and mesodermal First BA - Type I
elements
-usually present as abscess below mandible
-External: always superior to hyoid
-Course: variable relationship with CN VII and parotid
-Internal: terminates at bony-cartilaginous junction
First BA - Type II
589
Second Branchial Anomalies (most common type)
-external: anterior border of SCM

-internal: tonsillar fossae
-course:
-deep to second arch structures:
-external carotid artery, stylohyoid and posterior belly
of digastric
-superficial to third arch structures:
-lateral to CN IX and (XII)
-internal carotid artery (courses between carotid
vessels)
-cysts commonly in anterior triangle below hyoid
Third Branchial Arch Anomalies Second BA
-external as in 2nd BAA

-internal: piriform sinus (superior portion)
-course:
-deep to third arch structures:
-CN IX
-carotid vessels
-superficial to fourth arch structures:
-superior laryngeal nerve
-(CN XII)
-enter pharynx at thyrohyoid membrane
-cysts in anteroinferior cervical triangle
-lower in neck than second branchial
cyst
Third BA
Fourth Branchial Arch Anomalies
-internal: piriform sinus (inferior portion)

-translaryngeal course under thyroid ala, beneath inferior constrictor
-exits near cricothyroid joint
-superficial to recurrent laryngeal
-terminates in anteroinferior region of the neck
Laryngoceles
-external laryngocele
-air-filled herniation of saccule of laryngeal ventricle
Fourth BA
Pseudotumour of Infancy
-affects 0.4% of all newborns
-pathophysiology:
-intrauterine or birth trauma causing muscle injury, hematoma, and resultant fibrosis
-firm round mass within SCM 2-3 weeks after birth
-diagnosis made by US
-conservative treatment with 80-100% complete resolution by 1 ya
-physical therapy, observation and reassurance
590
MIDLINE NECK MASSES
Thyroglossal Duct Cysts

-develop from remnants of thyroid anlage that descends from foramen cecum
-may enlarge after URTI
-SSx:
-midline neck mass with cystic and solid components
-elevates with tongue protrusion
-typically inferior to hyoid bone and superior to thyroid gland
-dysphagia, globus sensation
-histology:
-respiratory epithelium
-squamous epithelium
-Sistrunk procedure to prevent recurrence rate
-reduces recurrence rate from 20% to less than 5%
-removing central portion of hyoid bone
Thymic Cysts
-thymus:
-third pharyngeal pouch derivative
-formed during sixth week of life
-remnants may persist as cords along path of migration from angle of mandible to midline of neck
Dermoid Cysts
-usually in submental region
-do not elevate with tongue protrusion
-formed along lines of embryologic fusion
-lined by epidermis, containing epidermal appendages
-treat with simple excision
Plunging Ranulas
-pseudocysts of the floor of mouth caused by mucous extravasation from blocked sublingual gland
-isolated submental mass or in association with visible sublingual ranula
Teratomas of the Neck

-acute respiratory symptoms in newborn period from tracheal compression
-large, semicystic, encapsulated lesion
-made of mature ectoderm, mesoderm, endoderm and immature embryonal tissue
-US: mixed echogenicity
-emergent surgical excision required
MASSES OF ENTIRE NECK
Lymphatic Malformations
-benign, multiloculated, soft, painless, compressive masses
-incidence 1.2-2.8 per thousand
-more common in posterior triangle of neck
-pathophysiology:
-abnormal development or obstruction of jugular lymphatics
-cosmetic deformity; masses in anterior neck may cause respiratory compromise
-US and CT: thin walled multi-loculated cysts
591
-high recurrence rate: 25-50%
Hemangiomas
-most common head and neck neoplasms in children
-<1/3 present at birth
-present first few months and enlarge over next 12 months
-involution occurs in 90%
-conservative treatment for most, surgery for deep seated tumours
-steroids and laser useful adjuncts
592
CONGENITAL ANOMALIES OF THE NOSE
EMBRYOLOGY
-third week of gestation, midline neural groove develops along dorsal surface of embryo forms neural
tube
-neural tube closure starts in mid-portion of embryo and progresses both anteriorly and posteriorly, leaving
neuropores at each end
-neural crest cells in lateral portions of neural tube begin migrating between tube and surface ectoderm into
mesenchyme
-anterior neuropore region especially vulnerable to developmental errors; it represents most distal end of
closed neural tube and most distal point of neural crest cell migration
-once neural crest cells reach their destinations, mesenchyme begins organizing and condensing into
mesodermal elements at various centers, which later fuse with one another and ossify
-potential spaces:
-fonticulus nasofrontalis: space b/n frontal and nasal bones
-prenasal space: space b/n nasal bones and nasal capsule
-foramen cecum: space b/n frontal and ethmoid bones; continuous with prenasal space
-spaces normally obliterate during fetal development
CONGENITAL ANOMALIES OF THE NOSE

Diagnosis Treatment Complications
Dermoid -fistulous tract on nasal dorsum, with or without cyst located -complete surgical -infection
from nasal tip to glabella excision -cosmetic deformity
-protruding hair, cheesy contents typical CT may show bifid -meningitis
septum or patent foramen cecum
Glioma -smooth, firm, intra- and/or extranasal mass not attached to -surgical excision -cosmetic deformity
skin -nasal obstruction
-meningitis
Encephaloceles -soft pulsatile mass -surgical excision -cosmetic deformity

-swell with straining or crying -meningitis
-probe cannot be passed between septum and intranasal mass -associated congenital
-CT shows bony skull base defect abnormalities possible
F.Ling - Congenital Anomalies of the Nose (1)
593
NASAL DERMOIDS
-range of nasal anomalies varying from short epithelium-lined tract on nasal dorsum to tracts extending
from nasal dorsal skin through septum to dura
-can contain epithelium and skin appendages such as hair, hair follicles, and sweat and sebaceous glands
Embryology
-theories suggests that dermoids represent clusters of epithelium that became trapped at time of fusion of
ectodermal process
-if skin maintains its attachment to fibrous tissues of nasal capsule in the prenasal space or at fonticulus,
epidermal elements can be drawn under developing bones, forming a tract
-sinuses and cysts generally occur in nasal midline
-pit, fistulous tract, or mass anywhere from nasal tip to glabella
-deeper involvement may occur and extension intracranially has been noted in 25-30% of cases
Evaluation
-CT and MRI are important in studying extent of lesion and if there is intracranial involvement
-CT findings that suggest deep extracranial involvement:
-fusiform swelling or bifidity of bony nasal septum
-widening of nasal vault
-glabellar erosion
-patent foramen cecum
-bifid crista galli
-MRI used to image soft-tissue masses in the sagittal plane
Treatment
-craniofacial approach if intracranial extension exists
-most dermoids do not have intracranial communication and can be safely approached externally
-approaches:
-vertical midline incision on nasal dorsum most efficient approach to extracranial dermoids
-medial osteotomies and outfracturing of nasal bones for exposure may be necessary
-external rhinoplasty approach:
-excellent cosmesis but limited exposure
-bicoronal flap approach:
-may be useful for dermoids at root of nose
-presence of epithelium in the stalk at skull base warrants an intracranial approach to completely and safely
excise entire tract
GLIOMAS AND ENCEPHALOCELES
-glioma are unencapsulated collections of glial cells in a connective tissue matrix that may retain
attachments to the dura
-encephaloceles are herniation of meninges with or without brain tissue through skull base and by
definition communicate with CSF-containing subarachnoid space
Embryology
-glioma and encephaloceles are developmentally related, with glioma representing pinched-off
encephaloceles
-theories of encephalocele formation:
594
-incomplete separation of closed neural tube from surface ectoderm, resulting in a mechanical
barrier to neural crest cell migration and resultant lack of bone formation in that area
-delay of migration of neural crest cells to their normal destinations failure of migration would
result in an area of mesenchyma devoid of neural crest cells necessary for normal bony formation,
leading to a defect in the cranium
-glioma:
-firm noncompressible masses that do not expand with straining or crying and do not
transilluminate
-external masses most common:
-glabellar masses (60%) may present as a lateral nasal mass
-intranasal mass (30%)
-combined (10%) dumbbell-shaped, with a connecting band passing through junction of
upper lateral cartilage and nasal bone
-may connect with dura
-encephalocele:
-consist of tissues prolapsed through a defect in cranium and are in continuity with CNS
-sincipital encephaloceles:
-aka frontoethmoidal encephaloceles
-skull base defect always between frontal and ethmoid bones at foramen cecum
-types:
-nasofrontal:
-sac passes directly forward between frontal and nasal bones
-nasal bones normal but displaced downward
-lesions located at glabella
-nasoethmoidal:
-sac passes downward below nasal bones and above upper lateral
cartilages to present as mass on lateral nose
-nasoorbital:
-sac extends under frontal and nasal bones to protrude through defect
in medial orbital wall
595
-basal encephaloceles:
-types:
-transethmoidal:
-sac herniates through defect in cribriform plate into superior meatus
and extends medial to middle turbinate
-sphenoethmoidal:
-sac extends through a cranial defect b/n posterior ethmoidal cells and
sphenoid to present in nasopharynx
-transsphenoidal:
-sac protrudes through a patent craniopharyngeal canal to present in
nasopharynx
-sphenomaxillary:
-encephalocele herniates through superior orbital fissure and then
through inferior orbital fissure to present in sphenomaxillary fossa
-occipital (75%) > sincipital (15%) > basal
-pulsatile, expand with crying or straining or with compression of jugular veins (Furstenberg
test)
-intranasal encephaloceles may resemble polyps but, unlike polyps, are located medial to middle
turbinate and are intimately related to nasal septum rather than to lateral nose
Evaluation
-any child presenting with external or
internal nasal mass requires careful
radiologic evaluation
Treatment
-glioma completely excised whenever
possible to minimize cosmetic deformity
and risk of meningitis
-extranasal glioma can be
approached through standard
external incision, depending on
location of mass
-combined lesions or intranasal
masses can be approached through
a lateral rhinotomy
-management of encephaloceles and those
glioma suspected to have intracranial
communications is primarily neurosurgical,
with excision of extracranial components
performed secondarily
596
CLEFT LIP AND PALATE:
EVALUATION AND TREATMENT OF THE PRIMARY DEFORMITY
INCIDENCE AND GENETICS
-most common congenital malformation of the head and neck

-CL +/- CP [CL(P)] genetically distinct from CP w/o CL [CP]
-CL(P): 1/1000; varies by ethnic group: native american > asian > caucasian > blacks; M:F = 2:1
-CP: 1/2000; constant among ethnic groups; M:F 1:2
-syndromic: eg. Apert, Stickler, Treacher-Collins, Waardenburg
-nonsyndromic: multifactorial inheritance - recurrence risk rates based on studies of clefting in populations
Risk of Cleft Lip or Palate

CL(P) CP
1 affected parent 2% 7%
1 affected sibling 4% 2%
2 affected siblings 9% 1%
1 affected parent and 1 affected sibling 15% 17%
ETIOLOGY
-teratogens: ethanol (FAS), anticonvulsants, steroids, chemotherapy, vitamin A excess

-maternal/intrauterine conditions: infant of diabetic mom, amniotic bands
-chromosomal abnormalities
-unknown
EMBRYONIC CONSIDERATIONS AND CLASSIFICATION
-Phase I: 4-5 weeks GA

-development of upper lip, nose primary palate (palate anterior to incisive foramen)
-frontonasal process forms:
-anterior labial component philtrum
-anterior palatal component forming alveolar part of premaxilla
-posterior palatal component forming portion of hard palate anterior to incisive foramen
-maxillary processes forms:
-lateral lip segments and nasal alae
-Phase II: 8-9 weeks GA
-development of secondary palate (hard and soft palate posterior to incisive foramen)
-medial growth of palatal shelves (mesoderm) from lateral maxillae
-shelves canted superiorly but eventually shift inferiorly and fuse at midline from incisive foramen and
progresses posteriorly toward uvula
-a cleft of the alveolus is always associated with a cleft of the lip

-cleft of lip may be isolated entity
F.Ling - Cleft Lip and Palate (1)
597
-submucous cleft:
-microform expression of cleft of secondary palate
-bifid uvula
-midline diastasis of levator muscles
-posterior hard palate notching due to loss of posterior nasal spine
Classification: (University of Iowa)

-Group I: CL
-unilateral right or left, or bilateral
-complete (extension to nasal floor) or incomplete (slight muscle diastasis at vermilion to small
bridge of tissue at the nasal sill)
-Group II: CP
-secondary palate only
-unilateral or bilateral
-Group III: CL(P)
-complete cleft palate: cleft of both primary and secondary palates; nearly always associated with
cleft lip
-Group IV: CP
-primary palate only
ANATOMIC DEFORMITY AND FACIAL GROWTH
Unilateral Cleft Lip

-orbicularis oris, blood supply and innervation generally follow external
form of the cleft lip
-complete cleft muscle fibers directed superiorly following cleft
margins and terminate at columella base medially and beneath nasal ala
laterally
-lateral maxillary segment displaced inferiorly
-maxilla is hypoplastic on cleft side
-alar base and lateral crus are displaced laterally and inferiorly
-columella displaced toward normal side
-cartilaginous septum and nasal spine are deflected away from cleft
-dome is lowered, horizontal naris on cleft side
-alveolar defect passes through developing dentition
Bilateral Cleft Lip

-orbicularis oris absent in prolabium (medial segment)
-short columella length
-widely flared alae with rotated and displaced lower lateral cartilages
-premaxilla protruded
-hypoplastic/posteriorly displaced maxillary segments
Cleft Palate
-muscle fibers of the palate follow medial margin of cleft and insert into medial cleft edges and posterior
edge of lateral bony hard palate
Facial Growth
-collapse of alveolar arches, mid-face retrusion malocclusion
598
GENERAL TEAM MANAGEMENT APPROACH
Initial Care and Psychosocial Issues

-counselling for family
Nursing Care and Feeding Issues

-complete CL(P) and CP children have significant feeding problems
-special nipples to assist feeding
-eg. Haberman feeder: elongated nipple that extends past cleft zone
-squeeze bottle mechanism decreases need for negative pressure suction from baby
SURGICAL MANAGEMENT OF THE PRIMARY DEFORMITY
Sequencing and Timing of Surgery
Lip Adhesion
-goal: convert a complete cleft lip into incomplete cleft lip, allowing definitive lip repair to be performed
with less tension
-performed at 2-4 weeks of age
-definitive lip repair at 4-6 months of age
-criteria:
-wide unilateral complete cleft lip and palate where closure with conventional lip repair might
produce excessive tension on the incision
-symmetric wide bilateral complete cleft lip with very protruding premaxilla
-introduction of symmetry to asymmetric bilateral cleft lip
-disadvantage: introduction of scar tissue
Cleft Lip Repair

-at 10-12 weeks of age
-“rule of tens”: 10 weeks old, weighs 10 pounds, haemoglobin of 10g
Cleft Palate Repair

-timing controversial
-desire to facilitate velopharyngeal competence for adequate speech favours relatively early closure,
whereas possible negative influence on maxillofacial growth and occlusion favours late closure
-technically more challenging in early closure
-usually completed at 9-12 months of age
Surgical Technique: Cleft Lip Repair

-rotation advancement method (Millard) - most commonly used
-interdigitation of triangular flaps (Tennison and Randall) - second most commonly used
-presurgical orthopaedics may be required before definitive lip repair to move premaxilla posteriorly
-nasoalveolar molding (NAM)
-assists in moulding and shaping complete clefts into a favourable position
-usually started shortly after birth by orthodontists
-molding plate worn 24h for several weeks prior to lip repair
Surgical Technique: Cleft Palate Repair

-techniques:
-Wardill-Kilner-Peet technique (VY advancement)
-suitable for clefts extending into hard palate and for wide clefts
599
-von Langenbeck technique
-Bardach two-flap technique
-flaps based on posterior descending palatine arteries
-complete two-layer mucosa closure of the entire cleft, with dissection, redirection, and suturing
of soft palate musculature (intravelar veloplasty)
-Furlow technique
-for narrow soft palate cleft and submucous cleft
-double-opposing Z-plasty
-advantage: lengthens soft palate with Z-plasty, and overlapping the mucomuscular flaps realigns
the levator sling
-disadvantage: increased operative time, dissection, and scarring within the soft palate, and
increased risk of fistula at junction of the hard and soft palates
-attention directed to approximation and repair of levator veli palatini
-most common postoperative complications:
-hypernasal speech: 30%
-oral-nasal fistulas: 10-20%
Common ENT Problems:
Eustachian Tube dysfunction:

-due to hypoplastic levator and tensor veli palatini muscles
-may lead to CSOM, cholesteatoma, CHL, speech delays
Velopharyngeal dysfunction:
-due to deficiencies in palatal and pharyngeal musculature and/or inadequate palatal length
-speech articulation difficulties; potential VPI
VPI:
-speech therapy when child is 6 months old
-dental prosthesis may improve palatal lift
-surgery:
-secondary palatal lengthening
-pharyngeal augmentation
-narrow the anteroposterior diameter of nasopharynx using soft tissue or implants
-pharyngeal flaps
-convert incompetent nasopharynx into two lateral “ports”
-require good lateral pharyngeal wall motion
600
TONSILLITIS, TONSILLECTOMY AND ADENOIDECTOMY
ANATOMY
Adenoids
-formed during 3rd-7th months of embryogenesis
-functional and mechanical obstruction of ET with adenoid inflammation play significant role in
development of middle ear disease
-blood supply:
-pharyngeal branches of external carotid artery
-minor branches from internal maxillary and facial arteries
-sensation: CN IX and X
-three types of surface epithelium:
-ciliated pseudostratified columnar
-stratified squamous
-transitional
Tonsils
-may extend down to hypopharynx
-hyperplasia:
-abnormal tongue position, tongue-thrust habit, aberrant speech patterns, altered orofacial growth
-blood supply:
-FAIL: facial, ascending pharyngeal, internal maxillary, lingual arteries
-upper pole:
-internal maxillary artery palatine branches ascending/descending palatine arteries
-ascending pharyngeal artery
-lower pole:
-facial artery tonsillar branch (most important)
-dorsal lingual artery
-ascending pharyngeal artery
-lymphatic drainage:
-superior deep cervical and jugular lymph nodes
-sensation: CN IX and branches of lesser palatine nerve via sphenopalatine ganglion
-no afferent lymphatics
-crypts lined by specialized antigen processing squamous epithelium
-histology:
-reticular cell epithelium
-squamous layer
-antigen presenting cells (M-cells)
-extrafollicular area
-T-cells
-lymphoid follicle
-Mantle zone (mature B-cells)
-germinal center (active B cells)
MICROBIOLOGY AND IMMUNOLOGY
Microbiology
-acute tonsillitis:
-classically GABHS (strep. pyogenes)
-other aerobic and anaerobic bacteria and viruses also implicated
F.Ling - T+ A (1)
601
-H. influenzae, S. aureus, S. pneumoniae, polymicrobial infection, BLPO, anaerobes
-viruses:
-initiators of mucosal inflammation, crypt obstruction and ulceration with secondary bacterial
infection
Immunology
-tonsils and adenoids involved in both local immunity and in immune surveillance
-no specific adverse effects with T+A; but still provide immune function
-tonsils and adenoids should be removed only for clearly defined clinical disease
PATHOGENESIS OF ADENOTONSILLAR DISEASE

-various theories
-viral infection with secondary bacterial invasion
-inflammation and loss of integrity of crypt epithelium chronic cryptitis and crypt obstruction
stasis of crypt debris and persistence of antigen
-other factors:
-environment, host factors, widespread use of antibiotics, ecological considerations and diet
CLINICAL CLASSIFICATION OF ADENOIDS AND TONSILS
Adenoids
Acute Adenoiditis:
-purulent rhinorrhea, nasal obstruction, fever, +/- otitis media
-loud snoring after episode of acute infection
Recurrent Acute Adenoiditis:
-4 or more episodes during 6 month period
-prophylactic Abx controversial
-daily low-dose (one half to one third full dose) or episodic prophylaxis (short course
with onset of URI)
Chronic Adenoiditis:
-nasal discharge, malodorous breath, PND, chronic congestion
-? role of extraesophageal reflux
Obstructive Adenoid Hyperplasia:
-chronic nasal obstruction (snoring and obligate mouth breathing)
-rhinorrhea
-hyponasal voice
Tonsils
Acute Tonsillitis:
-sore throat, fever, dysphagia, tender cervical nodes
-erythematous tonsils with exudates
Recurrent Acute Tonsillitis:
-4-7 episodes in 1 year
-5 episodes/year for 2 consecutive years
-3 episodes/year for 3 consecutive years
Chronic Tonsillitis
-no true consensus on definition
-symptoms > 4 weeks
F.Ling - T+ A (2)
602
Obstructive Tonsillar Hyperplasia
-snoring, dysphagia, voice changes (muffling or hyponasality)
-unilateral tonsillar hyperplasia should raise suspicion of malignancy
CLINICAL EVALUATION
Adenoids
-when medical therapy fails, adenoidectomy is the first step in controlling infection in the
nose/nasopharynx; about 67% of children show resolution
-sinusitis may take 2-3 months to clear after adenoidectomy
-nasality of speech:
-sounds that emphasize nasal emission: milkman, Mickey Mouse
-loss of appropriate nasality further supports obstructive adenoid hyperplasia
-lateral x-rays of limited use
-allergy evaluation
-r/o reflux
-r/o occult or overt submucous cleft palate risk of VPI with surgery
-occult cleft:
-bifid uvula
-abnormal movement of palate
-midline diastasis of muscles
-history of fluid regurgitation through nose
-nasopharyngoscopy:
-loss of midline bulge signifies absence of musculus uvulae associated with
higher risk of development of VPI postoperatively
Tonsils
-significant rare complications of GABHS:
-poststreptococal glomerulonephritis
-rheumatic fever
-obstructive tonsillar hyperplasia:
-snoring, choking and coughing, frequent
awakenings, restless sleep, dysphagia,
daytime hypersomnolence, behavioural
changes
-FTT, CHF (rare)
-unless significant (+3 or +4) hyperplasia, tonsils
should be left in situ (if no history of recurrent or
chronic infection)
-polysomnography:
-important to measure peak end-tidal CO2
if elevated then hypoventilation is present
-used mostly in child where diagnosis is
unclear or who has an unusual risk for
surgery
F.Ling - T+ A (3)
603
MANAGEMENT OF DISEASES OF THE ADENOIDS AND TONSILS
Adenoids
-recurrent or chronic cases treated with antibiotics effective against B-lactamase-producing organisms
-hyperplasia 6-8 wk course of intranasal steroids
-indications for adenoidectomy:
-obstruction
-AH with chronic nasal obstruction or obligate mouth breathing
-OSA
-FTT
-cor pulmonale
-swallowing abnormalities
-speech abnormalities
-severe orofacial/dental abnormalities
-infection
-recurrent/chronic disease
-recurrent/chronic otitis media with effusion
-chronic otitis media
-neoplasia
-contraindications for adenoidectomy:
-overt or submucous cleft palate (relative contraindications)
-lateral or superior adenoidectomy may suffice if severe OSA present
-neurologic or neuromuscular abnormalities with impaired palatal function
-anemia
-disorders of hemostasis
-complications:
-nasopharyngeal stenosis
-bleeding
-torticollis (Grisel’s syndrome)
-C-spine subluxations from hyperextension
Tonsils
-acute tonsillitis:
-first line antibiotics: penicillin
-chronic tonsilitis:
-clavulin or clindamycin for 3-6 weeks obviates need for tonsillectomy in 15% of children
-obstruction
-TH with chronic nasal obstruction
-OSA
-FTT
-cor pulmonale
-swallowing abnormalities
-speech abnormalities
-severe orofacial/dental abnormalities
-infection
-recurrent/chronic disease
-tonsilitis with: -peritonisllar abscess, abscessed cervical nodes, acute airway
obstruction, cardiac valve disease
-persistent tonsillitis with: persistent sore throat, tender cervical nodes, halitosis
-tonsilolithiasis
-recurrent/chronic otitis media
F.Ling - T+ A (4)
604
-neoplasia
-post-tonsillectomy:
-10-day course of amoxicillin to help reduce pain and malodorous breath
PERITONSILLAR ABSCESS
-secondary to infection of peritonsillar salivary gland (Weber gland) located between tonsil capsule and
muscles of tonsillar fossa
-tx: hydration, pain relief and antibiotics effective against Staph. aureus and oral anaerobes
LINGUAL TONSILS
-extraesophageal reflux is a prime contributor to chronic lingual tonsilitis
-surgical excision rarely necessary
UNILATERAL TONSIL HYPERPLASIA

-suspect unusual infection or neoplasia
-Mycobacterium tuberculosis, atypical mycobacteria, fungal organism, or actinomycosis
-lymphoma
F.Ling - T+ A (5)
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CONTROVERSIES IN TONSILLECTOMY,
ADENOIDECTOMY, AND TYMPANOSTOMY TUBES
Absolute Indications for Tonsillectomy/Adenoidectomy

-obstruction that result in OSA
-obstruction unresponsive to antimicrobial therapy and causing FTT
-suspected malignancy
-persistent/recurrent tonsillar haemorrhage
Relative Indications for Tonsillectomy

-recurrent acute tonsillitis
-chronic tonsillitis
-obstructive tonsils
-peritonsillar abscess
AAO-HNS - Indications for tonsillectomy

-3 or more episodes per year
-hypertrophy causing malocclusion
-upper airway obstruction
-peritonsillar abscess unresponsive to nonsurgical treatment
-halitosis not responsive to medical management
-suspected neoplasm
-individual considerations
Indications for observation

-age < 3
-OSA
-significant associated medical problems
-neurologic delay
-craniofacial abnormalities
-living long distance from hospital
-questionable caregiver at home
-known coagulopathy
-emesis or hemorrhage
-poor oral intake
Techniques for tonsillectomy

-electrocautery
-dissection snare
-intracapsular partial tonsillectomy
-uses microdebrider
-advantages:
-effective
-less pain, quicker return to normal diet
-disadvantages:
-tonsillar regrowth
-increased intraoperative blood loss
Adjuvant treatment
-perioperative antibiotics
-fewer episodes of fever, offensive odour
-improved oral intake
F.Ling - Controversies T+A, M+T (1)
606
-less pain, fewer days to return to normal activity
-perioperative steroids
-decreased post-op emesis
-decreased post-op pulmonary distress, subglottic edema
-pain reduction
Complications
-death, anaesthetic complications, endotracheal tube injury
-pulmonary edema
-atlantoaxial subluxations
-hemorrhage:
-primary bleeding: < 24H
-secondary bleeding: 7-10 days post-op
-dehydration
-Grisel’s syndrome
-vertebral body decalcification and anterior transverse ligament laxity from infection/inflammation
-causes pain and torticollis
-nasopharyngeal stenosis
Elective Indications for Adenoidectomy

-obstructive adenoids
-recurrent/chronic adenoiditis
-recurrent/chronic sinusitis
-recurrent acute otitis media and recurrent/chronic otitis media with effusion
Indications for Myringotomy and Placement of Tympanostomy Tubes
-chronic otitis media with effusion unresponsive to medical management for 3 or more months bilateral or
for 6 months or longer unilateral; earlier when significant hearing loss (eg. > 25 dB), speech/language
delay, severe retraction pocket, disequilibrium/vertigo, or tinnitus is present
-recurrent episodes of OME not meeting criteria for chronic disease, but cumulative duration excessive (eg
6 of 12 months)
-recurrent AOM, especially when ABx prophylaxis fails to reduce the frequency, severity and duration of
attacks; minimum frequency of three or more episodes in 6 months or four or more episodes in 12 months
with one being recent
-ETD, when persistent or recurrent signs and symptoms, disequilibrium/vertigo, tinnitus, or a severe
retraction pocket, unrelieved by medical treatment; patulous eustachian tube; and during hypobaric
treatment in patients with a prior history of otitis media/eustachian tube dysfunction, or when eustachian
tube dysfunction develops during treatments
-tympanoplasty when eustachian tube function is poor
-suppurative complication, present or suspected
Tubes Only vs Tubes and Adenoidectomy

-recommendations (Bluestone): first surgical procedure for chronic OME unresponsive to medical
treatment is only tubes and withold adenoidectomy unless child meets criteria for this procedure.
-if COME recurs following spontaneous extrusion of tubes, then recommend adenoidectomy irrespective
of size of the adenoids and a myringotomy and aspiration of the middle-ear effusion
F.Ling - Controversies T+A, M+T (2)
607
RANDOMIZED CONTROL TRIALS FOR
TONSILLECTOMY, ADENOIDECTOMY AND TYMPANOSTOMY TUBES
Evidence from RCTs
-tonsillectomy in children who meet the frequency severity and characteristics of episodes will be more
effective than not performing this operation
-adenoidectomy can reduce the frequency of recurrent acute otitis media in children who had had
tympanostomy tubes previously inserted, but continued to experience recurrent attacks after the tubes had
extruded
-lack of efficacy of adenoidectomy, +/- tonsillectomy, for children who had never received tympanostomy
tubes in the past
-adenoidectomy is efficacious in children who had COME, whether or not tympanostomy tubes had been
previously placed
-tympanostomy tube placement without addition of adenoidectomy is effective in the management of both
COME and recurrent AOM
-myringotomy alone for COME no more effective than no surgery
No RCT trials to date
-addressing efficacy and safety of tonsillectomy for chronic tonsillitis

-current recommendations:
-trial of antimicrobial agent may be beneficial in some children prior to recommending
surgical interventions, especially in infants and very young children, when the operation
has come increased risk; the clinician may be able to delay surgery until child grows
older, if the antibiotic treatment is successful
-peritonsillar abscess as an indication for tonsillectomy also has not been evaluated by a prospective
randomized clinical trial
-no prospective randomized clinical trails have demonstrated that adenoidectomy is effective in reducing
the morbidity of sinusitis in children. Benefit of adenoidectomy remains uncertain
-even though these studies are not available, adenoidectomy should still be considered on an
individualized basis for chronic sinusitis
608
CONGENITAL ANOMALIES OF THE AERODIGESTIVE TRACT
Development of the Respiratory Primordium

-at fourth week of development the respiratory primordium appears as an outgrowth (laryngotracheal
groove) from the ventral wall of the foregut (primitive pharynx)
-the laryngotracheal groove evaginates to form the laryngotracheal diverticulum dividing the forgut into a
dorsal protion (esophagus) and a ventral portion (larynx, trachea, and lung) separated by the
tracheoesphageal septum
-respiratory primordium (ventral portion) maintains open communication with the pharynx through the
laryngeal orifice
-epithelial proliferation obliterates the laryngeal lumen
-recanalization occurs by the tenth week (no recanalization results in stenosis)
-three tissue swellings surround the laryngeal orifice:
-median swelling behind hypobranchial eminence epiglottis
-two lateral swellings arytenoid cartilages
Common Congenital Anomalies of the AE Tract

Nose/nasopharynx Larynx
-usually present with stridor or -choanal atresia -laryngomalacia
feeding difficulties -choanal stenosis -cysts
-septal deformity -neoplasm
-note inspiratory, expiratory or -turbinate hypertrophy -cleft
biphasic stridor to localize -masses (glioma, -web
obstruction encephalocele, adenoid -stenosis
hyperplasia)
-inflammatory disorders almost never
Trachea
affect newborn; thus most stridor Oral/oropharynx -TEF
appearing in first few weeks of life -macroglossia -tracheomalacia
usually d/t congenital lesions -craniofacial deformity -vascular compression
(Apert, PRS) -congenital stenosis
-masses and cysts (TGD, (complete ring)
Investigations lingual thyroid, cystic -hemangioma
-CXR: PA/lat hygroma) -cyst
-barium swallow -neurologic deficit -genesis
-tracheal bronchus
-CT scan (choanal atresia)
-endoscopy Esophagus
-laryngoscopy -TEF
-bronchoscopy -vascular compression
-duplication
-esophagoscopy
ANOMALOUS CONDITIONS OF THE NOSE
Choanal Atresia/Stenosis
-bony atresia: transpalatal approach
-membranous atresia: transnasal endoscopic approach
ANOMALOUS CONDITIONS OF THE LARYNX
Laryngomalacia
-usually few symptoms at birth with gradual development of high-pitched inspiratory stridor and occasional
F.Ling - Aerodigestive Tract Anomalies (1)
609
feeding difficulties
-usually self-limited; complete resolution may take as long as 18 months
-intervention rarely necessary: tracheotomy or supraglottoplasty
Neoplasms
-most common lesions are vascular malformations
Vocal Cord Immobility

-unilateral: usually idiopathic
-bilateral:
-cardiothoracic anomalies
-neurologic anomalies: hydrocephalus and Arnold-Chiari malformation
-may require tracheotomy
Web
-due to incomplete recanalization at 8th week GA
-types:
-supraglottic (2%)
-glottic (75%)
-subglottic (7%)
-most commonly in anterior portion of glottis
->50% obstruction requires intervention
-may require lysis via external thyrotomy or internal endoscopic lysis
Congenital Subglottic Stenosis

-usually exacerbated by URTI
-severe cases: cricoid split vs tracheotomy
Hemangioma
-usually develops biphasic stridor towards third week of life
-50% have associated cutaneous hemangioma
-spontaneous regression often occurs after 12th to 18th month
-treatment options:
-observation
-steroids
-interferon-alpha
-CO2 laser
-tracheotomy
-surgery
Posterior (Laryngeal) Cleft

-due to failure of development of tracheoesophageal septum
-may cause significant aspiration
-types:
-I: interarytenoid
-II: cleft extends into cricoid
-III: cleft extends through entire cricoid into trachea
-IV: complete cleft involving entire posterior tracheal wall
-major clefts repaired by lateral approach or laryngofissure
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ANOMALOUS CONDITIONS OF THE TRACHEA
Tracheal Agenesis
-survival rare
Tracheomalacia
-collapse of anterior tracheal wall against soft posterior component
-most cases self-limited
-tx:
-observation (typically resolves with growth)
-correct GERD if present
-rarely requires tracheotomy or intubation; stent may be required
Tracheoesophageal Fistula
-5 types:
-esophageal atresia (EA) with distal TEF (85%)
-isolated EA (10%)
-isolated TEF (4%) “H-type”
-EA with proximal TEF (0.5%)
-EA with double TEF (0.5%)
-associated with VATER complex (Vertebral, Anal, Tracheal-Esophageal, Radial limb or renal defects)
-management requires surgical correction
Vascular Anomalies
-anomalous subclavian artery (Bayford syndrome)
-aberrant right subclavian artery arising from left descending aorta
-passes behind esophagus and trachea
-“dysphagia lusoria”
-barium swallow: compression passing obliquely up and to the right on AP view
-associated with nonrecurrent right recurrent nerve, aortic and subclavian aneurysm, and
diverticuli
-tx: ligate and reanastomose to right common carotid for severe symptoms
611
-double aortic arch
-most common vascular anomaly to cause stridor
-vascular ring encircles esophagus and trachea
-treatment: division of one component
-right aortic arch
-similar to double arch
-anomalous left common carotid artery
-innominate artery compression
-high innominate artery may cause anterior compression of trachea
-pulmonary artery sling
-left pulmonary artery originates from right pulmonary artery, slings around right mainstem
bronchus, then between trachea and esophagus
Tracheal Stenosis
-usually secondary to complete tracheal rings
-treatment conservative: steroids and Abx for URTIs
ANOMALOUS CONDITIONS OF THE ESOPHAGUS
Duplication
-foreguts cysts in superior or posterior mediastinum
-true duplications in lower 1/3 of esophagus
-mucosa contains acid-secreting cells bleeding and ulceration
-treatment: surgical removal
612
NEONATAL RESPIRATORY DISTRESS
NOSE
-obligate nasal breathers

-cyclical cyanosis: cyanotic episodes interrupted during episodes of crying
-feeding difficulties
-ddx:
-nasal dermoid
-encephalocele, glioma
-craniofacial anomalies: Treacher Collins syndrome, Apert syndrome
-piriform aperture stenosis
-nasolacrimal duct cysts
-choanal atresia
-nasopharyngeal tumour
OROPHARYNX/HYPOPHARYNX
-stridor worse supine, feeding and agitation

-besides difficulty with breathing, one of the features that best characterizes oropharyngeal and supraglottic
laryngeal airway obstruction is difficulty with feeding
-ddx:
-macroglossia, glossoptosis
-neoplasm: lingual thyroid, dermoid, vallecular cyst
-hemangioma, lymphangioma
-laryngomalacia
LARYNX
-abnormal cry; aphonia

-“brassy” type cough
-ddx:
-laryngomalacia
-webs, atresia, neoplastic disorders, stenosis, clefts
-laryngospasm
TRACHEA/BRONCHI
-normal cry, expiratory wheezing
-ddx:
-complete tracheal rings, transesophageal fistula, tracheal hemangioma
-vascular compression
-mediastinal cysts and neoplasms
F.Ling - Neonatal Respiratory Distress (1)
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RECURRENT RESPIRATORY PAPILLOMATOSIS
INTRODUCTION
-RRP caused by HPV types 6 and 11

-most common benign neoplasm in larynx among children
-second most common cause of childhood hoarseness
-(most common is vocal cord nodules from vocal abuse)
-diagnosis between 2-4 years
-incidence 4.3/100 000 children
ETIOLOGY
Human Papillomavirus
-specific viral types correlated with disease severity and clinical course:
-eg. HPV 11 more obstructive airway course early and greater need for tracheotomy
-adult-onset RP could reflect either activation of virus present since birth or an infection acquired in
adolescence or adult life
-HPV present in genital tract of as many as 25% all women of child-bearing age
Recurrent Respiratory Papillomatosis

-occurs exclusively in squamous epithelium
-pedunculated masses with finger-like projections of nonkeratinized stratified squamous epithelium
supported by core of highly vascularized connective tissue stroma
-koilocytosis: vacuolization of cytoplasm within HPV infected epithelial cells
-lesions occur at anatomic sites where ciliated and squamous epithelium are juxtaposed
-most commons sites
-limen vestibuli (junction between nasal vestibular and nasal cavity proper)
-nasopharyngeal surface of soft palate
-midline of laryngeal surface of epiglottis
-upper and lower margins of ventricle
-undersurface of vocal folds
-carina
-bronchial spurs
-iatrogenic squamociliary junctions
-tracheotomy: stoma and in mid-thoracic trachea
-3-5% of patients with recurrent growths undergo malignant transformation
EPIDEMIOLOGY
-childhood-onset RRP (CORRP)

-arbitrarily < 12 years of age
-most often diagnosed between 2-4 years of age
-more common, more aggressive, multiple lesions, airway compromise
-M:F = 1:1
-children diagnosed before 3 ya
-3.6x more likely to require > 4 surgical procedures per year
-2.1x more likely to have two or more anatomic sites involved
-spontaneous remission at puberty
F.Ling - Recurrent Respiratory Papillomatosis (1)
614
-adult-onset RRP (AORRP)
-peaks b/n 20-40 /w slightly higher male predominance
-solitary lesions
-airway obstruction less frequently observed
-recurrence less common
-risk factors:
-younger first time mothers (longer 2nd stage of delivery)
-lower socioeconomic status
-50% born from mother with condylomata acuminata
-oral sex; multiple sex partners
TRANSMISSION
-CORRP linked to mothers with genital HPV infections

-rate of transmission however is very low
-risk ~1/400 (ranges from 1/80 to 1/1500)
-insufficient evidence to support delivery by CS in all pregnant women with condylomata
-CS for newly infected mothers with condylomata present
-AORRP may be associated with oral-genital contact
CLINICAL FEATURES
-progressive hoarseness, stridor and respiratory distress

-any infant or young child with symptoms of voice change, along with obstructive airway symptoms or
recurrent croup, warrants laryngoscopy to r/o neoplasia
-dysphonia most commonly
-less commonly: chronic cough, recurrent pneumonia, FTT, dyspnea, dysphagia
-prolonged tracheotomy and presence of subglottic papilloma at time of tracheotomy associated with
increased risk of distal tracheal spread
-GERD a potential risk factor for disease persistence
-extralaryngeal spread:
-oral cavity
-trachea
-bronchi
Surgical Management
-no single modality consistently effective at eradication
-goal is to debulk as much disease as possible while preserving normal morphology and anatomy and
preventing complications of subglottic and glottic stenosis, web formation and diminished airway
-potential surgical modalities
-microlaryngoscopy with cup forceps removal
-microdebrider powerized resection
-CO2 laser
-KTP/ND:YAG laser
-Flash scan lasers
-avoid tracheotomy: may seed lower airway or stoma
-aim of therapy:
-reduce tumour burden
-decrease spread of disease
-create safe and patent airway
615
-improve voice quality
-increase time interval between surgical procedures
Laser Surgery:
-protective precautions*:
-eye protection, laser masks for OR personnel; warning signs outside OR door
-protection of pts eyes and face with wet cloth
-smallest possible laser-safe ETT used
-cuff of ETT filled with saline
-room set-up:
-full set of laryngoscopes
-two ventilating bronchoscopes
-pediatric tracheotomy set
-for lasering:
-laser not used until oxygen and mixture is between 26 and 30% - minimizes possibility
of laser-induced ETT fire
-moistened neuropatties placed in subglottis to decrease air lead and provide backstop for errant
laser shots
Jet Ventilation
-limitations/disadvantages/complications:
-possibility of transmission of HPV particles into distal airway
-pneumothorax
-pneumomediastinum
-inadequate ventilation
-excessive mucosal drying
-insufflation of air into stomach
-disseminating blood into tracheobronchial tree
Adjuvant Treatment Modalities
-criteria for use:

-surgery requirement of more than 4 procedures per year
-distal multisite spread of disease
-rapid regrowth with airway compromise
1. alpha-interferon
-most commonly recommended
-dose: 2mU/m2 per day or 4 mU/m2 every other day for 6 months
-discontinue if no response
-continue for additional 6 months if partial response
-continue for 3 months after complete response
-side effects:
-acute reactions:
-fever and flulike symptoms: chills, headache, myalgia
-chronic reactions:
-decrease growth rate
-elevation of liver transaminase
-leukopenia
-spastic diplegia
-febrile seizures
616
2. indole-3-carbinol
3. photodynamic therapy
4. cidofovir
5. acyclovir
6. ribavarin: antiviral drug used to treat RSV pneumonia
7. retinoic acid
8. mumps vaccine
9. methotrexate
Risk factors for malignant transformation

-tobacco
-prior history of XRT
-history of bleomycin use
-infection with HPV 16, 18
617
THE SYNDROMAL CHILD
DEFINITIONS
-Association:
-nonrandom occurrence in two or more individuals of multiple anomalies
-eg. CHARGE association
-Deformation:
-abnormal form, shape or position caused by mechanical forces
-eg. congenital torticollis and facial asymmetry from oligohydramnios
-Disruption:
-morphologic defect of organ resulting from extrinsic breakdown or interference of an originally
normal developmental process
-eg. facial clefting as a result of amniotic bands
-Dysplasia:
-abnormal organization of cells into tissues and its morphologic results
-eg. Hurler syndrome: coarse facies, corneal clouding, macroglossia, skeletal abnormalities
-Malformation:
-morphologic defect of organ resulting form intrinsically abnormal developmental process
-eg. isolated cleft lips and anencephaly
-Polytopic field defect:
-pattern of anomalies derived from disturbance of a single developmental field
-eg. velocardiofacial syndrome
-Sequence:
-pattern of multiple anomalies derived from a single known or presumed prior anomaly or
mechanical factor
-eg. Pierre Robin sequence - primary abnormality is micrognathia glossoptosis causes cleft
palate
-Syndrome:
-pattern of multiple anomalies pathogenetically related but not representing a single sequence or a
polytypic field defect
MENDELIAN INHERITANCE PATTERNS
-autosomal dominant:
-eg. Waardenburg syndrome and Treacher Collins syndrome
-autosomal recessive:
-eg. Usher syndrome, cystic fibrosis
METHODS OF SYNDROME DIAGNOSIS
-directed history:
-parental consanguinity and ethnicity, maternal and paternal ages, possible teratogen exposure,
outcome of prior pregnancies
-laboratory tests and karyotyping
-DNA analysis: eg. velo-cardio-facial syndrome
-dysmorphology database; ~ 30% of syndromal children will have private syndromes
F.Ling - The Syndromal Child (1)
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TERATOGENS
-may alter fetal development in a recognizable pattern
-eg. CMV 10% symptomatic children microcephaly, cerebral calcification and chorioretinitis
-eg. fetal alcohol syndrome
-mental retardation and developmental delay
-microcephaly, epicanthal folds, elongated and undefined philtrum and flattened nasal dorsum
SPECIFIC GENETIC SYNDROMES
Achondroplasia
-most common cause of short-limb dwarfism
-due to defect in FGF receptor-3
-autosomal-dominant
-shortened limbs, long narrow trunk, frontal bossing and mid-face hypoplasia, lumbar lordosis, limitation
of elbow extension, genu varum, trident hand
-obstructive sleep apnea common
-brainstem compression central ventilatory problems sudden death
Apert and Crouzon Syndromes

-craniosynostosis, hypertelorism, exophthalmos, parrot-beaked nose, maxillary hypoplasia, mandibular
prognathism
-syndactyly in Aperts
-Aperts mostly spontaneous mutations; Crouzon usually autosomal dominant
-upper airway obstruction a frequent problem
-fusion of cervical vertebra in Apert
Branchiootorenal Syndrome
-autosomal-dominant
-branchial cleft anomalies: cysts or fistulae
-otologic malformations: preauricular pits, malformed auricles, ossicular and cochlear malformations
-renal malformations: renal genesis, polycystic kidneys, duplicated ureter
Down Syndrome
-most common genetic disorder associated with mental retardation and developmental delay
-1/700-1000 live births
-trisomy 21
-increased maternal age a risk factor
-microcephaly, mid-face retrusion, upslanting palpebral fissures, epicanthal folds, macroglossia
-40% have congenital heart malformations
-delayed gross motor skills
-increased joint laxity (10-20%) atlantoaxial subluxations
Fragile X Syndrome
-X-linked
-second most common genetic cause of MR
-prominent ears, large jaw, long face
-high pitched, jocular speech
-hyperkinetic behaviour
-macroorchidism, joint hypermobility, flat feet, mitral valve prolapse
619
Goldenhar Syndrome
-oculoauriculovertebral spectrum
-facial asymmetry
-unilateral external and middle ear deformities:
-mildly deformed ears to complete anotia
-external canal atresias and ossicular deformities
-vertebral malformations
-most cases are sporadic
Neurofibromatosis Type 1
-prevalence of 1/3000-4000
-café au lait spots and cutaneous neurofibromas
-axillary freckling, optic glioma, Lisch nodules (iris hamartomas), sphenoid wing dysplasia
-cervicofacial plexiform neurofibromas resemble “bag of worms”
Neurofibromatosis Type 2
-central form of neurofibromatosis
-bilateral acoustic neuromas, meningiomas, spinal cord schwannomas
-mean age of presentation is 20 - unilateral or bilateral hearing loss common
-two types:
-Wishart type:
-early onset and rapid growth, with other fibromatous tumours other than AN
-Gardner type:
-slower rate of growth and onset and usually only bilateral acoustic neuromas
-autosomal dominant
Pierre Robin Sequence

-triad of glossoptosis, micrognathia and cleft palate
-25% later assigned to a known syndrome most commonly Stickler syndrome
Treacher Collins Syndrome

-mandibulofacial dystosis
-autosomal-dominant
-external and middle ear anomalies, zygomatic and mandibular hypoplasia, downslanting palpebral
fissures, lower lid colobomas, and cleft palate
-50% with hearing impairment from ossicular malformation or EAC atresia
Usher Syndrome
-SNHL and retinitis pigmentosa
-most common cause of combined deafness and blindness in the Western world
-three types:
-Ush 1: profound SNHL, vestibular dysfunction, retinitis pigmentosa
-Ush 2: mild to moderate SNHL, normal vestibular function, retinitis pigmentosa
-Ush 3: progressive SNHL, progressive vestibular dysfunction and retinitis pigmentosa
Velocardiofacial Syndrome
-almond shaped palpebral fissures, deficient nasal alae, tubular nose with bulbous nasal tip, small mouth
-variable degree of palatal clefting
-adenoidectomy VPI
Waardenburg Syndrome
-heterochromia irides, white eyelashes, white forelock and SNHL, dystopia canthorum
620
PEDIATRIC MALIGNANCIES
-lymphoma:
-lymphoproliferative disorder
-the most common pediatric malignancy of the head and neck (excluding retinoblastoma and
neoplasms of the CNS)
-risks:
-irradiation
-EBV (Burkitt’s lymphoma)
-HIV, immunosuppression
-organic toxins (phenols, benzene)
-immunological diseases (rheumatoid arthritis, celiac disease)
HODGKIN DISEASE
Epidemiology
-bimodal incidence:
-ages 15-34 years
-later adult years
-M:F = 2:1
-EBV associated in 40%
-80% with cervical lymphadenopathy
-cervical mass most common presentation
-spreads via contiguous lymph nodes
-mediastinal involvement tracheal or SVC compression
-B symptoms present in 30-40%
Pathology/Classification
-Reed-Sternberg cell:
-two or more nuclei and two or more large nucleoli
(“owl’s eyes”)
-large binucleated cells diagnostic for Hodgkin disease
-eosinophilic inclusions
-Rye Classification:
-lymphocyte predominant (2-10%): -abundant normal-appearing lymphocytes with rare
RS cells and no fibrosis
-associated with better prognosis
-mixed cellularity (20-40%) -pleomorphic infiltrate of lymphocytes, other
inflammatory cells, and more numerous RS cells
-nodular sclerosis (40-80%) -nodules of lymphoid infiltrates separated by bands
of collagen, containing lacunar cell variants of RS
cells
-more common in women
-lymphocyte depleted (2-15%) -paucity of lymphocytes, diffuse fibrosis, and bizarre-
appearing RS cells
-associated with poorer prognosis
F.Ling - Pediatric Malignancies (1)
621
Diagnosis and Staging
-excisional open biopsy usually required to establish diagnosis
-fresh sample required for immunochemistry
-Ann Arbor system:
-I: Single lymph node region or extralymphatic site (IE)
-II: Two or more lymph node regions or extralymphatic sides (IIE) on same side of
diaphragm
-III: Nodal regions, extralymphatic sites (IIIE), or splenic involvement (IIIS) on both sides of
the diaphragm
-IV: Disseminated disease
Treatment
-stage I and IIA: external beam XRT; 10-year survival rate 90%
-advanced disease: combination chemotherapy; complete response rate 44-87%
-MOP(P): mecholorethamine, oncovin (vincristine), prednisone, procarbazine
-ABVD: adriamycin, bleomycin, vinblastine, DTIC
-in children low dose radiation and chemotherapy recommended to limit toxicities and morbidity
Prognosis
-dependent on staging; overall >75% 5 year survival
-better prognosis for lymphocytic predominance types
-worse prognosis with presence of Reed-Sternberg cells, class B symptoms and higher staging
NON-HODGKIN LYMPHOMA
Epidemiology
-incidence increases throughout life
-increased risk in immunodeficiency states
-EBV appears to have role in pathogenesis
-cells of origin:
-85% NHL arise from B-cells
-15% NHL arise from T-cells
-rapidly growing extranodal disease primarily involving head and neck (29%) and mediastinum (26%)
-Waldeyer ring hypertrophy
-may present with respiratory distress or SVC syndrome
-hematogenous dissemination early
-CNS involvement: CN palsies, MS changes
Treatment
-tumour burden (clinical stage and serum LDH concentration) most important predictor of outcome
-primary treatment is systemic chemotherapy
-typically treated with CHOP: cytoxan, doxorubicin, vincristine, prednisone followed by radiation
to involved sites
-XRT limited to emergency situations involving airway, nervous, or vascular compromise
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RHABDOMYOSARCOMA
Epidemiology
-incidence at least equal to that of all other sarcomas combined
-most frequent soft-tissue malignancy of childhood
-head and neck involvement (35-40%)
-50% occur in children < 5ya
-rare distant metastasis
-orbit > nasopharynx > middle ear/mastoid > sinonasal cavity
-nasal obstruction, epistaxis, otorrhea, proptosis, cranial nerve palsies
-parameningeal sites:
-middle-ear-mastoid
-sinonasal
-nasopharyngeal
-infratemporal fossa
-may spread into meninges, less favourable prognosis
Pathology
-classified based on histopathology:
-Embryonal and botryoid variant (75%)
-most common types among infants and young children
-spindle-shaped cells containing abundant eosinophilic cytoplasm
-botryoid variant: forms condensed layer of cells immediately beneath mucosa and
produces a polyploid lesion
-Alveolar (20%)
-occurs predominantly in adolescents
-small, round cells separated into alveolar groupings by fibrous septa
-Pleomorphic
-usually in adults
-well differentiated, consists of spindle and “strap” cells
Diagnosis and Staging

-most common sites of metastatic spread: lungs, bones, and bone marrow
-CT scan of H+N, chest
-bone scan, bone marrow biopsies
-most important prognostic factor is presence or absence of metastatic disease
-factors associated with better prognosis:
-smaller tumour size and noninvasiveness
-orbital primary site
-embryonal histology
-absence of regional lymph node involvement
-complete resectability
-younger age at diagnosis (2-10 years)
623
-Group staging system (Intergroup Classification)
Group I:
-13%
localized disease with complete surgical resection and no evidence of regional nodal
involvement
Group II:
-20%
-Group IIA: grossly resected disease with microscopic residual disease and no regional
involvement
-Group IIB: complete resection with no residual disease, but they do show regional
disease with involved nodes
-Group IIC: containing patients with microscopic residual disease and regional nodal
involvement.
Group III:
-48%
-incomplete resection or biopsy only; gross residual disease
Group IV:
-18%
-distant metastasis at the time of diagnosis
TNM staging system

Stage I:
-Disease is localized and involves the orbit, the head and neck region (excluding
parameningeal sites), or the nonbladder/nonprostate genitourinary region
Stage II:
-localized disease of any unfavourable primary site not included in the stage I category
-primary tumour < 5 cm in diameter
Stage III:
-localized disease of any unfavourable primary site not included in the stage I category
-primary tumour > 5 cm in diameter and/or it involves regional lymph nodes
Stage IV:
-metastatic disease at the time of diagnosis
Risk classification
Low risk:
-Patients have embryonal RMS either (1) occurring at a favourable site (stage I), (2)
occurring at an unfavourable site with complete resection (group I), or (3) occurring at an
unfavourable site with microscopic residual disease (group II).
Intermediate risk:
-Patients have (1) embryonal RMS occurring at an unfavourable site with gross residual
disease (group III), (2) metastatic embryonal RMS and are younger than 10 years, or (3)
any nonmetastatic alveolar RMS at any site.
High risk:
-Those at high risk include any patient with metastatic disease unless he or she is younger
than 10 years and has embryonal metastasis.
Treatment
-complete resection has a large impact on survival
-increasing efficacy of chemotherapy and radiation therapy reduced indication for radical surgery
-combination surgery and chemoradiation therapy advocated
-long-term survival can approach 60-70%
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THYROID CARCINOMA
Presentation
-asymptomatic firm anterior neck mass
-signs/symptoms suggestive of malignancy:
-rapid growth
-new-onset hoarseness
-odynophagia
-hemoptysis
-fixation to surrounding tissues
-75% cervical lymphadenopathy
-5-10% pulmonary metastasis
Pathology
-usually papillary
-risk factors:
-radiation exposure
-Gardner syndrome (familial polyposis)
-Cowden syndrome (familial goiter and skin hamartomas)
Treatment
-controversial total vs hemi-thyroidectomy for papillary/follicular ca
-medullary ca:
-family screened - those positive undergo total thyroidectomy
-age 6 years for MEN type 2A
-shortly after birth for MEN 2B
NASOPHARYNGEAL CARCINOMA
-rare
-type I (keratinizing), type II (nonkeratinizing), type III (undifferentiated)
-type III most common in children
-most present with asymptomatic metastatic cervical disease
-XRT +/- chemotx for disseminated disease
-5-yr survival 40%
NEUROBLASTOMA
-newborns and children <10 ya; peak 2 ya - highest incidence in first 2 years of life
-most common malignancy in infants under 1 ya
-60% have metastatic disease
-signs/symptoms:
-painless cervical mass
-Horner syndrome
-heterochromia iridis
-pressure symptoms related to aerodigestive tract
-osseous metastasis:
-calvarium
-orbit
-ribs
-long bones
625
-diagnosis:
-IVP
-CXR, abdominal US, skeletal survey, liver-spleen scan, bone marrow aspirate
-urine vanillylmandelic acid (VMA)
-treatment:
-surgical excision
-chemotherapy for residual disease
Late complications in treatment of pediatric malignancy:

-leukemia
-growth retardation
-sarcoma
-recurrence
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OTITIS MEDIA WITH EFFUSION
DEFINITIONS AND TERMINOLOGY
-middle ear effusion

-liquid resulting from infection and mucosa inflammation
-serous, mucoid, purulent
-temporal sequence: acute (0-3 weeks), subacute (3 weeks - 3 months), chronic (> 3 months)
-acute otitis media (AOM):
-rapid onset of infection in middle ear
-fever, otalgia, hearing loss
-recurrent AOM:
-four or more episodes in 1 year
-three or more episodes in 6 month period
-otitis media with effusion (OME)
-presence of effusion behind intact TM without any signs of acute inflammation
-chronic suppurative otitis media (CSOM)
-persistence of purulent otorrhea through a TM perforation or tympanostomy tube
EPIDEMIOLOGY
-if a child has not had OM before age of 3 years statistically unlikely to develop severe or recurrent OM
-overall highest incidence of AOM in the 6-11 month age group
-mean duration of OME after AOM is 40 days
-incidence of OME appears to peak during second year of life, most prevalent during winter
months, and is associated with URIs
-most children have resolution of asymptomatic MEE within a few months without medical or surgical
intervention
-a very high incidence of middle-ear infections reported in Native Americans and Inuit
-strong genetic pre-disposition to OM
-other risk factors:
-low socioeconomic class
-day-care
-decreased breast-feeding
-second-hand smoke
-seasonal variation: more common in winter, fall, spring (correlation with URI)
RISK FACTORS FOR MIDDLE-EAR DISEASE
-cleft palate
-craniofacial disorders:
-Down’s syndrome, Apert syndrome, mucopolysaccharidoses
-congenital or acquired immunodeficiency
-hypogammaglobulinemia, IgA deficiency, DiGeorge syndrome, HIV, chemotherapy
-allergy, nasal obstruction, ciliary dysfunction, prolonged nasal intubation
-environmental:
-day-care attendance
-smoking in households
F.Ling - Otitis Media with Effusion (1)
627
PATHOPHYSIOLOGY
-abnormal function of ET
-ET in infants and children: shorter, more horizontal
-congestion of ET leads to increased negative middle-ear pressure influx of bacteria and viruses from
nasopharynx induces inflammatory response
-abnormalities of the palate and associated musculature (tensor veli palatini) may worsen ET function
MICROBIOLOGY
-most common pathogens:

-Streptococcus pneumoniae (30-50%)
-Haemophilus influenzae (20-30%)
-group A streptococci (1-5%)
-others:
-gram negative enteric organisms: E. coli, Klebsiella, Pseudomonas aeruginosa
-immunocompromised children:
-Mycobacterium tuberculosis Mycoplasma pneumoniae, Chlamydia trachomatis
-B-lactamase producing bacteria:

-30% of H. influenzae
-100% of M. catarrhalis
-Staphylococcus
-S. pneumoniae has other resistance factors
-anaerobic bacteria commonly seen in CSOM:
-peptostreptococcus, Fusobacterium sp., Propionibacterium acnes., Bacteroides sp.
EVALUATION
History
-otalgia, irritability, fever, lethargy, otorrhea
-hearing loss
-otorrhea
-pneumatic otoscopy
- mobility on both positive and negative pressure MEE
-movement only on negative pressure ET dysfunction
-colour of TM:
-yellow or blue MEE
-dark red trauma, haemorrhage
-red AOM or hyperaemia
Hearing Evaluation
-audiometric evaluation
-ABR in newborns
-behavioural observation audiometry (BOA) for infants 6 months to 1 year
-visual reinforcement audiometry (VRA) for 1-2 ya
628
-play audiometry for 2-5 ya
-standard audiometry > 5 ya
-immitance audiometry
TREATMENT AND PREVENTION

-AOM has spontaneous resolution rate of 60-80%
-however, several studies suggest that resolution rate is higher if antimicrobial are given from
beginning, and complication rate may be lower as well
-routine non-treatment of symptomatic AOM not advocated
-routine treatment of asymptomatic MEE is controversial
-watchful waiting may be appropriate
-MEE not necessarily sterile (bacteria in 30-70%)
-if MEE there > 3 months, then hearing evaluation and possible surgical intervention should be
considered
Medical Management: Antimicrobial Agents

-first line:
-Amoxicillin for 5-10 days; follow-up in 2-4 weeks
-40 mg/kg/day divided tid (250 mg/5ml)
-despite treatment, persistent MEE in 40% at 4 weeks, 20% at 8 weeks and 10% at 12 weeks
-second line:
-2nd generation cephalosporin, clavulin (40-50 mg/kg/day divided bind), macrolides (Azithromycin
10 mg/kg day 1 then 5 mg/kg daily days 2-5)
-for H.flu and M. catarrhalis
-“third line”:
-if failed above, then most likely penicillin resistant strep. pneumoniae
-use high dose amoxil or amoxil with clavulin
-“fourth line”:
-if failed above then consider ceftriaxone
-recurrent/frequent OM
-those who clear effusion between episodes
-Rx: -antibiotic treatment for each separate episode of AOM
-prolonged prophylactic antibiotic treatment (Amoxil and Septra)
-for those with 3-4 episodes in 6 months; 4-6 in 1 year
-risk of developing resistance
-BMT
-those with persistent effusion
-use of nasal steroids not established
-lack of evidence showing that decongestants (systemic and intranasal) effective in curing or preventing
middle ear disease
Prevention
-changes in environmental factors
-taking child out of daycare
-preventing exposure to second hand smoke
Surgical Therapy: Myringotomy and Tube Insertion

-indications:
-recurrent AOM unresponsive to medical therapy
-chronic OM with bilateral effusion greater than 3 months and conductive hearing loss (>30dB)
629
-negative middle-ear pressure with impending cholesteatoma
-intervention in presence of complications of OM
-other “soft” indications:
-recurrent OM (3-4 episodes in 6 months; 4-6 in 1 year)
-to improve quality of life but no real medical indication for this
-average time tubes remain in place and functional is 8-12 months
-complications:
-otorrhea
-persistent TM perforation (1-3%)
-tympanosclerosis
-plugging of tube
-formation of granulation tissue
-cholesteatoma
-extrusion into middle ear
-factors related to persistent perforation:
-tube retention beyond 36 months and multiple sets of tubes
Adenoidectomy and Tonsillectomy

-differing studies - some show decreased recurrence of effusion with adenoidectomy
-consider adenoidectomy in children > 4 years old with recurrent infection or hypertrophied adenoids
-no study showing tonsillectomy effective in preventing OM
COMPLICATIONS
-Intratemporal:
-hearing loss (conductive and sensorineural)
-if MEE > 3 months and bilateral hearing and communication skills should be evaluated
-TM perforation
-CSOM +/- cholesteatoma
-retraction pockets/atelectasis
-cholesteatoma
-adhesive otitis media
-tympanosclerosis
-ossicular discontinuity/fixation
-mastoiditis
-petrositis
-labyrinthitis
-facial paralysis
-cholesterol granuloma
-infectious eczematoid dermatitis
-Intracranial:
-meningitis
-subdural empyema
-brain abscess
-extradural abscess
-lateral sinus thrombosis
-otitic hydrocephalus
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GENETIC HEARING LOSS
-childhood SNHL:
-50% genetic factors
-75-80% autosomal recessive
-18-20% autosomal dominant
-X-linked ~2-4%
-mitochondrial < 1%
-20-25% identifiable environmental causes, prenatal, perineal or postnatal
-25-30% sporadic (“cryptogenic”)
STRUCTURAL MALFORMATIONS OF THE INNER EAR
-cochlea reaches full growth (2.75 turns) by end of 8th week GA
Michel Aplasia
-autosomal dominant trait
-structures of inner ear do not develop
-arrest/insult in development before end of 3rd week GA (otic placode formation)
-presents with anacusis
-hearing aids and cochlear implantation NOT useful
Mondini Aplasia
-autosomal dominant
-developmental malformation of cochlea
-second most common abnormal X-ray finding in SNHL
-only basal coil clearly identified
-absence of interscalar septum, endolymphatic aqueduct typically enlarged
-arrest/insult ~ 6-7th week GA
-association with syndromal and non-syndromal conditions (eg. CM) described
-associated with an increased risk of perilymphatic gushers and meningitis from a dilated cochlear
aquaduct
Scheibe Aplasia
-most common form of inner ear aplasia
-result in partial or complete aplasia of the pars inferior (cochlea and saccule) and normal pars superior
(SCCs and utricle)
-associated with other diseases such as Usher syndrome and Waardenburg syndrome
-normal bony labyrinth; malformation of membranous labyrinth
-organ of Corti poorly differentiated
-tectorial membrane malformed
-stria vascularis degenerated
-scala media compromised by collapse of Reissner membrane
-hearing aids useful
Alexander Aplasia
-aplasia of cochlear duct
-audio: high-frequency hearing los with adequate residual hearing in low frequencies
F.Ling - Genetic Hearing Loss (1)
631
Semicircular Canals
-lateral SCC are last to develop and have longest period of susceptibility to teratogenic insults
Enlarged Vestibular Aqueduct

-usually bilateral
-most common congenital cause for SNHL seen on X-ray
-VA > 1.5 mm at midpoint or > lateral SCC
-40% develop profound HL
-progressive hearing loss - possibly because of disruption of labyrinthine membrane
-surgery unsuccessful for prevention of progression
Bing-Siebemann Dysplasia
-complete membranous labyrinth dysplasia
-rare
AUTOSOMAL DOMINANT DISORDERS
Waardenburg Syndrome
-variable expressivity
-features:
-unilateral or bilateral SNHL
-pigmentary anomalies:
-white forelock, heterochromia irides (two different coloured eyes), premature graying
and vitiligo
-craniofacial features:
-dystopia canthorum (laterally displaced medial canthi), broad nasal root, synophrys
-two clinical types
-WS1 (presence of dystopia canthorum)
-20% with HL
-WS2 (absence of dystopia canthorum)
->50% with HL
-other types
-WS3 (Klein-Waardenburg)
-includes features of WS1 and skeletal malformations particularly in hands and forearms
-WS4 (Waardenburg-Shah)
-autosomal recessive
-features of WS2 with Hirschsprung megacolon
Stickler Syndrome
-associated with mutations of type II collagen gene (COL2a1) on Chr 12
-features:
-Pierre-Robin sequence
-severe myopia associated with retinal detachment and cataracts
-hypermobility and enlargement of joints with early adult onset arthritis
-progressive SNHL in 15%
Branchiotorenal Syndrome (Melnick-Fraser Syndrome)

-branchial anomalies
-otologic anomalies: sensorineural, conductive, mixed, Mondini aplasia or small cochlea
-renal anomalies: minor dysplasia to agensis and renal failure
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Treacher Collins Syndrome (Mandibulofacial dysostosis)
-high penetrance; new mutation in 60%
-treacle protein function in early craniofacial development
-features:
-microtia, aural meatal atresia, conductive hearing loss from ossicular malformation (~30%)
-SNHL and vestibular dysfunction may be present
-bilateral malar hypoplasia, downward slanting palpebral fissures, coloboma of lower eyelids,
hypoplastic mandible
Goldenhar Syndrome
-facial asymmetry
-unilateral external and middle ear deformities:
-mildly deformed ears to complete anotia
-external canal atresias and ossicular deformities
-vertebral malformations
-most cases are sporadic
Neurofibromatosis
-NF1(von Recklinghausen disease)

-prevalence of 1/3000-4000
-defect localized to chromosome 17
-café au lait spots and cutaneous neurofibromas
-axillary freckling, optic glioma, Lisch nodules (iris hamartomas), sphenoid wing dysplasia
-cervicofacial plexiform neurofibromas resemble “bag of worms”
-HL caused by neurofibroma encroaching on middle or inner ear, but marked deafness is rare
-acoustic neuroma in 5%
-NF2 (Central)
-central form of neurofibromatosis
-localized to defect in long arm of chromosome 22
-bilateral acoustic neuromas, meningiomas, spinal cord schwannomas
-mean age of presentation is 20 - unilateral or bilateral hearing loss common
Otosclerosis
-appears to be transmitted in an autosomal dominant pattern with decreased penetrance, so only 25% to
40% of gene carriers show the phenotype
-preponderance of affected females suggests a possible hormonal influence
Osteogenesis imperfecta (OI)

-features:
-bone fragility
-blue (clear) sclerae
-hearing loss (conductive, mixed, or sensorineural)
-hyperelasticity of joints and ligaments
-genes for OI have been identified, COL1A1 on chromosome 17q and COL1A2 on chromosome 7q.78
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NONSYNDROMIC AUTOSOMAL DOMINANT HEARING LOSS
Dominant Progressive Hearing Loss

-variable age of onset (usually earlier age of onset)
-four types described:
-early onset
-high frequency
-mid frequency
-low frequency
-represents a group of disorders
RECESSIVE DISORDERS
Usher Syndrome
-SNHL and retinitis pigmentosa
-~3-4 cases per 100,000 population
-most common cause of combined deafness and blindness in the Western world (affects one half of 16 000
deaf and blind persons in the US)
-three types:
-Ush 1: profound SNHL, vestibular dysfunction, retinitis pigmentosa (90%)
-Ush 2: mild to moderate SNHL, normal vestibular function, retinitis pigmentosa (10%)
-Ush 3: progressive SNHL, progressive vestibular dysfunction and retinitis pigmentosa
-ophthalmologic evaluation is integral to diagnosis (RP diagnosed with electro-retinography)
Pendred Syndrome
-due to mutations in SLC26A4/PDS (pendrin) gene
-defect in tyrosine iodination
-SNHL associated with abnormal iodine metabolism euthyroid goiter
-most patients have Mondini aplasia or enlarged vestibular aqueduct
-dx: abnormal perchlorate discharge test: abnormal organification of nonorganic iodine
-treat goiter with exogenous thyroid hormone
Jervell and Lange-Nielsen Syndrome

-SNHL associated with episodes of syncope caused by a cardiac conduction defect sudden death
-attributed to mutations in potassium channel gene
-HL variable but usually severe
-ECG: large T waves and prolongation of QT interval
-syncope as early as second or third year of life - can resemble seizures
-treatment: beta-blockers effective in managing the cardiac component of the syndrome
NONSYNDROMIC RECESSIVE SENSORINEURAL HEARING LOSS
-three subtypes:
-congenital severe-to-profound
-CX26 (GJB2 or DFNB2) gene defect most common; accounts for ~50% of recessive
nonsyndromic hearing loss
-produces gap junction protein connexin 26
-congenital moderate
-early-onset
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SEX-LINKED DISORDERS
Otopalatodigital Syndrome
-hypertelorism
-craniofacial deformity involving supraorbital area, flat midface, small nose and cleft palate
-short broad fingers and toes
-conductive hearing loss caused by ossicular malformation
Wildervanck Syndrome
-suspected X-linked dominant
-features: fused cervical vertebrae, sensorineural or mixed hearing loss (related to bony malformation of
inner ear), paralysis of 6th cranial nerve
Alport Syndrome
-SNHL associated with renal disease of varying severity
-progressive HL
-nephritis hematuria “red diaper” syndrome
-early diagnosis essential to facilitate management of renal disease
-X-linked d/t mutation of type 4 collagen gene (COL4A5)
MITOCHONDRIAL INHERITANCE
-mitochondrial diseases typically involve progressive neuromuscular degeneration with ataxia,

ophthalmoplegia, and progressive hearing loss
-disorders:
-Kearns-Sayre
-MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke)
-MERRF (myoclonic epilepsy with ragged red fibers)
-Lebers hereditary optic neuropathy
Probability of having a child with congenital hearing loss
Parental Mating No. deaf offspring Risk of having another affected

child
Hearing x hearing 1 9-17%

>1 25%
Hearing x deaf 0 5%
1 40-50%
Deaf x deaf 0 10%

1 60%
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PEDIATRIC AUDIOLOGY
HEARING SCREENING
Infant Screening
-endorses universal detection of infant hearing loss by 3 months of age and intervention by 6 months of age
-risk indicators:
-NICU admission
-syndrome associated with hearing loss: NF, osteopetrosis, Usher syndrome
-family history of hearing loss
-craniofacial anomalies
-in uteri infection: TORCH, syphilis
-parental concern of hearing or speech delay
-post-natal infections: meningitis
-hyperbilirubinemia requiring transfusions
-neurodegenerative disorder (eg. Hunter syndrome)
-head trauma
-recurrent or persistent otitis media with effusion for at least 3 months
-children with indicators of progressive or delayed-onset hearing loss should be examined minimum
q6months through 3 years of age
BEHAVIOURAL AUDIOMETRIC ASSESSMENT
General Test Considerations

-first method used to test children who are at least 5 months of age
-goal: establish hearing levels for each ear
Test Battery
-Immittance Testing
-tests middle ear function
-limitations:
-children less than 4 months have:
-incomplete ossification of canal wall, which increases volume and compliance
-unresolved mesenchyme in middle ear which increases resistance
-Speech Testing
-speech stimulation provides reference for frequency-specific testing
-broadband speech more meaningful to child - will respond at lower thresholds
-speech awareness threshold obtained
-speech recognition not attempted until 3 years of age
-Pure-tone Testing
-warble tones (younger children tend to respond better to this type of stimulus) in sound field
-pure tones with earphones (for older children)
-initial test frequency is 2000 Hz then 500 Hz signal (commonly affected in CHL)
BEHAVIOURAL TEST TECHNIQUES
Behavioural Observation Audiometry

-for children less than 5 months of age
-relies on reflexive responses and state changes
-imprecise
F.Ling - Pediatric Audiology (1)
636
-responses are reported as minimal response levels and are not considered true thresholds
Visual Reinforcement Audiometry

-5 months - 2 years
-child turns naturally or is trained to look for an auditory stimulus
-behaviour is reinforced with a flashing light
-allows used of a standard threshold technique to obtain hearing levels
Conditioned Play Audiometry

-2-5 years of age
-child trained to perform an activity in response to auditory stimulus
-standard threshold technique can be used and normal adult threshold levels are expected
Standard Audiometry
->5 years of age
SPECIAL TESTS
Auditory Brainstem Response Testing

-provides threshold estimate in the 1000-4000 Hz range
-500 Hz tone burst stimulus estimates low frequency hearing
-bone-conducted stimulus can be applied
-newborn ABR comprises waves I, III, and V (mostly look at wave V - the most robust)
-98% sensitive, 96% specific
-click stimulus at intensity levels b/n 30-40 dBnHL
Otoacoustic Emission Testing

-measures outer hair cell function
-performed over broad, frequency-specific range (1000-6000 Hz)
MANAGEMENT OF HEARING LOSS
Amplification
-critical range of hearing 0-15 dB for a young child
-unvoiced consonants: s, p, k, th, f, sh fall at or below normal adult hearing thresholds
-resonance frequency of infant ear canal much higher than adults (7200 Hz vs 2700 Hz)
-affect selection of gain and peak frequency responses
-therefore must monitor these effects to prevent discomfort or overamplification
-binaural amplification used to limit auditory deprivation in select cases
Assistive Devices
-FM systems used to decrease signal-to-noise ratio, reverberation and distance problems that degrade signal
received by hearing aid
CENTRAL AUDITORY PROCESSING DISORDERS
-definition:
-deficit in information processing of audible signals not attributed to impaired peripheral hearing
sensitivity or intellectual impairment
637
-refers to limitations in ongoing transmission, analysis, organization, transformation, elaboration,
storage, retrieval, and use of information contained in audible signals
-signs:
-easy distraction
-delayed responses
-frequent requests for repetition
-symptoms of hearing loss
-frequent reversals
-difficulty following directions
-inconsistent academic performance
-unexplained behavioural difficulties
-tests commonly used to diagnoses CAPD among children:

-monaural tasks
-speech in noise
-filtered speech
-pitch pattern sequence
-binaural tasks
-competing sentence test
-diotic speech in noise
-binaural fusion
-phonemic synthesis
-dichotic tasks
-staggered spondaic word test
-dichotic digit test
-dichotic consonant-vowel test
-pediatric sentence identification test
-electrophysiologic tests
-ABR
-middle latency response (MLR)
-late vertex response
-auditory P300 - endogenous evoked potential, elicited by an internal event such as
perception or cognition
-management:
-environmental modifications: preferential seating, increased visual cues
-compensatory strategies: cueing, repetition, review, etc..
-amplification with personal or classroom style FM systems
638
PEDIATRIC FACIAL FRACTURES
-controversial problems:
-elevation of functional matrix off underlying facial architecture to gain exposure to the fractures
may alter development
EPIDEMIOLOGY
-serious facial fractures amongst children rare (1.5-15%)

-nasal fractures most common
-mandibular fractures ~20-50% of pediatric facial #s
-condyle most vulnerable (40-70% of mandibular #)
-orbital fractures second most common midfacial fractures after nasal fractures
-type of fractures age related:
-<5 years: shearing and greenstick type; less comminution
-6-12 years: intermediate patterns of fractures
-adolescence: adult pattern of facial fractures
EMERGENCY MANAGEMENT
-ABCs - c-spine
-need for tracheotomy controversial for severe facial fractures
ETIOLOGY
-MVA most common cause of serious facial fractures

-bones of face not fully mineralized
-bony sutures not fused
-cortices are thin
-greater proportion of cancellous bone
-infant’s craniofacial complex is elastic but solid structure
-80% of cranial growth occurs during first 2 years of life
-after 2 ya, face begins to grow faster than skull
-by 7 ya, orbit and brain near completion of growth
FACIAL GROWTH AND TRAUMA
-alterations of growth and remodelling d/t trauma can cause facial deformities
-condyle:
-important site of mandibular growth
-injuries to this area however can, but do not consistently cause facial asymmetry
-crush injuries to condylar head before 5 ya predispose child to ankylosis and growth disturbances
-extensive remodelling of condylar fracture between ages 3-11 results in normal anatomic
features:
-injuries before 3 ya severe deformities
-injuries after 6 ya moderate deformities
-injuries during adolescence mild deformities
-midface more susceptible to developmental deformities from even minor trauma
F.Ling - Pediatric Facial Fractures (1)
639
-theories:
-loss of stimulus to normal growth
-mechanical restriction produced by scarring and loss of motion
-altered muscular activity
-interruption of vascular supply to teeth
Rigid Fixation
-concern about impairment of facial growth
-most data from animal studies but no firm conclusions
-use of bone grafts to bridge defects become incorporated into growing face
-rib grafts
-cranial bone grafts
-bone loss of buttresses of > 5mm should be bridged rigidly with calvarial bone grafts
-rigid fixation usually reserved in cases where fractures cannot be restored by any means
-minimally displaced fractures often best left alone or managed with closed reduction
-use as small plates as possible and do not cross more than one suture line
Surgical Approaches
-nasal or zygomatic arch fractures managed with closed or limited open techniques
-five basic incisions:
-lower gingivolabial sulcus incision:
-arch of mandible #
-coronal incision:
-upper third of face (zygomatic arches, upper orbital rims, nasoethmoidal region) #
-subciliary/trans conjunctival incision:
-inferior orbital rim and orbital floor #
-upper gingivolabial sulcus incision:
-maxilla #
-external:
-mandibular angle and ramus #
Nasal Fractures
-nose in children is soft - energy is dissipated easily
-septum more likely to be fractured
-nasal bones have little projection; children over 6 years more susceptible to bony fractures
-usually greenstick type #
-management:
-initial evaluation:
-often limited by swelling
-r/o septal haematoma cartilage necrosis saddle nose deformity
-treatment:
-usually 5-7 days post injury when swelling has subsided
-closed reduction
Mandibular Fractures
-infants younger than 2 years:
-accurate alignment with acrylic splints (dentist)
-wired in place with circum-mandibular wires for 2-3 weeks
-IMF not necessary
-children 2-5 years:
-may use arch bars for IMF
-piriform aperture suspension or circummandibular wiring may be necessary
640
-children 6-12 years:
-arch bars for IMF
Condylar Fractures
-three types:
-intracapsular crush fracture of head
-high condylar fracture through neck above sigmoid notch
-low subcondylar fracture (most common, often greenstick)
-treatment mainly conservative closed approach
-unilateral #:
-with normal ROM and normal occlusion: soft diet and movement exercises
-deviation with normal occlusion: arch bars with use of guiding elastic bands
-open bite deformity: 2-3 weeks of IMF followed by 6-8 weeks of guiding elastics
Arch of Mandible Fractures

-anterior fractures with minimal to moderate displacement: IMF
-bone-to-bone reapproximation : ORIF
-interfragmentary wiring or monocortical miniplate fixation
-body and angle fractures usually greenstick: soft diet and symptomatic therapy
Dentoalveolar Fractures
-incisors and canines most commonly injured
-avulsion of secondary tooth: survival depends on early reimplantation
Midfacial Fractures
-injury ranges from simple blowout fractures to highly comminuted injuries
-ophthalmology consult required
-more likely to cause problems with facial growth and development and to result in permanent deformities
if left uncorrected
Zygomaticomalar Complex Fractures

-usually do not occur before age 5 years - in keeping with development of maxillary sinuses
-Gilles’ reduction for isolated zygomatic arch fractures
-tripod fractures:
-triangulation required to control 3 main buttresses
-most fractures are medial displacements of malar fragment with only greenstick fractures of
frontozygomatic suture and zygomatic arch
-zygomaticomalar buttress fixation usually adequate
Nasoethmoidal Complex Fractures

-CT required for preoperative planning
-assess medial canthal integrity under general anaesthesia
-average intercanthal distance:
-4 ya: 25 mm
-12 ya: 28 mm
-adult: 30 mm
-intercanthal distances > 10 mm from average confirms diagnosis of displaced fracture of
nasoethmoid complex
-reconstruction of nasal maxillary buttress may be required
-intercanthal distance should be restored
-use of nasal dorsal bone grafts to manage midfacial crush injuries important
641
-steps for management of traumatic telecanthus:
-bicoronal incision
-explore central fragment reosteotomize
-reestablish nasomaxillary buttress with microplates
-transnasal wiring to reduce intercanthal distance
Orbital Roof, Supraorbital Rim, Frontal Bone Fractures

-usually delayed swelling - an important clue
-classification (Messinger):
-Type I: comminution of orbital roof but no displacement
-Type II: displacement of fragments toward anterior cranial fossa
-Type III: displacement inferiorly into orbit
-most children will need surgical repair of roof or superior orbital rim
-neurosurgical intervention takes priority
Floor of Orbit Fractures

-parallels pneumatization of maxillary sinus; unusual to see floor fractures before age 5 years
-most common isolated type of fractures of orbit among children older than 7 years
-ophtho consult required
-most children with isolated fractures are observed for 7-10 days
-exploration if continued exophthalmos, diplopia or pain
-entrapped muscle requires immediate repair
-large defects repaired with calvarial bone grafts
Maxillary Fractures
-Lefort system useful in predicting difficulty of reconstruction - but anatomic classification inadequate to
describe severity of injury and complexity of reconstruction needed
-functional classification
-type I: minimally displaced, usually not comminuted
-main buttresses cracked
-type II: moderately displaced with some area of comminution
-fragments large enough to accept plates and screws
-type III: severely displaced with multiple comminution
-requires stabilization and use of bone grafts for reconstruction
-maxillary fractures uncommon among children
642
CONGENITAL VASCULAR LESIONS
CHARACTERISTICS OF CONGENITAL VASCULAR LESIONS

Hemangioma Malformation
Clinical
-usually absent at birth, 30% present as red macule -all present at birth; may not be evident
-rapid postnatal proliferation -commensurate growth; rapid growth possible with hormonal
-slow involution changes, trauma or infection
-F:M = 3:1 -no involution
-F:M = 1:1
Cellular
-plump endothelium, increased turnover -flat endothelium, slow turnover
-increased mast cell count -normal mast cell count
-multilaminated basement membrane -normal thin basement membrane
-capillary tubule formation in vitro -poor endothelial growth in vitro
Radiologic
-angiographic findings: well-circumscribed intense lobular- -angiographic findings: diffuse, no parenchyma
parenchyma staining with equatorial vessels -low flow: phleboliths, ectatic channels
-MRI: intermediate signal intensity on T1 that increases on T2; -high flow: enlarged, tortuous arteries with arteriovenous
flow voids present shunting
-MRI: does not enhance on T2 images
Skeletal
-infrequent mass effect on adjacent bone; rare hypertrophy -low flow: distortion, hypertrophy or hypoplasia
-high flow: destruction, distortion, or hypertrophy
HEMANGIOMAS
-most common neonatal tumour

-~10% incidence
-stages:
-Proliferative:
-lasts 6-12 months
-rapid growth: endothelial hyperplasia
-Involuting:
-50% completely resolved by 5 years
-70% by 7 years
-Involuted:
-redundant skin, scarring, telangiectasia
-types:
-superficial: -raised and bright red
-subcutaneous (deep): bluish appearance
-mixed: both superficial and deep appearance
-complications:
-ulceration, airway obstruction, high output cardiac failure, cosmetic deformity
-Kasabach-Merritt Phenomenon:
-not real hemangioma
-platelet sequestration, ecchymosis, no female predominance
-actual lesion is either kaposiform hemangioendothelioma or tufted angioma
-supportive treatment; avoid used of blood products causes sequestration and produce rapid
tumour enlargement
F.Ling - Congenital Vascular Lesions (1)
643
Management of Hemangiomas
-indications for immediate treatment:
-affects swallowing or vision
-life threatening: associated with high output cardiac failure or respiratory difficulty
-primary objectives:
-limit tumour growth
-avoidance of complications
-primary medical treatment
-oral prednisone
-continue treatment until involution is well established
-steroid resistant lesions:
-intralesional steroids
-limited to smalls lesions
-avoid periorbital injections risk of retinal artery thrombosis
-interferon alpha-2a
-s/e: low-grade fever, LFTs, transient neutropenia, anemia, spastic diplegia
-surgery
-photocoagulation:
-used during early proliferative phase q4-6 weeks on superficial lesions
-ineffective for deep hemangioma
VASCULAR MALFORMATIONS
-occur when abnormal morphogenesis involved vascular channels

-types:
-low flow lesions: capillary malformations, venous malformations, lymphatic malformations,
combinations
-high flow lesions: arterial malformations, arteriovenous malformations
Capillary Malformations and Other Birthmarks

-capillary malformations = “port-wine stains”
-present at birth, gradually darken
-located in cutaneous superficial vascular plexus
-capillary and postcapillary venules
-treated because of commensurate growth and cosmetic deformity
-tx: pulsed dye laser at 585 nm
-provides selective absorption by oxyhaemoglobin which confines laser energy to vessel
walls
-other birthmarks:
-nevus flammeus:
-glabella “angel kiss”
-nape of neck “stork bite”
-irregular outline with distinct edges
-usually fade within first year of life; no treatment necessary
Lymphatic Malformations
-occur when lymphatic sacs fail to communicate with lymphatic vessels
-variable extent of involvement in the head and neck
-spontaneous regression not frequent
-MRI findings:
-low T1, high T2, no flow voids
644
-staging system:
-I: unilateral infrahyoid
-II: unilateral suprahyoid
-III: unilateral suprahyoid and infrahyoid
-IV: bilateral suprahyoid
-V: bilateral suprahyoid and infrahyoid
-infrahyoid usually macrocystic, easier to remove

-suprahyoid usually microcystic, more infiltrative, excision usually incomplete
-bilateral airway problems
-tx:
-surgery best
-sclerotherapy, I+D, aspiration, XRT unsuccessful
-OK432:
-lyophilized, low-virulence strain of Strep. pyogenes
-92% response rate for macrocystic lesions
-44% response rate for microcystic lesions
Venous Malformations
-dilated vascular channels lined by normal endothelium
-common on lips and cheek
-soft compressible
-low-flow phleboliths
-tx: sclerotherapy or surgery
Arteriovenous Malformations
-abnormal communications between arteries and veins that bypass the capillary bed
-characteristically associated with a thrill or bruit
-MRI:
-no enhancement on T2
-flow voids on both T1 and T2
-angiography:
-dilatation and lengthening of arteries with early shunting of enlarged veins
-tx: surgery with pre-op embolization if symptomatic
Associated Syndromes
-Sturge-Weber:
-facial capillary malformation involving CN V1 with ipsilateral vascular malformation of
leptomeninges and eye
-choroidal malformation in eye causes glaucoma among 30% of pts
-Klippel-Trenaunay:
-cutaneous capillary malformation with underlying venous and lymphatic malformation
-skeletal overgrowth of a limb and possible growth retardation
645
Embryology of the Face, Lips
and Palate Development of the Face and Lips
ENT Residents’ Academic Half-Day
May 9th 2003
Resident Coordinator: Francis Ling
4th week GA 5th week GA (early)

• By the end of the fourth week, • The paired maxillary swellings
all five swellings have appeared. enlarge and grow ventrally and
• The maxillary swellings can be medially.
distinguished lateral, and the • A pair of ectodermal
mandibular swellings caudal to thickenings called the nasal
the stomodeum placodes appear on the
• The frontonasal process is blue frontonasal process and begin to
in these illustrations. enlarge.
5th week GA (late) 6th week GA

• The ectoderm at the centre of • Each medial nasal process
each nasal placode invaginates begins to migrate towards the
to form an oral nasal pit, other and they fuse.
dividing the raised rim of a • The mandibular swellings have
placode into a lateral nasal now fused to create the
process and a medial nasal primordial lower lip.
process • The nasal pits deepen and fuse to
form a single, enlarged,
ectodermal nasal sac.
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1
7th week GA 10th week GA
• Lateral and inferior expansion of • Ectoderm and mesoderm of
each fused medial nasal process frontal process and each medial
forms the intermaxillary process. nasal process proliferate,
• The tips of the maxillary forming a midline nasal septum.
swellings grow to meet this This divides the nasal cavity into
process and fuse with it. two nasal passages which open
• The intermaxillary process gives into the pharynx, behind the
rise to the bridge and septum of secondary palate, through the
the nose, and the philtrum on the definitive choana.
upper lip.
10th week GA
• The philtrum is now formed, and
the lateral portions of the
maxillary and mandibular Development of the Palate
swellings fuse to create the
cheeks and reduce the mouth to
its final width.

• The floor of the nasal cavity • The tongue moves
at this stage is a posterior downward and the palatine
extension of the shelves rapidly rotate
intermaxillary process upwards towards the
known as the primary palate.
midline, growing
• The medial walls of the horizontally.
maxillary swellings begin to
produce a pair of thin medial
extensions, ' palatine shelves'
,
which grow inferiorly on
either side of the tongue.
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2
• The palatine shelves begin to • The ventral secondary palate
fuse ventrodorsally with becomes the bony hard
each other, the primary palate through mesenchymal
palate and the inferior nasal condensations (endochondral
septum. ossification).
• The dorsal secondary palate
becomes the soft palate
through myogenic
mesenchymal condensation.
Cleft Lip
• Underdevelopment of
mesenchyme of the
Abnormal Facial Development maxillary swelling, resulting
in inadequate contact with
the medial nasal process and
intermaxillary process. The
length and depth of the
resulting cleft can vary
considerably.
Cleft Lip Cleft Lip

• Pathogenetic factors such as • Etiology is multifactorial,
inadequate migration or however drugs such as
proliferation of neural crest phenytoin and vitamin A and
ectomesenchyme, or its analogs may induce the
excessive cell death during condition
maxillary swelling or nasal
placode development may
account for a cleft lip.
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3
Cleft Palate Cleft Palate
• Caused by inadequate • It may result from a wide
palatine shelf growth, range of congenital insults
incorrect shelf elevation, an and genetic errors.
excessively wide head, • Etiology is again
failure of shelves to fuse or multifactorial, with the same
rupture after fusion. teratogens as for cleft lip,
although an x-linked cleft
palate syndrome has been
described.
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4
Introduction
• “2% of livebirths have congenital anomalies”
ENT Problems in the • 70% congenital anomalies occur in head and neck region
and the hand
Syndromic Child • Several thousand distinct syndromic entities described
• Many have craniofacial and otolaryngologic components
Francis T.K. Ling MD (PGY-3)
University of Ottawa - Department of Otolaryngology • Frequent ENT consults
Grand Rounds • Syndromes search for suspected defects
Wednesday April 2, 2003
Introduction Introduction
• Minor anomalies • Multidisciplinary approach
• Defects without serious medical or surgical significance • ENT consulted to deal with problems that affect:
• Epicanthic folds, coloboma, small or protuberant ears, small nares, • Respiration
bifid uvula
• Swallowing
• Occur in 15% of the population
• Hearing
• Half of all known minor anomalies occur in the head and neck
region • Speech
• Three or more minor malformations Major malformation found • Facial appearance
in 90%
• Evaluate for cardiac, renal or vertebral defects
Definitions Definitions
• Malformation • Deformation
• Morphologic defect of an organ resulting • Abnormal form, shape or position of a body
from intrinsically abnormal developmental part caused by mechanical forces
process • Usually occurs late in development
• Three types: • Eg. Congential torticollis and facial
• Incomplete (eg. Cleft lip) asymmetry from oligohydramnios
• Redundant (eg. Ear tags)
• Aberrant (eg. Mediastinal thyroid)
• Initiated late in fetal development are
simple; those initiated early usually more
complex and severe
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1
Definitions Definitions
• Disruption • Sequence
• Morphologic defect of organ • Pattern of multiple anomalies derived from a single known or
resulting from extrinsic breakdown presumed prior anomaly or mechanical factor
or interference of an originally • Eg. Pierre Robin sequence
normal development process
• Syndrome
• Rare
• Greek: “running together”
• Eg. Facial clefting as a result of
amniotic bands • Pattern of multiple anomalies pathogenetically related but not
representing a single sequence
• Association
• Nonrandom occurrence in two or more individuals of multiple
anomalies not known to be a sequence or syndrome
• Eg. CHARGE association
Syndrome Diagnosis Syndrome Diagnosis

• Over 3000 syndromes described • Physical examination
• ~30% of syndromal children will have private syndromes • Head and neck examination
• Documentation of major and minor anomalies
• Directed history
• Family history at least over 3 generations (AD, AR, X-linked) • Database
• Parental consanguinity and ethnicity (recessive disorders) • Smith’s Recognizable Patterns of Human Malformations
• Maternal and paternal ages (trisomies, craniosynostosis • Genetics or dysmorphologist
syndromes) • Laboratory testing
• Possible teratogen exposure (fetal alcohol syndrome) • karyotyping
• Outcome of previous pregnancies • DNA analysis
• Miscarriages, still births, neonatal deaths, birth defects
Otolaryngologic Problems
• Hearing loss
• Speech disorders
• Airway obstruction
Otolaryngologic Problems
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2
Hearing Loss Hearing Loss
• Congenital
• Devastating effect on speech and intellectual development • Usually conductive
• High risk with craniofacial anomalies • External auditory meatus atresia
• Various degrees of obliteration of middle ear cleft
• Delayed detection • Ossicular deformity
• Assumed mental retardation rather than hearing loss • Ossicular fixation
• Acquired
• Usually conductive
• Most often consequence of eustachian tube dysfunction
• OME
Speech Disorders Speech Disorders
• Hypernasality • Hyponasality
• Causes: • Severe posterior displacement of midface
• VPI after cleft palate repair most common • Persistent congenital atresia or stenosis
• Anatomical anomalies involving nasal cavity and nasopharynx • Iatrogenic velopharyngeal stenosis from palatopharngoplasty
• Reduced with speech therapy
• Hoarseness
• Palatopharyngoplasty at 5 years of age if speech therapy
• Vocal cord nodules present in 20% of children with VPI
unsuccessful
• Increased laryngeal activity to compensate for loss of vocal power
Airway Obstruction Airway Obstruction

Neonatal Nasal Airway Obstruction Neonatal Nasal Airway Obstruction
• Neonates obligate nasal breathers until 3 months of life • Choanal Atresia
• Paradoxical cyanosis • Most common cause of neonatal nasal
obstruction
• Causes:
• Bilateral involvement life threatening
• Bilateral choanal atresia
• 1:5000 – 1:8000 neonates
• Midfacial hypoplasia
• Osseous (90%) or membranous (10%)
• Piriform aperture stenosis
• Unable to pass nasal catheter
• Relieved by oral airway until at least 3 months of age • May be seen in many syndromes
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3
Neonatal Nasal Airway Obstruction Neonatal Nasal Airway Obstruction
• CT findings • Treatment
• Narrowing of posterior choanae < • Surgical
0.34 cm in children under 2 years old • Transpalatal
• Inward bowing of posterior maxilla • Transnasal
• Fusion or thickening of vomer • Endoscopic
• Presence of bone or soft-tissue
septum extending across posterior
choanae

Neonatal Oropharyngeal Obstruction Neonatal Oropharyngeal Obstruction
• Glossoptosis: tongue falls back and obstructs oropharynx • Pierre Robin Sequence (PRS)
• Micrognathia or retrognathia • 1:8500
• Triad of glossoptosis, micrognathia and
• Occurs more readily when associated with cleft palate
cleft palate airway obstruction
• Long term sequelae • Pathogenesis:
• Cor pulmonale • Mandibular deficiency maintains
• Congestive heart failure tongue high in nasopharynx prevents
medial growth and fusion of palatal
• Arrhythmias
shelves cleft palate (U-shaped)
• Failure to thrive

Neonatal Oropharyngeal Obstruction - PRS Neonatal Oropharyngeal Obstruction - PRS
• Clinical Findings
• Marked anteroposterior mandibular
deficiency
• Small or retropositioned mandible
• Width of cleft greater on average than
isolated cleft palate
• Signs and symptoms of airway obstruction
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4
Neonatal Oropharyngeal Obstruction - PRS Neonatal Oropharyngeal Obstruction - PRS
• Airway Obstruction • Two categories:
• Neuromuscular impairment of • Nonsyndromic (80%): potential for catch-up growth
genioglossus and other parapharyngeal • Syndromic (20%): usually intrinsic defect
muscles • Stickler syndrome
• Anatomic abnormalities include • Velocardiofacial syndrome
retroposition of mandible and diminished • Fetal alcohol syndrome
effectiveness of genioglossus in exerting
anterior traction on the tongue

Neonatal Oropharyngeal Obstruction - PRS Obstructive Apneic Episodes
• Treatment • Various contributing factors:
• Positioning (up to 70% successful) • Adenoid hypertrophy
• Nasopharyngeal airway • Severe posterior displacement of midfacial structures
• Tracheotomy • Retrognathia
• Others: • Hypotonia
• Tongue-lip adhesion/glossopexy • Causes failure to thrive, pulmonary hypertension,
• Mandibular distraction osteogenesis
behavioural problems
• Subperiosteal release of floor of mouth
Airway Obstruction
Chronic Nasal Obstruction
• Distortion of midfacial anatomy
• Enlarged adenoids Specific Syndromes and
• Palatal clefts Associations
• Reduce caliber of nasal airway
• Distortion of nasal soft tissue
• Nasal mucosa edema
• Septal deviation
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Specific Syndromes & Association Branchio-
Branchio-oto-
oto-renal Syndrome
• Branchio-oto-renal Syndrome • Autosomal dominant
• Goldenhar Syndrome • Branchial cleft anomalies
• Down Syndrome • Cysts
• Treacher-Collins Syndrome • Fistulae
• Velocardiofacial Syndrome • Family history of “fish parts” removed from neck
• CHARGE Association • Otologic malformations
• Craniofacial Syndromes • Preauricular pits (75-85%)
• Apert • Malformed auricles
• Crouzon • Ossicular and cochlear malformations
• Pfeiffer • Hearing loss highly variable
Branchio-
Branchio-oto-
oto-renal Syndrome Goldenhar Syndrome
• Renal malformations • Oculoauriculovertebral spectrum
• Renal agenesis • Facial asymmetry
• Polycystic kidneys • Hypoplastic mandibular ramus and condyle
• Duplicated ureters • Maxillary, malar and temporal bone smaller on
• Hydronephrosis one side
• Mastoid poorly pneumatized
Goldenhar Syndrome Down Syndrome

• Unilateral external and middle ear • Most common genetic
deformities disorder associated with
• Mildly deformed ears to complete anotia mental retardation and
• External canal atresias and ossicular developmental delay
deformities • Trisomy 21
• Vertebral malformations • 1/700-1000 live births
• Hemivertebrae and fused vertebrae described
• Increased maternal age a
risk factor
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Down Syndrome Down Syndrome
• Microcephaly • Otologic Disease
• Flat nasal bridge • Congenital:
• Midface retrusion • Increased incidence of congenital temporal bone anomalies
• Conductive, sensorineural and mixed
• Upslanting palpebral fissures
• Acquired:
• Epicanthal folds
• External canal stenosis
• Macroglossia • Immature immunologic development
• Congenital heart malformations • Defective eustachian tube cartilage and musculature
(40%) • Chronic ear disease
• Delayed gross motor skills
• Hypotonia and increased joint laxity

• Airway Obstruction • Airway Obstruction
• Common • Predisposing factors
• Obstructive sleep seen in 50-100% • Midface and mandibular hypoplasia
• Frequently overlooked/missed • Abnormally small upper airway and superficially positioned tonsils
• May be a component of central sleep apnea • Relatively large adenoids with contracted nasopharynx
• Macroglossia
• Increased secretions
• Obesity
• Generalized hypotonia

• Other Considerations
• Subglottic Stenosis • Cervical Spine Abnormalities
• Incidence of congenital • Atlantoaxial instability
narrowing of subglottis • 15-20% of DS
higher • Odontoid hypoplasia and laxity of
• More likely to acquire transverse ligament of first and
subglottic stenosis second vertebrae
• Smaller airway • Can cause compression of spinal
cord
• Increased likelihood of
major surgery • Precautions for adentotonsillectomy
• Smaller ETT used when and major otologic surgery
intubating children with DS
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Treacher-
Treacher-Collins Syndrome Treacher-
Treacher-Collins Syndrome
• 1/25000 to 1/50000 • Prominent nasal dorsum
• Retrusive mandible
• Mandibulofacial dystosis
• Zygomatic and mandibular
• Autosomal dominant hypoplasia
• Bilateral, symmetric • Downslanting palpebral fissures
• Lower lid colobomas
abnormalities of first and
• Cleft palate (Pierre Robin
second branchial arch sequence)
structures • External and middle ear
anomalies
• 50% with hearing impairment
from ossicular malformation or
EAC atresia
Treacher-
Treacher-Collins Syndrome Velocardiofacial Syndrome
• Airway Issues • Common multiple anomaly syndromes
• Size of nasopharynx 50% smaller than • 22q11 microdeletion
normal
• Maxillary hypoplasia with choanal
• AD with variable expressivity
stenosis • 186 reported clinical features
• Micrognathia and retropositioned • 50 ENT related
tongue • Many are minor anomalies
• Prone to OSA and SIDS
• Characterized by craniofacial anomalies, conotruncal heart
• Difficult intubation
defects, immune deficiencies, and learning disabilities
• May require tracheostomy
Velocardiofacial Syndrome Velocardiofacial Syndrome

• Craniofacial Anomalies – • Speech Abnormalities
Facial Structure • High frequency of severe
• “Characteristic Facies” hypernasality
• Almond shaped palpebral • Platybasia increases depth of
fissures pharynx
• Deficient nasal alae
• Tubular nose with bulbous
nasal tip
• Small mouth
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Velocardiofacial Syndrome Velocardiofacial Syndrome
• Speech Abnormalities • Airway Obstruction
• Palatal abnormalities • Generalized hypotonia
common (75%) • Pharyngeal hypotonia
• 20% overt clefts • Retrognathia
• 80% submucous clefts
• Laryngomalacia
• Classic bifid uvula or
notching of hard palate • Laryngeal web
• Occult • Vascular rings
• Adenoidectomy • Anomalous subclavians compressing trachea
significant VPI
• PRS
CHARGE Association CHARGE Association

• Coloboma • Cause unknown
• Heart defects • Pathogenesis thought to be secondary to abnormal
• Atresia (choanal) development of neural crest during embryogenesis
• Retarded growth and/or • Otologic problems
development • High risk for severe hearing loss
• High proportion of facial nerve palsies
• Genital hypoplasia
• Ear abnormalities and/or
deafness
CHARGE Association Craniofacial Syndromes

• Airway Complications • Craniosynostosis and craniofacial synostosis
• Bilateral choanal atresia CHARGE Association (~50%) • Premature fusion of cranial sutures
• Other airway abnormalities • Fusion of bones of skull base and face
• Laryngomalacia • Common syndromes
• Subglottic stenosis
• Apert
• Larygneal clefts
• Crouzon
• Tracheomalcia
• Pfeiffer
• Asher et al (1990)
• Higher propensity for airway complications in CHARGE (56%)
• Early repair of bilateral choanal atresia rarely successful
• Proposed early tracheotomy instead of early choanal atresia repair
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Craniofacial Syndromes Craniofacial Syndromes
• Common features • Major complications
• Craniosynostosis • CNS:
• Hypertelorism • Progressive hydrocephalus
• Exophthalmos • Cerebellar herniation
• Parrot-beaked nose • Increased intracranial pressures
• Maxillary hypoplasia • Ophthalmologic

• Exposure keratitis
• Mandibular prognathism
• Optic nerve atrophy

• Apert • Apert
• Clinical triad of • Clinical triad of
craniosynostosis, midface craniosynostosis, midface
hypoplasia, symmetric hypoplasia, symmetric
syndactyly syndactyly
• Syndactyly: fusion of digits • Syndactyly: fusion of digits
2,3,4 2,3,4
• Spontaneous mutation • Spontaneous mutation
• Increased paternal age • Increased paternal age
• Fusion of cervical vertebrae • Fusion of cervical vertebrae

• Crouzon • Pfeiffer
• Craniosynostosis, • Craniosynostosis, midface
brachycephaly, shallow deficiency, broad thumbs,
orbits and maxillary broad toes, brachydactyly,
hypoplasia variable syndactyly,
• No syndactyly radioulnar fusion
• Autosomal dominant
659
10
• Pfeiffer • Pfeiffer
• Craniosynostosis, midface • Craniosynostosis, midface
deficiency, broad thumbs, deficiency, broad thumbs,
broad toes, brachydactyly, broad toes, brachydactyly,
variable syndactyly, variable syndactyly,
radioulnar fusion radioulnar fusion

• Airway Problems
• Maxillary height, nasal • Risk of impaired respiratory
cavity width, bony function, obstructive sleep
nasopharyngeal height, and apnea, cor pulmonale and
nasopharyngeal airway sudden death
reduced • Central apnea caused by
• Severe compromise of increased intracranial
nasopharyngeal and hypertension
oropharyngeal space
• Reduced patency of
posterior choanae
• Long floppy soft palate

• Tracheal Cartilaginous Sleeve (TCS)
• Surgical options • Rare
• UPPP • Exclusively in CS syndromes
• Soft palatal split • Fusion of tracheal rings solid
cartilaginous tube
• Adenotonsillectomy
• Makes airway more susceptible to
• LeFort III advancement
obstruction
osteotomy
• “kinking off”
• Tracheostomy • Ineffective cough and poor
mucociliary clearance
• Internal lining more susceptible to
granulation
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11
• Tracheal Cartilaginous Sleeve (TCS) • Tracheal Cartilaginous Sleeve (TCS)
• Rare • Diagnosed by bronchoscopy
• Exclusively in CS syndromes • Associated with increased morbidity
• Fusion of tracheal rings solid and mortality
cartilaginous tube • Longer length sleeves seem to be
• Makes airway more susceptible to associated with shorter life
obstruction expectancies
• “kinking off” • Treatment: tracheal resection
• Ineffective cough and poor
mucociliary clearance
• Internal lining more susceptible to
granulation

• Treatment • Phase I – patients under 6 months
• Involves multidisciplinary team • Respiratory distress
• Craniofacial team including plastic surgeon and otolaryngologist • Intubation, tracheotomy
• Surgeries must be timed appropriately for maximum results • Sleep apnea
• Multiple phases of repair • Central or obstructive
• Needs sleep study
• Central: increased intracranial hypertension
• Poor nutrition
• Nasal obstruction feeding problems
• Nasogastric feeding or gastrostomy tubes

• Phase II – 6-9 months • Phase III – 9 months to 3
• Fronto-orbital advancement years
• Decreasing bitemporal • Additional cranial vault
distance remodelling
• Increasing anteroposterior • Monobloc or craniofacial
dimension of anterior advancement
cranial vault • Advancement of cranium
• Increasing superior orbital and midface
simultaneously
coverage
• Reserved for children with
combined ocular and
respiratory threats
• High complication rate
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12
Craniofacial Syndromes Summary
• Phase IV – 3-5 years • Syndromes = frequent ENT consults
• LeFort III Advancement • The usual problems
Osteotomy
• Improves facial • Hearing
appearance • Speech
• Corrects exorbitism by • Airway
enlarging orbital
cavities • Basic knowledge of common syndromes
• Expands epipharynx • Other hidden major anomalies
• Restores dental
occlusion • Reduce morbidity and mortality
• Reduces symptoms of • Pass some exam questions
OSA
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13
MIDDLE EAR AERATION
OTITIS MEDIA PATHOPHYSIOLOGY
Anatomy of Eustachian Tube
-diff b/w adult and pediatric -

compared to adult, the infant’s tube
is:
-one half adult size -
reaches adult size by age 7
-osseous portion longer
and wider in diameter
-tensor veli palatini muscle
less efficient
-density of elastin in
cartilage is less (not as stiff
therefore more
collapsible), but cartilage
cell density is larger
-volume of Ostmann’s fat
pad is less
-angle:
-adult: 45o in relation to
horizontal plane
-peds: 10o
-mucosal lining:
-continuous with
nasopharynx and middle ear
-characterized as respiratory epithelium - mucociliary clearance
-mucous glands predominate at nasopharyngeal orifice - graded change to a mixture of goblet,
columnar and ciliated cells near tympanum
-folded lining to increase surface area
-mucosa-associated lymphoid tissue present
-muscles of ET:
-tensor veli palatini: active dilatation (innervated by V3)
-levator veli palatini: adds support and contributes to ET function by elevating medial arm of the
cartilage
-salpingopharyngeus: does not appear to have any physiological function
-tensor tympani: does not appear to be involved in the function of the tube
-closure attribute to passive reapproximation of tubal walls by extrinsic forces exerted by

surrounding deformed tissues, by recoil of elastic fibers within tubal wall
Physiology of Eustachian Tube
-function:
-pressure regulation
-protection from NP sound pressure and secretions
-clearance
F.Ling - Eustachian Tube and Otitis Media (1)
663
-surface tension factors
-experiments using surfactants shown to enhance clearance of middle ear and its function
-compared to atmosphere, middle ear is relatively hypoxic and hypercarbic
Pathophysiology of Eustachian Tube
-failure of opening mechanism

-edema and congestion of respiratory mucosa causes narrowing of ET lumen increase in
negative middle-ear pressure, causing influx of bacteria and viruses from nasopharynx
inflammatory response
-aspiration of gas into the middle ear is possible because negative middle-ear pressure develops
slowly as gas is absorbed by the middle-ear mucous membrane
-abnormal patency
-infants anatomically have a shorter ET than adults, which would make reflux more likely to occur
in the infant
-insufflation of nasopharyngeal secretions into the middle ear occurs more readily if the ET is
abnormally distensible
-nonintact middle ear and mastoid system (eg perforation, radical mastoidectomy cavity)
-following radical mastoidectomy, a patent ET could cause troublesome otorrhea
-allergy: relationship not clear; presumed to be related to ET obstruction
-cleft palate
-specific abnormalities
-deficient tensor veli palatini
-timing maturation
-effect of mastoid aeration
Clinical Tests of ET Function
-intact TM
-Valsalva, Politzer tests
-inflation of the eustachian tube and middle ear
from the nasopharynx end of the system by one
of these classic methods is an assessment of tubal
patency only and not function, and failure to
inflate the middle ear does not necessarily
indicate a lack of patency of the eustachian tube.
-Toynbee’s test
-closed nose swallowing
-if negative pressure (even transitory in the
absence of a patulous tube) develops in the
middle ear during closed-nose swallowing,
eustachian tube function can be considered most
likely to be normal
-9-step tympanometric test (see figure)
-non intact TM
-inflation/deflation test
-same principle as 9-step tympanometric test
except measures pressure changes within middle
ear cavity
664
OTITIS MEDIA
Classification
-effusions:
-serous
-mucoid
-purulent
-acute (0-3 weeks)
-subacute (3-12 weeks)
-chronic (> 12 weeks)
-acute otitis media (AOM): fever, irritability, otalgia, hearing loss

-recurrent AOM: > four episodes in a year; > three episodes in 6 months
-otitis media with effusion (OME): effusion behind intact TM
-chronic otitis media with effusion (COME): effusion behind intact TM > 3 months
-chronic suppurative otitis media (CSOM): persistence of purulent otorrhea through perforation or
tympanostomy tube
Epidemiology
-if a child has not had OM before the age of 3 years, he is statistically unlikely to develop severe or
recurrent OM
-highest incidence of AOM for both sexes was in the 6-11 month age group
-mean duration 40 days
-incidence of OME peaks during second year of life, is most prevalent during the winter months, and is
associated with URIs
-resolution of OME after first episode of AOM:
-8 weeks: 80% cleared middle ear
-12 weeks: 90% cleared middle ear
Risk Factors
-anatomic abnormalities (affecting ET function):
-craniofacial anomalies: cleft palate, Apert, Down, mucopolysaccharidoses
-congenital or acquired immunodeficiencies
-hypogammaglobulinemia, IgA deficiency, DiGeorge syndrome, HIV, drug-induced
immunodeficiency
-nasal conditions:
-allergy, nasal obstruction (sinusitis, adenoid hypertrophy, nasal/nasopharyngeal tumours), ciliary
dysfunction, prolonged nasal intubation
-host factors:
-immature/impaired immunology
-familial predisposition
-sex/race
-environmental factors
-day-care attendance
-smoking in households
-other:
-bottle feeding
-reflux
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Microbiology
Bacterial:
-acute (adults)
-non-typable Hemophilus influenzae (20-30%)
-group A streptococci (1-5%)
-acute (neonates and infants)
-non typable Hemophilus influenzae (20-30%)
-Staph. aureus, group B streptococci, gram negative enteric pathogens (up to 20%)
-chronic suppurative
-P.aeruginosa
-S.aureus
-corynebacterium
-Klebsiella pneumonia
-anaerobes: peptostrptococcus, fusobacterium, propionibacterium acnes, bacteroides
-persistent effusion
-S.pneumoniae, H.flu, M.catarrhalis, group A strp in 30-50%
-resistance:
-Beta lactamase:
-30% H.flu
-100% M.catarrhalis
-pneumococcal resistance
-chromosomal alterations lead to decrease in penicillin binding proteins and increasing
resistance to sulfa, chloramphenicol, tetracycline, and TMP
-risk factors to resistance:
-multiple and prolonged courses
-not taking entire prescribed course
-inappropriate administration
Viral
-RSV, rhinovirus, influenza, adenovirus, enterovirus, parainfluenza virus
-may potentiate possibility of nasopharyngeal colonization with bacteria
-found in 17% of AOM
-bacteria and viruses in 9%
Diagnosis
-audiometry:
-< 6 months: ABR
-6 months to 1 year: behavioural observation audiometry (BOA)
-1-2 years: visual reinforcement audiometry (VRA)
-2-5 years: Play audiometry
-over 5 years: conventional audiometry
-tympanometry
-tympanoscentesis (indications)
-neonate (< 4 weeks) with otitis media; fever of unknown origin
-immunocompromised
-guide treatment in the presence of highly resistant organisms
-relief of acute pain not responding to analgesics
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Management
-"watch and wait"
-treat with antibiotics if:
-< 24 months (increased risk for developing meningitis)
-immunocompromised
-systemic symptoms or complications
-TM perforation with otorrhea
-temperature > 38.5oC
-otherwise treat symptomatically with analgesia (tylenol) for 48-72 hours, providing adequate
follow-up assured
-treat with antibiotics after 48-72 hours if worse or not better
-recurrent OM:
a) those who clear fluid between each infection
-antibiotic treatment for each separated episode
-prolonged prophylactic antibiotic (falling out of favour because of resistance)
-M+T
b) those with persistent effusions: (see COME section)
-antibiotics, pneumococcal resistance
-amoxicillin first line agent for a first episode of OM
-10 day treatment with follow-up in 2-4 weeks
-tubes
-indications:
-treatment of recurrent AOM unresponsive to medical therapy
-chronic OM with bilateral persistent effusion greater than 3 months and conductive
hearing loss
-negative middle-ear pressure with impending cholesteatoma
-intervention in the presence of complications of OM
-complications:
-risk of TM perforation:
-1-2% first set
-2-3% second set
-in place for > 2 years risk is 8-10%
-adenoidectomy
-results of studies evaluating efficacy of adenoidectomy in preventing or decreasing middle-ear
disease vary widely
-Prevnar:
-heptavalent pneumococcal vaccine
-reduced otitis visits by 7.8% and antibiotic prescriptions by 5.7%
-10% reduction in OM in the risk of 3 visits within 6 month period
-26% reduction in the risk of 10 visits within 6 month period
-tube placements reduced by 24%
-lack of evidence for other strategies such as decongestants/antihistamines, mucolytics, allergy therapy, ET
inflation, xylitol chewing gum, Valsalva’s manoeuvre etc..
COME
-persistent MEE present for > 3 months, hearing evaluation and possible surgical intervention should be
considered
-medical/surgical management
-treatment if fluid present > 3 months and:
-disease is bilateral, very symptomatic and associated with significant conductive hearing
loss
667
-significant TM changes such as deep retraction pockets or middle-ear changes such as
adhesive otitis or ossicular involvement
Complications
-CHL
-perforation
-tympanosclerosis
-describe pathology
-Tympanosclerosis is thought to be a complication of otitis media in which acellular
hyalin and calcified deposits accumulate within the tympanic membrane and the
submucosa middle ear. In most patients, these plaques are clinically insignificant and
cause little or no hearing impairment. Tympanosclerotic plaques within the tympanic
membrane appear as a semicircular crescent or horseshoe-shaped white plaque within the
tympanic membrane
-cholesteatoma
-cholesterol granuloma
-adhesive OM
-labyrinthitis
-facial paralysis
-acute mastoiditis
-petrositits (Grandenigo’s syndrome)
-meningitis
-sigmoid sinus thrombosis
-extradural abscess
-brain abscess
-otic hydrocephalus
668
CLEFT PALATE REPAIR
-Goals:
-separation of the nasal and oral cavities
-construction of a watertight and airtight velopharyngeal valve
-preservation of facial growth
-development of aesthetic dentition and functional occlusion
-Timing:
-controversial
-advantages: providing normal speech; better result with velopharyngeal competence the earlier the repair
-disadvantages: surgical effect on facial growth and dental occlusion
-most centers complete palate closure by 18 months of age if not by 12 months

-equally effective results may be obtained by dental obturation
-for children 3-4 years of age
-Palatoplasty techniques
-important to reconstruct muscular sling improves subsequent palatal and eustachian tube function
Schweckendiek’s technique
-primary veloplasty
-closure of only the soft palate cleft
-incisions are made in the soft palate, muscle bundles
are dissected, a levator sling is reconstructed, and the
soft palate is closed.
-usually performed at age 3 to 12 months
-delayed closure of the hard palate at a later date
-advantages:
-construction of a velopharyngeal valve at an
early age
-minimal disturbance in future facial growth
-disadvantages:
-necessity of an additional operative procedure
and hospitalization
-required dental prosthesis
-technique is rarely indicated.
Von Langenbeck’s palatoplasty

-bipedicle mucoperiosteal flaps of the hard and soft palate for repair of the defect
-anteriorly and posteriorly based bipedicle flaps are
advanced medially to close the palatal cleft
-advantages:
-easy technique to perform
-disadvantages:
-failure to provide any additional palatal length
-inability to close complete clefts of the primary
and secondary palate
-poorer speech in more extensive palatal clefts
669
V-Y push-back
-Oxford method
-creation of two posteriorly based unipedicle flaps
with single or double (depending on the extent of
the cleft),anteriorly based, unipedicle, palatal flaps
-anterior flaps are advanced or rotated medially,
and the posterior flaps are retrodisplaced ith a V to
Y technique
-increases length of the reconstructed palate
-advantages:
-lengthening of palate
-improved speech resulting in more extensive palatal clefts than those obtained by Von
Langenbeck’s method
-disadvantages:
-failure to provide mucosal coverage of the retrodisplaced palate’s nasal surface reduces the
palatal lengthening obtained in the final result secondary to scar contracture of the raw nasal
surface
-difficulty of closing the cleft’s alveolar portion
-fistulas in the thin mucoperiosteal membrane near the hard/soft palate junction
Furlow’s palatoplasty
-double reversing Z-plasty operation
A to E, Furlow palatoplasty.
A Two mirror-image Z-plasties are drawn with the cleft as their central limbs.
B The oral-side Z-plasty flaps are elevated with the levator-palatopharyngeus muscle in the posteriorly based flap. Only the
mucosa is elevated in the anteriorly based flap.
C The nasal flaps are elevated with the remaining muscle in the posteriorly based flap.
D, E Transposing the two sets of flaps overlaps the palatal muscles and lengthens the soft palate
-lengthens the velum and creates a functional levator muscle sling

-technically difficult to perform in wide clefts
-four triangular flaps are created.
-speech appears to be good, and the results in 2- to 3-year-old submucous cleft palate children with
velopharyngeal insufficiency are encouraging.
Two-flap palatoplasty
-creation of two posteriorly unipedicle-based flaps that
extend to the alveolar portion of the cleft
-these flaps are rotated and advanced medially to
reconstruct the defect
-does not allow closure of the alveolar cleft or lengthen
the palate unless a Z-plasty is used in the soft palate
670
-technique:
-a single mucoperiosteal flap is elevated from each palatal shelf
-flap is based posteriorly on the descending palatine artery
-palate is closed in three layers:
-nasal layer by a vomer mucoperiosteal flap to a palatal mucoperiosteal flap and velar
mucosa posteriorly
-palatal muscles are carefully approximated
-oral mucosa into close approximation
Complications
-most common complication of palatoplasty is hypernasal speech
-up to 30% to 40% of cleft patients
-fistula formation reportedly occurred in up to 21% of patients after palatoplasty
-anteriorly on the lingual surface of the maxillary alveolus and posteriorly at the hard/soft palate
junction
671
NON-GENETIC HEARING LOSS
INFECTIONS
Congenital CMV Infection

-CMV affects ~1% of live newborns
-only 10% exhibit signs of CMV inclusion disease:
-mental retardation
-severe to profound hearing loss
-ocular problems (eg. chorioretinitis with optic atrophy)
-other: language or learning disabilities, cerebral palsy, HSM, jaundice, microcephaly, growth
retardation
-15% who are asymptomatic at birth most commonly develop progressive bilateral SNHL
-onset after 1st year of life
-essentially all infants with symptomatic congenital CMV are products of pregnancies involving primary
maternal infection
-investigations to determine prenatally infected newborns are difficult because perinatally infected infants
commence excreting virus as early as 3 to 12 weeks
Congenital Toxoplasmosis
-cats are primary reservoirs
-HL occurs in ~25% of untreated cases
-diagnosis by detecting specific antibodies in serum, plasma, SSF and intraocular fluid
-intensive therapeutic intervention with primarily infected expectant mothers and postnatal treatment of
congenitally infected infants minimizes fetal damage and may prevent the emergence of sensory deficits
Congenital Syphillis
-classic picture:
-SNHL, interstitial keratitis, Hutchinson’s teeth (notched incisors), nasal septal perforation
-positive fistula test (Hennebert’s sign)
-Tullio’s phenomenon: disequilibrium in the presence of loud sounds
-otosyphilitic SNHL in children varies in severity and assumes bilateral flat configuration
-HL may be sudden in onset
-speech discrimination disproportionately impaired compared to pure tones
-dx: fluorescent treponema antibody absorption test; may remain positive after treatment
-tx:
-parenteral penicillin
-conjunctive steroids help stabilize or improve auditory acuity in ~50% of otosyphilitic patients
Rubella
-SNHL, congenital heart defects, ocular defects, microcephaly, HSM, thrombocytopenia, mental or motor
retardation, interstitial pneumonitis, encephalitis, low birth weight
-second-trimester rubella resulted in deafness
-midfrequency SNHL from moderate to severe
-25% demonstrated progressive loss over time
-immunization has eradicated rubella in developed world
Measles and Mumps

-vaccines have decreased incidence of these infections
-unilateral profound SNHL w/o vestibular symptoms mos common auditory sequelae of mumps
F.Ling - Non-Genetic Hearing Loss (1)
672
Herpes Simplex Encephalitis
-primary maternal genital herpes infection during pregnancy may result in spontaneous abortion, premature
labor, CNS damage or IUGR
-fetal infection occurs transplancentally or via an ascending route from infected genitalia
-associated SNHL in encephalitis attributed to CNS mechanisms
-tx: intensive antiviral drugs for infant infected with herpes simplex virus
Bacterial Meningitis
-HL generally appears early in clinical course child with meningitis who exhibits a normal ABR after
first few days of antibiotic therapy is unlikely to develop SNHL later
TOXIC DRUGS AND CHEMICALS
Aminoglycosides
-vestibulotoxic: streptomycin
-cochleotoxic: amikacin, kanamycin, neomycin
-gentamicin: vestibulotoxic in 2/3; cochleotoxic in 1/3
-pathogenesis:
-cause outer hair cell degeneration initially, with later inner hair cell damage commencing at basal
cochlear coil an proceeding apically
-synergistic effect with loop diuretics
-in preterm infants, complicated perinatal course and prolonged or high-dose aminoglycoside treatment
enhances risk of ototoxicity
Loop diuretics
-used to treat bronchopulmonary dysplasia
-can have prolonged effects in low birth weight infants
-effects generally rapid in onset and quickly reversible with furosemide
Retinoids
-treatment of severe recalcitrant cystic acne
-cause malformations in embryos
Antimalarials
-quinine and chloroquinine have ototoxic potential
-varying degrees of severe to profound SNHL
Cisplatin
-produces high-frequency SNHL, tinnitus, peripheral neuropathy, and dose-related renal insufficiency
-careful audiologic monitoring is indicated when dosage levels of 400 mg/m2 or greater are reached
HYPOXIA AND ANOXIA

-associated with increased rates of SNHL
-neonatal risk indicators:
-acidosis, meconium staining, primary apnea, resuscitation at birth, history of prolonged
ventilatory assistance
HYPERBILIRUBINEMIA
-elevated bilirubin crossing BBB deposits in basal ganglia (ie. ventrocochlear nucleus) SNHL
-treatment with fluorescent lighting or exchange transfusion
673
RECURRENT OTITIS MEDIA AND MASTOID DISEASE
NEONATAL INTENSIVE CARE

-premature infants (bw < 2500 g) experience 20 fold increased risk for SNHL
EAR OR TEMPORAL BONE TRAUMA

-see temporal bone fractures
PERILYMPHATIC FISTULA
-discontinuity in bony or membranous enclosure that normally surrounds perilymphatic spaces of inner ear
can produce fistula
-risk factors:
-ear surgery, head or ear trauma, noise trauma, barotrauma, significant physical exertion, cranial
or inner ear anomalies, ossicular or middle ear deformities
-symptoms:
-aural fullness, sudden fluctuating or progressive SNHL, fluctuating speech discrimination scores,
roaring tinnitus, balance disturbances
-exacerbated by nose blowing, straining, Valsalva manoeuver, ET dysfunction or physical exertion
-fistula test:
-apply negative and positive pressure to EAC while monitoring of nystagmus
-helpful if positive, but inconclusive if negative
-surgical exploration may not yield a definitive diagnosis
NOISE-INDUCED HEARING LOSS
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PEDIATRIC TRACHEOTOMY DECANNULATION
-adults and children with very short-duration tracheotomy (less than 1 month) can be decannulated by removing the
tube and covering the stoma with an occlusive dressing
-most children, are more difficult to decannulate because of many factors, including suprastomal collapse and
granulation, the relative size of the airway, and possibly psychologic attachment to the tracheotomy tube
-a more controlled process, ward decannulation, is used in these children
Ward Decannulation
-recent endoscopy with suprastomal granulation removal required
-suprastomal collapse should be excluded
-tracheotomy tube is downsized in a controlled stepwise manner, usually one size smaller each day
-child should be kept on the ward and carefully observed at night
-once smallest tracheotomy tube has been tolerated, tracheotomy tube can be blocked for 12 hours during
the day and for 24 hours the next day and night
-tube can be safely removed and stoma covered, although the child still needs to be kept on the ward for
observation for about 5 days
-it this approach fails, the child needs to undergo endoscopy again to exclude cord fixation, cord palsy,
stomal granuloma, stomal collapse, and tracheomalacia
Surgical Decannulation
-endoscopy before decannulation shows significant suprastomal collapse
-entails formal closure of the stoma, sometimes with additional support from cartilage, is followed by
intubation
-tracheocutaneous fistula is excised preserving the tracheal wall unless a cartilage graft is required
-if cartilage is not required (mild to moderate collapse only), the stoma is closed and sutured laterally to the
sternomastoid to prevent collapse of the repair
-if cartilage is required, it is harvested from a rib and carved to a boat shape as for laryngotracheal
reconstruction
-postoperatively, the patient is intubated for 24 to 48 hours
F.Ling - Tracheotomy Decannulation (1)
675
SENSORINEURAL HEARING LOSS
-Screening for SNHL in :

1. Family history of hereditary childhood SNHL
2. In utero infection, such as cytomegalovirus (CMV), rubella, syphilis, herpes, and toxoplasmosis
3. Craniofacial anomalies, including those with morphologic abnormalities of the pinna and ear canal
4. Birth weight less than 1500 g (3.3 lbs)
5. Hyperbilirubinemia at a serum level requiring exchange transfusion
6. Ototoxic drugs including but not limited to aminoglycosides used in multiple courses or in combination
with loop diuretics
7. Bacterial meningitis
8. Apgar scores of 0 to 4 at 1 min or 0 to 6 at 5 min
9. Mechanical ventilation lasting 5 days or longer
10. Stigmata or other findings associated with a syndrome known to include an SNHL or conductive
hearing loss
-most common prenatal cause of hearing loss is intrauterine infection (CMV)

-common causes of perinatal hearing loss: hypoxia, hyperbilirubinemia, infection, medication toxicity
-most common postnatal cause of hearing loss: meningitis
F.Ling - Sensorineural Hearing Loss (1)
676
EVALUATION OF THE HEARING-IMPAIRED CHILD
-requires multispecialty team

-history:
-detailed prenatal, birth, and postnatal history
-TORCH infections
-gestational age, birth weight, IUGR, APGAR scores
-perinatal infections
-hyperbilirubinemia
-ICU admission
-PMHx:
-meningitis
-head trauma
-ototoxic medications
-development
-school performance
-complete family history
-hearing loss; speech or language disorders; ear, nose, and throat disorders; craniofacial
deformities; and such syndromic features as kidney disorders, sudden death at a young
age, thyroid disease, intracranial tumors, progressive blindness, and café au lait spots
-physical examination:
-ear examination
-search for subtle findings (e.g., preauricular or branchial pits, heterochromia irides, blue sclerae,
dystopia canthorum, facial asymmetry, café au lait spots)
-investigations:
-CBC: -acute myelogenous leukemia
-FT-Abs -syphilis
-thyroid function -Pendred
-lipid profile -hyperlipidemia
-glucose -diabetes
-urinalysis/BUN/Cr -Alports
-ECG -Jervell and Lange-Nielsen
-serologic tests -CMV, rubella, toxoplasmosis
-ESR, ANA, RF -autoimmune disease/vasculitis
-69-kD inner ear antigen -autoimmune disease
-CT temporal bones -EVA, Michel, Mondini
-ophthalmology -early detection of coexisting retinitis pigmentosa with
electroretinography
-Usher (RP)
-Cogan’s (IK)
-connexin 26, 30
-audiology:
determine the type of hearing loss (i.e., conductive, sensorineural, or mixed); degree of
loss (i.e., mild, moderate, severe, profound, and anacusic); the audiometric configuration
and symmetry of the impairment; and finally, with serial assessment, the stability or
progression of the loss.
A diligent search for etiology of SNHL in a child using state of the art techniques will prove inconclusive
in 30% to 40% of cases
F.Ling - Sensorineural Hearing Loss (2)
677
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The first 8 weeks constitutes the period of greatest embryonic development of the
head and neck.
There are 5 arches (pharyngeal or branchial). Btw these arches are the clefts
externally and the pouches internally.
Each pouch has a ventral or dorsal wing.
The derivatives of arches are usually mesoderm origin.
The cleft is lined by ectoderm, the pouch is lined by endoderm
The adenoids are colonized with bacteria soon after birth, enlarge early and middle
childhood form antigenic challenges and should regress by early adulthood.
Hypertrophic tonsils are rare in adults and suggest chronic infection or lymphoma.
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The tonsil is nestled in a fossa formed by the muscular anterior and posterior
tonsillar pillars (palatoglossus and palatopharyngeus) and lying superficial to the
superior constrictor muscle; preservation of these muscular condensations and the
overlying mucosa is critical to maintaining physiologic function of the palate
postoperatively.
The tonsil is contiguous inferiorly with the lingual tonsil. The point of attachment
(plica triangularis) must be transected during tonsillectomy. In pts with marked
hypertrophy, this extension is freq quite large and can result in troublesome
bleeding at the pt of transection at the base of the tongue.
The adenoid is positioned in the midline of the posterior wall of the NP immediately
inferior to the rostrum of the sphenoid and extending laterally to but not onto the
lateral wall of the NP. It makes up the most rostral portion of the pharyngeal
lymphoid tissue termed Waldeyer’s ring. The space created lateral to the adenoid
and posteromedial to the ET orifice is termed the FOSSA of Rosenmuller.
Gerlach’s tonsil is lymphoid tissue within lip of the fossa of Rosenmuller; goes into
ET.
Inferiorly, the adenoid extends nearly to the superior margin of the superior
constrictor…Passavant’s ridge.
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Tonsillar branch of the facial artery is the main supply of the entire tonsil.
Facial artery:
• Tonsillar art
• Ascending palatine art
Lingual art
•dorsal lingual branch
IMA
• Desceding palatine
• Greater palatine
Ascending pharyngeal (ECA)
Venous drainage of the tonsil is thru lingual and pharyngeal veins which empty into
the IJ.
In most people the ICA lies 2cm posterolateral to the deep surface of the tonsil;
however in 1% of the population, it is found just deep to the superior constrictor.
Adenoids: Ascending palatine, ascending phayrngeal, pharyngeal br of IMA,
ascending cervical branch of thyrocervical trunk
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The luminal surface of the tonsil is covered by stratified squamous epithelium (E)
which deeply invaginates the tonsil; the base of the tonsil is separated from
underlying muscle by a dense collagenous hemi-capsule (Cap). The parenchyma
contains numerous lymphoid follicles (F) dispersed just beneath the epithelium of
the crypts.
The surface of the adenoids differs from the tonsils in that the adenoids have deep
folds and few crypts , while the tonsils have from 10-30 crypts and the surface of
the adenoids is composed of ciliated pseudostratified columnar epithelium which
functions in mucociliary clearance. With chronic infection, this layer is thinned,
resulting in stasis of secretions and increased exposure of the tissue to antigenic
stimuli. Deep to the surface epithelium lies a stratified squamous layer followed by
a transitional layer. The SS layer thickens with chronic infection. The transitional
layer is responsible for antigen processing.
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1. MC bacteria:
Beta streptoccoci, staphylococci, streptoccocus pneumoniae, hemophilus
2. Prevalence of beta-lactamase producing organisms is rising:
from 2 % in 1980 to 44% in 1989 (FIND STUDY)
3. Prevalence of anaerobic org is also rising
Asymptomatic streptococcal pharyngitis responsible for at least 1/3 of ARF in 3rd
world. Gold std is throat culture.
Blood agar plate with septra more sensitive than plain agar plate.
Culture both tonsils; if only one, may miss 25%.
Rapid streptococcal antigen test, 12 min.; highly specific but variable sensitivity;
must confirm negative result with a throat cx.
• Newer solid-phase enzyme immunoassay
• Older latex agglutination test
Treat with 10 day course of PCN if high clinical suspicion (augmentin, clinda, pcn +
rifampin for recurrence)
Post treatment culture: high risk RF, remain symptomatic, recurring symptoms; if
asymptomatic but positive cx, treat if h/o RF or if FH of RF
Suspect infectious mononucleosis if sore throat and malaise persist despite abx
treatment; order WBC and Paul-Bunnell. Characterized by white membrane
covering one or both tonsils and hypersensitivity to ampicillin. Look for atypical
mononuclear cells and positive Paul-Bunnell blood test.
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Core species do not always correlate with surface bacteria. 90% correlation with
H.influenza, 73% strept pyogenes
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Yellow spicules due to hyperkearatineized areas of epithelium are sometimes

extensive over the tonsil. It is important to probe the tonsil to be certain these areas
are not exudate. No treatment is required unless assoc with tonsillitis.
Tonsilloliths are yellow gritty particles in crypts, more commonly seen in adults
with a h/o recurrent tonsillitis.
Elongated styloid process causes pain exacerbated during maximal deglutition and
deep breathing…. 2nd branchial arch derivitative, approx 2.5 cm long, located btw
internal and ECA just lateral to tonsillar fossa.
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Diagnosis of OSA is based on H & P (snoring, restless sleep, FTT, daytime

symptoms… poor mentation, decreased attn span, poor scholastic performance,
dysphagia, nocturnal enuresis, chronic mouth breathing; predisposing conditions
craniofacial abnormalities, NM disorders, FTT, cor pulmonale, Downs syndrome)
MC symptom in kids is snoring (adults is daytime somnolence).
Obtain sleep study when PE does not correlate with history ($1600), or when
suspect central component.
Apnea (10s breathing pause)from complete obstruction is uncommon in children.
Children tend to have a continuous partial obstructive hypoventilation that is
characterized by decreased oxygen saturation, hypercapnia, labored paradoxical resp
efforts, and snoring.
Controversy over how to interpret sleep study in kids… few normative data.
Marcus et al.(1992) studied normal resp patterns in children during sleep.
Abnormal values: >1 obstructive apnea of any duration per hour
central apnea assoc with desat <90%
Pco2>53 or Pco2>45 for more than 60% test time
fall of o2 sat < 92%
No consensus on indications for surgery for those without severe obstruction/apnea.
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Apparent: tonsil sits in more medial position, displacement medially by PTA or

parapharyngeal space mass.
Chronic infections: tubercular tonsillitis, actinomycosis, and congenital syphilis
Congenital include teratoma, hemangioma, lymphangioma, and cystic hygroma.
Neoplastic:
Benign papillomas
Lymphoma (usually non-Hodgkins B-cell) and squamous cell
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Instability is caused by laxity of transverse ligament.

Neck pain, muscular problems.
Hyperactive DTR, clonus
atlas-dens interval > 4.5mm
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Von Willebrand’s disease is the most common inherited coagulopathy (AD with
variable expression) (1% population) and is caused by a deficiency in Factor
VIII:VW complex necessary in platelet activation. 3 types… type 1 is the most
common (80-90%) with subnormal levels of qualitatively normal vWF and most
will respond to desmopressin. Type 2 is a defect in the factor, type 3 is complete
absence of the factor.
DX elevated PTT, BT, decreased vWF antigen, factor VIII procoagulant activity,
ristocetin cofactor activity; measure response of levels to desmopressin
(0.3microg/kg IV)
RX give IV over 30 min preop (peak levels 45-60 min), 12 hr postop, then q am
until eschar completely sloughed and fossae completely healed; also give
aminocaproic acid or tranexamic acid preop and postop to decrease fibrinolysis (oral
cavity high conc of fibrinolytic enzymes); not useful type 2/3
adverse effects… Na <132 or tachyphylaxis, d/c desmopressin, give cryoprepipitate
or vWF-containing antihemophilic factor
ITP:
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From 1971-1994 the Children’s Hospital of Pittsburgh conducted parallel

randomized and nonrandomized clinical trials to determine
1. efficacy of tonsillectomy in reducing the frequency and severity of episodes of
pharyngitis,
2. the efficacy of adenoidectomy in reducing the freq/severity of OM, and
3. the effect of adenoidectomy of the course of nasal obstruction due to large
adenoids
Findings:
1. Histories of recurrent throat infections that are undocumented do not validly
predict recurrence; need documentation by physician before performing
tonsillectomy
2. Using the selection criteria, the incidence of throat infection during the first 2
years of f/u was significantly lower in the surgical groups
3. Many pts in the nonsurgical group had fewer than 3 episodes of infx, and most
cases were mild… therefore, treatment should be individualized, taking into
consideration pt/parental preference, anxieties, tolerance of illness, tolerance of
antimicrobial drugs, child’s school performance in relation to illness-related
absence, accessability of health-care services, out-of-pocket costs, nature of
available anesthetic and surgical services/facilities
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Contraindications:
Tonsillectomy
Acute infection
Anemia
Disorders of hemostasis
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Mortality 1 in 16,000 to 35,000 (anesthetic and hemorrhage); Hemorrhage 0.1-

8.1%; 76% occur within first 6 hrs; 0.04% require transfusion; 0.002% mortality
(mc for primary); Etiology: retained adenoid tissue, damage to post pharyngeal wall
muscle; Increased incidence winter, age > 20
Anesthetic: kinking, extubation, fire, laryngospasm
Resp compromise: sudden loss of PEEP… pulmonary edema; avoid sedating
analgesics
Assess for loose teeth… post op CXR to r/o aspiration if loss of tooth
Draping to avoid burns… avoid towel clips (penetration); avoid tape (accidental
extubation when take drapes off)
Sore throat: increased with increased age, electrocautery, KTP/ less with CO2 lasere
and periop/postop antibiotics (4.4 to 3.3 days)
Otalgia: referred from IX, r/o otitis, ET tube injury or edema
Fever: normal in 1st 36 hr… watch for dehydration
Dehydration: n/v 2nd to anesth, swallowed blood; decreased po intake with pain,
esp younger kids less cooperative and smaller volume reserve; single intraoperative
steroid earlier return to nl diet
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VPI: usu transient; sig in 1 in 1500-3000; only 1/3 identified preop as increased risk;
> 2mo speech therapy; > 6-12mo pharyngeal flap
NP stenosis: circumferential contracture of pharynx Waldeyer’s ring, T AND A;
syphilis; increased risk with excessive mucosal excision; difficult to rx
AA subluxation.. Grisel’s syndrome vertebral body decalcification and laxity of
anterior transverse ligament secondary to infection in the nasopharynx… may cause
spontaneous subluxation 1 week postoperatively…pain and torticollis (traumatic
adenoidectomy or injection of local anesthestic into prevertebral space)
15-28% tonsil tags; 6% recurrent pharyngitis
adenoids may grow from adjacent lymphoid tissue… incomplete removal?
Laceration of ICA usu occurs medially and near the skull base.
Pseudoanerusym of ICA requires embolization and proximal ligation.
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Anesthetic induction is hazardous…. Hypovolemic, underestimated blood loss (T

&C). Risk of aspiration, stomach full of swallowed blood… tracheotomy if active
hemorrhage prevents intubation.
ECA ligation via lateral neck incision, retraction of SCM posteriorly if unable to
stop bleeding.
Angiography if ECA ligation fails…

ICA and ECA communicate via opthalmic/angular nasal arteries and via middle
meningeal artery
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Paradise:
Parallel randomized and nonrandomized clinical trials of
213 children who developed recurrence of OM after extrusion of t-tubes;
In both trials, over a period of 2 years, 28-35% fewer episodes than controls.
Gates: 578 children with chronic middle ear effusion. Adenoidectomy combined
with myringotomy or with t tube placement proved to be more effective thatn
myringotomy or tube placement alone in preventing recurrences of OM over a 2
year period
* differences were small (31 vs 36 weeks as mean cumulative times with effusion in
2 treatment groups over 2 yr f/u).
TT surgery alone is assoc with higher rate of repeat surgeries, increased rate of
otorrhea, greater expense and human cost of illness than initial adenoidectomy and
myringotomy
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Contraindications:
Adenoidectomy
Overt or submucous CP
Neurologic or neuromuscular abnormalities with impaired palatal function
Anemia
Disorders of hemostasis
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Submucous cp 1 in 1200
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59
Carotid Body Tumours
Introduction:
-Paraganglionic tissue of the head and neck:
-embryologically derived from the neural crest
-develops in the paravertebral region in association with arterial vessels and cranial nerves
-associated with the autonomic nervous system
-Glenner and Grimley classification (based on location):
-branchiomeric
-intravagal
-aorticosympathetic
-visceroautonomic
The Carotid Body:

-Von Haller in 1743
-Embryology:
-derived from mesodermal elements of the third branchial arch and neural elements originating from the
neural crest ectoderm
-Location:
-bifurcation of the common carotid artery, on the adventitia of the posterior medial side of the ECA
-fibrous capsule attached to bifurcation by Mayer’s ligament
-Size: 5x 3x 1.5 mm
-Blood supply: external carotid artery
-Nerve supply: glossopharyngeal nerve (DeCastro, 1928)
-Function:
-regulation of pulmonary ventilation
-monitors and responds to changes in blood oxygen, CO2, and pH levels
-afferent input from the glossopharyngeal nerve producing sympathetic stimulation to the medullary
reticular formation
-hypoxia, hypercapnia and acidosis tidal volume and respiratory rate and sympathetic tone
Tumours of the paraganglia:

-Various terms:
-non-chromaffin paragangliomas - they do contain catecholamines
-glomus tumours - true glomus tumours are mainly located in the skin and superficial soft tissues of the
extremities
-chemodectoma - no chemoreceptor function is known for these tumours
-Carotid body paragangliomas:
-most common tumours of head and neck paraganglia (60% to 67% of the total)
-rare lesions, only 1000 reported cases in the literature by 1990
Epidemiology:
-incidence less than 0.02%
-same frequency in male and female patients
-occur in all ages
-primarily occur in the fifth decade of life (45 to 50 years)
-greater incidence of carotid body tumours in:
-people who live at high altitudes
-higher predilection for female patients (8.3:1 vs 2:1)
-chronic hypoxia
-two forms of the disease:
1. Sporadic (~90%):
-5% incidence of bilateral carotid tumours
2. Familial (~10%):
737
-autosomal-dominant pattern
-32% incidence of bilateral tumours
-often associated with other paragangliomas (ie. glomus jugulare, glomus vagile)
Other Associations:
-medullary carcinomas of the thyroid
-neurofibromatosis
-parathyroid adenomas and hyperplasia
-suggests that such an association may represent another variable expression of the MEN syndrome
-Carney’s triad:
-extra-adrenal paraganglioma, gastric leiomyosarcoma, pulmonary chondroma
-rare and occurs predominantly in young girls
Pathology:
-grossly tumours vary from 2.0 to 9.0 cm with most being approximately 4.0 cm
-composed of nests of epithelial cells arranged in clusters : Zellballen
-two receptor cell types:
1. Chief cells (type I, epithelioid cells)
-contain 60-300 catecholamine-bound neurosecretory granules
2. Sustentacular cells (type II, supporting cells)
-more concentrated on the peripheral aspect of cell clusters
-devoid of neurosecretory granules
-cell clusters encased in a network of myelinated nerve fibers mixed with a rich vascular plexus
-lack a true capsule
Clinical presentation:
-palpable neck mass:
-most common presenting symptom
-often asymptomatic
-long history: average of 2 to 8 years; some for as long as 47 years
-others (fewer than 30% in one series)
-due to size of mass:
-neck pain/discomfort, dysphagia, dyspnea
-due to involvement of cranial nerves
-hoarseness (vagus), dysphagia (vagus), tongue weakness (hypoglossal)
-dizziness and hearing loss have been reported
-Horner’s syndrome (sympathetic chain): rare
-few documented cases presenting with cerebral ischemia
-functional tumours: secretion of catecholamines
-only 12 cases of functional CBT reported in the literature
-can produce paroxysmal hypertension mimicking pheochromocytoma:
-palpitations, flushing, dizziness, syncope, hypertension, fever
-preoperative administration of alpha-blockers and the intraoperative use of propranolol for beta-adrenergic
blockade have been advocated in the prevention of cardiovascular complications during the induction of
anesthesia and surgery
-on examination:
-mass located below the angle of the jaw deep to SCM
-sign of Fontaine: laterally mobile but vertically fixed - not that helpful
-may be pulsatile - bruit is infrequent
Differential diagnosis:
-branchial cleft cyst, carotid artery aneurysm, primary or metastatic carcinoma, enlarge lymph node, parotid gland
tumour, thyroid tumour
738
Natural History:
-tend to grow relentlessly if not resected
-slow growth at a rate of ~ 0.5 cm per year (2.5 cm in five years)
-no cases of spontaneous resolution have ever been reported
-without resection, 75% asymptomatic patient will eventually develop symptoms
-inferiorly, the fascia of the carotid sheath tends to restrict growth
-superiorly, there is no restriction
-extension to skull base infiltration of CNS
-medially and anteriorly:
-displacement or encasement of vagus, hypoglossal, or sympathetic chain by tumour
-incidence of cranial nerve involvement up to 20% (usually vagal or hypoglossal nerves)
-death can occur either from metastatic disease or from progressive growth:
-from strangulation or through intracranial extension and cranial neuropathies
-some have reported a 30% mortality from untreated, or inadequately resected carotid body tumours
Malignancy:
-literature ranges from 2.6% to 50%
-overestimated rate:
-histological appearance (based on nuclear atypia, nuclear to cytoplasmic ratio) does not correlate with
growth behaviour
-only admissible criteria for malignancy is the presence of distant metastases
-rate considered to be approximately 2 to 5% - most likely less than 3%
-commonly to regional lymph nodes
-also to brachial plexus, cerebellum, lungs, bone, abdomen, pancreas, thyroid, kidney, breast
-long survivals with disseminated disease are seen
eg. patient with spinal metastasis living for decades
Diagnosis and Investigations:

-absolutely no open biopsy should be done
a) Complete bilateral cerebral angiography

-enhancing oval mass widening the angle of the bifurcation with displacement of the internal and external
carotid arteries: essentially pathognomonic of CBT
-blood supply:
-primarily from bifurcation and external carotid artery
-contributions from internal carotid artery, vertebral artery and thyrocervical trunk also
occurs
-advantages:
1. knowledge of blood supply aids in exposure and hemostasis
2. extent of tumour blush will also indicate the cephalic extent of the tumour and help in
planning surgical exposure and approach
3. evaluation of concurrent atherosclerosis and collateral flow
4. identification of multicentric paragangliomas of the contralateral carotid body
5. essentially 100% accurate
-was historically used to diagnose the tumour and detect bilateral or multiple paragangliomas, its current
role is primarily limited to the evaluation of tumours with indeterminate MR or CT findings, or to provide
access for preoperative embolization
b) Contrast-enhanced CT
-well marginated, ovoid mass which splays the internal and external carotid arteries at the level of the
bifurcation and demonstrates intense homogeneous enhancement following the IV administration of
iodinated contrast.
-useful in demonstrating the lateral and medial extent of the tumour
-useful in accurately estimating size
739
c) Intravenous digital subtraction angiography
-safer than conventional angiography
-generally does not provide the same detail
d) Ultrasonography (colour flow doppler)

-non-invasive diagnostic test
-highly vascularized, well-delineated mass spreading the carotid bifurcation
-can be well-differentiated from avascular or hypovasuclar masses
-Muhm (Arch Surg 1997; 132:279-284):
-considered the first imaging procedure to be used in patients with suspected carotid body tumours
because it is a noninvasive method of high sensitivity and specifity.
-most useful screening test both in sporadic and familial cases for early detection and diagnostic
confirmation of the presence of CBTs
e) MRI
-signal voids: “salt and pepper” appearance due to highly vascularized parts with a fast blood flow
-better show the relation of the tumor to the adjacent internal jugular vein and carotid artery
-avoidance of ionizing radiation and iodinated contrast media
d) MRA
-direct vascular imaging showing the displacement of the carotid arteries, the vessels afferent to the mass
and the highly vascular tumor
-no exogenous contrast is administered
-spatial resolution of MR angiography is typically less than that of conventional angiography
-only the larger, more rapidly flowing feeding vessels will be identified extending to the tumour
-the lack of “tumour blush” on MRA is the norm rather than the exception, and should not exclude the
diagnosis of carotid body tumour
-although angiography has been the gold standard to diagnosing CBTs, recent reports in the literature are
increasingly advocating the use of CT/MRI as well as duplex doppler as first line investigative modalities.
Other Investigations:
-functional tumours:
-urinary metanephrines and vanillylmandelic acid (VMA)
-metaiodobenzylguanidine I 131 (131I MIBG) scan can determine the source of catecholamine production
and/or functional state of the tumor
-Brain flow studies:
-reserved for extensive tumours that are intimately associated to the carotid artery
-tumours larger than 3 cm
-recurrent carotid body tumours
-history of antecedent carotid injury
-any vascular tumour that invades the cavernous sinus or involves the ICA circumferentially
-carotid balloon occlusion with Xenon CT scan or EEG monitoring
-transcranial doppler
-SPECT
Treatment:
-Historical perspective:
-1880 - Reigner first attempt at surgical extirpation - patient did not survive
-1886 - Maydl successfully removed a CBT, leaving the patient aphasic and hemiplegic
-1889 - Albert; 1891- Marchand; 1903 - Scudder: first successful removal with preservation of the carotid
artery complex
-1940 - Gordon-Taylor demonstrated that there was a safe subadventitial plane of dissection
-1953 - Morfit et al added arterial reconstruction techniques
740
-1971 - Shamblin et al grouped these tumours based on extent of encirclement of carotid arteries
-Classification of CBT: Shamblin, et al (review of 90 cases):

I: relatively small tumours with minimal attachment to carotid vessels
-surgical excision with minimal difficulty
II: larger with moderate arterial attachment; always a plane where normal carotid could be identified
-required precise surgical dissection (were the most common in their series)
III: larger neoplasms encasing the carotid arteries
-removal would require arterial resection and grafting
-because of the rather slow growth rate, one controversy over the years has been whether or not these lesion need to
be removed.
-early complication rates:
-Early mortality rates from 5 to 15% and as high as 29%
-cerebrovascular sequelae in 8 to 20%
-incomplete excision up to 30%
-cranial nerve injuries 32 to 44%
-Advances in pre-operative diagnosis and localization, intra-operative management of the carotid and cerebral
circulation, along with better anaesthetic management lead to marked decreased mortality rates:
-Chambers and Mahoney (1968):
-37/38 tumours without mortality, significant complications or permanent CN palsies
-Williams et al (1986-1990):
-0.6% (1/177)operative death
-2.3% (4/177)strokes
-29% (51/177)cranial nerve dysfunction
-The major series reported in the literature from 1991 to 1995 show further reduction of the overall
incidence of morbidity to 24.2% (stroke in 1.9% and peripheral nerve palsy in 22.3% of patients) without
any mortality.
-Recognition of their tendency for relentless growth and improved technical aspects of their surgical resection
favour surgical removal in most cases.
-Davidge-Pitts and Pananowitz have correlated size with Shamblin class:
-tumours larger than 4 to 5 cm tend to have partial or complete encirclement of carotid arteries,
and operative complications are much more frequent
-significantly increased incidence of postoperative morbidity with tumours larger than 5 cm
-early removal of an asymptomatic tumour is advocated to minimize potential cranial nerve and
carotid artery injury
-surgery is the current mainstay of therapy for carotid body tumours
-indications for conservative approach:
-patient’s age and medical condition
-patient with bilateral CBT and previous resection with resulting vagus nerve injury
Surgical technique:
1. Oblique neck incision made anterior to SCM
-subplatysmal flap elevation to provide wide exposure of the carotid system
2. Limited selective neck dissection is performed
-sampling of regional nodes for metastasis
-spinal accessory nerve is identified
-hypoglossal nerve identified - with division of ansa cervicalis, CN XII can be retracted superiorly
-vagus nerve identified
3. Common, external and internal carotid arteries proximal and distal to the tumour are controlled
-if the external carotid is involved within the tumour, it can be sacrificed
4. Subadventitial dissection in the plane of Gordon-Taylor
-tumour is dissected away from the surface of the internal carotid
741
-excessive bleeding may be avoided by ligation of the small tumour-feeding vessels on the posterior aspect
of the carotid bifurcation
-the tumor freed from the bifurcation is retracted superiorly to allow dissection of the superior laryngeal
nerve away from the deep surface of the tumour
5. If more exposure is needed superiorly, the digastrics is taken down along with the stylohyoid muscle
6. If the carotid is involved with the tumour, it is sacrificed and replaced with either a venous or synthetic graft
Postoperative complications:
-Mainly cranial nerve injuries
-vagus and hypoglossal most commonly affected
Adjunctive treatment:
1. Preoperative embolization:
-embolization is performed by the introduction of polyvinyl alcohol beads into the microvasculature of the
paraganglioma and gelfoam into the arterial branch itself to obliterate the flow
-operation within 48 hours after embolization is recommended to minimize revascularization edema or
local inflammatory responses.
-risks: TIA, stroke
-benefits: reduce hemorrhage during surgery and provide a more visible operating field; reduce the need
for transfusion
-controversy:
-La Muraglia et al (J Vasc Surg 1992;33(4):454-6) 11/17 preoperative embolization, the
significant difference in the intraoperative blood loss (372+213 ml compared with 609+564ml of
patients that were not embolized). However operative times were equivalent in both groups (4.1 h
vs. 4.5 h)
-Berguer and Kieffer disagree because of the high risk of stroke during embolization. They have
not found that the dissection is any less demanding than in those cases who did not have
preoperative embolization
-Litle VR et al (annals of Vasuclar Surgery 1996;10(5):464-8)
11 embolized vs 11 non-embolized
-no differences in blood loss, number of blood transfusion, operative time or perioperative
morbidity
-overall hospital stay was similar but the EMB group had a significantly longer preoperative
stay compared to the N-EMB group
-concluded that preoperative embolization does not significantly improve outcome in patients
undergoing resection of carotid body tumours measuring 4 to 5 cm
-some authors suggest the use be limited to tumours greater than 5 cm in diameter
2. Radiation therapy:
-still much controversy as to the effectiveness of radiation therapy
-usually reserved for inoperable, bulky and recurrent tumours although CBTs have been considered radio-resistant
-a number of reports have indicated excellent control of these tumours; long term follow-up is not available
-it is accepted that radiation (40-50 Gy) produces fibrosis of the tumours, controlling the tumour growth
but not curing it
-complications:
-necrosis of mandible, carotid artery, and larynx
-should not be considered alternative, but complementary to surgery
Follow-up:
-yearly follow-up with ultrasound or CT scan to measure progression if conservative route taken
-recurrences are uncommon, occurring in approximately 10% os cases
742
HEMANGIOMAS AND VASCULAR ANOMALIES
OF THE HEAD AND NECK
(Cumming’s)
Objectives:
1. Understand classification of hemangiomas and vascular malformation. Subclasses of vascular

malformations.
2. Understand pathology and pathophysiology of hemangiomas
3. Understand the difference between superficial and deep hemangiomas.
4. Understand the different complications that can arise from hemangiomas.
5. What are the management options for hemangiomas: surgical and medical.
6. Treatment approach to subglottic hemangiomas.
7. Understand the histology of the different vascular hemangiomas: capillary, venous malformations and
lymphatic malformations.
8. Understand the different presentations and diagnosis of vascular malformations.
9. Identify treatment options for each type.
10. What is the difference between AVM and vascular malformations.
11. What is the treatment of AVMs.
12. What are the magnetic resonance characteristics of vascular anomalies.
CLASSIFICATION
(1) hemangioma:
-a lesion that grows rapidly in early infancy
-characterized by endothelial proliferation and invariably undergoes slow regression
(2) vascular malformation:

-a lesion that is present at birth
-characterized by a normal rate of endothelial cell turnover and grows commensurately with the child
-structural anomalies, errors of vascular morphogenesis
-‘‘slow-flow’’: capillary, venous, lymphatic, or combined forms

-‘‘fast-flow’’: arteriovenous fistula [AVF] and arteriovenous malformation [AVM]) lesions.
F.Ling - Hemangiomas and Vascular Anomalies (1)
743
DISTINGUISHING CHARACTERISTICS: HEMANGIOMA VERSUS VASCULAR MALFORMATION
Clinical
-hemangioma
-usually not seen at birth
-rapid postnatal growth (proliferative phase) for first 8-12 months of life
-slow regression over 5 to 8 years (involutive phase)
-vascular malformations
-by definition, are present at birth
-grows proportionately with the child
Cellular
-hemangioma:
-proliferating phase: rapidly dividing endothelial cells forming syncytial masses with and without
lumina
-mast cells significantly increased in proliferating hemangioma and return to normal late in
involuting phase; their role angiogenesis is poorly understood
-during involutive phase, endothelial cell activity diminishes and cellular parenchyma is replaced
by fibrofatty tissue
-vascular malformations:
-no cellular proliferation but rather a progressive dilation of vessels of abnormal mural structure
-lined by flat, quiescent endothelium lying on a thin single laminar basement membrane
Radiographic
Magnetic resonance imaging characteristics of vascular anomalies

T1-weighted T2-weighted Contrast (gadolinium) Gradient
Hemangioma Soft-tissue mass, Lobulated soft-tissue Uniform intense High-flow vessels within
isointense or mass, enhancement and around soft-tissue
hypointense, flow voids increased signal, flow mass
voids
Venous Malformation Isointense to muscle, Septated soft tissue Diffuse or No high-flow vessels
possible high-signal mass, high signal, signal inhomogeneous
thrombi voids (pheleboliths) enhancement
Lymphatic Malformation Septated soft-tissue Soft-tissue mass, high Rim enhancement or no No high-flow vessels
mass, low signal signal, fluid/fluid levels enhancement
AVM Soft-tissue thickening, Variable increased Diffuse enhancement High-flow vessels

flow voids signal, flow voids throughout abnormal
tissue
Skeletal
-hemangiomas only rarely cause bone or cartilaginous hypertrophy
-slow-flow vascular anomalies, specifically lymphatic, venous, or lymphatovenous types, can cause
significant hypertrophy and distortion of the craniofacial skeleton
-fast-flow anomalies typically cause interosseous destruction
744
HEMANGIOMA
Diagnosis and natural history

-majority during first 6 weeks of life
-macular patch, blanched spot, or localized area of telangiectasia surrounded by a halo
-80% isolated; 20% multiple
-head and neck most commonly involved: most common tumour of infancy
-superficial:
-skin raised with a vivid bright-red colour
-well circumscribed
-deep:
-proliferate in lower dermis or subcutaneous tissue with little involvement of superficial or
capillary dermis
-overlying skin is smooth with a bluish hue
-mixed:
-both deep and superficial skin layers involved
-“capillary-cavernous hemangioma”
-hemangioma is firm and rubbery and difficult to compress
Radiologic imaging
-order of investigations: US (with Doppler flow study) > MRI (occ CT) > angiography
Complications
-Obstruction
-Visual
-can result in deprivation amblyopia and failure to develop binocular vision
-Subglottic hemangioma
-usually presents after first 6 weeks of life
-more than half of these infants have an associated cervicofacial cutaneous hemangioma
-biphasic stridor - insidious onset of respiratory distress
-lateral radiograph of neck or a fluoroscopic study of upper airway:
-smooth, usually posteriorly based round swelling in subglottic space
-dx: requires direct laryngoscopy: smooth, easily compressible mass in subglottic space
-biopsy of not necessary for diagnosis
Ulceration and bleeding

-d/t penetration of epidermal basement membrane
-ulceration common in hemangiomas of lips
-usually responds to daily cleansing and application of topical antibiotic ointment
Alarming complications
Congestive heart failure

-typically seen with multiple cutaneous hemangiomas and with hemangiomatous proliferation
within the viscera, typically the liver
-overall mortality rate 54%
Platelet-trapping coagulopathy (Kasabach-Merritt syndrome)

-large hemangiomas may cause platelet trapping
745
-profound thrombocytopenia (2000 to 40,000/mm3)
-purpura and life-threatening bleeding into the pharynx, gastrointestinal tract, and/or brain
-occurs in 1% of infants with hemangiomas
-mortality of 30% to 40%
Management
-complete resolution of hemangiomas occurs in over 50% by age of 5 years and in over 70% by age of 7
years
-skin exhibits mild atrophy after involution
-for small hemangioma in an inconspicuous location, nothing should be done
Subglottic hemangioma
-lesion occupying < 20% of airway: no treatment required; await involution
-classically for respiratory distress, tracheotomy for 2 years until sufficient involution
-corticosteroid therapy:
-60% respond to corticosteroids
-dose: prednisone (2 to 3 mg/kg/day); lower dosage or an alternate-day regimen may be continued
for 4 to 6 weeks or longer
-CO2 laser:
-failed corticosteroid therapy
-CO2 laser beam used in intermittent mode at a setting of 0.05 seconds at 20 watts
-circumferential subglottic hemangiomas removed in stages to prevent subglottic stenosis, or
tracheostomy may become necessary
-surgical resection:
-via laryngofissure approach
-shell out tumour sub-mucosally
Pharmacologic therapy for alarming complications
Corticosteroid
-high-dose corticosteroids remain premier pharmacologic agent for control of endangering
hemangiomas
-dosage: oral prednisone (2 to 3 mg/kg/day); IV in infants with respiratory complications
-if no response in 7 days, lesion is considered steroid unresponsive drug discontinued
-steroid dosage usually lowered slowly over several weeks if responsive or patient can be
switched to alternate-day therapy
-intralesional corticosteroids for small protuberant hemangiomas on face (upper-eyelid and
nasal-tip lesions)
-dose of triamcinolone and betamethasone no more than 40 and 6 mg, respectively
-one to five injections are necessary, spaced 4 to 6 weeks apart
Interferon-a-2a
-used in infants with life-threatening hemangiomas that do not respond promptly to corticosteroids
-agent of choice for patients with Kasabach-Merritt syndrome
Surgical therapy
-excision for removal of fibrofatty residuum or skin laxity post-involution
-indications for earlier operative intervention:
-hemangioma causing visual problems and is unresponsive to corticosteroid therapy
-early excision of an obstructing subglottic hemangioma using a CO2 laser
-pedunculated and ulcerated lesions removed rather than waiting for involution to occur
746
-evidence of psychosocial problems d/t body or facial image (lip and nasal tip)
-if skin removal will be necessary in the future either because of colour, quality, or contour,
notwithstanding the final result of involution
VASCULAR MALFORMATIONS
Capillary malformation
Histology
-abnormally dilated capillaries or venule-sized vessels in superficial dermis
-lesion may become raised and nodular with progressive vascular ectasia
Clinical features
-Sturge-Weber syndrome:
-port-wine stain within V1 area at serious risk for choroidal and intracranial vascular anomalies
-cerebral angiography: capillary, venous, and arteriovenous anomalies of leptomeninges
-leads to progressive degeneration and atrophy of cerebral hemispheres
Management
Laser therapy
-management of choice; causes thermal thrombosis
-argon laser used for adult patients
-flashlamp pulsed tunable-dye laser preferred for young children, patients with light-coloured
port-wine stains, and those whose skin is sensitive to heat
Surgical excision
-used in selected cases
Venous malformation
Histology
-dilated or ectatic vascular channels lined by normal endothelium
-thrombosis common (phleboliths)
Clinical features
-soft, compressible nonpulsatile mass with rapid refilling
-expansion on compression of jugular vein or Valsalva’s manoeuver
-phlebothrombosis recurrent pain and tenderness
Management
Sclerotherapy
-sclerosing agents: 95% ethanol or sodium tetradecyl sulfate (1% or 2%) injected into epicenter
Surgery
-for large or symptomatic venous anomalies
-subtotal resection to reduce bulk and improve contour and function or relieve pain
747
Lymphatic malformation
-once transected, however, lymphatic malformation have tendency to proliferate into surgical scar
Histology
-multiple dilated lymphatic channels lined by a single layer of flattened endothelium
-walls of variable thickness and are fibromuscular, with both striated and smooth muscle components
Clinical features
-may have wide infiltration
-associated with hypertrophy of both bone and soft tissue
-Type I lymphatic malformations

-located below level of mylohyoid muscle and involve anterior and posterior cervical triangles
-have large cystic structures without infiltration of surrounding soft tissue
-Type II lymphatic malformations
-found above level of mylohyoid muscle and involve the oral cavity, lip, and tongue
-smaller lymphatic channels with infiltration of surrounding tissue
Management
-surgical resection is management of choice
-laser reserved for disease not readily resectable by sharp dissection
-oral cavity and tongue lesions
-supraglottic region
-intralesional injection of OK-432
Arteriovenous malformation
Histology
-arteriovenous shunts
-dysmorphic arteries are thick-walled and of irregular caliber
-fragmentation of internal elastic lamina and highly disorganized smooth muscle in the media
-veins: progressive reactive hypertrophy, intimal thickening, and sclerosis caused by increased blood
Clinical findings
-manifest during late childhood, adolescence, or early adulthood
-throbbing pain, buzzing, or pulsatile tinnitus
-involved skin has elevated temperature, and a thrill may be felt
Management
-MRI and angiography for evaluation
-angiography: superselective embolization (pre-op)
-total resection
748
MALIGNANT LESIONS OF THE ORAL CAVITY
(Cummings)
-order of prevalence of SCCa based on subsite:

-oral tongue > floor of mouth > alveolar ridge (lower>upper) > buccal mucosa > retromolar trigone > hard
palate
ANATOMY
Lymphatic Drainage
Lips:
-lower lip:
-bilateral metastasis
-medial portion: submental lymph nodes
-lateral portion: submandibular lymph nodes
-upper lip:
-preauricular, infraparotid, submandibular, and submental lymph nodes
-no crossing of midline has been documented for mucosal lymphatics
-submental, submandibular, and periparotid areas drain into lymph nodes of upper and occasionally middle
jugular lymphatic chain
Buccal Mucosa:
-submental and submandibular triangle lymph nodes
Alveolar Ridges:
-buccal aspect of upper and lower alveolar ridges:
-submental and submandibular lymph nodes
-lingual aspect of upper and lower gingiva:
-chiefly to upper deep jugular and lateral retropharyngeal lymph nodes
-lingual surface of the lower alveolus also may end in submandibular nodes
F.Ling - Malignant Lesion of the Oral Cavity (1)
749
Retromolar trigone:
-upper deep jugular chain of lymph nodes; some to subparotid and lateral retropharyngeal lymph nodes.
Hard palate:
-sparse
-upper deep jugular (subdigastric) or lateral retropharyngeal nodes
-primary palate: prevascular and retrovascular group of submandibular nodes
Floor of mouth:
-superficial mucosa
-ipsilateral and contralateral preglandular lymph nodes
-deep collecting
-ipsilateral preglandular nodes
-most anterior collecting vessels of the deep system cross the midline
-posterior portion drain directly into the jugulodigastric and jugulocarotid nodes
Tongue:
-all vessels drain ultimately into deep jugular
lymph nodes
-nearer the tip of the tongue the lymphatics arise,
the lower is the first-echelon node; and the
farther posterior, the higher the node
-anterior (apex) submental nodes
-lateral or marginal trunks submandibular
nodes
-central trunks deep jugular nodes
-tongue base jugulodigastric nodes
MANAGEMENT
Radiotherapy
-four general principles:

-most SCCs are radioresponsive, although high doses of radiation are required for local control
-well-oxygenated neoplasms are more radioresponsive than hypoxic ones
-bone or deep muscle invasion decreases radiocurability
-large cervical metastases are better managed by neck dissection, with or without adjunctive
radiotherapy
-total dose of radiotherapy usually 65 to 75 Gy
-conventional fractionation external-beam XRT administered at 1.8 to 2.0 Gy per fraction 5x/week
-hyperfractionation:
-smaller than conventional dose fractions given twice a day to a greater total dose
-presently unclear whether hyperfractionation enhances locoregional control; it may even increase
incidence of late complications
-interstitial irradiation (brachytherapy) is frequently used in combination with external radiotherapy to treat
cancers of the tongue and floor of the mouth
750
Prophylactic neck irradiation
-radiotherapy of N0 neck with 50 to 55 Gy will control occult disease and prevent later occurrence of
cervical metastases
-although prophylactic neck irradiation appears to be at least as effective as elective neck dissection in the
management of occult neck disease, prospective randomized studies are needed for conclusive evidence in
support of one modality or the other
Surgery
-local surgical excision for lesions < 2.0 cm

-if initial tumor is small, surgery alone would reserve radiotherapy for use in a combined regimen to
manage subsequent primary neoplasms that might warrant management of greater magnitude
-surgery indicated in pts who have completed XRT and demonstrate persistent tumor or suffer recurrence
at primary site or in neck
-if radiotherapy controls primary tumor continued palpable lymphadenopathy, neck dissection without
resection of the primary site is indicated
Neck dissection
-N0 necks but extensive primary lesions (T2, T3, or T4) high probability of neck metastases
-supraomohyoid neck dissection (zone I, II and III) warranted
-if no metastases, no radiation
-if metastases improved regional control with addition of XRT
-N1, N2, or N3 require a comprehensive neck dissection for optimal disease control and should undergo
postop XRT
-midline lesions may cause bilateral metastases
-if both are clinically N0, bilateral extended supraomohyoid neck dissections can be performed as
staging procedures
Combined therapy
-combination of radiotherapy and surgery in treating advanced stage III and IV disease of the oral cavity in
hopes of reducing local recurrence and improving survival rates
-pre- or postoperative radiotherapy has been shown to reduce neck recurrence
-Preoperative irradiation:
-45 to 50 Gy delivered at 2.0 Gy per day
-surgery is initiated after a 4-week interval following radiotherapy
-theoretic advantages:
-tumor cells may have better oxygenation before surgery and thus be more sensitive to
irradiation
-malignant cells at periphery of neoplasm are destroyed
-tumor seeding at the time of resection may be decreased
-may be fewer and less viable cells intravascularly and within lymphatics at time of
surgery, which could lower frequency of distant metastases.
-disadvantages:
-wound healing problems, which increase as preoperative doses exceed 40 Gy
-increased incidence of tissue necrosis, wound infection, and fistula formation occurs
when surgery is performed in a radiated region
-reconstruction usually is more difficult because of fibrosis and inflammation and
reduced blood supply
751
-changes in size of neoplasm as well as general inflammatory responses elicited by the
radiotherapy may obscure tumor margins
-Postoperative radiotherapy:
-begun 3 to 4 weeks following surgery
-theoretic advantages:
-safer administration of a higher total dose of irradiation
-destruction of subclinical residual tumor, which may remain following surgery
-fewer wound infections
-distinct tumor margins facilitating more accurate and complete surgical removal
-ability to direct radiation to specific areas observed intraoperatively where tumor-free
surgical margins are questionable
-disadvantage:
-surgery may interrupt blood supply of remaining tumor cells and lessen their sensitivity
to radiotherapy
-wound breakdown or other operative complications may delay onset or prevent delivery
of radiotherapy
Chemotherapy
-not effective for cure

-used for palliation for unresectable disease or distant metastases
-agents used: cisplatin, 5-fluorouracil, methotrexate, bleomycin, paclitaxel, and topotecan
-no benefit in survival with the use of induction chemotherapy
-adjuvant chemotherapy failed to show any difference in survival between the groups
-however did reveal a decreased incidence of distant metastases
752
PRINCIPLES OF CHEMOTHERAPY IN
THE MANAGEMENT OF HEAD AND NECK CANCER
-relative success of chemotherapy depends on tumour burden, percentage of tumour cells in a

chemotherapy-responsive phase of the cell cycle, and number of cells with inherent or acquired resistance
to chemotherapeutic agents
TYPES OF CHEMOTHERAPEUTICS
-alkylating agents:
-cross-link DNA and interfere with DNA replication
-nitrogen mustard, cyclophosphamide, chlorambucil
-cisplatin, doxorubicin, bleomycin, mitomycin C
-antimetabolites:
-interfere with cellular metabolism
-methotrexate, 5-fluorouracil, hydroxyurea, gemcitabine
-microtubule disruption:
-vincristine, vinblastine, vinorelbine
-microtubule stabilizers:
-paclitaxel, docetaxol
-topoisomerase I inhibitors:
-prevent unwinding of DNA
-irinotecan, topotecan
CLINICAL TRIALS
-phase I:
-tolerance and pharmacologic properties of newly developed compounds are studied
-end point is determination of maximally tolerated dose
-phase II:
-determine therapeutic activity, or efficacy, of a new drug in a specific disease and stage
-end point is definition of activity measured as response rate, at an acceptable rate of toxicity
-phase III:
-new drug or combination is compared with current standard therapy
ROLES OF CHEMOTHERAPY IN HEAD AND NECK CANCER
-1/3 pts with SCC present with early-stage lesions no chemotherapy needed
-for all other pts, chemotherapy may have a role
-metastatic disease and for those with locoregional recurrences that cannot be managed with
further surgery or radiation, chemotherapy has a palliative role
-advanced stage III and IV cancer:
-may improve survival and organ preservation
F.Ling - Chemotherapy (1)
753
STANDARD CHEMOTHERAPY FOR RECURRENT OR METASTATIC CANCER
-response rates of various drugs ~30% or less with responses that are almost exclusively partial and of
short duration
-primary goal is palliation of symptoms, including pain, disfigurement by a mass, or decreased organ
function d/t invasive cancer
Methotrexate
-antimetabolite: interferes with intracellular folate metabolism
-binds to dihydrofolate reductase
-prevents conversion of folic acid to tetrahydrofolate inhibition of DNA synthesis
-active only during S phase
-side effects minimized with leucovorin
-toxic reactions: myelosuppression, mucositis, dermatitis, nausea, vomiting, diarrhea and hepatic fibrosis
-produces partial response rate of ~10%
Cisplatin
-antitumor activity results from intracellular binding to form bifunctional covalent links that interfere with
normal DNA function
-side effects:
-renal toxicity common
-nausea and vomiting, peripheral neurotoxicity, ototoxicity, and cumulative myelosuppression
-partial response rates of ~15-30%
-analogues:
-Carboplatin: decreased nephrotoxicity and neurotoxicity
5-Fluorouracil
-S-phase-specific uracil analogue
-sequential phosphorylation and incorporation into RNA
-activation to 5-fluorodeoxyuridine monophosphate, which blocks thymidylate synthase and
blocks conversion of uridine into thymidine compounds
-cells unable to synthesize DNA
-side effects:
-myelosuppression, mucositis, dermatitis, diarrhea, cardiac toxicity
Paclitaxel and Docetaxel

-taxanes
-stabilize tubulin polymers and prevent cell division
-response rates ~ 30-40%
COMBINATION CHEMOTHERAPY
-in the management of head and neck cancer, most combinations have been based on methotrexate or
cisplatin
-combinations produce statistically significantly higher response rates than do single agents, including
methotrexate
-cisplatin and infusional 5-FU produce higher response rates than do single agents or other combinations
-in no comparison group is survival time meaningfully lengthened
-toxicities of cisplatin and infusional 5-FU are significantly greater than those of single agents
754
Summary:
-methotrexate in weekly low doses, cisplatin, infusional 5-FU, paclitaxel and docetaxel are most active
single agents
-response rate is 20-40% and response lasts for 1-6 months
-combination chemotherapy produces higher response rates, although long-term survival rarely is achieved
OTHER ROLES OF CHEMOTHERAPY
-benefits and mechanisms of chemoradiotherapy:

-drugs and irradiation may be active against different tumour cell subpopulations because of cell
cycle specificity, pH, and oxygen supply
-cells resistant to one modality of treatment can be eradicated with the other
-combination therapies can increase tumour cell recruitment from G0 into radiation therapy-
response cell cycle phase
-tumour shrinkage can decrease interstitial pressure and therefore increase drug and oxygen
delivery
-early eradication of tumour cells prevents emergence of drug or radiation resistance
-cell-cycle synchronization increases the effectiveness of both therapies
-chemotherapy inhibits repair of sublethal radiation damage and inhibits recovery from potentially
lethal radiation damage
-unresectable locoregionally advanced cancer, chemoradiation therapy clearly better than radiation therapy
alone in most settings
-studies suggest that intensive chemoradiation therapy can be at least equivalent to surgery plus radiation
therapy for medically fit pts
Nasopharyngeal Cancer
-chemotherapy is important in management of NPC
-considered standard therapy
-metastatic undifferentiated carcinoma, or lymphoepithelioma (WHO III) of the nasopharynx is highly
sensitive to chemotherapy
-Phase III Intergroup Study 0099 showed increased survival benefit with chemoradiotherapy (cisplatin/5-
FU) over radiotherapy alone for stage III and stage IV nasopharyngeal cancer (J Clin Oncol 1998;
16:1310-1317)
-76% versus 46% 3-year survival, P <0.001
Unresectable Head and Neck Cancer

-long-term survival rate with XRT alone for unresectable cancer historically 10-30%
-in general, most single-agent chemotherapeutic drugs given concomitantly with XRT, locoregional control
and survival are better than with XRT alone
-most frequently used, and perhaps best single-agent chemotherapeutic drugs, are 5-FU and cisplatin
-risk of acute mucositis, dermatitis, and chemotherapy-specific side effects is greater than with either mode
of therapy alone
-Phase III Multicenter Study showed increased survival benefit with concomitant chemotherapy
(cisplatin/5-FU) and radiation therapy over radiation therapy alone for advanced head and neck cancer
(48% versus 24% 3-year survival, P<0.0003)(J Clin Oncol. 1998;16:1318-1324.
Postoperative Adjuvant Chemoradiation Therapy

-in a few studies, combined modality groups had both improved locoregional control and improved overall
survival rate
755
Resectable Cancer of the Head and Neck
-use of chemoradiation in the management of resectable cancer of the head and neck has not yet gained
widespread acceptance
-although some studies suggest that results on locoregional control and survival are comparable to surgery
and radiation
Induction (Neoadjuvant) Chemotherapy

-goal is to improve likelihood of organ preservation or cure
-advantages:
-drug delivery to cancer cells is unimpaired
-macroscopic response may predict response of microscopic disease. Prompt elimination of
micrometastases may aid in cure
-tumour may shrink, allowing more successful surgery or radiation therapy with less radical
treatment
-pt performance status at surgery may be improved
-disadvantages:
-original extent of tumour may be obscured
-performance status may decline
-tumour may grow during chemotherapy
-duration, toxicity, and cost of treatment increase
-most extensively used and studied combination is a regimen of cisplatin and 5-FU
-general conclusions of studies:
-overall response rates exceeding 80% are frequently achieved
-complete response rates usually range from 20-50%, most trials showing approximately 30%
-toxicity usually is moderate to severe, but administration of subsequent standard local therapy is
not compromised
-pts achieving complete responses have a better prognosis, particularly if the responses are
confirmed histologically
-organ preservation is possible at least in laryngeal and hypopharyngeal carcinoma
-survival assessed in randomized studies, generally does not improve
-most pts died of complications of locoregional disease; therefore the decreased rate of distant
metastasis did not translate into a survival benefit
-Department of Veterans Affairs Laryngeal Cancer Study (N Engl J Med 1991; 324:1685-1690):
-advanced laryngeal cancer
-standard tx: sx + XRT
-study tx: three cycles of neoadjuvant cisplatin and 5-FU followed by XRT
-findings: overall survival rates were identical in two groups - 68% 2-year survival, P=0.98
-high rate of preservation of the larynx (64% of pts in chemotherapy arm had larynx
preserved)
-similar rate of disease-free survival with laryngeal preservation (28%) was achieved in another
study with similar design in which pts had hypopharyngeal cancer
-Piriform Sinus Cancer Organ Preservation (J Natl Cancer Inst. 1996; 88:890-899):
-Phase III European Organization for Research and treatment of Cancer (EORTC)
-showed no significant change in survival with induction chemotherapy (cisplatin/5-FU) followed
by adjuvant radiation therapy over surgical management for advanced hypopharyngeal cancer (30-
35% 5-year survival)
-approximately half of patients who were alive at 3 years in the induction chemotherapy arm
retained their larynx
-study shows that all pts with laryngeal or hypopharyngeal carcinoma should be offered organ
756
preservation therapy
-neoadjuvant chemotherapy has not conclusively improved survival and therefore continues to be
investigational therapy for dz of sites other than larynx and hypopharynx
CHEMOTHERAPY EMERGENCIES
Complications
-nausea, vomiting -antiemetics, fluids, relaxation, support
-diarrhea -control of infection, antidiarrheal therapy
-alopecia -none
-mucositis -mouth care, narcotic therapy
-myelosuppression
-neutropenia -GCSF, IV Abx, hospitalization if pt has fever
-thrombocytopenia -platelet transfusion if count is 10-20/ul or bleeding at <50/ul
-anemia -control of bleeding, erythropoietin therapy, transfusions
-nephrotoxicity -hydration, support, dialysis
-electrolyte wasting -repletion
-neurotoxicity -mainly supportive
-allergic reaction -antihistamine, steroids, epinephrine
-pulmonary toxicity -support, steroids, management of specific cause
-hepatotoxicity -mainly supportive
Emergencies
-neutropenia fever
-fever, chills, symptoms of infection plus absolute neutrophil count < 500/ul
-hospitalization, antibiotics (broad spectrum antipseudomonals), with or without GCSF
-thrombocytopenia
-platelet count <10-20/ul, petechia, overt bleeding
-transfusion, determining source of bleeding, avoidance of ASA and NSAIDs
-allergic reaction
-esp to paclitaxel or bleomycin
-rash, hives, stridor, hypotension
-antihistamine, glucocorticoid, epinephrine
-extravasation
-eg. vincristine or doxorubicin can cause necrosis of skin
-redness, swelling, pain
-subcutaneous epinephrine or hyaluronidase
-overdose
-drug dependent
-supportive, antidote if available
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PRINCIPLES OF RADIATION ONCOLOGY
RADIATION PHYSICS
Terminology
-Rad (Radiation Absorbed Dose)
-amount of energy deposited by ionizing radiation per gram of tissue
1 rad = 1 erg/cm3
1 Gy = 100 rads
External Beam Irradiation

-most patients treated with megavoltage x-rays or gamma rays (photons)
-H+N cancer can be managed with 4-6-MeV x-rays or cobalt 60 gamma rays
-15-25-MeV x-rays occasionally used for boost to certain H+N cancers (eg. BOT, NP)
-have skin sparing properties
-electron beams used for superficial lesions
-have less skin sparing properties
Brachytherapy
-radioactive sources are placed within or close to target volume
-interstitial therapy: source placed into tumour and surrounding tissues
-intracavitary: within body cavities
-surface molds: onto epithelial surfaces
-advantages:
-radiation confined to implant volume greater dose delivered with lesser dose to adjacent tissue
-continuous delivery of radiation at a low dose rate
-avoids morbidity of XRT to other tissue structures
-disadvantages:
-tumour must be accessible and relatively well demarcated
-cannot be used as only treatment if there is high risk of regional lymph node metastasis
-usual dose:
-70-80 Gy to target volume for 5-7 days
RADIOBIOLOGY
Cell Death
-radiation cell “kill” is expressed as a logarithmic cell survival curve
-radiation does not kill a certain number of cells but a percentage of cells
-cells are considered “killed” when they lose clonogenic survival
-direct effect: secondary electron interacts with DNA to produce damage
-when a critical number of double stranded and single stranded breaks occur, then the cell
undergoes necrotic cell death or apoptosis
-indirect effect: secondary electron interacts with molecule in vicinity to produce a free radical which
damages the cell
Determinants of Sensitivity of Radiation Therapy

-larger tumours have a more hypoxic center, therefore are less sensitive to radiation because less free
radicals are generated
-1 cm tumour = 109 cells
-3 cm tumour = 1010 cells
F.Ling - Principles of Radiation Oncology (1)
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-oxygenated cells are more susceptible to radiation than hypoxic cells
-exophytic tumours are typically well vascularized and therefore more susceptible to radiation
injury, ulcerative and infiltrative tumours are less vascularized and therefore more resistant to
radiation
The Four R’s

-therapeutic advantage hypothetically is gained by means of the following mechanisms:
-repair (sublethal injury)
-reoxygenation (tumour cell hypoxia)
-redistribution (cell cycle effects)
-repopulation
Sublethal Injury (Repair)

-sublethal injury can be repaired by a cell if no further hits are incurred
-because of this, a greater dose is needed to produce a biologic effect when it is given in several
fractions than when given as single fraction
-the greater number of fractions, the greater opportunity for repair between dose fractions and the greater is
the total dose needed to produce the same level of biologic effect
-important because certain tumours have more capacity for repair may appear to be radioresistant
-may need to treat with hypofractionation (few large fractions)
-reason for fractionation:
-allows repair of injured normal tissue, which ultimately reduces late complications
Tumour Cell Hypoxia (Reoxygenation)

-presence of oxygen at time of irradiation increases effect of ionizing radiation
-formation of free radicals that damage DNA
-dose of radiation needed to kill hypoxic cells is 2.5-3 times greater than that needed to kill well-
oxygenated cells
-hypoxic tumour cells usually reoxygenate during course of fractionated irradiation and therefore
will become more sensitive to radiation therapy
Cell Cycle Effects (Redistribution)

-cells in S phase (DNA synthesis) more radioresistant than other cells in cell cycle
-cells surviving each fraction redistribute themselves into more sensitive phases of cell cycle,
making them more susceptible to eradication by subsequent fractions
-redistribution is greatest for cells that are rapidly cycling (ie tumour cells)
-cells tend to be more radiosensitive in mitosis and late G1 and early S-phases
Repopulation
-if tumour cell population is reduced, malignant cells respond with accelerated repopulation
-accelerated treatment schedules with twice-daily fractionation and combined accelerated-hyperfractionated
schedules have been developed to diminish the opportunity for repopulation of rapidly proliferating
tumours
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LOCAL CONTROL AS A FUNCTION OF RADIATION DOSE AND SIZE OF TUMOUR
Radiation Primary Site and Clinical Stage Regional Lymph Nodes

Dose
(Gy) T1 T2-3 T3-4 Subclinical 1-3 cm 3-5 cm
30-40 ~60-70%
50 60% nasopharynx ~90% ~50%
55 30% supraglottic larynx
60-65 90% tonsillar fossa 80% tonsillar fossa 50% tonsillar fossae
90% RMT, ATP 75% supraglottic larynx
100% supraglottic 55% glossopharyngeal
larynx sulcus
88% base of tongue
70 100% tonsillar fossae 90% RMT, ATP 65% tonsillar fossa 90% 70%
100% glossopharyngeal 80% glossopharyngeal
sulcus sulcus
75 80% base of tongue 90% tonsillar fossa

100% glossopharyngeal
sulcus
Regression Rates
-tumour regression rate is related to cycling time of tumour cells
-lethally injured cells and surviving cells are morphologically indistinguishable:
-biopsy is of little value in early postirradiation period
-positive biopsy result usually not reliable indicator of persistent disease until about 3 months
after treatment
TREATMENT
Contraindications to XRT
-patients with collagen vascular disease
-pregnant women
-previous XRT to head and neck region
Selection of Treatment Modality

-modalities:
-sole treatment
-adjunctive treatment:
-radiation treatment is needed for cure
-adjuvant treatment:
-treating probability of microscopic disease
-treatment may or may not be needed for cure
-palliative treatment
-early stage cancer usually effectively managed with either surgery or radiation alone
-larger cancers usually managed with combination therapy
-in general, surgery more effective in salvaging radiation therapy failures than vice versa
760
Doses Required for SCCa to control disease in > 90% of patients
-subclinical disease (<106 cells): 4500-5000 cGy
-microscopic disease (>106 cells): 6000-6500 cGy
-clinically palpable tumours:
-T1: 6000 cGy
-T4: 7500-8000 cGy
Radiation Therapy Alone

-external beam, interstitial implant or a combination
-tumours that can be primarily treated with XRT
-all H+N cancers that are T1-T2 and N0-N1 necks
-exceptions:
-nasopharynx
-tumours of salivary glands and FOM generally treated primarily with surgery
-neck nodes are irradiated if there are clinically positive nodes or if there is considerable risk of subclinical
lymph node metastasis
-small cancers usually 60-65 Gy in 6-6.5 weeks
-larger tumours: 65-70 Gy in 6.5-7.5 weeks
-shrinking field technique:
-initial tumour dose of 45-50 Gy delivered in 4.5-5 weeks through large portals
-1st field reduction boosts the field to encompass gross tumour with some margin (additional 15-20
Gy for a total dose of 60-72 Gy in 6-7.5 weeks)
-2nd field reduction boosts again for highly infiltrative primary tumours or large nodes; total dose
is 70-75 Gy
-spinal cord limited to 45 Gy to avoid risk of radiation myelitis
Combined Surgery and Radiation Therapy

-surgical failures usually are caused by residual microscopic disease
-radiation failures usually are caused by inability to eradicate bulky masses
-post-op dose of 58-66 Gy in 5-6.5 weeks is effective if tumour has been reduced to microscopic level
-indications for adjuvant XRT:
-T3-T4 tumours
-extracapsular spread
-multiple lymph node involvement
-positive resection margins
-recurrent disease
Preoperative Radiation Therapy

-arguments in favour:
-unresectable lesions can be made resectable
-extent of surgical resection can be diminished
-before surgical intervention, treatment portals usually are smaller than those needed
postoperatively
-microscopic disease is more radiosensitive preoperatively because it has a better blood supply
-viability of tumour cells disseminated through surgical manipulation is diminished, so risk of
distant metastasis decreases
-disadvantages:
-slower wound healing
-if there is residual disease after surgery, difficult to give more radiation
-typical dose is 45 Gy in 4.5 weeks
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Postoperative Radiation Therapy
-arguments in favour:
-anatomic extent of tumour can be determined surgically; easier to define treatment portals
-greater dose of irradiation can be given postoperatively than can be given preoperatively
-total dose given can be based on residual tumour burden after surgery
-surgical resection easier and healing is better in tissue that is not irradiated
-disadvantages:
-radiation may need to be postponed secondary to postoperative complications
-typical dose is 60-65 Gy in 6-7 weeks
-higher doses needed if residual disease or positive margins
-reduces risk of recurrence in surgical field
-results are poorer if postoperative radiation therapy is delayed more than 6 weeks
Fractionation Schemes
-Standard fractionation:
-usually 2 Gy per day x 25 days (5 days/week x 5 weeks)
-Hyperfractionation:
-increasing number of doses (BID dosing)
-decreasing intensity per dose (~1.0-1.2 Gy per fraction)
-higher total dose
-treatment time constant
-higher probability of tumour control without increasing the risk of late complications
-increased acute side effects
-Accelerated fractionation:
-multiple fractions of 1.5-2 Gy daily (higher daily dose)
-decreased overall treatment time
-decrease total dose ~10%
-increases acute side effects and decreases late side effects
-increases tumour cell kill (prevents tumour cell proliferation)
-Hypofractionation:
-smaller number of larger fractions
COMPLICATIONS
Acute Tissue Reactions

-appear in second week of irradiation
-subside several weeks after completion of treatment
Late Tissue Reactions

-xerostomia
-from irradiation of salivary glands
-dental caries
-soft-tissue radionecrosis
-mucosal ulceration from damage to vascular connective tissue
-osteoradionecrosis and cartilage radionecrosis
-caused by overlying soft tissue necrosis
-hypocellularity, hypovascularity, and ischemic of tissue (not infectious)
762
-fibrosis
-principal dose-limiting factor of XRT
-ocular complications (cataracts, retinopathy, optic nerve injury, lacrimal gland injury)
-serous otitis media, SNHL
-spinal cord injury
-Lhermitte syndrome: transitory syndrome characterized by electric shock sensations triggered by
flexing the cervical spine
-radiation myelopathy
-transverse myelitis
-brain injury (somnolence syndrome: transient condition characterized by lethargy, nausea, headache,
cranial nerve palsy or ataxia, brain necrosis)
-rare
-radiation induced cancer:
-increased risk of thyroid, salivary gland cancer, leukemia, sarcomas (may have lag period of 20
years)
-post-radiation hypothyroidism
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CUTANEOUS MALIGNANCY
-descending order of incidence

-BCC accounts for 90% of all cutaneous neoplasms in H+N region
-SCC
-melanoma
RISK FACTORS
-sun exposure:
-UV B - 280-320 nm range
-host factors:
-fair complexion
-light hair
-blue eyes
-inability to tan
-propensity to sunburn
-history of multiple or severe sunburns
-Celtic ancestry
-other factors:
-chronic chemical exposure: arsenic
-radiation therapy
-trauma: burns, ulcers and scars (ie. Marjolin’s ulcer)
-immunosuppression
-HPV
-genetic syndromes:
-xeroderma pigmentosum (AR)
-nevoid BCC syndrome (AD) - aka Gorlin’s syndrome
-BCC beginning in childhood
-jaw cysts (odontogenic keratocyst), bifid ribs, scoliosis, MR and frontal
bossing
BASAL CELL CARCINOMA
Epidemiology
-most common malignancy in humans
-comprises approximately 65% of all epithelioid tumours
-20% of all cancers in men and 10-15% of all cancers in women
-86% of lesions occur initially in the head and neck, with 25% of all primary lesions occurring on the nose
-more common in men than in women
-most frequently between ages 40-60 years
-rare metastasis
Evaluation
-five clinical forms:
-nodular or noduloulcerative
-morphealike or sclerosing
-superficial multicentric
-pigmented
-fibroepithelioma
F.Ling - Cutaneous Malignancy (1)
764
-nodular (Noduloulcerative):
-most common
-discrete, raised, circular lesion, pink, waxy with visible capillary network (telangiectasias)
-“central ulceration with rolled border”
-superficial:
-scarring and atrophy with threadlike waxy border; scaly
-more common on trunk and extremities
-morphealike:
-most dangerous
-macular, whitish plaque
-indistinct margins makes excision difficult
-aggressive, higher rate of recurrence
-worst prognosis
-pigmented:
-less common
-may resemble nevus or melanoma
fibroepitheliomas:
-firm pedunculate lesions that resemble fibromas
Histopathology
-large, oval nucleus with relatively little cytoplasm
-resemble basal cells of epidermis
-peritumoral lacunae: proliferation of stroma oriented in parallel bundles around the tumour masses
-mucinous stroma
-four histologic patterns:
-solid:
-proliferation of basaloid cells that extend into the papillary dermis, peripheral columnar
cells arranged in palisades
-keratotic:
-differentiated to hair-like structures
-cystic:
-differentiated to sebaceous gland-like structures
-adenoid:
-differentiated to tubular structures, lace-like histological pattern
Treatment Options
-excisional curettage (small lesions < 2 cm)
-cryosurgery (small lesions < 1 cm)
-scalpel excision (4 mm margins)
-XRT
KERATOTIC BASAL CELL CARCINOMA
-basosquamous cell carcinoma or metatypical carcinoma

-features of both squamous and basal cell
-thought to be more biologically aggressive than other types of BCC
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SQUAMOUS CELL CARCINOMA
Evaluation
-accounts for 10% of skin malignancies
-related to chronic sun exposure
-erythematous, ulcerated, crusting lesion
-granular friable base
-hyperkeratotic patch or an area of crusting
-occasionally a nodular exophytic lesion
-1-4% to 30% metastatic potential
Characteristics of high-risk squamous cell carcinoma

-Invasion to reticular dermis or adipose
-Poorly differentiated histology
-Immunosuppressed host
-Tumour size 2 cm in diameter or greater
-Location on the lip or ear
-Tumour arising in scar, radiated skin, or chronic ulcer/sinus tract
-Recurrent tumour
-Perineural invasion
-Rapid growth
Histopathology
-features:
-hyperchromatism
-pleomorphism
-increased mitotic activity
-intercellular bridges
-irregular masses of epidermal cells that proliferate downward and invade dermis
-differentiated tumours: keratin pearls
-actinically induced: more benign course with low incidence of metastasis
-de novo lesions: more aggressive behaviour, greater potential for metastasis
-regional metastasis:
-Clarkes level IV or V associated with 20% regional metastasis rate
-histologic variations:
-generic
-adenoid
-bowenoid
-verrucous
-spindle-pleomorphic types (sarcomatoid)
Treatment Options
-surgical excision
-XRT
-Moh’s
-neck dissection and superficial parotidectomy for clinically positive nodes only
PREMALIGNANT LESIONS
Actinic Keratoses
-most common premalignant lesion of H+N
766
-chance of malignant progression: 20%
-“sandpaper-like scale”
-atypical squamous cells extend past dermal-epidermal junction into papillary dermis
-tx: superficial shave excision, cryosurgery, topical 5FU, TCA peel
Bowens Disesase
-carcinoma in situ of the skin
-full-thickness dysplasia of epidermis without evidence of invasion
-common in pts with chronic arsenic ingestion
-metastasize in 20-35% of cases; 30% develop invasive SCCa
Keratoacanthoma
-benign usually self-limited epithelial tumour
-in males and older pts
-rapid growth 2-6 months
-involution usually within 2-6 months
-most common area affected: nose
-surgical excision recommended because of lack of predictability
PROGNOSIS
Tumour Behaviour
-see table
Recurrent Cutaneous Lesions

-location of recurrences:
-midface region: 57.6%
-nose: 25.5% to 41%
-auricular and preauricular: 13.4%
-relative risk: FACTORS ASSOCIATED WITH HIGH-RISK
-nose > ears > periorbital areas > face > neck CUTANEOUS MALIGNANCIES
and scalp
Histology
-most common area for recurrent skin cancer: -de novo SCC (vertical growth)
-alar-nasolabial junction -BCC morphea type
-other risk factors for recurrence: -keratotic BCC
-size > 3 cm
Location (“H” zone on the face)
-involvement deeper than skin and -nose, nasolabial sulcus, floor of nose, columella
subcutaneous fat -auricular, postauricular, preauricular
-four or more previous treatments without -periorbital region, embryonic fusion planes
control
Size
-proven metastatic disease ->2 cm
Predisposing factors
TNM CLASSIFICATION OF SKIN CARCINOMA -genetic predisposition or syndrome
-history of arsenic use
-tumour arising in burns or scars
Tx: unknown -tumours arising in area of radiodermatitis
T0: no evidence of primary
Tis: carcinoma in situ Other factors
-recurrent tumours
T1: < 2cm -immune status
T2: 2-5 cm -tumours with significant tissue invasion
T3: > 5 cm
767
T4: tumour invades extradermal structures (cartilage, skeletal muscle, bone)
Nx: nodes cannot be assessed

N0: no regional node metastasis
N1: regional node metastasis
Stage:
I: T1 N0 M0
II: T2 N0 M0
T3 N0 M0
III: T4 N0 M0
Any T, N1 M0
IV: Any T, Any N, M1
MANAGEMENT
Curettage with Electrodesiccation

-most common treatment for BCC < 2 cm
-used by dermatologists - cure rates 92-98%
-advantages:
-maximal sparing of normal tissue, ease of performance and expediency
-disadvantages:
-open wound, depressed or hypertrophic scarring, delayed bleeding
-contraindications:
-lesions with deep invasion, morphealike and sclerotic BCC
-recurrent tumours
Cryosurgery
-for some basal lesions
768
-liquid nitrogen
-advantages:
-high cure rate, tissue-sparing capabilities, expedience
-disadvantages:
-prolonged healing phase and wound care
-hypopigmentation and scarring can occur
Radiation Therapy
-uses: -poor operative candidates, surgical adjunct or for palliation
-curative in select patients
-advantage:
-ability to treat wide field of tumour and avoidance of surgery
-disadvantage:
-protracted treatment course, expense, adjacent tissue effects, limited effectiveness if tumours
involve cartilage or bone, radiodermatitis, delayed carcinogenesis
Photodynamic Therapy
-photosensitizing drug that selectively localizes in tumours exposure to light preferential tumour
necrosis
-still investigational modality
-lack of predictability
Interferon-Alpha
-investigational:
-BCC (nodular and superficial) have excellent responses
-intralesional injection 3x/week
-associated with leukocytopenia and thrombocytopenia
Excisional Surgery
-93-95% successful
-small, primary, well-demarcated nodular BCC:
-3- to 5-mm margin usually sufficient
-multicentric, large, or recurrent tumours, aggressive growth pattern BCCs, and SCC:
-excisional margins should be greater (1-2 cm)
-advantages:
-tissue for diagnosis and to assess completeness of excision
-excellent cosmesis
-disadvantages:
-time consuming, inconvenient
Mohs’ Surgery
-indications:
-recurrence
-morphea type
-high risk of recurrence (H zone)
-cosmetic regions in which reconstruction is difficult
-chemical fixative applied to cancer, fixing it in situ and permitting careful serial excision with examination
of entire specimen histologically
-maps extension of residual tumour so that reexcision of these pockets of cancer were possible
-96-99% cure rates
-advantages:
-examine resection margins in their entirety
769
-microscopic foci of tumour identified, mapped and reexcised
-highest cure rate in management of advanced, high-risk or recurrent lesions
-disadvantages:
-time consuming
-expertise required
Carbon Dioxide Laser

-for multiple premalignant lesions
Treatment for Metastatic SCC
-80-90% of metastases from cutaneous SCCs occur first to the regional nodes
-N0 neck:
-monitoring for clinical nodal disease
-prophylactic radiation to primary site and primary draining lymph nodes reserved for very
high-risk lesions or those with neurotropism
-prophylactic node dissection is usually not recommended for those with no clinical evidence of
regional metastases
-if extension to the parotid capsule elective superficial parotidectomy should be considered
-N+ neck:
-therapeutic options include radiotherapy, surgical lymphadenectomy, or a combination of lymph
node dissection and radiotherapy
RECONSTRUCTION
-if confronted with indistinct deep margins or a high probability of recurrence, consider skin grafting and
observation for 6-12 months
-if possible, place incisions in a facial crease, hair-bearing areas, junctions of facial units, and parallel to
relaxed skin tension lines
-always plan reconstruction from simple to more complex microvascular patterns: primary closure skin
770
graft > local flap > regional flap > free flap
-if using a local facial flap, consider the donor site defect and its effect on functional structures (eg. eyelid,
mouth)
771
MALIGNANT MELANOMA
EPIDEMIOLOGY
-worldwide incidence increasing

-leading cause of death from malignancies of the skin
-2% of all cancer deaths in US
-2:1 M:F
-median age of diagnosis 55y
-15-30% melanomas arise within head and neck
CLINICAL PRESENTATION AND DIAGNOSIS
-pigmented lesion that changes over weeks to months

-increased diameter or height, variations in border, colour, ulceration, itching, pain, and bleeding
-10% may lack melanin
-risk factors:
-UV-B
-fair skin (blue-green eyes)
-history of childhood sun exposure with episodes of severe sun burning
-FHx of cutaneous malignancies
-familial dysplastic nevus syndrome
-immunosuppression
-previous melanomas
-pre-existing pigmented lesions
-age
-radial (intraepithelial) vs. vertical (intradermal- invasion through dermal-epidermal junction) growth
-ABCD’s of melanoma:
-A: asymmetry - irregular shape
-B: border irregularity; bleeding and ulceration
-C: colour variation
-D: diameter (>1 cm, increasing in size)
-four clinicopathologic types:

-lentigo maligna
-premalignant pigmented lesion in head and neck of elderly pts
-Hutchinson melanotic freckle
-5% progress to LM melanoma - 6-10% of melanoma lesions
-excise with 0.5 cm margins
-slow radial growth phase - may take 10 years to progress
-superficial spreading
-most common melanoma (65-75% cases)
-radial growth for 5-7 years then may become invasive
-high cure rates when detected in radial growth phase
-nodular
-10-15% of all melanomas
-occurs in both exposed and non-exposed skin
-most invasive, poorer prognosis
-acral lentiginous
-most common seen in blacks
-soles of feet and hands and oral/anogenital mucosa
F.Ling - Melanoma (1)
772
-differential diagnosis:
-seborrheic keratosis
-benign nevi
-haemangioma
-blue nevi
-pyogenic granuloma
-pigmented basal cell carcinoma
MUCOSAL MELANOMA
-rare; 2% of all H+N melanomas

->50% within nasal cavity
-also sinuses, nasopharynx, oral cavity, oropharynx
-depth of invasion has little or no prognostic impact
-wide excision mainstay therapy; XRT suggested
DESMOPLASTIC MELANOMA
-accounts for fewer than 1% melanoma cases overall

-histologic variant
-75% occur in H+N
-high propensity for neural invasion
-wider resection margins with adjuvant XRT considered
STAGING AND CLASSIFICATION
Clark staging
Level I - All tumor cells above basement membrane (in situ)
Level II - Tumor extends into papillary dermis
Level III - Tumor extends to interface between papillary and reticular dermis
Level IV - Tumor extends between bundles of collagen of reticular dermis (extends into reticular dermis)
Level V - Tumor invasion of subcutaneous tissue
Breslow classification (thickness)

Melanoma 5-year survival and metastasis potential based on
Less than or equal to 0.75 mm pathological staging
0.76-1.5 mm
1.51-4 mm Breslow 5-year survival Nodal Mets Distant Mets
1 >95% 2-3%
Greater than or equal to 4 mm
2 80-94% 20-25% 8%
3 40-84% 57% 15%
AJCC groupings based on TNM 4 10-30% 62% 72%
classification (Buzaid et al)
Stage 0 - pTis, N0, M0
Stage I - pT1, N0, M0; pT2, N0, M0
Stage II - pT3, N0, M0
Stage III - pT4, N0, M0
Any pT, N1, M0
Any pT, N2, M0
Stage IV - Any pT, any N, M1
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T classification (thickness)
T1a - 1 mm without ulceration and level II or III
T1b - 1 mm with ulceration or level IV or V
T2a - 1.01-2 mm without ulceration
T2b - 1.01-2 mm with ulceration
T3a - 2.01-4 mm without ulceration
T3b - 2.01-4 mm with ulceration
T4a - Greater than 4 mm without ulceration
T4b - Greater than 4 mm with ulceration
N classification
N1 - 1 node positive for metastasis
N1a - 1 node positive for micrometastasis
N1b - 1 node positive for macrometastasis
N2 - 2-3 nodes positive for metastasis
N2a - 2-3 nodes positive for micrometastasis
N2b - 2-3 nodes positive for macrometastasis
N2c - Intransit met(s) or satellite(s) without metastatic nodes
N3 - 4 or more metastatic nodes or matted nodes or intransit metastases or satellite(s) with
metastatic node(s).
M classification
M1a - Distant skin, subcutaneous, or nodal metastases, normal LDH level
M1b - Lung metastases, normal LDH level
M1c - All other visceral metastases or any distant metastases with an elevated LDH level
REGIONAL NODAL STAGING
-nodal drainage basins are unpredictable

-risk of regional metastasis varies directly with tumour thickness
-< 0.75 mm: no risk
-0.76-1.49 mm: 25% risk
-1.5-3.9 mm: 60% risk
-> 4.0 mm: > 65% risk
-number of lymph nodes involved more predictive of treatment outcomes than size of lymph nodes
-once the presence of lymph node involvement is confirmed, a therapeutic lymph node dissection is
recommended
-lymphoscintigraphy may provide adjunctive method of defining pathways of regional metastasis

-helpful with midline tumours
Imaging and Occult Nodal Disease

-lesions < 1mm and Clark levels < IV w/o palpable nodes are observed
-lesions > 1mm and Clark levels IV or V
-might benefit from surgery or radiation
-use of U/S, CT or MRI are still not completely reliable in distinguishing regional metastatic
disease from reactive adenopathy
Elective Lymph Node Dissection

-ELND recommended for melanomas beyond level II
-survival benefit to ELND in pts < 60 ya or those who had lesions 1-2 mm in depth
774
-neck dissection usually functional
-radical neck dissection for clinically positive nodes
-no survival benefit seen in those with lesions > 4mm thick
-for lesions > 1 mm thick and for ulcerated lesions without regional metastasis, excision is offered along
with a procedure to assess the status of regional lymph nodes
-development of sentinel lymph node biopsy may enhance sensitivity and specificity of ELND
-lymphoscintigraphy may provide an adjunctive method of identifying sentinel lymph nodes and defining
routes of lymphathic spread, especially in patients with primary tumours located in the midline that have
predicted drainage basins that are ambiguous or include both parotid glands
Sentinel Lymph Node Identification and Biopsy

-ultimate role in H+N still to be determined
-based on concept that there is an orderly progression of lymphatic drainage from first class echelon or
sentinel node to nodes of lower echelons
-if one can identify the sentinel lymph node in a basin at risk for spread from a melanoma and find
it to be free of metastasis, then the remainder of nodes in that basin should also be free of
metastatic tumour
-indications:
-patients at risk for nodal metastasis:
-Breslow > 1.0 mm
-thin melanomas (<1.0 mm) with poor prognostic features (Clarke level III and IV)
-techniques:
-injection of primary site with isosulfan blue dye or hand-held gamma probe to find nodes that
take up a radioactive colloid tracer
-sample first echelon node (4-8% false positive rate):
-if node positive for melanoma complete neck dissection
-if node negative observe
-can focus a more extensive evaluation of lymph nodes at risk for subclinical metastasis
-can increase sensitivity in detection of nodal metastases, thereby improving selection of pts who
receive regional and systemic treatment
-role of SLNB has yet to be fully defined in the management of melanoma of the head and neck due to the
complexity of drainage patterns
TREATMENT
Treatment Overview
-Superficial (<0.76 mm)

-excision with 1 cm margin down to fascia
-ELND not indicated no N0 neck
-Intermediate (0.76-3.99 mm)
-excision with 2 cm margins
-may consider interferon as adjuvant therapy
-N0 neck: may consider SLNB if positive ELND; several studies indicate that ELND confers
survival advantage for intermediate thickness tumours
-N+ neck: neck dissection (may require superficial parotidectomy); may consider chemotherapy
-Deep (>4.0 mm)
-excision with 3 cm margins
-consider interferon
-N0 neck: elective neck dissection not indicated
-N+ neck: neck dissection (may require superficial parotidectomy); may consider chemotherapy
775
Primary Excision
-surgical resection is the mainstay of therapy
-resection margins: -in situ: 0.5 cm
-1-2 mm: 1.0 cm
-2-4 mm: 2.0 cm
->4 mm: > 2.0 cm (3.0 cm)
-frozen sections of analysis for surgical margins had sensitivity and specificity of 100% and 90%
respectively
Regional Lymphadenectomy
-therapeutic neck dissection and parotidectomy
-neck dissection recommended for clinically positive nodes
-extent of neck dissection remains area of controversy
-type tailored to site of primary tumour:
eg. primary of face, ear and anterior scalp: parotidectomy and LND levels I-IV
postauricular and posterior scalp and neck: levels II-V
Radiotherapy
-traditionally thought that melanoma was radioresistant; but this can be overcome by increasing the
individual dose fraction (hypofractionation)
-XRT generally not recommended for primary treatment of melanoma
-exceptions:
-elderly pts who are poor candidates for surgical resection
-extensive facial LM melanoma that precludes adequate surgical resection
-XRT very effective in post-operative adjuvant setting in achieving high rates of local-regional control
-pts should be considered for XRT either to primary site and/or regional nodal basins whose
primary lesions measure 1.5 mm or greater or are ulcerated
-pts with regional metastasis should be offered radiotherapy after excision of primary tumour and
neck dissection
-dosages of 6 Gy are delivered twice weekly over 2.5 weeks to a total of 30 Gy
Systemic therapy
-indications:
-for adjuvant treatment for those completed local-regional therapy and have no evidence of local,
regional, or systemic disease but are at high risk for systemic relapse
-presence of distant metastasis
-high risk patient:
-primary lesions that are ulcerated
-primary lesions > 4 mm or Clark level IV
-pts with satellitosis
-pts with in transit disease
-pts with nodal disease
Interferon
-has yet to be shown unequivocally to improve overall survival
-used for deep primary (> 4mm) or regionally metastatic melanoma
-intensive daily IV dose x 1 month
-3x/week daily maintenance dose for next 48 weeks
-adverse effects:
-cardiac and hepatic toxicity
-constitutional symptoms
-myelosuppression
776
Tumour Vaccination
-strategies stimulate immune system to overcome immune tolerance to tumour antigens and enhance the
immune surveillance of tumour cells
Systemic Therapy for Metastatic Disease

-metastasis to brain, liver, bone: median survival of 3-4 months
-chemotherapy and immunotherapy being studied
-results anticipated
-eg. dacarbazine (DTIC); BCNU, cisplatin, lomustine, hydroxyurea; DTIC with cisplatin and vinblastine
SURVEILLANCE
-those with melanoma:

-55-70% recurrences appear within
first 2 years of therapy
-80% of recurrences will be diagnosed
in the first 3 years after treatment
-PE, LFTs and CXR will detect most of these
recurrences; routine screening with CT is not
recommended
777
NEOPLASMS OF THE NOSE AND PARANASAL SINUSES
EPIDEMIOLOGY
TUMOURS OF THE SINONASAL
-less than 1% of all malignancies TRACT
-risk factors:
Epithelial
-exposure to industrial fumes
-benign
-wood dust (hardwood only) -keratotic papilloma
-nickel-refining processes -fungiform papilloma
-leather tanning -inverted papilloma
-cylindrical papilloma
-mineral oils -adenoma
-chromium and chromium compounds -malignant
-isopropyl oils -squamous cell carcinoma
-lacquer paint -transitional cell carcinoma
-adenoid cystic carcinoma
-soldering and welding -adenocarcinoma
-radium dial painting -melanoma
-previous radiation -olfactory neuroblastoma
-chronic infection -undifferentiated carcinoma
-EBV Burkitt’s lymphoma Non-epithelial
-smoking not a significant etiologic factor -benign
-most common malignant nasal tumours: -fibroma
-SCCa -chondroma
-osteoma
-adenocarcinoma -neurilemoma
-adenoid cystic carcinoma -neurofibroma
-hemangioma
-malignant
-soft tissue sarcoma
EVALUATION -rhabdomyosarcoma
-leiomyosarcoma
Diagnosis -fibrosarcoma
-nasal obstruction, epistaxis, nasal discharge -liposarcoma
-angiosarcoma
-asymptomatic in 9-12% -myxosarcoma
-regional and distant metastases infrequent -hemangiopericytoma
-cervical metastases 1-26% (most series report <10%) -connective-tissue sarcoma
-infraorbital or supraorbital numbness suggests malignant -chondrosarcoma
-osteosarcoma
invasion -lymphoreticular tumours
-proptosis, chemosis, EOM impairment, mass effect in cheek, -lymphoma
loose dentition -plasmacytoma
-giant cell tumour
-CT or MRI for evaluation Metastatic carcinoma
-CT: -good for demonstrating bone erosion
-MRI: -differentiates adjacent tumour from soft
tissue
-differentiates secretions in an obstructed sinus from space-occupying lesion
-demonstrates perineural spread
-less artifact effect with dental fillings
-imaging in sagittal plane
-no ionizing radiation
F.Ling - Neoplasms of Nose and Sinuses (1)
778
PARANASAL SUBSITES
Paranasal Sinuses:
-maxillary sinus most common site involved
-ethmoid sinus second most common
-typically presents in an advanced stage
Nasal Cavity:
-less than 10% regional metastatic potential
-60% 5-year survivial
Anterior Cranial Fossa:

-bordered posteriorly by the lesser wing of the sphenoid and optic chiasm and extends to the
frontal bone
-floor contains the orbital plates of the frontal bone, fovea ethmoidalis, and cribriform plate
Pterygopalatine Fossa:
-pyramidal-shaped space below the apex of the orbit and between the posterior wall of the
maxillary sinus and pterygoid plates
-contains foramen rotundum, vidian nerve, sphenopalatine nerve, lesser and greater palatine
nerves, sphenopalatine ganglion, and internal maxillary artery
-invasion of this space carries a poor prognosis
Infratemporal Fossa:
-bounded anterior by the maxilla, postiorly by the glenoid fossa and mandible, and medially by the
lateral pterygoid plates
-roof contains the foramen ovale and spinosum
-also contains the pterygoid muscles
Orbital Cavity:
-invasion into bony orbit or orbital apex requires orbital exenteration
PATHOLOGY
Benign Epithelial Tumours
Papilloma
-may extend beyond site of origin and destroy bone
-three types:
-fungiform (50%)
-septum
-HPV 6 and 11
-22-50% recurrence rate
-3-5% associated with malignancy
-inverted (47%)
-lateral wall
-13% (10-15%) associated with malignancy; degenerates to non-keratinizing
SCCa
-HPV 16 and 18 weakly associated with malignant degeneration
779
-cylindrical (3%)
-lateral wall
15% associated with malignancy
-treatment of inverted papilloma:
-resection via lateral rhinotomy-medial maxillectomy approach
-endoscopic resection
Adenoma:
-arise from septum
-recurrence rate low after complete removal
Malignant Epithelial Tumours
SCC:
-risk factor: nickel exposure
-most common tumour of sinonasal tract (~80%)
Adenocarcinomas
-risk factors: wood dusts, leather tanning
-4-8% of all sinonasal tumours
-originate at ethmoid sinuses
-high (higher incidence of metastasis) and low (tend to recur locally) grades
Adenoid cystic carcinoma

-20% of all ACC arising in head and neck
-early neurovascular invasion
-grades:
-low: less than 30% solid architecture
-high: more than 30% solid architecture
-higher incidence of local recurrence and metastasis
Melanoma
-primary (<1%) or metastatic
-early vascular and lymphatic invasion
-median survival 36 months
Olfactory neuroblastoma
-arises from olfactory epithelium
-bimodal frequent at 10-20 and 50-60 ya
-histopathology:
-homogenous small cells with uniform round-to-oval nuclei
-true rosettes (Flexner-Wintersteiner [FW]):
-ring of columnar cells circumscribing a central oval-to-round space, which
appears clear on traditional pathological sections
-pseudorosettes (Homer Wright [HW]) rosettes:
-looser arrangement and the presence of fibrillary material within the lumen
-immunohistochemistry:
-positive for S-100 protein and/or neuron-specific enolase
-negative for cytokeratin, desmin, vimentin, actin, glial fibrillary acidic protein,
UMB 45, and the common leukocytic antigen
780
-Kadish Staging System:
-A: confined to nasal cavity
-B: in nasal cavity extending to PNS
-C: extending to orbit, base of skull, cranial cavity or with cervical/distant
metastasis
-UCLA Staging System:
-T1: involving nasal cavity and/or PNS, sparing most superior ethmoidal air cells
-T2: involving nasal cavity and/or PNS with extension to or erosion of cribriform
plate
-T3: extending into orbit or protruding into anterior cranial fossa
-T4: involving brain
-treatment: craniofacial resection +/- post-op XRT
Sinonasal undifferentiated carcinomas (SNUC)

-rapid progression, usually advanced stage at presentation
-treatment: surgery, radiation, chemotherapy
Benign Nonepithelial Tumours
Fibroosseous lesions
-osteomas, fibromas, chondromas most common
Sinonasal nerve sheath tumours

-2/3 schwannomas; 1/3 neurofibromas
-total removal usually advocated
Malignant Nonepithelial Tumours
Neurogenic sarcoma
-rare - most commonly associated with NF
Rhabdomyosarcoma
-embryonal, alveolar and pleomorphic types
-tumours involving PNS classified as nonorbital parameningeal - behave more aggressively
-treatment: usually radical surgery with intensive radiation and chemotherapy
Fibrosarcoma
-arises from fibroblasts
-etiologic factors: radiation and trauma
-treatment: wide surgical resection; XRT for positive margins or recurrent tumours
Hemangiopericytoma
-arises from pericytes of Zimmermann
-considered low grade malignancy
-vascular, rare
-treatment primarily surgical
Osteogenic sarcoma
-etiologic factors:
-ionizing radiation, fibrous dysplasia, trauma, Paget disease, gene associated with
retinoblastoma
-treatment: surgical excision
781
Chondrosarcoma
-slow-growing
-surgical removal with wide margins
-metastatic potential and oncologic outcome of sarcomas is variable, however local behaviour is similar
-sarcomas are infiltrative
-often incompletely resected
Lymphoma
-usually non-Hodgkin type
-treatment: XRT for localized lesions and chemotherapy for systemic involvement
Extramedullary plasmacytoma
-found in H+N 80-90% of cases, 40% in sinonasal tract
-prognosis unpredictable
-most lesions respond to XRT
STAGING
Maxillary Sinus
TX -primary tumour cannot be assessed

T0 -no evidence of primary tumour
Tis -carcinoma in situ
T1 -tumour limited to antral mucosa with no erosion or destruction of bone
T2 -tumour with erosion or destruction of infrastructure, including hard palate and/or middle nasal
meatus
T3 -tumour invades: skin of cheek, posterior wall of maxillary sinus, floor or medial wall or orbit, or
anterior ethmoid sinus
T4 -tumour invades orbital contents and/or any of the following: cribriform plate, posterior ethmoid
or sphenoid sinuses, nasopharynx, soft palate, pterygomaxillary or temporal fossae, or base of
skull
Ethmoid Sinus
T1 -confined to ethmoid with or without bony destruction

T2 -spread into nasal cavity
T3 -involvement of anterior orbit and/or maxillary sinus
T4 -intracranial, intraorbital, sphenoid, frontal, skin of external nose
Ohngren’s Line
-imaginary line drawn between medial canthus and angle of mandible
-tumours arising below this line have better prognosis than tumours arising above this line
-staging for soft-tissue sarcomas based on histologic features
782
PRINCIPLES OF TREATMENT
Concepts
Early stages:
-single modality primarily with surgical resection for early maxillary or nasal cavity tumours
(except for small cell carcinoma, lymphoma, rhabdomyosarcoma)
-primary radiation therapy
Advanced stages:
-multimodality treatment:
-primary surgery with postoperative XRT
-primary XRT with surgical salvage
-Unresectable/Nonoperable candidates;
-may consider primary radiation, chemotherapy, or combination radiochemotherapy
Surgery
-approaches:
-endoscopic excision:
-low morbidity, no external scar, limited to benign small lesions
-lateral rhinotomy
-incision begins at medial aspect of eyebrow, follows along lateral nasal wall, around alar
crease to the philtrum and a sublabial incision
-may extend incision to include the lip for exposure of hard palate
-midfacial degloving approach
-incisions:
-transfixion incision
-intercartilaginous incision
-gingivobuccal incision -from midline to maxillary tuberosities
-for lesions that are inferior and involve medial maxillary walls
-limited superior and posterior visualization
-avoids external incisions and allows bilateral exposure
-Weber-Ferguson incision:
-addition of subciliary incision and lip splitting incision to lateral rhinotomy incision
-transpalatal:
-for tumours involving floor of nose/inferior portion of maxilla
-infratemporal fossa approach:
-access obtained via a preauricular or postauricular incision with extension in a
hemicoronal and cervical fashion
-may gain additional exposure by retracting the TMJ
-Raveh approach - anterior craniotomy
-anterior craniofacial resection for anterior tumours
-resection types
-medial maxillectomy
-removes lateral nasal wall and medial maxilla
-standard resection for inverting papillomas
-partial maxillectomy
-tumours confined to floor of antrum inferior maxillectomy
-preservation of orbital floor
783
-total maxillectomy
-removal of entire maxillary bone
-radical maxillectomy
-total maxillectomy with orbital exenteration
-craniofacial resection
-en bloc removal of the anterior cranial base including the cribriform plate and ethmoid
sinuses
-may require dural excision
Radiation Therapy
-may be used as single modality, adjunct to surgery, or as palliative therapy
-usually for unresectable or lymphoreticular tumours, poor surgical candidates
Chemotherapy
-usually used for palliation; limited reports based on non-randomized studies
Combination Therapy
-for positive margins, perineural, perivascular invasion
-positive lymph nodes or recurrent tumour
Treatment of SCCa by Site of Origin
Nasal Cavity
-usually detected earlier associated with better prognosis
-SCCa most common malignant tumour in this area
-tumours extending to PNS, larger than 2 cm, or positive margins: post-op radiation
-5-year survival > 60%
Maxillary Antrum
-most common site of origin for malignancies of the sinonasal tract
-usually diagnosed at advanced stages: combination therapy
-5-year survival 40-50%
Ethmoid Sinus
-earlier diagnosis and better prognosis
-combination therapy recommended
Sphenoid Sinus
-extremely rare
-gross total removal and postop XRT
Frontal Sinus
-rare
-managed by combination therapy
784
MANAGEMENT OF ADVANCED TUMOURS
Orbital Invasion
-pathways of invasion:
-direct bony erosion (eg. medial wall or floor)
-perivascular or perineural invasion (eg. infraorbital or ethmoidal NV bundles)
-preformed pathways (eg. infraorbital fissure, nasolacrimal duct)
-bone erosion does not constitute an absolute indication for orbital exenteration
-prognosis is dismal palliation
-meta-analysis: no statistically significant difference in survival rate of patients who had orbital
exenteration compared to those that did not
-resection of medial an inferior orbital walls produces severe exophthalmos and hypophthalmos
-rigid reconstruction of bony orbit using titanium mesh +/- calvarial bone grafts
Cervical Metastasis
-incidence: 3-16% (10%)
-poor prognostic indicator
-elective neck dissection or irradiation for N0 neck not justified
-cervical metastasis usually during first 48 months after initial treatment sign of tumour recurrence
Pterygopalatine Fossa
-incidence 10-20%
-presence of tumour in this area a risk factor for recurrence
-radical surgery and radiation therapy advised
Infratemporal Fossa and Skull Base

-invasion by direct, bone erosion or preformed pathways (eg. cribriform plate, superior orbital fissure,
foramen lacerum), NV structures (V2, V3)
-craniofacial resection
-absolute contraindications (treatment offers no benefit; increases mortality and morbidity):
-medical or nutritional problems (poor surgical candidate)
-presence of distant metastases
-invasion of prevertebral fascia
-invasion of cavernous sinus
-involvement of carotid artery in a high-risk patient
-bilateral invasion of optic nerves or optic chiasm
-invasion of dura and intracranial involvement of neural structures by adenoid cystic carcinoma
-overall 5-year survival 50-60%
RECONSTRUCTION OPTIONS
-fascial, temporalis muscle, pericranial/galea flaps

-provides additional support for watertight closure of skull base and dural defects
-regional or microvascular free flaps
-soft tissue bulk
-prosthetic obturator
785
COMPLICATIONS
Orbital
Surgical
-epiphora
-from stenosis of lacrimal sac
-tx: DCR or cannulation of lacrimal canaliculi for 12 weeks
-diplopia
-from limitation of EOM
-may be secondary to entrapment in craniofacial osteotomies
-tx: observe, release EOM if entrapped
-blindness:
-from compression of optic nerve
-tx: high-dose steroids and emergent surgical decompression
-exophthalmos or hypophthalmos
-tx: support globe with bone grafts and/or titanium mesh
Radiation Therapy
-full eye irradiation:
-dry eye will decompensate rapidly, leading to severe keratitis, panophthalmitis and
blindness within 1 year enucleation recommended
-100% of eyes receiving 5800 rad will develop severe panophthalmopathy and severe
corneal ulceration
-post-radiation retinopathy or optic neuropathy
Wound
-bleeding: packing, arterial ligation, or embolization
-infection: antibiotics/debridement
-loss of reconstructive flaps or skin grafts: debridement
Skull Base
-CSF leak
-observation, bed rest
-reconstructive flap for persistent leak
-meningitis
-antibiotics, correct CSF leak
-pneumocephalus
-aspiration if at tension and diversion of nasal airway with use of ETT, nasal trumpets or a
tracheotomy
-osteomyelitis: antibiotics, debridement, HBO
-frontal lobe syndrome: changes in patient’s affect
-cranial nerve injuries
EMERGENCIES ASSOCIATED WITH SINONASAL TUMOURS
Bleeding
-tx: -cauterization/packing
-arterial ligation/embolization in case of massive tumour where packing is impossible
-transoral ligation of internal maxillary artery and transorbital ligation of ethmoidal
arteries
786
Visual Impairment
-blindness d/t compression or stretching of optic nerve, its arterial supply or its venous drainage
-decompression of orbit or optic nerve
-radiation for lymphoreticular tumours
Infection
-acute bacterial sinusitis and possible orbital and intracranial complications
-treat with antibiotics and debridement
CSF leak or Pneumocephalus

-may occur after destruction of skull base and disruption of dura mater
-unlikely to resolve spontaneously and should be managed by prompt craniofacial resection, dural grafting
and pericranial flap
-tension pneumocephalus treated by transcutaneous needle aspiration
-emergency extirpative surgery
787
ORBITAL TUMOURS
-primary tumours
-hemangioma, NHL, inflammatory tumours, meningioma, optic nerve glioma
-secondary tumours
-invasion from other structures
-12% of orbital lesions; 33-45% of orbital neoplasms
-mucoceles, SCCa, meningioma, vascular malformations, BCC
-metastatic disease
-adenocarcinoma of lung and breast
-2-8% of orbital tumours
-pediatric group
-most are benign
-orbital dermoids, vascular tumours, optic nerve glioma, and inflammatory tumours
-10-30% malignant
-most common is rhabdomyosarcoma
-metastatic neuroblastoma, leukemic orbital involvement, Ewing sarcoma, extension of
retinoblastoma
-symptoms and signs:

-proptosis most common
-axial proptosis: occurs d/t tumours inside EOM cone
-non-axial proptosis: extraconal tumour
-EOM dysfunction, diplopia
-vision changes, conjunctival injection and chemosis, pain, pupillary changes
VASCULAR TUMOURS
Cavernous Hemangioma
-most common primary intraconal orbital neoplasm found in adults
-slowly progressive, painless, unilateral proptosis over many years
-CT/MRI for diagnosis
-discrete round or oval mass without associated inflammation or infiltration
-usually enhances with IV contrast
-tx: complete surgical excision with excellent prognosis
Capillary Hemangioma
-most common vascular tumour of orbit and periocular tissue in infancy and childhood
-upper eyelid most common periocular location
-usually first noted during first month of life and grows to maximum size by 12-18 months of age
-spontaneous involution by age 4-8 years
-50% at 5years; 90% at 7 years
-complications:
-have potential to cause derivational and anisometropic amblyopia
-cosmetic cutaneous deformities
-proptosis and corneal exposure
-bony malformations
-CT/MRI:
-diffusely infiltrating nonencapsulated mass
-conformation to surrounding orbital structures
F.Ling - Orbital Tumours (1)
788
-treatment for:
-amblyopia, proptosis with corneal exposure, optic nerve compression, bony deformities
-intralesional injections of corticosteroids, systemic steroids or careful debulking surgeries
Lymphangioma
-arise from pluripotent mesodermal tissue of the orbit and surrounding structures
-multiple, variably sized, thin-walled, endothelial-lined vascular channels
-superficial, deep, or both
-superficial:
-more common: involve conjunctiva and eyelids
-enlargement from bleeding, URTI
-CT: multiple, contiguous, dilated cystic spaces within orbit
-may be confused with a varix (dilated orbital vessel)
-varix is connected with normal circulation: enhances with contrast and enlarges with Valsalva
-resection difficult d/t infiltrative nature
-surgical debulking and cyst drainage are mainstays of treatment
HEMATOPOIETIC TUMOURS
Lymphoid Tumours
-represent 4-13% of all orbital tumours
-development of systemic lymphoma:
-20% with lymphoid tumours of conjunctiva
-35% with orbital tumours
-67% with eyelid disease
-orbital lymphoid lesions:
-almost exclusively in adults
-slowly progressive painless proptosis over several weeks to months
-CT:
-“putty-like” molding of tumour around other orbital structures
-no bony destruction
-most extraconal
-superior orbit most common location
-lacrimal gland involved in 40% cases
-biopsy needed for diagnosis
-most lymphomas are of monoclonal B-cell origin
-most reactive orbital lymphoid lesions are composed of a majority of T cells and polyclonal B
cells
Leukemia
-orbit can harbour malignant leukemic cells
-more common in children and often bilateral
-may resemble orbital cellulitis
-granulocytic sarcoma:
-collection of immature myeloid cells forming a mass in the orbit
-more common in children and may be seen in both acute and chronic myelogenous leukemia
-poor prognosis
-radiotherapy often used to treat orbital lesions
789
Langerhans Cell (Histiocytosis X)
-Langerhans cell is a macrophage that normally resides in epidermis of skin
-dz characterized by one or more destructive bone lesions of skull, ribs, sternum, long bones, vertebrae or
pelvis
-orbit rarely affected
-frontal and zygomatic bones most commonly involved orbital structures
-CT: circumscribed lytic bone lesion without sclerosis
-excision of isolated orbital bone lesions often curative
NEURAL TUMOURS
Schwannoma (Neurilemmoma)
-accounts for ~1% of all orbital tumours
-progressive visual loss or RAPD may be cause by tumours located in orbital apex
-more commonly located in intraconal space
-CT:
-well-circumscribed elongated ovoid mass that displaces surrounding structures
-may have areas of cystic degeneration and calcification
-small degree of enhancement after intravenous contrast injection
-MRI:
-hypointense on T1
-hyperintense on T2
-histology:
-schwann cells with characteristic patterns:
-Antoni A: orderly palisading arrangement of elongated spindle-shaped cells
-Antoni B: loose myxoid arrangement of ovoid or stellate cells
-tx: complete surgical excision
Optic Nerve Gliomas

-5th most common primary intraorbital tumour
-2nd most common orbital tumour found in children
-cell responsible: fibrillary astrocyte
-associated with NF in 18-50% of cases
-presentation:
-mean age 8 years
-axial proptosis and vision loss
-optic nerve head edema
-CT: -fusiform or lobular, isodense, homogeneous enlargement of the optic nerve
-MRI:
-to evaluate extension of tumour into optic canal and chiasm
-hypointense relative to brain in T1
-hyperintense in T2
-treatment:
-observation and monitoring for pts with tumours confined to orbit along with good vision
-progressive growth resection of optic nerve from posterior surface of globe to optic chiasm
Orbital Meningiomas
-arise from optic nerve
-3% of all orbital tumours
-75% are female; 4th-7th decade; rare in children
790
-presentation:
-proptosis and visual complaints
-optic disk pallor, optic nerve head edema, diplopia, headaches, optociliary shunt vessels, ptosis
-CT:
-focal exophytic mass at any point along optic nerve
-may have calcification of tumour in subarachnoid space along optic nerve tissue “railroad
track” appearance
-cannot be removed from surface of optic nerve without causing severe vision loss
-tumours usually followed in elderly patients
-radiotherapy and hormone therapy used in some patients
MESENCHYMAL TUMOURS
Mesodermal and Muscle Tumours
Rhabdomyosarcoma
-most common primary malignant tumour of orbit in children
-most common soft-tissue malignancy of childhood
-presentation:
-progressive, painless, unilateral proptosis
-ptosis and palpable mass
-conjunctival chemosis, ophthalmoplegia, choroidal folds, optic disk edema, dilated retinal vessels
-CT:
-poorly defined homogeneous orbital mass
-25% intraconal
-bone destruction and sinus invasion present
-types:
-2/3 are embryonal
-alveolar most malignant and has predilection for inferior orbit
-pleomorphic most well-differentiated and carries best prognosis
Fibroosseous Tumours
Fibrous Dysplasia
-replacement of normal cortical bone with a cellular fibrous stroma containing multiple nests of immature
woven bone
-orbital and facial bone involvement more typical of monostotic form
-orbital roof most common site of orbital involvement
-presentation:
-proptosis, globe and orbit displacement, facial asymmetry
-CT:
-involved bone appears thickened and deformed
-multiple areas of lucent-appearing lytic spaces and “ground glass”-appearing sclerotic zones
-treatment:
-usually observation
-surgical removal if causing significant cosmetic deformity or vision loss secondary to
compressive optic neuropathy
-debulking the only option for some large tumours
791
Osteoma
-known to arise from bones of paranasal sinuses
-most originate from frontal bone
-unilateral solitary lesions
-r/o Gardner syndrome:
-familial condition associated with soft-tissue tumours and colon carcinoma
-CT: smooth rounded or lobulated mass with density similar to normal bone
-small tumours observed; larger tumours resected
Osteosarcoma
-more commonly affects long bones
-rare orbital involvement
-gene responsible of osteosarcoma and retinoblastoma discovered on chromosome 13
-presentation: orbital pain, numbness and vision loss
-extremely poor prognosis
-surgical resection and systemic chemotherapy
LACRIMAL GLAND TUMOURS
-proptosis and medial and inferior globe displacement

-most masses d/t inflammatory disease
-infection:
-acute dacryoadenitis
-bacterial: staph and strep species most common
-viral: herpesvirus, mumps, mononucleosis
-lymphoproliferative disorders:
-benign reactive lymphoid hyperplasia
-atypical lymphoid hyperplasia
-malignant lymphoma
-leukemia
-epithelial neoplasms
-pleomorphic adenomas
-50% of epithelial neoplasms
-proliferations of both epithelial and mesenchymal elements
-CT: round well-circumscribed mass in anterior portion of superior lateral orbit
-pressure of lacrimal gland fossa w/o bony destruction
-tx: complete surgical resection without incisional biopsy (prevents recurrence)
-other 50% carcinomas:
-adenoid cystic
-most common malignant epithelial neoplasm of lacrimal gland
-malignant mixed carcinoma
-adenocarcinoma
-mucoepidermoid carcinomas
-pain and numbness common

-CT demonstrates bony destruction; calcification more likely in malignant lesions
-mortality > 50%
-tx: complete resection, exenteration, removal of adjacent bone, postoperative
radiotherapy
792
INFLAMMATORY TUMOURS
-idiopathic orbital inflammation

-dull and poorly localized orbital pain often exacerbated by eye movement
-eyelid swelling, conjunctival chemosis, diplopia
-vision loss in 20%
-CT: multiple tissues in orbit affected
-MRI: T1 isointense with muscle and enhance with contrast; T2 isointense to hyperintense to
surrounding orbital fat
-treatment:
-oral corticosteroids
-may require immunosuppressive medications
-orbital vasculitis
-rare
-associated with many systemic vasculitic syndromes:
-WG, PAN, giant cell arteritis
-suspected idiopathic orbital inflammation that does not respond as expected to oral prednisone
demands a biopsy for histologic examination
CYSTS
-most common primary: dermoids
-most common secondary: mucocele
-dermoid cysts:
-arise from bits of embryonic ectoderm trapped within suture lines between orbital bones
-superficial dermoids: frontozygomatic, frontoethmoid, or frontolacrimal sutures
-subcutaneous mass at lateral portion of eyebrow
-deep orbital dermoids: sphenozygomatic or sphenoethmoid suture
-present with painless progressive proptosis and globe displacement
-CT:
-round, well-defined, thin-walled structure with non-enhancing lumen
-may have dumbbell shape as they extend through suture into temporalis fossa, sinuses or
cranial vault
-histology:
-stratified squamous epithelium with presence of dermal appendages
-treatment: surgical resection if symptomatic
SECONDARY TUMOURS
-account for 44% of all orbital tumours

-mucocele
-most common mass lesion of orbit originating in the paranasal sinuses
-usually from frontal and ethmoid sinuses
-SCCa:
- most common sinus tumour invading orbit
-maxillary sinus site of origin in 80% of cases
-meningioma:
-most common tumour extending from cranial vault
-arise from sphenoid ridge
-CT: hyperostosis of involved bone
-MRI: enhances with contrast
793
-BCC, sebaceous cell carcinomas, SCCa: most common eyelid neoplasm
-BCC: most common eyelid malignancy
-usually involving lower eyelid and medial canthus
-orbital exenteration and postop XRT advocated for orbital invasion
-SCCa and melanoma:
-most common lesions of conjunctiva
-choroidal melanoma:
-most common intraocular tumour
-retinoblastoma:
-malignant neoplasm of sensory retina
-most common intraocular tumour in children
-treatment combination of surgical excision, radiotherapy and chemotherapy
METASTATIC TUMOURS

-breast cancer represents 50% of metastatic lesions (most common)
-other malignancies
-lung carcinoma, prostate, GI, renal cell, thyroid, malignant melanoma
-most common metastatic tumour in children is neuroblastoma
-CT:
-most common site of metastasis is intraconal space
-well-defined infiltrative mass that enhances with contrast
-bones of orbit another common site osteolytic and osteoblastic lesions
-poor prognosis
-tx: radiotherapy and/or chemotherapy
794
SALIVARY GLAND NEOPLASMS
-major salivary glands: parotid, submandibular, sublingual glands

-minor salivary glands: 600-1000 glands distributed throughout upper aerodigestive tract
Theories of Salivary Gland

Neoplasms
Multicellular Theory:
-neoplastic cells originate
from their secretory unit
counterparts
-eg. oncocytic tumours
from striated ducts,
acinic cell carcinoma
from acinar cells
Bicellular Theory:
-all neoplastic cells
differentiate from basal
(reserve) cells in
excretory and
intercalated
Origin of various salivary gland neoplasms according to Multicellular Theory
-Adults:
-80% parotid; 80% benign
-10-15% submandibular; 50% benign
-5-10% sublingual and minor salivary
glands; < 40% benign
-95% salivary gland neoplasms in adults
-Children:
-68% benign; 32% malignant
-most common benign mesenchymal
tumour: haemangioma
-most common benign epithelial tumour:
pleomorphic adenoma
-most common malignant: mucoepidermoid
carcinoma
-benign: mixed (48%), hemangioma (31%),

neurofibroma (6%), misc (15%)
-malignant: MEC (37%), acinic cell (22%),
rhabdomyosarcoma (9%), lymphoma (9%),
misc (23%)
F.Ling - Salivary Gland Neoplasms (1)
795
BENIGN NEOPLASMS
Pleomorphic Adenoma
-65% of all salivary gland neoplasms
-parotid > submandibular > minor salivary glands
-smooth, lobular
-histology:
-myoepithelial component:
-spindle shaped with hyperchromatic nuclei
-epithelial (ductal luminal) component:
-varied growth patterns
-stromal component
-products of myoepithelial cells
-myxoid, chondroid, fibroid, or osteoid
components
-incomplete encapsulation and transcapsular growth with pseudopod extensions high rate of recurrence
after surgical enucleation
Warthin’s Tumor
-papillary cystadenoma lymphomatosum
-second most common benign neoplasm of parotid gland
-6-10% of all parotid tumours
-men, 4th-7th decades
-10% bilateral; malignant tumours rare
-histology:
-multiple cystic spaces with thick mucinous material
-epithelial component:
-papillary epithelium
-double layer of oxyphilic granular cells
-inner or luminal cells, non-ciliated, tall
columnar nuclei at luminal aspect
-outer or basal cells are round, cuboidal with vesicular nuclei
-lymphoid component:
-lymphoid stroma projecting into cystic spaces
-treatment: surgical excision; recurrence uncommon
Oncocytoma
-only in parotid gland
-<1% of all salivary gland neoplasms
-M=F; 6th decade of life
-histology:
-granular eosinophilic cells with small indented nuclei
-granularity from abundant mitochondria
-EM: mitochondria-filled cytoplasm
-tx: superficial parotidectomy
Monomorphic Adenoma
-benign, non-aggressive tumours
-basal cell adenoma (most common), clear cell adenoma, glycogen-rich adenoma
-well-circumscribed and encapsulated
-histology:
-rows of peripheral palisading cells with thick basement membrane
796
MALIGNANT NEOPLASMS
-most common malignant tumour of parotid (adults and children)
-second most common of submandibular
-60-70% located in parotid gland; palate next most frequent site
-low-grade:
-higher ratio of mucous cells to epidermoid cells
-behave like benign neoplasms
-small and partially encapsulated
-histology:
-aggregates of mucoid cells separated by
strands of epidermal cells
-macrocystic tumour foci
-intraluminal papillary projections
-positive keratin and mucin staining
-tx: superficial parotidectomy
-high-grade:
-higher proportion of epidermoid cells; may resemble SCCa
-aggressive neoplasms
-larger and locally invasive
-histology:
-few mucoid elements; very few cystic foci
-more solid nests of cells
-isolated foci of squamous keratinocytes and mucous secreting cells
-prominent clear cell may be present
-positive keratin and mucin staining
-tx: parotidecotmy with selective neck dissection (N0), radical neck dissection (N+), +/-
postoperative XRT

-“cylindroma”
-6% of salivary gland neoplasms
-most common malignancy of submandibular gland and minor salivary glands
-M=F; 5th decade
-most often presents as asymptomatic mass; facial paralysis and pain in small percentage of cases
-histology:
-basaloid epithelium arranged in cylindric formations in an eosinophilic hyaline stroma
-perineural invasion a typical feature
-low grade:
-cylindromatous (tubular) pattern (grade I)
-cribriform pattern: nests of cells with round
spaces “Swiss cheese” appearance (grade II)
-high grade: (worse prognosis)
-solid pattern (grade III)
-tx:
-complete surgical excision and postoperative radiation
-radical neck dissection for N+ only
-progresses in slow relentless fashion; long-term
survival even with mets
797
-local recurrence and persistence:
-70% 5-year survival
Acinic Cell Carcinoma

-low grade salivary gland malignancy
-1% of all salivary gland neoplasms
-2-4% of parotid gland neoplasms
-95% occur in parotid gland
-composed of serous cells
-F>M; 5th decade of life
-second most common salivary gland malignancy in childhood
-bilateral involvement in 3%
-histology:
-“blue dot” tumour abundance of basophilic granules
-serous acinar cells
-PAS stain (stains glycogen) brings out
granules
-cells with clear cytoplasm
-patterns: solid, microcystic, papillary cystic, follicular
-benign course in early years; decline in survival approaching 50% at 20 years
-tx: total parotidectomy with facial nerve preservation (unless nerve is directly involved)
-prognosis:
-most favourable prognosis and survival
-with recurrence 20 year survival ~50-60%
Adenocarcinoma
-commonly occurs in minor salivary glands
-aggressive; likely metastasize
-histology:
-no clear histomorphologic features diagnosis of exclusion
-cylindric cells of variable height form papillae, acini, or solid masses
-mucinous staining; differentiate from MEC by lack of keratin staining
-grading based on degree of glandular formation
Polymorphous Low-Grade Adenocarcinoma

-second most common malignancy of minor salivary glands
-palate, buccal mucosa, upper lip
-F>M; 6th decade
-histology:
-variable tumour cell differentiation and
organization
-cells arranged in solid lobular islands, diffuse
sheets, islands with internal ductules, cribriform and
papillary arrangements
-frequent perineural invasion characteristic
-spindle and clear cell areas stain positive with S-
100
-tx: wide total excision
-prognosis: indolent invasive and persistent course; metastasis uncommon
798
Carcinoma Ex-Pleomorphic Adenoma
-tumour arising from pre-existing pleomorphic adenoma
-2-5% of salivary gland tumours
-slowly growing mass that suddenly increases in size; usually been present for 10-15 years
-histology:
-characteristics of a mixed tumour
-malignant portion may appear as an adenocarcinoma, SCC, undifferentiated carcinoma, or some
other form of malignancy
-local and distant metastasis common
-poor prognosis
-overall 5-year survival is 40%
-tx: combination surgery and radiation recommended

-rare
-submandibular > parotid
-50% are metastatic SCCa from skin
-M>F; 7th decade
-histology:
-intracellular keratinization, intercellular bridges, keratin pearl formation
-produce no mucous
-poor prognosis 35% 5-year survival
-tx: parotidectomy with postoperative radiation
Undifferentiated Carcinoma
-rare
-M=F; 7th decade
-Greenlandic Eskimos: high incidence related to EBV
-aggressive with early metastasis and low survival rates
Sarcoma
-rare
-rhabdomysarcomas and fibrosarcomas most common histopathologic types
Lymphoma
-primary lymphoma rare (no known extrasalivary lymphoma)
-arises from intraglandular lymphoid tissue that occurs during embryonic development
-prognosis generally good
Metastatic tumours to the parotid

-most common source is lungs
799
ASSESSMENT AND DIAGNOSIS
Etiologic Factors
-smoking not associated with most salivary neoplasms
-associated with development of Warthin’s tumour
-radiation-induced
-latency ~15-20 years
-most important etiologic factor
-most commonly pleomorphic adenoma
-most common malignancy is mucoepidermoid carcinoma
-occupational exposure to wood and furniture industries linked to minor salivary gland neoplasms
(adenocarcinoma of nasal cavity and paranasal sinuses)
History
-asymptomatic masses common
-pain associated with neural invasion
-head and neck exam
-facial nerve function
-multiple masses, invasion of surrounding tissue, and associated cervical lymphadenopathy should raise the
suspicion of malignancy
Fine-Needle Aspiration Biopsy

-accurate aid in diagnosis
-depends on skill of cytopathologist
Radiology
-CT/MRI useful for assessment of tumours involving parapharyngeal space
Diagnostic Surgery
-excisional biopsy and enucleation is associated with high rates of tumour recurrence
-proper approach is parotidectomy with preservation of facial nerve
-normal anatomic structures mimicking neoplasm:
-masseter, transverse process of atlas, processes of mandible
-inflammatory diseases; chronic sialadenitis
-nutritional deficiencies
-infections
-cystic lymphoepithelial lesions (HIV)
-metastasis: melanoma and SCC
-necrotizing sialometaplasia: benign but mimics SCC
800
MANAGEMENT
Surgery
-superficial parotidectomy
-tumour removed with a cuff of normal tissue
-also curative for low-grade malignancies
-eg. low-grade MEC, acinic cell carcinoma
-management of tumours involving the facial nerve (controversial):
-facial nerve resection if involved with tumour followed by immediate nerve grafting
-if facial nerve is functioning and able to sharply dissect tumour off, then try to save nerve
-modified neck dissection performed for histologically positive nodes
-no neck dissection for adenoid cystic carcinoma because no nodal metastasis
Anatomic Landmarks for facial nerve identification

-tragal pointer (nerve is 1 cm anterior inferior)
-tympanomastoid suture (nerve is 6-8 mm deep to and inferior )
-digastric muscle attachment to digastric groove
-retrograde dissection from distal nerve branch
-nerve within mastoid bone
Radiation Therapy
-in combination with surgery improves locoregional control and survival
-neutron beam XRT appears to be better than conventional photon therapy for adenoid cystic carcinoma
-radiation therapy is recommended postoperatively for all pts with malignant salivary gland tumours
(especially if residual disease and high grade tumour)
-exceptions: T1 or T2N0 disease with low-grade histology and negative resection margins
Chemotherapy
-currently no proven benefit of adjuvant chemotherapy in improving locoregional tumour control or
survival for malignant tumours
-current role is palliation of symptomatic unrespectable recurrent disease after XRT
-pain relief in ~50% of pts
Treatment Summary (Options)

-low grade:
-superficial parotidectomy
-high grade (T1, T2) N0:
-total parotidectomy
-postoperative XRT
-high grade (T3, N0) or N+:
-total parotidectomy
-modified radical neck dissection
-postoperative XRT
-+/- nerve resection if involved
-T4 tumour:
-radical parotidectomy
-radical neck dissection
-postoperative XRT
801
COMPLICATIONS
Early complications:
-facial nerve paralysis
-temporary paresis in 10-30%
-permanent paralysis in < 3%
-marginal mandibular branch the most at risk for injury
-(passes over facial artery at anterior border of masseter)
-haemorrhage or haematoma
-infection
-skin flap necrosis
-trismus
-fibrosis and scarring of masseter muscle
-improves with jaw-opening exercises
-salivary fistula or sialocele
-common
-self-limited; treated with pressure dressings +/- aspiration
-seroma
Long-term complications:
-Frey’s syndrome
-reported in 30-60% of pts; only 10% have symptomatic Frey’s syndrome
-gustatory sweating
-related to aberrant regeneration of nerve fibers from post-ganglionic secretomotor
parasympathetic innervation of parotid gland to severed postganglionic sympathetic fibers that
supply sweat glands of skin of face and auriculotemporal region
-tx:
-antiperspirant
-topical anticholinergics: eg. 1% glycopyrrolate
-botox injection
-Jacobson neurectomy
-surgery SCM/fascia flap
-recurrent tumour
-cosmetic deformity
-soft-tissue deficit
-hypertrophic scar/keloid
Complications of Submandibular Gland Excision:

-haemorrhage
-infection
-marginal mandibular branch injury
-hypoglossal nerve injury
-lingual nerve injury
-scar
PROGNOSTIC FACTORS
-factors affecting survival:

-tumour stage, location, histopathology, size, recurrence, regional and distant metastasis
-facial nerve paralysis, skin involvement, pain, gender also affect prognosis
-minor salivary gland > submandibular > parotid in terms of aggressivity
802
Histopathology
-survival rates continue to decrease after 5 years for all tumour types except low-grade malignancies, acinic
cell carcinoma, and low-grade mucoepidermoid carcinoma
Tumour Size
-major prognostic indicator
-larger size related to poor prognosis, decreased survival and high rates of regional, distant metastasis and
recurrence
Facial Nerve Paralysis

-indicates poor prognosis
-associated with high incidences of local and regional metastasis
-salivary gland cancers presenting with facial nerve abnormality:
-malignant mixed
-high-grade MEC
-squamous cell carcinoma
-polymorphous low grade adenocarcinoma
Skin Involvement
-associated with decreased survival
-requires excision of involved structures
Regional Lymphatic Metastases

-associated with poorer prognosis
-high rates of cervical metastasis:
-HG-MEC, SCC, adenoca
-low rates of cervical metastasis:
-acinic cell, adenoid cystic
Distant Metastasis
-occurs in ~20% of parotid malignancies
-occurs most frequently in adenoid cystic and undifferentiated carcinoma
-lung > bone > brain
Recurrence
-diminished survival rate
803
Pain
-6.5% of malignant tumours
-ominous sign
Gender
-men have poorer outcomes
Location
-no difference in survival based on location
-parapharyngeal space involvement associated with a poor prognosis
-for adenoid cystic carcinoma, major salivary gland tumours have better prognosis than minor tumours
804
LIP CANCER
FUNCTIONAL ANATOMY
-functions:
-maintaining oral competence
-speech articulation
-contribute to appearance and facial expression
-upper lip: CN V2
-oral commissure: buccal branch of CN V3
-lower lip: mental branch of CN V3
-motor innervation: CN VII
-blood supply:
-superior and inferior labial arteries from facial arteries
-located just between submucosa and orbicularis oris at vermillion cutaneous junction
-lymphatics:
-upper lip:
-drainage to ipsilateral preauricular, infraparotid, submandibular and submental lymph
nodes
-no contralateral drainage because of embryonic fusion plane of central frontonasal
process separates lateral maxillary processes and their associated neurovascular and
lymphatic connections
-lower lip:
-drainage to submental and submandibular nodes
-drainage is bilateral
-upper deep jugular nodes (level II)
-middle deep jugular nodes (level III)
CLINICAL EVALUATION
-most common malignant tumour of oral cavity (25-30%)

-90% SCC, 90% occur on lower lip
-risk factors:
-sun exposure
-pipe and cigarette smoking
-poor dental hygiene
-chronic alcoholism
-Panorex or CT:
-ipsilateral enlargement of mental nerve foramen: sign of mandibular invasion via mental nerve
-obliteration of fat in masticator space, pterygopalatine fossa, or along mandibular canal
-basal cell carcinoma:

-more common than SCC on upper lip
-usually from direct extension from perioral skin lesion
-slow growth, rarely cervical metastasis
-minor salivary gland tumours:
-unusual
-upper lip in 85% cases
F.Ling - Lip Cancer (1)
805
-most commonly pleomorphic adenoma (67%)
-17% are malignant
-keratoacanthoma:
-benign self-limiting epithelial neoplasm
-initial rapid growth phase then spontaneous regression over weeks to months
-incisional biopsy
-premalignant lesions:
-chronic actinic changes: hyperkeratosis, leukoplakia, angular cheilitis
-associated with SCC 46%
-ulcerative inflammatory lesions:
-viral stomatitis
-primary syphilis
-other:
-melanoma
-microcystic adnexal carcinoma
-Merkel cell carcinoma
-malignant fibrous histiocytoma
-malignant granular cell tumours
Prognostic Factors
-poor indicators:
-large primary tumour (> 3cm)
-cervical node metastasis
-recurrent tumours
-perineural invasion
-poorly differentiated histology
-mandibular invasion
-commissure lesions (?)
-size:
-<2cm: 5yr-sr 90%
->3cm: 5yr-sr 64%
-mandibular involvement: 5y-sr <50%
-tumour thickness:
->5mm associated with significantly higher rate of cervical lymph node metastasis
-cervical nodes positive: survival is 25-50%
-grade:
-well-differentiated: 86-95% survival rates
-poorly differentiated: 38-71%
-recurrence: 5yr-sr decreases by 50%
-location: poorer prognosis associated with upper lip and commissure involvement
806
TREATMENT
-XRT: 5y-sr 80-90%

TREATMENT OF LIP CANCER
-noninvasive but treatment times
long T1 N0 M0 surgery or radiation equally effective
-whistle deformity may result T2 N0 M0 surgery or radiation
T3 N0 M0 surgery and radiation
-risk of ORN of mandible T4 N+ M0 surgery and postoperative radiation
-might limit future reconstructive
options
-most useful in treatment of early commissure lesions
-surgery: 5y-sr 90% for early lesions
-excision with 8-10 mm margins
-surgery usually chosen as primary modality treatment for early cancer
-management of the N+ neck

-strategies:
-clinically palpable level I node: selective ND (1-IV)
-clinically palpable level II-V nodes: radical or modified radical ND
-bilateral nodes: IJV preserved on less involved side if N1
-bilateral N2-N3 disease: staged radical or modified radical ND 3 weeks apart
-N0 neck: elective neck dissection rarely indicated except in large recurrent lesions
-management of the N0 neck
-controversial
-risk of cervical metastasis based on size of primary
-T1 lesions 5% (no treatment to neck required)
-T2 lesions 5-10% (no treatment to neck required)
-T3 and T4 lesions 67% (requires treatment to neck)
-staging suprahyoid neck dissection indicated when significant risk (20-30%) of occult metastasis
present:
-large T2 lesions (3-4 cm) with N0 neck or larger
-recurrent disease at primary site
-ipsilateral N1 disease present, contralateral neck is N0, and postoperative radiation
therapy not planned
-indications for postoperative radiation:
-T3 or T4 primary
-recurrent tumour
-pathologically confirmed nodal metastases, extracapsular spread, or perineural invasion
-positive margins
-multiple positive neck nodes
LIP RECONSTRUCTION
Defects < ½ Lip

-vermillion mucosal defects reconstructed with mucosal advancement flaps from inside mouth
-full-thickness defects usually closed primarily with shield or V excision
Defects ½ to 2/3 Lip

-Karapandzic labioplasty
-orbicularis oris myocutaneous flap
-preserves motor and sensory innervation of the lip
-may result in microstomia and unsightly scars
807
-Abbe-Estlander flaps
-transfer full-thickness tissue from one lip to the opposite lip
-second stage procedure usually required
-width of flap should be half width of tissue excised
-Abbe flap originally designed to close medial defects
-can be medially or laterally based
-Estlander flap originally deigned to reconstruct defects near corner of mouth
Defects > 2/3 Lip

-Karapandzic labioplasty
-Abbe-Estlander flap
-Bernard cheiloplasty
-full-thickness advancement flaps from adjacent cheek tissue
-Webster modification: use of Burrow triangles in melolabial fold; vermillion border
reconstructed with mucosal advancement flap
808
-repair with distant flaps for defects involving entire lip
-RFFF with use of palmaris longus tendon for structural support
-others:
-pectoralis major myocutaneous flap
-radial forearm or fibular osseocutaneous flap for anterior mandible and lip defects
-iliac crest or scapular osseomyocutaneous flap for larger defects including floor of
mouth, tongue or cheek
809
COMPLICATIONS
Surgical
-wound infection and dehiscence
-incompetent oral sphincter
-microstomia
-poor cosmetic result
Radiation
-whistle deformity
-osteoradionecrosis
810
NEOPLASMS OF THE ORAL CAVITY
ANATOMY
-tissue layers of cheek:

-mucosa
-pharyngobuccal fascia
-buccinator fat pad
-buccinator muscle
-subcutaneous tissue
-skin
-incisive foramina:
-house palatine nerves (V2) and nasopalatine arteries
-lie posterior to maxillary incisors
-provide route for tumour spread from palate into anterior nose
-palatine foramina:
-house greater palatine vessels and nerves
-potential routes for spread for hard palate neoplasm through the pterygopalatine fossa to skull
base
-primary routes of lymphatic spread deep jugular and/or lateral pharyngeal nodes
-primary palate drains to submandibular nodes
-referred otalgia results from innervation of V3, the lesser palatine nerve and the glossopharyngeal nerve
-lymph drainage:
-tip of tongue submental nodes
-lateral two thirds of tongue submandibular and jugulodigastric nodes
-medial tongue jugulomyohyoid nodes
-unlike base of tongue, oral tongue does not have bilateral lymphatic drainage
EVALUATION, ASSESSMENT, AND DIAGNOSIS
Epidemiology
-95% of malignancies are SCCa
-4% of cancers in males; 2% of cancers in females
-average age 60 years
-with continued smoking, pts cured of first primary carcinoma have 40% chance of developing second
H+N cancer or recurrence
-75% of cases SCCa involve only 10% mucosal surface of mouth
-mainly floor of mouth where flow and pooling of carcinogen-contaminated saliva occurs
-risk factors:
-alcohol and tobacco
-reverse smoking: carcinomas of the hard palate
-HPV subtype 16 estimated to be present in up to 22% of cases of oral carcinoma
-betel-nut chewing
-tobacco chewing
-poor dental hygiene
-chronic irritation; oral leukoplakia and erythroplakia
-Plummer-Vinson syndrome
F.Ling - Oral Cavity Neoplasms (1)
811
Evaluation
-onset, duration and progression of lesion; painful
-trauma or caustic ingestion; risk factors for malignancy (weight loss, smoker, alcohol abuse,
family history, etc); history of connective tissue diseases, autoimmune disorders,
immunodeficiency, diabetes, radiation therapy, other malignancies
-taste disturbances, persistent sore throat (>3weeks), odynophagia, dysphagia, halitosis,
hoarseness, trismus, fever, malaise, persistent otalgia
-biopsy of primary
-all chronic leukoplakia or ulcerative lesions that fail to heal after 1-2 weeks should undergo
excisional biopsy
-FNA of possible neck metastasis
-imaging studies
-CXR
-CT/MRI
-Panorex
-barium swallow
-laboratory tests: baseline LFTs
-consultations:
-radiation therapy - for adjuvant or definitive therapy considerations
-dental - pre-radiation dental treatment and posttherapy cases
-panendoscopy
Differential Diagnosis (other rare tumours in oral cavity)

-granular cell myoblastoma
-benign lesion that can be mistaken for well-differentiated carcinoma
-minor salivary gland tumours:
-adenoid cystic carcinoma, adenocarcinoma, mucoepidermoid carcinoma
-sarcomas: rhabdomyosarcoma and liposarcoma
-malignant fibrous histiocytoma
-malignant melanoma
-Hodgkin and non-Hodgkin lymphomas
-HIV:
-Kaposi sarcoma, non-Hodgkin lymphoma and SCCa now recognized as being prevalent in HIV-
infected pts
-hairy leukoplakia: d/t EBV; uniquely localized to lateral tongue border
812
Differential diagnosis of Benign Pigmented Oral Lesions
-generalized pale mucosa: -anemia, thalassemia
-black/brown discolouration: -bismuth and arsenic intoxication
-blue-gray gingival margin (Burton’s line) -lead intoxication
-generalized redness -polycythemia vera, hepatic insufficiency
-perioral melanotic macules -Puetz-Jeghers syndrome (GI hamartomatous polyps)
-small yellow spots -Fordyce’s disease (sebaceous gland histology)
-black-hair tongue -elongated (hyperplastic) filiform papillae
-telangiectasia -Osler-Wever-Rendu
-diffuse hyperpigmentation of mucosa -Addison’s disease
Precancerous Lesion and Prevention

-erythroplakia: red plaque
-higher risk of malignancy (25% malignant potential)
-leukoplakia: white plaque
-hyperkeratosis and dysplasia
-types:
-Keratotic: adherent, insidious development, protracted course, nonerosive surface
(higher risk of carcinoma)
-Nonkeratotic: nonadherent, acute onset, erosive and ulcerative features (higher risk of
acute infection)
-tx: -surgical, laser excision
-topical bleomycin in DMSO
-retinoids: stabilizing effect on oral mucosa (oral etretinate; etretinate paste therapy; 13-
cis-retinoic acid)
-all require biopsy
PATHOLOGY
Gross Pathology
-four forms of SCCa:
-exophytic
-ulcerative (most common)
-infiltrative
-verrucous
MANAGEMENT
Prognostic Factors
-size of lesion
-extent of nodal disease
-regional metastases portend a worse prognosis
-5-year survival rate ~50% lower than that in patients without clinical evidence of
metastases
-prognosis worse with multiple cervical metastases
-extracapsular spread = lower rate of survival; reduces survival rate by further 50%
-tumour thickness:
-depth of penetration
-significant correlation with treatment failure
-FOM tumours 2-3 mm thick better prognosis than thicker ones
813
-oral cavity tumours > 5mm significant metastatic rates
-perineural, perivascular and intralymphatic invasion
-DNA ploidy: nondiploid tumours worse prognosis
-overexpression of c-erbB-2 correlated with nodal dz and metastasis
-verrucous carcinoma better prognosis; tends not to metastasize
Radiation Treatment
-XRT = surgery for controlling small T1 lesions
-provides better functional result with speech and swallowing
-disadvantages: taste, xerostomia, protracted nature of treatment course
-FOM cancers: highest rate of XRT complications: 56% ORN of mandible

-Stage III or IV: combination XRT and surgery
-treatment of N0 neck
-metastatic potential >30% for T2-T4 lesions
-XRT vs surgery based on institution preference
-there are differences in T1 lesions in which some require neck therapy in addition to treatment of
primary lesion
-advantage of preop vs postop XRT not answered
-one study showed no significant difference wrt overall survival, disease-free survival
and surgical complications
General Treatment Guidelines for Oral Cavity SCCa:

-T1 tumours: primary surgical excision
-T2 tumours: primary surgical excision +/- supraomohyoid neck dissection +/- XRT
-T3/T4 tumours: combined therapy
-primary surgical excision
-supraomohyoid neck dissection
-pre- or post-operative XRT
BUCCAL CANCER
-ulcerative lesions penetrate early
-tumours <6mm have significantly better survival rates
-risk of metastasis:
-regional metastasis: 50% for all stages
-occult neck metastasis ~10%
-T1 lesions: surgery or XRT
-3-yr survival: 80%
-T2 lesions:
-3-yr survival: 60%
-Stage III and IV: surgery plus XRT
-3-yr survival (surgery or XRT alone): 41% (III); 15% (IV)
-3-yr survival (surgery and XRT): 60% (III); 35% (IV)
Verrucous Carcinoma
-predilection for buccal mucosa
-extension of lesion into underlying connective tissue deep to normal epithelium (“pushing margins”)
-treatment: surgical excision
-rarely metastasizes, therefore no neck dissection needed
814
HARD PALATE NEOPLASMS
-uncommon
-SCCa = salivary gland malignancies (1:1)
-India: incidence (40%) d/t reverse smoking
-incidence of nodal metastases is low (10%) - unnecessary for prophylactic neck dissection
-T4 lesions: 25% incidence of nodal metastasis - prophylactic neck irradiation can be considered
-tx: -XRT as effective as surgery for T1 and T2 lesions
-surgery preferred
-combination surgery (total or partial maxillectomy) and XRT for T3 and T4 lesions
-prognosis (5-yr survival): T1: 85%; T4: 30%
RETROMOLAR TRIGONE LESIONS
-composed of mucosa and periosteum over posterior and ascending ramus of mandible
-underlying mandible should be included in specimen
-often presents at an advanced stage
-regional metastasis ~10-20% at early stage
-treatment:
-T1 lesions: surgery or XRT
-T2 lesions: includes resection of soft palate swallowing problems
-XRT often treatment of choice
-T3 and T4 lesions: combined therapy
-composite resection (incl. partial mandibulectomy and neck dissection
-pre- or postoperative XRT
ALVEOLUS CARCINOMA
-rare (10% of all malignancies in oral cavity)

-80% lower jaw; most posterior third of dental arch (mandible)
-treatment:
-mainly surgical +/- XRT
-Stage I and II disease:
-surgery alone: 2-yr dz free survival rates 80% (I) and 70% (II)
-partial maxillectomy or mandibulectomy
-Stage III and IV:
-XRT for N0 neck
-modified neck dissection + XRT for N+ neck
-2-yr survival rates: 60% (III) and 50% (IV)
-segmental mandibular resection required for significant mandibular invasion
ORAL TONGUE CANCER
-excluding lip cancer, oral tongue is the most common site of oral cancer
-T1 and T2: surgery or XRT
-most are treated with surgery (partial glossectomy) because of morbidity of XRT
-control rates of 86% (T1) and 75% (T2) with XRT alone
-surgical management of a T2 primary must also include elective treatment of the ipsilateral N0
neck (treat levels I-IV)
815
-T3 and T4: combination therapy
-surgery with post-operative radiation
-overall survival rates: 30-35%
-controversy still exists for prophylactic neck therapy for T1 lesions
-no clear indicators exist
-significantly increased risk of neck metastases with tumour thicknesses of > 2-5 mm
-measurement of tumour thickness can be made with frozen-section analysis and can be used to
guide elective therapy of the N0 neck
-perineural invasion at primary site increases recurrence and mortality
-reconstruction:
-tongue flaps provide worst functional reconstructive results; should be avoided
-STSG provides good functional results
-myocutaneous or free flap
FLOOR OF MOUTH CANCERS
-T1 lesions:
-surgery alone; 5-yr survival 70%
-XRT alone; 3-yr dz free survival 85%
-T2 lesions: XRT or surgery +/- neck dissection
-high rate of occulte nodal disease: 23-50%
-highest complication rate if XRT used for cure
-3-yr dz free survival 64%
-40% occult metastatic rate
-Stage III and IV:
-T3: 70% occult metastases
-combination therapy
-survival rates: 30-35% (III) and 20-25% (IV)
SURGICAL TREATMENT AND RECONSTRUCTION
-STSG for resurfacing small to moderate defects

-pectoralis major flap
-excellent soft tissue for large FOM and tongue resections
-reliable
-SCM and platysma flap
-small to moderate oral defects
-not as reliable
-free-flap transfer
-osteocutaneous groin flap
-jejunal transfer
-RFFF
816
817
ODONTOGENIC CYSTS, TUMOURS,
AND RELATED JAW LESIONS
Radicular cysts, dentigerous cysts, OKC: make up 80% of dental cysts
ODONTOGENIC CYSTS
-two categories: inflammatory and developmental
Inflammatory Cysts:
-non-keratinising stratified squamous epithelium lining an inflamed collagenous cyst wall

-periapical (radicular) cyst most common (65%)
-develop in response to irritants escaping form necrotic pulp through the apical foramen
-radiologically: well-defined circular radiolucency epicentered around root apex
F.Ling - Odontogenic Lesions (1)
818
Developmental Cysts:
-dentigerous (follicular) cyst:

-cystic enlargement of the follicle of an impacted tooth
-radiolucency at crown of an unerupted tooth
-second most common (24%)
-may cause displacement or resorption of adjacent teeth, infection, and pathologic jaw fracture
-mucous metaplasia rare source of central mucoepidermoid carcinoma
-histology:
-outer thin connective tissue wall with a thin stratified squamous epithelial layer
-treatment: enucleation and curettage
-odontogenic keratocyst (OKC):

-5-8% of all odontogenic cysts
-capable of considerable bony destructiveness and frequent recurrence after surgery (25-40%)
-distinct histopathology:
-well-polarized hyperchromatic basal layer
-at surface undulating layer of refractile parakeratin
-malignant transformation rare
-treatment: enucleation and curettage
-Basal cell nevus syndrome: (Gorlin syndrome)

-autosomal dominant
-multiple keratocysts (5% of individuals with OKC)
-early development of multiple basal cell carcinomas
-bifid ribs, frontal bossing, depressed midface, wide nasal bridge, hypertelorism, relative
mandibular prognathism, calcification of falx cerebrii
-orthokeratinizing variant of OKC:

-without parakeratin
-recurrence rate much less (~2%)
-developmental lateral periodontal cyst

-innocuous
-1.5% of odontogenic cysts
-should be biopsied to r/o OKC
-glandular odontogenic cyst:

-capable of considerable growth and recurrence rate of up to 25%
-preference for anterior mandible and present as multilocular or unilocular radiolucencies
NON-ODONTOGENIC CYSTS
-incisive canal cyst (nasopalatine duct cyst, median anterior maxillary cyst)
-most common developmental jaw cyst
-Stafne bone cyst (lingual salivary gland depression):
-not a true cyst but an anatomic depression of the lingual aspect of the posteroinferior body of the
mandible that contains normal salivary gland tissue
-traumatic bone cyst:
-not a true cyst; represents an empty cavity within cancellous bone
819
-surgical ciliated cyst of the maxilla
-iatrogenic lesion
-entrapment of sinus epithelium during a previous Caldwell-Luc procedure
ODONTOGENIC TUMOURS
-classified into three groups based on germ cell layer of origin: epithelial, mesenchymal, and mixed
Epithelial Odontogenic Tumours:
-ameloblastoma:
-most common epithelial odontogenic tumours
-rare: ~1% of all tumours/cysts of jaws
-arise from odontogenic epithelium or enamel organ
-benign but locally invasive
-thought of as the oral counterpart to basal cell carcinoma
-peak occurrence 3rd to 4th decade (mean 40 years)
-large expansile multilocular or soap-bubble radiolucency
-posterior mandible (80%)
-immature adnexal neoplasm with infiltrative growth and limited metastatic potential
-cause cortical thinning and perforation, pathological fracture, and soft-tissue penetration
-types:
-central: arise in bone (intraosseous)
-plexiform unicystic:
-more aggressive central variant, occurs in the lining of follicular cysts or
impacted teeth
-peripheral:
-arise in soft tissue around
alveolar bone, much less
aggressive, may be treated
with local excision
-histology:
-tall columnar cells with reversed
nuclear polarity
-types: -follicular
-basal cell
-granular cell
-plexiform
-acanthomatous
-desmoplastic
-calcifying odontogenic cyst (COC) or Gorlin Cyst

-can attain considerable size and can displace or resorb teeth
-encapsulated, behaves in a benign fashion
-no malignant transformation
-calcifying epithelial odontogenic tumour (CEOT) aka Pindborg Tumour

-benign infiltrative tumour showing predilection for mandibular molar region
-malignant transformation not expected
-growth restriction less aggressive than ameloblastoma
-histology:
-sheets or islands of epithelial cells with eosinophilic cytoplasm
820
-may contain amyloid with concentric calcifications or psammoma-like bodies
(Liesegang rings)
Mesenchymal Odontogenic Tumours:
-odontogenic myxoma:
-benign slow-growing, expansile tumour
-arise from periodontal ligament, dental papilla or dental follicle
-gelatinous solid tumour
-recurrence rate 25%
-malignant transformation not expected
-cementomas:
-class of benign tumours that secrete cementum
-types:
-periapical cemental dysplasia
-more common in black females, multiple lesions, develops through varying
stages (osteolytic, cementoblastic, and maturation)
-cementoblastoma:
-true benign tumour of cementoblasts of the tooth root, usually form first
mandibular tooth
-cementifying fibroma:
-similar to ossifying fibroma
PEDIATRIC ODONTOGENIC TUMOURS
-unicystic ameloblastoma:
-expansile clinically non-infiltrative cystic neoplasm
-presents as an expansile well-demarcated unilocular radiolucency resembling a large dentigerous
cyst
-treated by curettage 15% recurrence
-may progress to infiltrative ameloblastoma if not treated
-adenomatoid odontogenic tumour (AOT):

-uncommon benign self-limited growth
-2/3 in females in the first two decades
-ameloblastic fibroma:
-uncommon benign neoplasm
-odontoma:
-mature histodifferentiation but disorganized morphodifferentiation
-production of enamel, dentin, cementum and pulp haphazardly admixed within a collagenous
capsule
821
RELATED JAW LESIONS
Giant Cell Lesions
-central giant cell granuloma:

-reactive process capable of swelling, bone destruction and recurrence
-mandible involved in 70% of cases
-at biopsy, a solid, reddish brown, liverlike tissue is suggestive of the diagnosis
-nonaggressive and aggressive types
-brown tumour of hyperparathyroidism:

-local manifestation of systemic metabolic disease
-histologically identical to central giant cell granuloma
-true giant cell tumour:

-capable of persistent recurrence and metastasis
-extremely rare in jaws
-aneurysmal bone cyst:

-rare giant cell lesion in jaws that features spongelike, cavernous blood-filled spaces
-lytic “blow-out” lesion of the affected jaw is seen
Fibroosseous Lesion
-fibrous dysplasia:
-affects maxilla more frequently than mandible
-developmental disturbance of bone formation that may be confined to one bone or multiple
skeletal sites
-formation of dysplastic bone that is unresponsive to physiologic demands
-fusiform swelling with indistinct blending borders that incorporate cortical bone
-ossifying fibroma:
-true neoplasm of the medullary portion of the jaws
-rapid growing bony hard mandibular swelling
-well-demarcated radiolucent or mixed lesion that diverges dental roots and displaces anatomic
structures at its expanding periphery
OTHER SIGNIFICANT JAW LESIONS
-intraosseous haemangioma or AVM:

-uncommon
-ill-defined honeycombed mandibular radiolucency
-presurgical needle aspiration recommended before entering any mandibular radiolucency
-lymphomas
-myelomas
-appears in the jaws in 30% of cases
-multiple radiolucent lesions without sclerotic borders present
-metastatic malignancies
-osteogenic sarcoma
822
MANAGEMENT
Evaluation
-slow-growing tumours compensatory changes in alveolar processes occlusion maintained
-fast-growing tumours can produce significant malocclusion
-dysethesia neural compression or invasion suggests malignancy
-appearance patterns on Panorex:
-well-demarcated lesions outlined by thin sclerotic borders suggest slow growth
-expansion, root displacement and/or resorption, and cortical thinning suggest rapid growth
-FNA to rule out vascular lesion
-open biopsy:
-excisional enucleation for smaller cysts
-incisional procedure for larger lesions
Treatment
-basic treatment modalities:

-simple enucleation
-marginal or segmental resection
-composite resection
Dentigerous Cysts
-minimal recurrence potential
-removed by conservative enucleation and curettage (E&C) of cystic lining from osseous defect
-other lesions amenable to E&C:
-lateral periodontal cyst, residual cyst, gingival cyst, paradental cyst, COC (Gorlin cyst), traumatic
bone cyst, surgical ciliated cyst of the maxilla
-AOT, ameloblastic fibroma, central odontogenic fibroma
Odontogenic Keratocysts
-association with impacted tooth requires removal of both cyst and tooth
-must remove any tiny shards of cystic lining that may persist after cyst removal
-resection of overlying mucosa, rotary burr reduction of osseous walls of cyst cavity, and
intracavitary destructive measures:
-chemical tissue fixation with Carnoy solution
-intracavitary cryotherapy with liquid nitrogen
-if mandibular defect > 4cm, immediate transoral bone grafting recommended to avoid pathologic
fractures
-may require marginal or segmental mandibulectomy for larger lesions
-other lesions with similar treatment approaches:
-glandular odontogenic cyst, small localized odontogenic myxomas and Pindborg tumours
Amelobastoma
-mandibular resection with adequate zone of radiographically normal-appearing trabecular bone around
main tumour mass
-1-1.5cm margin of adjacent radiographically uninvolved bone
-soft tissue extension requires resection - neck dissection not needed
-postoperative follow-up critical - 50% recurrences found within first 5 years
-treatment principles also apply to:
-odonotameloblastoma, larger or recurrent Pindborg tumours (CEOT), odontogenic myxoma
-unicystic variant of ameloblastoma:
-satellite lesions at cyst periphery or extension of intramural ameloblastoma through
823
fibrous wall of cyst
Malignant Ameloblastoma
-resection of primary tumour
-neck dissection for demonstrable metastasis
-aggressive resection of pulmonary metastasis
Ameloblastic Carcinoma
-radical surgical resection as for SCC with neck dissection reserved for demonstrable lymphadenopathy
Related Jaw Lesions
Central Giant Cell Granuloma

-initial treatment by curettage
-larger defects may require bone grafting
-non surgical options:
-injection of triamcinolone acetonide with local anesthetic
-daily calcitonins therapy for 1 year
Fibrous Dysplasia
-total resection and reconstruction
Ossifying Fibroma
-complete removal required
Intraosseous Vascular Lesions

-preoperative embolization
-resection of involved jaw striction
COMPLICATIONS
-recurrence most common complication

-secondary infection
-delayed pathologic mandibular fracture
824
NECK DISSECTION
ANATOMY
F.Ling - Neck Dissection (1)
825
-marginal mandibular branch of facial nerve:
-1 cm in front of and below the angle of mandible
-overlies facial artery and vein
-spinal accessory nerve:
-medial to digastric and lateral or immediately posterior to IJV
-usually within 1cm above Erb’s point (posterior border of SCM where greater auricular nerve
turns around it)
Anterior Cervical Triangles:

-boundaries:
-midline of neck, posterior border of SCM,
inferior border of mandible
-submandibular triangle:
-inferior border of mandible, anterior and
posterior digastric muscles
-submental triangle:
-anterior belly of digastric, hyoid bone, and
midline of neck
-carotid triangle (superior carotid triangle):
-omohyoid muscle, posterior belly of
digastric, posterior border of SCM
-muscular triangle (inferior carotid triangle):
-omohyoid muscle, midline neck, posterior
border of SCM
Posterior Cervical Triangles

-boundaries:
-clavicle, posterior border of SCM, anterior
border of trapezius
-occipital triangle:
-posterior border of SCM, anterior border of trapezius, omohyoid
-subclavian triangle:
-posterior border of SCM, clavicle, omohyoid muscle
DIAGNOSTIC EVALUATION
-error rate in assessing presence or absence of cervical lymph node metastasis by palpation ranges from 20-
50%
-CT/MRI have higher sensitivity and specificity in detecting mets in nodes > 1-1.5 cm
-33% of all mets from SCC of H+N in nodes < 1 cm
-circular enlarged nodes more likely to be malignant
-if tumour involvement of common or internal carotid artery is suspected angiography to determine status
of contralateral intracerebral circulation
-most malignancies in the neck are from metastasis (~85%)
-primary neck cancers in the neck are less common (~15%) - usually from salivary tumours, thyoird
cancers or lymphoma
Fine-Needle Aspiration
-specificity: 94-100%
-sensitivity: 92-98%
826
STAGING
Nodal Levels
I: -submental and submandibular triangles
II: -upper third (superior to hyoid bone or carotid bifurcation to base of skull); contain upper jugular
lymph nodes; upper limit is digastric muscle
III: -middle third (superior to omohyoid muscle to hyoid bone); contain middle jugular lymph nodes
IV: -lower third (superior to clavicle to omohyoid muscle); lower limit is transverse cervical vessels
V: -posterior triangle
VI: anterior neck between carotid sheaths
AJCC Staging
N0: -no regional lymph nodes
N1: -single ipsilateral lymph node < 3 cm
N2a: -ipsilateral lymph node between 3 and 6 cm
N2b: -multiple ipsilateral lymph nodes < 6 cm
N2c: -bilateral or contralateral lymph node; < 6 cm
N3: -lymph node > 6 cm
CLASSIFICATION OF NECK DISSECTIONS
Radical
Modified radical (I, II, III)
Selective
-lateral
-anterolateral (supramylohyoid or supraomohyoid)
-posterolateral
-anterior
Extended
Radical Neck Dissection

-includes:
-levels I-V
-spinal accessory nerve, IJV, SCM
-Rationale
-need to remove lymphatic of neck completely
-not indicated in absence of palpable cervical metastasis
-Indications
-multiple clinically obvious lymph node metastasis
-esp. posterior triangle nodes closely related to spinal accessory nerve
-advanced nodal disease: large metastatic tumour mass or matted nodes (risk of entering nodes)
-involvement of SCM, IJV or spinal accessory nerve
-recurrence or radiation failure
-Results
-recurrence rates:
-tumour-free nodes: 3-7%
-positive nodes: 20-71%
-prognostic factors:
-number of positive nodes: >4 nodes significantly worse survival
-extracapsular spread higher recurrence
-level of nodal involvement: multiple levels higher recurrence rate
827
-combined use of RND and XRT can decrease recurrences in the ipsilateral side of the neck and
prevent recurrence in the contralateral side in pts with cervical lymph node metastasis who have
combinations of poor prognostic factors
Modified Radical Neck Dissection

-includes:
-levels I-V
-Type I: spinal accessory is preserved
-Type II: spinal accessory and IJV is preserved
-Type III: spinal accessory, IJV and SCM preserved; “functional neck dissection” (Bocca)
Modified Radical Neck Dissection, Type I:

-for elective treatment of neck in pts with SCC of upper aerodigestive tract
-no need for such an extensive operation in pts with N0 neck
-surgical treatment of neck in selected pts with clinically obvious lymph node metastasis
-Andersen et al: preservation of spinal accessory nerve did not adversely affect survival and tumour control
in the neck
Modified Radical Neck Dissection, Type II:

-tumour noted to be adherent to SCM but away from accessory nerve and jugular vein
-eg. seen in hypopharyngeal and laryngeal malignancy with metastasis under middle third of SCM
Modified Radical Neck Dissection, Type III:

-treatment of the N0 neck; especially when primary tumour is in the larynx or hypopharynx
-treatment of the N1 neck when the metastatic nodes are mobile and no greater than 2.5-3 cm
-differentiated thyroid carcinoma with palpable lymph nodes
Selective Neck Dissections

-removing only those groups at highest risk of containing metastasis
-Anterolateral neck dissection
-supraomohyoid: levels I-III removed en bloc
-extended supraomohyoid: levels I-IV
-Lateral neck dissection
-levels II-IV
-Posterolateral neck dissection
-levels II-V
-Anterior neck dissection
-removal of pretracheal and paratracheal node groups
Rationale:
-lymph node groups most frequently involved in pts with carcinoma of the oral cavity are the
jugulodigastric and mid-jugular nodes
-submandibular triangle: carcinoma of floor of mouth, anterior oral tongue, buccal mucosa
-in absence of metastasis to first-echelon nodes, tumours of oral cavity and oropharynx rarely
involved low jugular and posterior cervical nodes
-Shah et al:
-tumours of oral cavity metastasized most frequently to levels I, II, and III
-tumours of oropharynx, hypopharynx, and larynx involved mainly nodes in levels II,
III and IV
-selective ND are associated with less postoperative morbidity
828
Indications:
-supraomohyoid ND:
-SCC of oral cavity staged T2-T4N0 or TxN1 when palpable node is < 3cm, clearly
mobile and located in levels I or II
-bilateral if anterior tongue and floor mouth malignancy
-SCC of lip or skin of midportion of face associated with clinically discrete single
metastasis to submental or submandibular nodes
-in conjunction with parotidectomy in pts with SCC, Merkel cell carcinoma, selected
stage I melanomas (thickness b/n 1.5-3.00 mm) in cheek and zygomatic regions of the
face
-lateral ND:
-tumours of larynx, oropharynx and hypopharynx staged T2N0, selected T3N0 and TxN1
when palpable node is located in levels I or II
-usually bilateral
-posterolateral ND:
-melanomas, SCC or other skin tumours that originate in posterior and posterolateral
aspects of the neck and occipital scalp
-anterior neck dissection:
-differentiated thyroid cancer
-esophageal and tracheal tumours and in laryngeal cancers with subglottic extension
Results:
-supraomohyoid and lateral ND:
-recurrence rate:
-negative nodes: 3.4% at 2 years
-positive nodes: 12.5% at 2 years (multiple nodes, extracapsular spread)
-important to dissect nodes in level IV in pts with cancer of oral tongue: “skip metastasis” in
15.8% to level IV or III
-important to dissect nodes out of retro-accessory triangle
Extended Neck Dissections

-extension to include:
-retropharyngeal, paratracheal and pretracheal lymph nodes
-hypoglossal nerve
-levator scapulae muscle
-(carotid artery)
-controversy exists about the advisability of resecting the common or internal carotid artery
-high morbidity and mortality and advanced disease
-however some feel that better patient selection is available to reduce the morbidity of resection
-patients with frank involvement of carotid wall whose preoperative evaluation indicates
intolerance to carotid ligation should have carotid resection and reconstruction
SEQUELAE OF NECK DISSECTION
-removal of spinal accessory nerve:

-decreases abduction of shoulder above 90 degrees
-dissection along the nerve will cause significant decrease in shoulder function; however in the
long term, function improves (usually by 12 months)
-when compared with radical neck dissection, preservation of spinal accessary nerve is associated
with less neck and shoulder pain and fewer physical problems and better shoulder function and
overall quality of life
829
COMPLICATIONS OF NECK DISSECTION
Air Leaks
-circulation of air through a wound drain
Wound Infections and Wound Breakdown

-risk factors:
-irradiated tissue
-soilage of wound by saliva, tracheal aspirates or gastric secretions
-tight wound closure
-immunocompromised and malnourished states
-hematoma or seroma
-treatment:
-aggressive antibiotic regimen, monitor for fistula, control diabetes, maximize nourishment,
meticulous wound care
Flap Necrosis
-from poorly planned incision that compromises vascular supply, wound infection, fistulas
Cranial Nerve Injury

-accessory shoulder syndrome
-vagus dysphagia, hoarseness, aspiration
-marginal mandibular branch
Bleeding
-haematoma:
-early milking of drains may evacuate accumulation of blood
-may require evacuation in OR
-failure to evacuate haematoma may predispose patient to wound infection
Chylous Fistula
-attempt to ligate intraoperatively
-post-op chylous fistula occurs after 1-2% of neck dissections
-adverse sequelae:
-electrolyte abnormalities
-malnutrition
-immune dysfunction
-treatment:
-conservative management unlikely successful if > 600 ml drains in 24h
-amount of output: Fistulas with higher output that cause more physiologic derangements
may require earlier aggressive therapies.
-conservative management:
-closed wound drainage
-pressure dressings
-low-fat nutritional support (medium chain fatty acids)
-correct electrolyte abnormalities
-nutritional therapy:
-enteral diets with fat restriction or the use of medium chain triglycerides:
-medium-chain triglycerides are absorbed directly from the gut into the portal
venous circulation.
-TPN affords full caloric and nitrogenous support while allowing bowel rest
-bowel rest achieves a decrease in chyle flow, allowing healing to occur
830
-surgical therapy:
-surgical ligation of the leaking lymphatic vessels
-other forms of therapy to plug the leak have included fibrin glue or the use of chemical
irritants such as tetracycline
Facial or Cerebral Edema

-bilateral ligation of IJV
-attempt for prevention by preserving at least one external jugular vein
-cerebral edema d/t increased cerebral venous pressure
-may cause SIADH hyponatremia ICP (ie. vicious cycle)
-treatment (cerebral edema):
-Neurosurgery consult
-consider corticosteroids, lumbar drainage, hyperventilation, mannitol, diuretics
Blindness
-rare
-intraorbital optic nerve infarction
Apnea
-carotid body denervation after bilateral neck dissection
-phrenic nerve injury
Jugular Vein Thrombosis

-87% patency rate
-radiation therapy influences patency rate
-18% patency rate for modified RND and radiation therapy
-88% for neck dissection alone
-57% for radiation alone
EMERGENCIES
Carotid Artery Rupture

-fistula formation and flap breakdown more likely in presence of malnutrition, diabetes and prior radiation
therapy
-perioperative antibiotics and free and pedicled vascularized flaps used to prevent rupture
-likelihood of rupture high in large cutaneous defects or large high-output fistulae in previously irradiated
patients, therefore must cover with vascularized tissue early
-manual pressure immediately and to OR for surgery: artery exposed and ligated proximally and distally to
area of rupture
Jugular Vein “Blow-out”

-usually complication of pharyngocutaneous fistula
-surgical exploration and ligation of jugular vein above and below level of rupture
831
TREATMENT PLANNING DECISIONS
Surgical Treatment of the N0 Neck
-Areas of controversy:
-superiority of elective treatment over observation and treatment only when lymph node metastasis become
clinically apparent
-indications for elective treatment
-extent of cervical lymph node dissection
-selection of elective surgical treatment versus elective neck irradiation
Elective Treatment versus Observation

-no good prospective trials - inadequate number of patients studied
-two studies show no survival advantage of elective neck dissection - but there were design flaws
-eg. “elective” neck dissection occurred within 2 months of primary treatment not at the same
time; inadequate follow-up time; insufficient patient numbers
-because of unreliability of patient follow-up, most physicians prefer to treat the neck electively rather than
expectantly, even though this preference remains controversial
Elective Treatment of the Neck
Indications
-based on the likelihood of occult lymph node metastasis associated with a given primary tumour
-elective neck dissection if:
-primary tumour associated with high risk of occult metastasis
-neck is entered for reasons of surgical approach
-possibility of occult lymph node metastasis is 20% or higher
Site of Origin
-overall incidence of nodal metastasis
-SCC of oropharynx > oral cavity
-lower lip and buccal mucosa < floor of mouth and oral tongue
-supraglottic >> glottic
Thickness and Depth of Invasion of Primary Tumour

-in oral cavity tumours, thickness and depth highly correlated with lymph node metastasis (LNM)
(Fukano et al.)
->5mm: rate of LNM 65%
-<5mm: rate of LNM 5.9%
-oral cavity, oropharynx, and hypopharynx
-invasion > 4mm LNM 4x more likely
Vascular and Perineural Invasion

-significant statistical correlation found
Cellular DNA Content

-remains controversial
-?aneuploid SCC of H+N more likely to have cervical LNM - but no correlation in some studies
Tumour Angiogenesis
-immunostaining of endothelial cells for factor VIII-related antigen (marker for angiogenesis) was
strongly related to probability of metastasis
832
Extent of Elective Cervical Lymph Node Dissection
-MRND, Type III or selective ND are currently preferred operations for elective surgical treatment of the
N0 Neck
-removal of SCM, IJV or posterior triangle of neck not done unless obviously involved by tumour
Elective Neck Dissection versus Elective Neck Irradiation

-risk of developing clinically positive LNM in N0 neck reduced to 5% using XRT
-elective neck irradiation used in:
-patients whose primary tumour is treated with radiation
-patients whom postop irradiation is indicated on basis of characteristics of primary tumour alone
(T4 and infiltrating T3 tumours) when these can be adequately resected without entering the neck
-otherwise elective ND preferable
Surgical Treatment of the N+ Neck
-neck dissection is mainstay treatment

-exceptions:
-LNM from SCC of nasopharynx
-particularly non-keratinising carcinomas; usually respond to XRT
-lymphoepitheliomas of tonsillar fossa
-may also respond to XRT
-lymphomas
Surgical Treatment
-may require removal of hypoglossal nerve, carotid, and overlying skin if involved with tumour
-preservation of adjacent structures should be pursued only when clearly identifiable plane exists between
tumour and such structure
-results of selective ND and MRND appear comparable to those of RND
Postoperative Radiation Therapy

-rate of tumour recurrence in neck is decreased by addition of radiation when multiple nodes are involved
at multiple levels of neck and when extracapsular spread is found
-it is recommended that pts with advanced head and neck cancer treated with daily fractions of 1.8 Gy
receive a minimum postoperative dose of 57.6 Gy to the entire operative bed
-sites of increased risk for recurrence should be boosted to 63 Gy
-some studies have suggested that a delay in initiation of radiation therapy beyond 6 weeks may
compromise tumour control
833
CONTROVERSIES IN MANAGEMENT OF N0 NECK IN SQUAMOUS CELL
CARCINOMA OF THE UPPER AERODIGESTIVE TRACT
-three options:
-close observation
-elective radiation therapy
-elective neck dissection
ELECTIVE TREATMENT OF CERVICAL METASTASIS
-controversy stems partly from uncertainty about actual risk or occult adenopathy and accessibility of at-
risk lymphatics for any particular tumour
-no biologic marker currently available to identify involved nodes
-theoretic benefit of elective neck treatment must be weighed against morbidity of treating pts who do not
have metastasis
-micrometastasis can occur in small lymph nodes
Option 1: Observation of the N0 Neck

-proponents claim that this reduces the number of N0 neck that would otherwise have been treated
unnecessarily
-believe that treatment with combined modality therapy when palpable disease develops in the
neck has similar efficacy if careful follow-up is provided
-~2/3 of pts who receive elective treatment may not need it
-Yuen et al:
-END provided no significant benefit for eventual nodal control
-however, outcomes of pts who failed in the neck was poor
-observation of the N0 neck requires better methods of staging through addition of imaging studies:
-CT: sens 83%; spec 83%
-physical examination: sens 74%; spec 81%
-sensitivity improved to 91% when physical exam is combined with CT
-histologic features that may be predictors of cervical metastasis:
-tumour thickness > 4 mm in oral cavity
-microvascular invasion
-grade of differentiation
Option 2: Elective Neck Irradiation

-proponents believe that morbidity of radiation is less than that of surgery and that similar cancer control
results are possible
-Mendenhall et al:
-ENI reduced neck failure rate in pts with N0 neck with controlled primaries (1.9%)
-failure rates much higher when primary was not controlled (25% with ENI, 67% w/o)
-some other studies show no benefit from ENI
-it is usually necessary to treat both necks when radiation alone is used for primary site
-exceptions include early glottic cancer and rarely other unilateral primary sites where the field
would not prevent later irradiation to the neck if needed
-disadvantages of ENI:
-increases both short-term (mucositis, pain) and long-term (fibrosis, xerostomia) morbidity
-increases risk of complications if salvage surgery is needed
-may mask recurrence in neck, delaying salvage surgery until incurable disease is present
F.Ling - Controversies in N0 Neck (1)
834
Option 3: Elective Neck Dissection
-proponents believe the prognostic information gained and potential for increased regional disease control
and survival justify the small amount of added operative time and low morbidity of the procedure
-several END studies demonstrated a high incidence of occult metastasis
-MD Anderson:
-overall occult metastasis rate of 25% in N0 necks
-6% had extracapsular spread of tumour in nodes
-several studies suggest that number and size of positive nodes are significant prognostic factors and that
ECS is an independent prognostic variable
ELECTIVE NECK DISSECTION VERSUS OBSERVATION
Randomized Prospective Trials

-75 pts with oral cavity cancer:
-39 pts: radical END
-36 pts: observation with therapeutic ND when metastasis appeared
-results: histologic presence of ECS was double in therapeutic group (25% vs 13%); no
statistically significant difference in survival curves
-recommendations: neck dissection should be considered for pts in whom regular follow-up is
difficult
-Kligerman:
-early oral cavity cancer
-33 pts resection alone 49% survival
-34 pts with resection + END 72% survival
-conclusions: neck dissection mandatory in early oral cancer, particularly with thicker tumours
Decision Analysis
-Weiss:
-suggested that elective treatment should be considered if probability of occult cervical metastasis
was greater than 20%
-relative utility of surgery over radiation became apparent if probability was greater than 50%
-recommended the choice of radiation versus surgery should be predicated on treatment of the
primary
RATIONAL AND CONTROVERSY: SELECTIVE NECK DISSECTION
Selective Neck Dissection

-attempts to minimize shoulder dysfunction by preserving spinal accessory nerve
-recent evidence indicates SND, combined with postop radiation when appropriate, is effective in
controlling neck disease in selected pts with limited metastasis in the upper neck
-however, the concept of limiting neck dissection by additional preservation of certain lymph node groups
is more recent and not as globally accepted
-results based on retrospective uncontrolled studies
-controversy centers mainly around need for END when primary is treated surgically
-secondary controversies exist regarding extent of END, role of bilateral END, and role of
adjuvant therapy when occult metastases are found histologically
835
SPECIAL CONSIDERATIONS IN MANAGEMENT OF THE N0 NECK FOR SPECIFIC PRIMARY
SITES
Oral Cavity
-supraomohyoid neck dissection (I-III) frequently used
-skip metastases occur in more than 15% some advocate including level IV in the dissection
-it has been observed that 33% of oral tongue and 40% of FOM failures occurred in contralateral
undissected neck
-ASHNS clinical practice guidelines:
-T1 and T2 oral cancers:
-unilateral neck dissection should be performed for clearly unilateral lesions, and
bilateral neck dissections should be performed for lesions at tip of tongue approaching or
crossing midline
-T3 and T4 tumours:
-ipsilateral or bilateral neck dissection or ENI recommended (5000 rads)
-neck not electively treated in T1 and T2 lesions of the lower lip
-bilateral neck dissection (regions I-III) appropriate for anterior tongue and floor of mouth cancer
-region V included if suspicious nodes are present
-unilateral neck dissection recommended for RMT lesions > T2
-early lip, buccal mucosa, and hard palate cancers do not require neck dissections because of low
metastatic rate
Oropharynx
-region II most commonly involved
-Shah: recommended elective dissection of regions II-IV
-cancers of base of tongue and pharyngeal wall had occult metastatic rates of 33% and 46% respectively
-bilateral modified neck dissection removing regions 1-V in base of tongue cancers with N0 necks is
appropriate
-clinical practice guidelines recommend with the exception of early tonsil cancer, radiation
Hypopharynx
-have high incidence of nodal metastasis
-regions II and III at highest risk
-pts with cancer of medial pyriform, midline hypopharyngeal wall, and postcricoid region are at high risk
for bilateral involvement
-guidelines recommend that all pts be treated with END or ENI but are not more specific
-bilateral SND (II-V) recommended for these pts
-pts with tumours involving only the lateral hypopharynx can be treated with unilateral neck dissection if
ipsilateral neck does not have suspicious nodes
-elective region I dissection can be considered optional in hypopharyngeal cancer
Larynx
Supraglottic Cancer
-regions II, III and IV are at high risk for occult metastasis from laryngeal cancers
-clinical practice guidelines recommend bilateral neck dissection unless radiation is given
-region VI dissection and ipsilateral thyroid lobectomy should be considered when supraglottic cancer
becomes transglottic
Glottic Cancer
-clinical practice guidelines indicate that T1 and T2 lesions should have delphian node treatment in the
narrow field laryngeal radiation portal
836
-no indication for END
-T3 and T4 not specifically addressed in the guidelines
Subglottic Cancer
-SND of regions II, III, IV and VI bilaterally is appropriate for primary subglottic cancer
-involves subtotal thyroidectomy
MINIMUM NECK DISSECTION IF ELECTIVE NECK DISSECTION IS PERFORMED

Indication Minimum Neck Dissection
T1-4 oral cavity

-tongue -I-IV
-floor of mouth -I-III (bilateral for lesions involving or approaching midline)
T1–4 oropharynx (excluding T1 tonsil) -I-IV

-I-V preferred, bilateral preferred unless T2 tonsil
T3, T4, and transglottic T2 glottic cancer -II-IV

-II-IV, VI preferred
T1-4 supraglottic -bilateral II-IV

-consider ipsilateral V and VI
T1-4 hypopharynx -bilateral II-IV

-consider ipsilateral V and VI, excluding lateral pyriform where unilateral is adequate
Nasopharynx
-clinical practice guidelines currently favour radiation therapy for treatment of nasopharyngeal carcinoma
-chemotherapy improved survival (72% 5-year-sr cf 54% with XRT alone)
-radiation field should include levels II-V and retropharyngeal nodes bilaterally
Nasal/Ethmoid and Maxillary Sinus

-clinical practice guidelines suggest that elective treatment of both sides of neck should be done only if
tumour extends to soft palate or nasopharynx
ADJUVANT THERAPY FOR THE DISSECTED NECK
-clinical practice guidelines for all sites tend to agree that all T4 cancers require postop irradiation
-T1-T3 indications:
-multiple levels of lymph node involvement
-more than two or three positive nodes
-ECS
-intravascular or perineural invasion
-positive margins
837
HYPOPHARYNGEAL CANCER
From Ch 112 - Cummings -

Malignant Tumours of the Larynx and Hypopharynx
RISK FACTORS FOR HYPOPHARYNGEAL CANCER
-history of heavy alcohol ingestion

-heavy alcohol consumption
Plummer-Vinson or Paterson-Brown-Kelly syndrome

-dysphagia, hypopharyngeal and esophageal webs, weight loss, and iron deficiency anemia
-achlorhydric, cheilitis
-women aged 30 to 50 years of age (85% of pts are women)
-early management can reverse process:
-bougienage, iron replacement, and vitamin therapy can reverse disease process
-barium swallow:
-hypopharyngeal web, most commonly in low hypopharynx or area between postcricoid region
and thoracic esophagus
-in a series of 322 women who developed postcricoid carcinoma, 1/3 to 2/3 Paterson-Brown syndrome
-malignancy began just proximal to the web, possibly because of chronic irritation
Second primary malignancies

-coexisting second primary malignancies are found in 4% to 8% of patients who have one head-and-neck
primary malignancy
-20% to 25% of patients with head-and neck-primary malignancies develop a second cancer within 5 years
-hypopharyngeal area was 3rd most common site for patients with FOM cancers to develop a second
primary malignancy
Diagnosis
-rich lymphatic network in submucosal tissue surrounding the hypopharynx allows early spread to regional
lymph nodes and direct extension into adjacent soft tissues
-risk of occult nodal metastasis: 30-40%
-78% of patients have palpable cervical metastases at presentation
-most patients with hypopharyngeal cancers (70%) manifest stage III disease
ANATOMY OF HYPOPHARYNX
-three subsites:
-piriform fossa
-posterior pharyngeal wall
-postcricoid area
-lymphatics:
-rich submucosal lymphatic network exits through
thyrohyoid membrane superior and middle jugular lymph
nodes
-inferiorly paratracheal lymph nodes and low jugular nodes
-metastasis to retropharyngeal nodes, paratracheal nodes,
paraesophageal nodes, and parapharyngeal space nodes
occurs
F.Ling - Hypopharyngeal Cancer (1)
838
-nerve supply:
-superior and middle constrictor muscles:
-superior laryngeal nerve and pharyngeal plexus (including pharyngeal branches of vagus
and glossopharyngeal nerves and contributions from superior cervical ganglion)
-inferior constrictor muscles:
-branches from external and recurrent laryngeal branches of vagus nerve
-piriform sinus:
-internal branch of superior laryngeal nerve
TNM STAGING SYSTEM FOR HYPOPHARYNX
Tumor size (T)

Tis - Carcinoma in situ
T1 - Tumor confined to one site and < 2 cm
T2 - Extension of tumor to adjacent region (two subsites) and between 2 and 4 cm
T3 - Extension of tumor to adjacent region or site with fixation of hemilarynx or > 4 cm
T4 - Massive tumor in invading bone or soft tissues of neck
Nodal involvement (N)

-see other notes
Distant metastasis (M)

-see other notes
DIAGNOSIS
-history of heavy alcohol ingestion; heavy smoking; and persistent dysphagia, persistent sore throat, or a
FB sensation in throat
-average duration of symptoms before presentation: 2-4 months
-referred otalgia via Arnold’s nerve, a division of CN X
-suggests malignancy hypopharynx, base of tongue, or supraglottic larynx
-20% have an asymptomatic neck mass: jugulodigastric or midjugular lymph node
-associated symptoms: weight loss, hemoptysis and hoarseness
-FNL: ulcerative lesion, pooling of secretions, fixation of vocal cords if advanced
PROGNOSIS
-pathologically positive cervical adenopathy related to tumor size:
-tumours < 4 cm 50% incidence of positive nodes
-tumours > 4 cm 85% incidence of positive nodes
MANAGEMENT OF HYPOPHARYNGEAL CANCER
-management modalities:
-full-course XRT with surgical salvage
-surgery alone
-combination pre- or post-XRT with surgery
-chemotherapy preceding or during surgery or radiotherapy
839
Surgery
-indications for nonresectability:
-involvement of carotid artery
-fixation of posterior pharyngeal wall (prevertebral fascia invasion)
-evidence of distant metastatic disease
-causes of surgical failure:
-tumor extension into thyroid gland, paratracheal nodes, and upper mediastinal lymph nodes
-submucosal extension inferiorly into cervical esophagus
Primary radiotherapy
-used for:
-(1) patients who have early malignancies, often confined to medial wall of piriform sinus,
particularly exophytic tumors without extension into piriform apex
-(2) patients who have primary malignancy of posterior pharyngeal wall
-(3) those who refuse surgical resection or are too ill to undergo resection
-(4) palliation to reduce bulk of extensive nonresectable malignancies and alleviate pain
-local control rate:
-T1 lesions: 79%
-T2 and T3 lesions: 56%
Results
-XRT alone insufficient management for patients with cervical metastases:
-5-year survival rate: 8%
-pts with T2 lesions: 69% had positive node findings at presentation
-survival decreased by 50%
-Pingree et al:
-5-year survival:
-surgery alone: 41%
-radiation alone: 21%
-combined surgery and XRT: 33%
-5-year survival for stage I and II hypopharyngeal cancer:
-surgery alone: 48%
-combined surgery and XRT: 40%
-Spector et al:
-69% of patients presented with positive metastatic disease
-87% of patients presented with stage III or IV disease
-overall incidence of distant metastases was 17.7%, and 6.2% of patients developed a second
primary cancer
Surgical/Reconstruction Options
-lateral pharyngotomy for a limited posterolateral pharyngeal wall lesion or medial piriform sinus lesion
-supracricoid hemilaryngopharyngectomy
-total laryngopharyngectomy:
-Pectoralis major myocutaneous flap
-Deltopectoral flap
-Radial forearm free flap
-Free jejunal graft
-Gastric pull-up
-mortality is 8%-15%, complication rate is 26-50%
-Colon transposition
840
MANAGEMENT OF THE NECK
-incidence of occult neck disease: 30%-40%

-issues of controversy:
-surgery alone, radiation alone or combination for clinically N0 neck
-decision often based on management of primary tumor
-N0 neck:
-must address and manage zones II, III and IV
-usually via modified or anterior neck dissection
-eg. piriform sinus tumours: levels II and III primarily involved
-N+ neck:
-comprehensive neck dissection (levels I-V)
-most studies support use of postoperative XRT for local control, although increased survival has not been
shown, for patients with N1 and N2 cervical disease
-radiation control:
-N0 neck: minimum dosage of 5000 rad
-N1 neck: minimum dosage of 6500 rad
-presence of contralateral node 4x greater in pts with palpable ipsilateral adenopathy
-control of contralateral neck: 6000 rad
-contralateral neck dissection is reserved for patients who have palpable nodal disease or if tumor
extends across midline
COMBINED MODALITY THERAPY
-need to administer postoperative radiotherapy within 8 weeks of surgery has been a major argument of
advocates of preoperative radiotherapy
-El-Badawi et al:
-surgery-only group: 25% survival rate
-combined surgery and post-op XRT: 40% survival
-recurrence above clavicle:
-T1-2: 18%
-T3-4: 33%
-distant metastasis after treatment:
-N0-1: 16%
-N2-3: 28%
-Garden et al:
-primary XRT:
-local control:
-89% of T1 and 77% of T2 lesions
-surgical salvage only successful in 6 of 19 primary recurrences
-5-year survival rates:
-68% for T1 lesions and 46% for T2 lesions
-protocol: twice-daily hyperfractionation
841
LYMPHOMAS OF THE HEAD AND NECK
(Non-Hodgkin)
-risk factors:
-congenital immunodeficiency disease
-acquired immunodeficiency
-HIV/AIDS
-immunosuppression from organ transplantation
-autoimmune disorders
-Hashimoto thyroiditis
-Sjogren lymphoma of salivary glands
-rheumatoid arthritis
-celiac disease
-EBV nasal lymphoma, Burkitt’s lymphoma
-organic toxins (phenol, benzenes)
Sites and Presenting Symptoms

-NHL: 10% occurrence in extranodal sites of H+N
-Waldeyer ring (50%) - tonsils > nasopharynx > tongue base (submucosal)
-paranasal sinuses, nasal cavity, larynx, oral cavity, salivary glands, thyroid and orbit
-B symptoms: fever, night sweats, weight loss
Site Symptoms
Tonsil tonsillar swelling, throat pain
Nasopharynx cervical mass, obstruction
Base of tongue FB sensation
Paranasal sinus exophthalmos, diplopia, pain
Nasal cavity obstruction, rhinorrhea
Oral cavity local swelling, pain
Larynx hoarseness, dyspnea, dysphagia
Salivary glands Mass
Thyroid Mass
Orbit Swelling, pain, proptosis, ptosis
Diagnosis and Histologic Classification

-FNA cannot assess whether lymphoma is follicular or diffuse, an important factor in determining grade
and prognosis
-immunohistochemical stains to differentiate from other cancers:
-antikeratin antibodies carcinoma
-anti-S100 protein melanoma
-panleukocyte antibodies lymphoma
-express either B-cell or T-cell markers
-B-cell lymphomas express a single class of light chains
-classification:
F.Ling - Lymphomas of the Head and Neck (1)
842
-Working Formulation (separates lymphomas according to natural histories):
-architectural pattern (follicular or diffuse)
-predominant cell type (large cell, small cleaved cell, mixed small and large cell, small
noncleaved cell, lymphoblastic)
-low- (12%), intermediate- (72%), high-grade (16%)
-with time, lymphomas can transform from low- to intermediate-grade type
-WHO classification takes into account immunophenotypic characteristics
-not useful in guiding treatment or predicting clinical behaviour
Working Formulation WHO Equivalents
Low grade
-small lymphocytic (consistent with CLL) -B-cell small lymphocytic or extranodal marginal zone
-follicular small cleaved cell -follicular lymphoma, grade 1
-follicular mixed -follicular lymphoma, grade 2
Intermediate grade
-follicular large cell -follicular lymphoma, grade 3
-diffuse small cleaved cell -mantle cell, lymphoplasmacytic
-diffuse mixed -diffuse large B cell, peripheral T cell
-extranodal NK/T cell
-diffuse large cell -diffuse large B cell, peripheral T cell
(rapidly fatal; most common NHL type in the -extranodal NK/T cell
head and neck)
High grade
-immunoblastic -diffuse large B cell, peripheral T cell
-extranodal NK/T cell
-lymphoblastic (usually T-cell origin) -lymphoblastic
-small noncleaved cell (EBV + HIV associated) -Burkitt lymphoma/Burkitt-like
Clinical Assessment
-staging tests:
-biopsy and pathologic review (open)
-complete physical examination
-indirect laryngoscopy
-CBC
-LFT
-HIV
-CXR hilar adenopathy
-CT/MRI head and neck
-upper GI series with small bowel follow-through
-association of Waldeyer ring and GI tract in 3-11%
-CT abdomen
-lymphangiogram (if available)
-lumbar puncture
-paranasal sinus higher propensity for CNS involvement
-bone marrow biopsy
-18% of pts with extranodal H+N lymphomas have BM involvement at presentation
Staging System
-Ann Arbor staging system (see Pediatric Malignancies)
-found more useful in predicting disease-free survival
843
MANAGEMENT
-primary treatment is radiation therapy, chemotherapy or a combination of the two

-radiation:
-2 Gy daily fractions to total dose of 30 to 40 Gy for low-grade lymphomas, 49-50 Gy for
intermediate-grade lymphomas
-chemotherapy:
-cyclophosphamide, chlorambucil, vincristine, prednisone, doxorubicin, bleomycin, methotrexate,
fludarabine
-delivered until complete response is achieved followed by two cycles of consolidation
chemotherapy
-CVP: cyclophosphamide, vincristine, prednisone
-CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone
Low-grade
Stage I or II
-involved-field or extended-field radiation therapy
-5-y: -65% disease free
-75% alive
-10-y sr: 60-65%
Stage III or IV
-CVP or chlorambucil
-complete response in 60-80%
-most eventually relapse
-fludarabine (purine analogue) for relapses
-Rituximab (minimally toxic monoclonal antibody directed against CD20 B-cell)
-interferon-alpha
-observation until patients become symptomatic with bulky disease
Intermediate-grade
Stage I or II
-age, performance status, stage, bulk of disease, number of extranodal sites, and serum LDH
influence prognosis
-CHOPx3 XRT CHOPx3
-CHOPx3 XRT
-5-y: -disease free: 80-100% (I); 75-80% (II)
-overall survival: 75-90% (I and II)
-poor outcome for pts with lymphoma of PNS or with NK phenotypes
Stage III or IV
-chemotherapy is the primary treatment
-usually CHOP or other combination chemotherapy
-complete response rate: 50-85%
-5-y: -disease-free: 30-60%
-overall survival: 35-70%
-XRT used to consolidate areas of bulky disease or for urgent treatment of airway obstruction
844
High-grade
-lymphoblastic lymphoma
-intensive combination chemotherapy
-60% can be cured
-small noncleaved cell lymphoma
-combination chemotherapy with escalated doses of cyclophosphamide, doxorubicin, vincristine,
prednisone, methotrexate, etopsoside, cytarabine, and intrathecal methotrexate
-at risk for tumour lysis syndrome
-65% are alive at 2 years
Thyroid Lymphomas
-XRT primary treatment of stage IE and IIE
-poor prognostic factors:
-bulky tumour, extracapsular extension, fixation and retrosternal involvement
-add CHOPx3-6 with radiation
-chemotherapy mainly for stage III and IV disease
Orbital Lymphomas
-low grade: XRT alone @ 30-35 Gy
-70% disease-free survival
-intermediate grade: XRT @ 36-40 Gy +/- chemotherapy
-high grade: XRT + chemotx
-advanced stage: combination chemotx
HIV-associated Lymphomas
-typically intermediate- or high-grade with advanced stage and frequent extranodal involvement
-common sites: gingiva, oral mucosa, parotid gland, conjunctiva
-overall survival generally poor
COMPLICATIONS OF THERAPY
Radiation Therapy
-major acute toxic effect is mucositis mouthwash
-xerostomia sialogogues, oral pilocarpine
-hypothyroidism thyroid replacement
Chemotherapy
-myelosuppression
-neutropenia or thrombocytopenia
-alopecia
-nausea and vomiting
-haemorrhagic cystitis (cyclophosphamide)
-cardiac arrhythmias/dysfunction (doxorubicin)
-neurologic (vincristine):
-neuropathy, constipation, ileus, hoarseness
-pulmonary fibrosis (bleomycin)
845
EMERGENCIES
-oropharyngeal/laryngeal lymphoma
-airway obstruction
-tumour lysis syndrome
-hyperuracemia, hyperkalemia, hyperphosphatemia, hypocalcemia
-cardiac arrhythmia, renal failure, death
-tx: allopurinol, IV hydration, alkalinization of urine
-febrile neutropenia
-sepsis, shock, death
-leptomeningeal lymphoma
-cord compression, confusion, cranial neuropathies
-paralysis, coma
846
THYROID DISEASE AND SURGERY
EMBRYOLOGY
-17th day GA:

-originates from foramen cecum migrates to pharynx via thyroglossal duct
-reaches mid-anterior neck by 3rd week
-TGD disappears by 10th week
-athyreosis = absent thyroid gland (rare)
-ectopic thyroid:
-may be found anywhere along thyroid duct from tongue as lingual thyroid to sternal notch
ANATOMY
-each lobe attached to trachea via lateral suspensory (Berry) ligament

-arterial supply:
-external carotid superior thyroid artery
-thyrocervical trunk inferior thyroid artery
-aortic arch or innominate artery thyroidea ima artery
-venous supply:
-superior, middle and inferior thyroid veins anterior facial and IJV
-inferior and ima veins innominate veins
-isthmus and inferior lateral lobes paratracheal and lower deep cervical nodes
-superior lobes superior pretracheal and cervical nodes
PHYSIOLOGIC CONSIDERATIONS
-paraventricular nuclei of hypothalamus TRH pituitary TSH iodine uptake by thyroid

-organification: iodination of thyroglobulin forms mono-iodotyrosine (MIT) and diiodotyrosine (DIT)
molecules
-MIT and DIT molecules link together to form triiodothyronine (T3) or thyroxine (T4) stored within the
colloid
-thyroglobulin T4 (90% of thyroid output) T3 (active cellular hormone)
-T4 measures thyroid function
-thyroglobulin assay used to measure completeness of thyroid ablation after surgery or radioisotope therapy
-elevated levels may indicate recurrent carcinoma
-Hashimoto thyroiditis autoimmune disease
TSH Effects on Thyroid

-increases vascularity
-stimulates iodide trapping
-increases release of thyroid hormone
-activates growth of thyroid gland (size and secretory activity of follicular cells)
-increased proteolysis of thyroglobulin
-increased iodination of tyrosine
-increased coupling of iodinated tyrosine
F.Ling - Thyroid Surgery (1)
847
Thyroid Hormone Effects
-elevates metabolic rate (thermogenesis, increases oxygen consumption)
-essential for normal neural and skeletal development (stimulates chondrocytes, bone reabsorption, growth
of neuronal tissue)
-increases sympathetic activity (increases heart rate and contractility)
-releases steroid hormones
-stimulates erythropoiesis
PATHOLOGY
Benign Lesions
-F:M = 5:1
-~1% of women develop disorders of thyroid function
-nodules very common: 3-7% of population with palpable nodules 5% of these nodules are malignant
-categories:
-nontoxic
-diffuse and multinodular goitre
-toxic
-toxic multinodular goitre, solitary toxic adenoma, diffuse toxic goiter (Graves disease)
-inflammatory
-acute, subacute, chronic thyroiditis
-most common benign neoplasm: follicular adenoma
-malignancy usually cannot be determined by cytology or intraoperative frozen sections requires
evidence of capsular invasion, blood vessel invasion or metastatic disease
Thyroid Cysts:
-typically arises from degenerated nodules, may result from cystic degeneration of malignancy
-may observe for regression, FNA relieves pain and acquires cells for cytology
-may consider lobectomy for recurrent cysts that are recalcitrant to drainage or bloody aspirates
Multinodular Goiter:
-more common in women
-pathophysiology:
-iodine deficiency TSH hypersecretion stimulates chronic thyroid hyperplasia and
involution multinodularity
-toxic nodular goiter: variation of diffuse colloid goiter in which one nodule is hyperfunctional
resulting in hyperthyroidism
-dx: FNA of a prominent nodule, TFT to confirm euthyroid sate (may be hypothyroid)
-tx: iodine replacement (reverses goiter), hormonal suppression (controversial), radioactive iodine
therapy or surgical excision (considered for cosmesis, decompression, concern for malignancy, or
toxicosis)
Malignant Tumours
-thyroid cancers account for 1.5% of all cancers
-death rate low: 1200 pts in US die annually
Papillary Adenocarcinoma
-most common type: 80% of all thyroid ca
-occurs earlier in life - peak in 3rd and 4th decade
-F > M ~ 3x
-4-10% have history of prior neck irradiation
848
-histologic features:
-papillary structures
-follicles
-Psammoma bodies - present in 40-50%
-presence in lymph nodes strongly
suggestive of PTC
-intranuclear vacuoles - “Orphan Annie-eyed” or
ground glass nuclei
-internuclear clefting, nuclear groove
-multicentric
-subtypes:
Papillary thyroid carcinoma with Psammoma body
-usual papillary (70%) (arrow). Note papillary structure and cells with “Orphan
-encapsulated (10%) Annie-eyed” nuclei.
-follicular (10%)
-tall cell (10%) - more aggressive variant
-diffuse sclerosis (3%)
-oxyphilic (2%)
-others (1%): columnar cell, clear cell, insular, lipomatous, trabecular
-clinical behaviour similar amongst various subtypes
-multicentric: both lobes affected in 80% of cases
-lymphatic spread
-locoregional metastasis high: 37-65%; micrometastasis in 90% lymph nodes
-impact on prognosis controversial: increases risk of recurrence but only slightly
increases mortality rate
-angioinvasion and distant metastases occur less frequently (2-17% of cases)
-prognosis:
-70-95% 5-year survival
-additional mortality rate of 10-20% over a 10-20 year period
-excellent prognosis for occult papillary carcinoma (<1.5cm) and papillary microcarcinomas
(<1.0cm)
Follicular Carcinoma
-10% of all thyroid cancers; occur almost exclusively in pts > 40 ya
-F > M ~ 3x
-requires open biopsy for diagnosis:
-capsular invasion or angioinvasion must be
demonstrated for diagnosis of FTC
-unifocal; multicentricity uncommon
-factors related to poor prognosis:
-increased degree of angioinvasion
-older age of onset
-distant metastasis at time of diagnosis
-metastasis:
-lymph node metastasis not a prevalent feature
(occur in < 20%)
-distant metastasis in 65%
-prognosis:
-70% 5-year survival; 40% at 10 years
-20% if distant metastasis at initial diagnosis
-50-60% of pts with FTC die of their dz
849
Hurthle Cell Tumours
-type of follicular tumour composed predominantly of
Hurthle cells
-large polygonal
-indistinct borders
-large pleomorphic hyperchromatic nuclei
-granular, eosinophilic/oxyphilic
-may be malignant (carcinoma) or benign (adenoma)
-capsular invasion and solid pattern of growth predict a
more aggressive behaviour carcinoma
-more aggressive variant of follicular carcinoma
with poorer prognosis
-at presentation: Hurthle cells demonstrating oxyphilic cytoplasm
-intrathyroidal (70%)
-cervical lymph node metastasis (20%)
-distant metastasis (10%)
-tx:
-hemithyroidectomy for Hurthle cell tumours lacking histologic criteria of malignancy
-total thyroidectomy with postoperative ablation for malignant lesions
-post-operative suppressive therapy recommended for all pts with Hurthle cell carcinoma because
they usually produce thyroglobulin and have TSH receptors
Medullary Carcinoma
-5-7% of thyroid carcinomas
-M=F
-types:
-Sporadic: 60-80% (usually unilateral, unilateral, worse prognosis)
-Familial: 10-40% (usually bilateral) - better prognosis than sporadic
-MEN type IIA: MTC, pheochromocytoma, hyperparathyroidism
-MEN type IIB: MTC, pheochromocytoma, neurofibromatosis
-originate from C-cells (derived from neural crest)
- produce calcitonin and carcinoembryonic antigen (CEA)
-also secrete gastrin, ACTH, substance P
-histology:
-nests of small, round cells
-amyloid production
-dense, irregular areas of calcification
-metastasis:
-early cervical lymph node metastasis in 50%
-involve central, paratracheal, and
jugular nodes
-distant metastasis to mediastinum, liver, lung
and bone in 8%
-diagnosis:
-measurement of calcitonins levels, with aid of Medullary thyroid carcinoma with amyloid stroma
pentagastrin stimulation used to:
-determine therapeutic success
-indicate recurrence
-screen family members for disease
-CEA a less sensitive marker for MTC
-screening with RET proto-oncogene
-can exclude 50% family members from further testing
850
-false negative rate 5%
-if positive >90% will develop MTC within first 2 decades of life
-monitoring for recurrence:
-persistently elevated calcitonin
-CT scan to look for lymph node metastasis
-octreotide scanning if unable to visualize nodes on CT
-PET scan (future)
-treatment:
-prophylactic treatment:
-total thyroidectomy in children with RET mutation by age of 5-6 years
-total thyroidectomy and cervical lymph node dissection
-prophylactic ipsilateral neck dissection for MTC > 2cm (nodal metastasis > 50%)
-neck dissection for persistently elevated calcitonins levels curative in 10-20%
-not sensitive to radioactive iodine
-prognosis:
-50-80% 5- and 10- year survival
-46% 10- year survival if cervical lymph node metastasis present
Anaplastic Carcinoma
-1-5% of all thyroid carcinoma
-mainly affects pts > 65 years
-usually present as large, fixed masses with vocal cord paralysis, compression of trachea or esophagus and
distant metastasis
-histology:
-giant and spindle cells in various proportions
-often represents the transformation of well-
differentiated carcinoma that was present for
many years
-small cell type responsive to radiation
-prognosis:
-average survival after diagnosis: 3-6 months
-effective treatment rarely feasible
-surgical debulking of tumour (controversial)
-most patients treated by combinations of
irradiation with surgery or chemotherapy
-multimodal treatment incl. doxorubicin Anaplastic thyroid carcinoma
and actinomycin D
Lymphoma
-associated with chronic lymphocytic thyroiditis and
Hashimoto’s thyroiditis
-dx: difficult to distinguish lymphoma from chronic
lymphocytic thyroiditis by FNA alone, therefore a
confirmational open biopsy is required along with
lymphoma staging work-up
-treatment:
-radiotherapy to neck and superior mediastinum
-surgical excision considered if tumour is
confined to the thyroid
Large cell lymphoma of thyroid
851
EVALUATION
Selection of Thyroid Nodules for Surgery
Clinical Parameters
-strong suspicion of malignancy
-firm or hard nodules
-homolateral vocal cord paralysis
-obvious metastatic disease
-other factors:
-history of irradiation early in life (40% risk of malignancy)
-presence of other endocrine tumours
-genetic syndromes (eg. Cowden disease and Gardner syndrome)
-coexisting thyroid disease
-FHx thyroid carcinoma
-solitary nodule: 4-33% malignant
-50% malignant in children; 85% with ca will have cervical adenopathy
-likelihood of malignancy within a solitary nodule is higher in male than female
-thyroid suppression strategies
-decreased volume of thyroid nodules by at least 50% in as many as 40% of pts
-goal to maintain TSH levels between 0.1 and 0.5 mIU/L with 0.125 and 0.15 mg thyroxine OD
-failure to respond to suppression is an indication for further investigations or surgery of the
nodule
-FNA and imaging investigation must be accomplished as a prerequisite
Needle Aspiration Cytology

-most accurate preoperative diagnostic modality; <5% false-positive rate
-reports classified as: benign, atypical, suspicious or malignant
-interpretation and management:
-benign: observation
-uniform follicular epithelium and abundant colloid: suggests nodular or adenomatous goiters
-inflammatory cells: suggests thyroiditis
-papillary cells (psammoma bodies, giant cells): suggests papillary carcinoma
-follicular cells: may be adenoma or carcinoma, requires q hemithyroidectomy to examine
architecture for differentiation (extracapsular spread, lymph or vascular invasion, or metastasis
indicate carcinoma)
-amyloid deposits (stained with Congo red): suggests medullary carcinoma
-undifferentiated, bizarre cells: suggests anaplastic carcinoma
Radioisotope Scanning
-evaluates function of nodule
-also to identify ectopic thyroid tissue (including retrosternal goiter, lingual thyroid and metastasis)
-hot nodules identified in 26% of thyroid cancers
-sensitivity and specificity low
Ultrasonography
-most sensitive in defining thyroid lesions
-identifying and monitoring nodules
-differentiates cystic from solid nodules in more than 80% of cases
-7% malignant in cystic lesions
-12% malignant in solid-cystic lesions
852
Computed Tomography
-not routinely used
-mainly to evaluate substernal goiter
-to evaluate cervical lymphadenopathy, airway and vascular displacement, tumour invasion
Other Diagnostic Studies

-CXR:
-rim or eggshell calcification suggestive of benign lesion
-bilateral calcification in superolateral aspect of thyroid indicative of MTC
-laryngoscopy
TREATMENT
Hemi- or Total Thyroidectomy

-identification of RLN one of key tasks
-RLN crosses inferior thyroid artery at roughly a right angle, superficial, deep or within its
branches
-be aware of possible non-recurrent laryngeal nerve (NRLN)
Management of Well-Differentiated Thyroid Carcinoma
Issues of Controversy
-selection of procedure: hemi- vs total thyroidectomy
-no prospective study to examine treatment outcome
-various recommendations, but no consensus:
-Hay et al: higher risk of locoregional recurrence - therefore total thyroidectomy in pts
with AMES low-risk PTC
-Wanebo et al: total thyroidectomy in high-risk pts showed no benefit over partial
thyroidecomy
853
-management of cervical nodes
-should a procedure be performed?
-occurs predominantly on right side
-found in < 1% of pts
Risk Factors
-Age
-one of most significant factors
-F<50 and M<40 have better survival rates than older pts
-mortality rates:
-<20ya: 2%
-20-40 ya: 5%
-40-50 ya: 8%
->50 ya: 34%
-Size of Primary
-lesions > 5cm have significantly poorer prognosis
-Unifocal or Multifocal Disease (PTC)
-microscopic foci of papillary carcinoma may remain clinically unapparent for a lifetime
-incidence of recurrence in opposite lobe has been shown to be low
-none of patients with recurrent disease in opposite lobe died of dz
-Extrathyroidal extension
-unfavourable prognostic sign
-associated with increased recurrence (local, regional and distant)
-Cervical Metastases
-increased risk of cervical recurrence without any increase in mortality
-Distant Metastases
-greatly increases risk of mortality
Risk Profiles for Selection of Therapy
-AMES:
-age, metastasis, extent of disease, size of lesion
-classified as low- or high-risk
-low-risk:
-7.7% recurrence rate, 1.8% mortality rate
-high-risk:
-59.1% recurrence rate, 46% mortality rate
854
-other classification systems:
-AGES (Mayo Clinic): age, histologic grade, extent, size
-MACIS: metastasis, age, completeness of surgical resection, extrathyroidal invasion, size
Low-Risk Patients
-mortality rates due to tumour are same regardless of extent of resection
-hemithyroidectomy appropriate for low-risk pts but restricted to those with lesions < 1.5 cm
High-Risk Patients
-more aggressive surgery
-total thyroidectomy reduces recurrence and increases survival
-tumour mortality rates as high as 42% out weigh increased morbidity associated with total
thyroidectomy:
-incidence hypoparathyroidism: 3-32%
-permanent RLN injury 1-11%
Treatment of Lymph Node Metastases

-paratracheal and upper mediastinal nodes, accessible through cervical incision, should be excised at time
of thyroidectomy
-elective neck dissection is not indicated for treatment of the lateral neck
-MRND for palpable lymph node metastasis
Radioiodine Therapy
-total thyroidectomy is often followed by ablation of residual thyroid tissue with 131I
-less than 10% of thyroid tissue should remain for ablative treatment
-pts in higher risk groups treated with postop ablative tx lower recurrence and overall mortality
-risks of therapy:
-dose dependent (but rare)
-acute myelogenous leukemia
-cancer of the bladder and female breast
-neonatal genetic and chromosomal abnormalities
-pre-iodine ablation treatment:
-no thyroid replacement for 6 weeks then RAI therapy
-alternatively, replace with T3 (cytomel) for 4 weeks and stop 2 weeks before RAI therapy
COMPLICATIONS OF THERAPY

-hypoparathyroidism
-airway obstruction
-haematoma compression
-bilateral vocal cord paralysis
-haematoma or seroma
-thoracic duct injury
855
HYPERTHYROIDISM
Clinical Features and Types

-Graves disease and toxic nodular goiter constitute > 90% of cases
-Graves disease:
-3rd or 4th decade
-F>M ~7x
-diffusely enlarged thyroid gland; hyperplasia, increased colloid material
-autoantibodies detectable:
-thyroid stimulating antibodies: thyroid receptor autoantibody (IgG)
-extrathyroidal manifestations: exophthalmos, pretibial myxedema, thyroid acropachy
-dx: thyroid stimulating antibodies, elevated T3, T4, RAIU and thyroglobulin; decreased TSH
-Toxic nodular goiters:

-single or multiple
-most in those >50ya; F>M ~8x
-autonomously functioning nodules, suppressing remaining gland
Treatment of Hyperthyroidism
Suppressive Therapy
-first line in attempt, non-destructive
-thionamides: PTU, methimazole, carbimazole
-inhibits T3 conversion and the oxidation and organification of iodine
-may cause hepatitis, agranulocytosis, parotitis
-iodides: KI, Lugol’s solution
-excess iodine inhibits thyroid hormone (Wolff-Chaikoff Effect)
-lithium:
-inhibits thyroid hormone release
-contraindicated in renal failure and cardiovascular disease
-beta-adrenergic blockers: propranolol, nadolol
-used to control peripheral manifestations of sympathetic overactivy
Ablative Therapy with Radioactive Iodine

-failed suppressive therapy
-131I treatment
-earliest age for treatment ranges from 20-40 years; pregnancy is a contraindication
-80-90% pts cured with single ablative dose; 10-20% cured with two doses
-hypothyroidism major complication; almost all eventually develop hypothyroidism
Surgery
-indications:
-failure of non-surgical management
-massive goiter with or without local symptoms
-florid disease
-desire for rapid control of toxic process
-patient bias
-pharmacologic intolerance
-suspicion of malignancy
856
-Preoperative preparation
-must establish euthyroid function and prevent thyroid storm in postoperative period
-thyroid storm: massive outpouring of T4 and adrenergic hormones that may prove fatal
-most regimens:
-thionamide antithyroid agents thyroid function is restored, followed by -
iodine solution administered for 10-14 days before surgery
-beta-adrenergic blocking agent effective for rapid preoperative preparation
-Surgical Approach:
-Graves disease: subtotal thyroidectomy
-unilateral toxic nodular goiter: lobectomy
-bilateral goiter: subtotal thyroidectomy
THYROIDITIS
Subacute Thyroiditis
-pathophysiology:
-viral (mumps, coxsackievirus) decreased iodine uptake
-painful enlarged thyroid, self limiting, malaise, associated URI
-treatment:
-symptomatic therapy, observation
Hashimoto’s (Chronic Autoimmune Thyroiditis)

-associated with lymphoma, neoplasms, other autoimmune disease
-pathophysiology:
-anti-thyroglobulin and anti-microsomal antibodies anti-TSH receptor transient hyperthyroid
then hypothyroidism
-risks:
-women, genetic susceptibility (HLA-DR3), Sjogren’s, DM, pernicious anemia
-histopathology:
-fibrosis, lymphocytic infiltration
-Ssx: slowly enlarging goiter, painless
-dx:
-antimicrosomal antibodies, ESR, TFT (may have elevated, normal, or low serum levels of T4 and
857
TSH), FNA only for prominent nodules suspicious of carcinoma or lymphoma that do not resolve
-treatment:
-long term thyroxine therapy with TFT monitoring
-surgical excision for compressive symptoms, suspicious nonfunctioning nodule
Riedel’s Thyroiditis
-thyroid fibrosis of unknown origin
-“rock hard” thyroid
-produces local pressure and hypothyroidism
-treatment: hormone replacement, may consider surgical release at isthmus
858
PARATHYROID DISEASE AND SURGERY
EMBRYOLOGY AND ANATOMY
-5th week GA:

-4th brachial pouch upper parathyroid glands
-less variable location
-shorter migration
-3rd brachial pouch/arch thymus gland and lower parathyroid gland
-more variable location
-longer migration
-size ~ 30-40 mg
-blood supply:
-subclavian artery thyrocervical trunk inferior thyroid artery inferior and superior
parathyroid arteries
-superior parathyroid:
-most commonly located in posterolateral aspect of superior pole, 1 cm above intersection of
recurrent laryngeal nerve and inferior thyroid artery
-inferior parathyroid:
-most commonly located 1-2 cm from entrance of interior thyroid artery into lower thyroid pole
-aberrant sites:
-anterior mediastinum, usually in thymus (3rd arch derivative)
-posterior mediastinum (4th arch derivative)
-aorta pulmonary window (3rd or 4th)
-retroesophagus, prevertebral
-tracheoesophageal site
-intrathyroidal site
-carotid bifurcation
CALCIUM PHYSIOLOGY
-Parathyroid Hormone:
-increases serum calcium and decreases serum phosphate
-stimulates osteoclastic resorption of bone
-increased calcium absorption and phosphate excretion by kidney
-increases rate of conversion of 25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin D3 in kidney
-increases gastrointestinal absorption of calcium by enhancing vitamin D synthesis
-Vitamin D:
-stimulates calcium and phosphate absorption in the intestine
-promotes bone osteoclast activity
-promotes retention of calcium by the kidneys
-Calcitonin:
-inhibits calcium resorption by osteoclasts
-increases kidney clearance of calcium and phosphate
F.Ling - Parathyroid Disease (1)
859
-hyperparathyroidism:
-primary:
-caused by adenoma or hyperplasia
of parathyroid glands
-other causes:
-parathyroid carcinoma
-familial hypocalciuric
hypercalcemia
-secondary:
-glands that are hyperplastic
because of malfunction of another
organ system
-causes:
-chronic renal failure
-Paget’s disease
-osteogenesis imperfecta
-multiple myeloma
-pituitary adenoma
-bone metastasis
-tertiary:
-occurs when PTH production is
irrepressible in patients with
normal or low serum calcium
levels
-persistent hyperfunction despite correction
CLINICAL MANIFESTATIONS OF HYPERPARATHYROIDISM
-hypercalcemia (only manifestation in 50% of

pts)
-osteitis fibrosis cystica (brown tumours)
-nephrocalcinosis
-manifestations:
-constitutional: fatigue, weight loss,
anorexia
-MSK: bone and joint pain, muscular
weakness
-Renal: colic from stones, hematuria
-GI: pancreatitis, constipation, peptic
ulcer disease, nausea
-Neuro: headache, memory loss,
psychotic behaviour, insomnia,
depression, confusion
-Skin: pruritus, brittle nails
History
-low-dose radiation exposure implicated
-Lasix increases urinary excretion of calcium hypocalcemia and hyperplastic parathyroid glands
-?FHx of MEN syndromes
860
Laboratory Evaluation
-electrolytes:
-serum calcium levels should be elevated on at least three occasions
-magnesium (usually low)
-chloride (usually elevated from PTH induced bicarburia)
-phosphate (usually low)
-if serum albumin is abnormal, calcium level should be adjusted to it
-measure ionized calcium levels and PTH
-others:
-ALP: suggests bone disease
-BUN/creatinine: renal function
-urine calcium:
-elevated in primary hyperparathyroidism
-low levels in familial hypocalciuric hypercalcemia
-thyroid function tests
-ACE levels: sarcoidosis
-serum prolactin and gastrin and urine catecholamines and metabolites: evaluate for MEN
syndromes
Preoperative Localization Tests

-non-invasive tests:
-Sestamibi or thallium 201-technetium 99m subtraction parathyroid scanning
-non-invasive, least expensive
-accurate in 85-90% of pts
-disadvantages:
-accuracy of only 35% in multiple gland hyperplasia
-false positive results with thyroid disease
-suppressive thyroid medication does not allow good subtraction of technetium
-unable to detect adenomas < 200 mg or < 5 mm
-Ultrasound:
-cannot localize retrotracheal, retroesophageal or mediastinal adenomas
-cannot detect small adenomatous glands (<5mm)
-CT:
-provide poor resolution of glands less than 1 cm
-do not differentiate parathyroid intimately associated with thyroid gland
-invasive tests:
-angiography
-selective venous catheterization for PTH
-reserved for patient who failed exploration
-time consuming
MEDICAL MANAGEMENT OF HYPERCALCEMIA
-95% success rate after surgery

-in chronic renal failure, however, surgical success rate is 50-85%
-hypercalcemia d/t sarcoidosis responds to steroids (blunts the synthesis and effects of elevated 1,25-OH2
vitD3 and decrease serum calcium levels
-saline/furosemide diuresis for severe hypercalcemia
-mithramycin and calcitonins to reduce bone resorption and hypercalcemia
-biphosphonates: inhibit bone resorption; toxic side effects include thrombocytopenia, hepatic dysfunction
and renal failure
861
-glucocorticoid: inhibit calcium intestinal absorption, may be effect for hypercalcemia secondary to
malignancy
-gallium nitrate: inhibits bone resorption, used for parathyroid carcinoma
-hemodialysis: indicated for life-threatening conditions
SURGICAL MANAGEMENT OF HYPERPARATHYROIDISM
-the longer the pathologic process of hyperparathyroidism are unchecked, the more severe demineralization
of the skeleton, nephrocalcinosis, and other symptoms will become
-if ALP is elevated, pt may need calcium supplementation during postoperative period while bone
metabolism equilibrates
-be prepared to resect from 1 to 3.5 glands or perform total parathyroidectomy and autotransplantation of
20 mg of tissue into a muscle bed
-superior parathyroid are more constant in their position:
-posterior aspect of thyroid lobe at point where recurrent laryngeal nerve passes under the
cricothyroid muscle
-inferior parathyroid usually found within 1-2 cm of inferior thyroid artery
-NIH Consensus Conference indications for parathyroid surgery:

-markedly elevated serum calcium concentration (>11.5 mg/dL)
-previous episode of life-threatening hypercalcemia (hypercalcemic crisis)
-reduced renal function (creatinine clearance reduced by 30% compared with age-matched
normals)
-radiologic evidence of kidney stones or nephrocalcinosis
-24-hour urine calcium > 400 mg/dl
-reduction in bone density >2 standard deviations for age-, gender-, and race-matched normals
-medical surveillance not suitable or desirable
Treatment Options:
-removal of adenoma and identification of other glands with biopsy of one normal gland
-subtotal parathyroidectomy with or without autotransplantation
-total parathyroidectomy with autotransplantation
-cryopreservation of parathyroid tissue and later transplantation
Operative technique
-if one enlarged gland is found frozen section adenoma one other gland is sampled
if normal, surgery is completed
if hyperplasia then assume parathyroid hyperplasia and perform subtotal parathyroidectomy
3.5 glands are removed
-measuring intra-operative PTH
-half-life of PTH is 4 minutes
-baseline PTH level measured preop
-after gland removed, rapid assay PTH measured after 10 minutes
-if more than 50% decrease in level, it is assumed that the pathologic gland has been
removed
-primary hyperparathyroidism in pregnancy:
-uncommon
-neonatal tetany may occur d/t precipitous drop in calcium postnasally
-pregnant women should undergo surgery during second trimester to avoid miscarriage
862
Surgery for parathyroid carcinoma
-carcinoma rare
-0.5% to 4% among pts with primary hyperparathyroidism
-wide excision required; local recurrence rate = 30%; regional and distant metastasis ~25-30% of these
patients
-structures needed to be excised:
-parathyroid gland, ipsilateral thyroid lobe
-skeletonization of tracheoesophageal groove, excision of paratracheal lymph nodes
-radical neck dissection reserved for palpable nodes
-primary radiation inadequate
Hyperparathyroidism after surgery

-recurrent or persistent hyperparathyroidism seen in 5%
-causes:
-usually ectopic gland
-missed adenoma (most commonly in posterior mediastinum)
-supernumerary gland
-second adenoma
-failed recognition of parathyroid hyperplasia
-incorrect diagnosis
-residual adenoma
-noninvasive sestamibi-thallium-technetium scans and invasive arteriography with selective venous
sampling for PTH helpful for localization of residual disease
Autotransplantation of parathyroid tissue

-devascularized glands cut into 1- to 2- mm pieces
-separate muscle bed created for each piece
-graft is neovascularized and functioning within 2-3 months
COMPLICATIONS
-haemorrhage and seroma promotion

-hypocalcemia temporary or permanent
-when multiple serum calcium levels are taken within the first 24h, a steep and fast decrease in
calcium usually portends the need for calcium supplementation
-symptomatic hypocalcemia treated with calcium and vitamin D
-2-4g calcium gluconate diluted in dextrose and water can be given IVq6h slowly over
30-45 mins
-must correct hypomagnesemia
-persistent hypercalcemia
863
NASOPHARYNGEAL CANCER
ANATOMY
-boundaries of nasopharynx
-superior: base of skull; basisphenoid and basiocciput
-posterior: bodies of atlas and axis
-anterior: choanal
-inferior: soft palate
-lateral: pharyngobasilar fascia and superior pharyngeal constrictors
-anatomic subsites:
-lateral wall:
-eustachian tube
-fossa of Rosenmuller (pharyngeal recess) - located posterosuperiorly to ET
-superior:
-foramen lacerum internal carotid artery cavernous sinus
-anterior:
-CN V3 crosses skull base through foramen ovale
-posterior:
-1.5 cm from jugular foramen (CN IX-XI)
-lies at apex of parapharyngeal space; at convergence of fascial planes that
separate space into three compartments:
-maxillary artery and lingual and inferior alveolar nerves
-retrostyloid compartment:
-carotid sheath contents
-retropharyngeal compartment:
-nodes of Rouviere
-access to nodes of the opposite neck
-path of least resistance for cancer spread
F.Ling - Nasopharyngeal Cancer (1)
864
-posterosuperior wall:
-rectangular region between Rosenmuller’s fossa
-anterior wall:
-narrow region of tissue bordering posterior choanae
-mucosa:
-at birth: pseudostratified columnar epithelium (PSCE)
-eventually replaced by squamous epithelium (SE); lateral walls, small patches of PSCE remain
-transitional epithelium:
-contains globular or cuboidal cells
-located where PSCE and SE meet
-lymphoid tissue and minor salivary glands
-nasopharyngeal carcinoma:
-85-95% of malignancies in nasopharynx
-remainder are lymphomas
-amplification of c-erbB-2 gene associated with poor prognosis
HISTOPATHOLOGY
-WHO Classification; three types:
-Type I: Keratinizing SCCa

-presence of intracellular bridges and prominent keratin formation
-25% of NPC in NA
-Type II: Non-keratinizing SCCa

-exhibit definite maturation sequence characteristic of squamous epithelium but display no
evidence of keratin formation
-least frequently encountered type
-Type III: Undifferentiated or “lymphoepithelioma”

-60% of NPC in NA; >95% of all cases in endemic areas
-cells of varying morphology that share common features:
-vesicular nuclei
-prominent nucleoli
-syncytia (fused multinucleated giant cells)
-intermixed strands or clumps of benign T-cells
EPIDEMIOLOGY
-NA and European white populations: 1/100 000

-African, North African, North American Inuit, Polynesian: 2-4/100 000
-southern Chinese: 30/100 000
-first-generation descendants to areas of low incidence: 15/100 000
-combination of genetic and environmental factors responsible for increased susceptibility to NPC
-NPC susceptibility genes linked to HLA region on chromosome 6
-dietary factors:
-salt-preserved foods; dried salted fish
-cigarette smoking (not a strong association)
865
-EBV:
-80-90% of non-keratinizing SCCa have abnormally increased antibody titers to EBV
viral capsid antigen (VCA) and early antigen (EA)
CLINICAL EVALUATION
-most common presentation: neck mass located at mandibular angle (60-70%)

-top 5 signs/symptoms:
-neck mass (60%)
-aural fullness (41%)
-hearing loss (37%)
-epistaxis (30%)
-nasal obstruction (29%)
-other:
-serous otitis media (33%)
-PND, H/A, tinnitus
-cranial nerve deficits (12-18%):
-superior spread of tumour (retrosphenoidal pathway)
-through foramen lacerum cavernous sinus
-CN VI and V (most common CN deficits)
-paralysis of cranial nerves III and IV; Horner’s syndrome
-foramen ovale or rotundum:
-diplopia
-pain or paresthesias involving lower two thirds of face
-spread to jugular foramen (retroparotid pathway)
-deficits in CN IX, X and XI
-distant metastasis (3-7%):
-bones > lungs and liver
Examination
-fiberoptic examination:
-friable exophytic, frankly malignant-appearing mass
-smooth submucosal bulge
-no abnormality seen (6%)
-smooth, submucosal and midline masses usually represent
embryologic remnants:
-eg. Tornwaldt cysts, pharyngeal bursa remnants
-FNAB of neck masses valuable
-CT scan with contrast the imaging study of choice
Laboratory Tests
-serologic testing may help establish diagnosis of NPC in pt with
unknown primary
Friable exophytic mass in nasopharynx
-those with occult or early (stage I) WHO type II or III NPC:
-86% positive EA (IgG) titers
-82% positive VCA (IgA) titers
-EBV titers in type I NPC not significantly increased
-screening in high-risk Chinese populations are valuable
-antibody-dependent cellular cytotoxicity (ADCC assay)
-provides prognostic information (except for type I); high titers associated with good prognosis
-EA and VCA have not shown to have prognostic value
866
Diagnostic Surgery
-biopsy
Staging
-shortcoming of various staging systems:
-eg. AJCC system: 80% of all pts placed into stage IV at presentation
-precise extent of NPC primary often difficult clinically because submucosal spread beneath
normal-appearing mucosa is common
-cervical metastasis:
-Ho et al:
-no significant difference in survival of patients with upper neck nodes compared with
pts whose disease is limited to nasopharynx
-Ho’s line:
-defines a line that begins at lateral border of trapezius insertion into occiput and
extends diagonally to sternal head of clavicle effectively separating levels I, II
and III from areas IV and V
-disease below line markedly worse prognosis; significantly increased risk of
distant metastasis
-Neel et al
-presence of unilateral compared with bilateral nodal disease had no prognostic
significance
-prognostically significant factors (Ho’s criteria):

-extensive tumour within nasopharynx
-number and duration of symptoms (seven or more symptoms)
-level of positive lymph nodes (low in neck)
-presence of metastasis
-histologic grade (WHO type I)
-keratinizing SCCa carries significantly worse prognosis than other histologic types (not
as radiosensitive)
-ADCC titer < 1:960
-symptoms > 2 months
-low Kornofsky scores
MANAGEMENT
TNM Staging
T1 -limited to nasopharynx
T2a -extension to nasal cavity or oropharynx; no parapharyngeal space involvement
T2b -extension to nasal cavity or oropharynx; with parapharyngeal space involvement
T3 -bony and/or paranasal sinus involvement
T4 -cranial nerve, intracranial, orbital, infratemporal fossa, hypopharyngeal involvement
Stage I: T1 N0
Stage II:
A: T2a N0
B: T2b or N1
Stage III: T3 or N2
Stage IV:
A: T4 B: N3 C: M1
867
Radiation Therapy
TREATMENT OF NASOPHARYNGEAL CANCER
-cobalt 60 or 4-6 MeV photons
-4500 cGy in 180-200 cGy fractions Radiation therapy
via paired lateral apposed fields -External beam supervoltage radiation
-primary treatment mode: field includes primary tumour,
covering nasopharynx and neck
first echelon lymph nodes, and all clinically involved
bilaterally nodes plus prophylactic radiation of supraclavicular
-lateral apposed boost fields are lymph nodes
directed at primary tumour site -Intracavitary brachytherapy
-may supplement external irradiation as part of primary
-critical to successful eradication of
treatment or for management of residual recurrent
primary tumour is ensuring that tumour
entire volume receives 6000 to 7000
cGy of 60Co-equivalent photon Surgical treatment
-plays limited role in management
energy
-surgical procedures (infratemporal fossa approach,
-brachytherapy used for recurrent NPC to transparotid temporal bone approach, transpalatal approach)
avoid overdose of adjacent normal tissues may be preferable to radiation for local recurrence
-high activity gold 198 or iridium
Other treatment
192 seeds via endotracheal tube -chemotherapy
-permanent implants of high-activity -proven efficacy regarding survival
iodine 125 into tumour bed via large -may help palliate intractable pain
spinal needle -immunotherapy
-impact on long-term survival obscure
-chemotherapy an adjunct to radiation therapy -vaccines
-combined-modality results in a -future potential development of vaccines for EBV-
significant decrease in distant related diseases
metastasis but little or no
improvement in local control or
disease-free survival* (new evidence suggests otherwise)
-drawback is toxicity that may lead to breaks in radiation treatment
-split-course XRT results in decreased survival compared with continuous course XRT
-cisplatinum-containing regimens (hematologic toxicity) does not overlap with radiation therapy
(mucosal damage)
-combined therapy yields slightly higher absolute survival rates
-chemotherapy already has been well established as a valuable modality for palliation of
unresectable disease
Surgical Treatment
-most frequently indicated surgical procedure:
-neck dissection to remove clinically positive cervical disease that has not been eradicated by full-
course radiation therapy
-surgical approaches for recurrent or residual disease:
-transparotid temporal bone approach
-infratemporal fossa approach
-maxillary swing procedure
General Treatment Options

-Stage I: EBRT or LR
-Stage II: EBRT
-Stage III-IVa: concomitant chemoradiation +/- MRND
-Stage IVB: concomitant chemoradiation + MRND
868
PROGNOSIS
-overall 5-year survival rate: 30-48% in most series

-modern radiation fractionation schedules:
-5-year actuarial survival rate of 57% and disease-free survival rate of 42%
-Neel and Taylor: 5-year survival rate of 50% (27% type I, 56% for types II and III)
-*Phase III study of concurrent chemoradiotherapy versus radiotherapy alone for advanced nasopharyngeal
carcinoma: positive effect on overall and progression-free survival. Journal of Clinical Oncology.
2003;21:631-637.
-treatment group: treated with fluorouracil and cisplatin plus radiation therapy
-control group: radiation therapy alone
-five years following treatment
-cancer relapses: 26% cf 46%
-overall survival at 5 years: 72% cf 54%
-progression-free survival at 5 years: 72% cf 53%
COMPLICATIONS
-xerostomia
-salivary tissue cannot tolerate > 3500 cGy of radiation
-tx: artificial saliva, water, Pilocarpine
-dental caries
-eustachian tube dysfunction: d/t postradiation fibrosis in nasopharynx
-serous otitis media resistant to conservative measures
-trismus, discomfort, induration of neck and entrapment neuropathy of CN IX, X, XI, and XII
-inappropriate shielding
-hypopituitarism, hypothyroidism, optic neuritis, radiation retinopathy
-temporal lobe necrosis, transverse myelitis
-chemotx related:
-5-FU: acute toxic response in mucosa is exacerbated
-bleomycin: aggravates soft-tissue fibrosis in irradiated areas
-cisplatin: SNHL (~30% of patients)
869
OROPHARYNGEAL CANCER
-<1% of all new cancers
-peak incidence 6th-7th decade; M>F
->90% SCCa
ANATOMY
-boundaries:
-anterior: circumvallate papillae (base of tongue), anterior tonsillar pillars, junction of hard and
soft palates
-lateral: tonsillar regions
-posterior: posterior pharyngeal wall
-superior: soft palate
-inferior: pharyngoepiglottic folds
-anatomic subsites:
-base of tongue
-tonsils
-tonsillar pillars
-soft palate and uvula
-posterior and lateral pharyngeal walls
-glossotonsillar sulci
-sensory and motor supply:
-CN IX (glossopharyngeal nerve) and CN X (vagus nerve)
-motor and most sensory innervation to soft palate: CN V2 and V3
-blood supply: branches of external carotid artery
-levels II and III
-central structures (BOT, soft palate, posterior pharyngeal wall) drain bilaterally
-tonsillar region and posterior pharyngeal wall retropharyngeal nodes upper level II nodes
-parapharyngeal space:
-divided by layer of fascia running from tensor veli palatini muscle to styloid into two
compartments:
-fat, variable portions of deep lobe of parotid, small branch of trigeminal nerve
to tensor veli palatini
-poststyloid compartment:
-carotid artery, jugular vein, cranial nerves IX to XII, sympathetic chain, lymph
nodes
-vagus and glossopharyngeal nerves have tympanic and auricular branches (Jacobson and Arnold nerves)
referred otalgia
PHYSIOLOGY
-normal speech production, respiration, deglutition

-four phases of swallowing: oral preparatory, oral, pharyngeal, esophageal
-poor speech production, dysphagia or aspiration post-surgery
-d/t VPI, pharyngeal stenosis, inappropriate functioning of tongue base from tethering or volume
reduction, decreased pharyngeal contraction or delayed triggering of pharyngeal swallow 2o
decreased sensation
F.Ling - Oropharyngeal Cancer (1)
870
ETIOLOGY
-alcohol and tobacco use (#1)

-HPV and EBV may have a role
-poor nutrition, poor oral hygiene, syphilis, occupational exposure, previous irradiation (minor)
HISTOPATHOLOGY
-premalignant lesion on soft palate and anterior tonsillar pillars

-leukoplakia, erythroplakia, lichen planus
-SCCa (>05% of oropharyngeal cancer)
-verrucous carcinoma
-fungating, slow-growing tumour with well-differentiated keratinizing epithelium and rare cellular
atypia
-rarely metastasize
-lymphoepithelioma
-rapid growth
-readily metastasizes
-usually in tonsillar region of young adults
-adenoid squamous, adenosquamous, basaloid SCCa: aggressive but rare
-other:
-lymphoma, minor salivary gland tumours, mucosal melanomas, sarcoma
NATURAL HISTORY
-lymphatic metastasis at presentation common

-orderly fashion: level II III retropharyngeal
-order may be altered by obstruction of lymphatic channels caused by inflammation, previous
surgery, radiation, or large metastatic deposits
-both necks usually involved
-rate of occult neck metastasis greater than 20% for all lesions larger than T1
-tumours generally advanced
DIAGNOSIS
History
-alcohol and tobacco abuse
-pain (most common presenting symptom)
-dysphagia
Physical
-nodal enlargement (primary symptom in 30%)
-trismus
-cranial nerve deficits
Biopsy of primary lesion and FNAB of enlarged nodes
871
Imaging studies
-CXR
-CT scan/ MRI
-assessment of advanced stage tumours or when involvement of mandible, parapharyngeal space,
prevertebral fascia, neck nodes, or retropharyngeal nodes is suspected
-Panorex
Laboratory studies
-CBC and chemistry
-LFTs
-ECG
Examination under anaesthesia

-examination of all aerodigestive mucosa for second primaries (seen in 8%)
-assessment of submucosal spread, mandibular invasion, and tumour fixation
TREATMENT
-routine use of chemotherapy remains debatable

TREAMENT OROPHARYNGEAL CANCER
-use of organ preservation protocols and neoadjuvant
or adjuvant chemotherapy remains investigational Primary tumour treatment
-T1 and T2: surgery or radiation (equally effective)
-T3 and T4: combined modality
-all pts with oropharyngeal SCC more extensive than
-primary surgery with addition of
T1 require some treatment of the neck because of high brachytherapy or chemotherapy
rate of clinically positive nodes and occult nodal -primary radiation with surgical salvage
metastasis at presentation Neck treatment
-N0 and N1: surgery or radiation
-N2 and N3: combined modality
Squamous Cell Variants and other Oropharyngeal Cancers -both necks are treated with central lesions
-spindle cell variant: clinically and biologically similar -retropharyngeal nodes are always treated
to SCC
-verrucous carcinoma: requires wide local excision INDICATIONS FOR POST-OP RADIATION
-lymphoepithelioma:
-exquisitely sensitive to radiation Tumour factors
-XRT is primary treatment -close or involved resection margins
-perineural or vascular invasion
-adenoid squamous, adenosquamous, basaloid -T3 or T4 tumours
squamous cell carcinoma: Neck factors
-combined surgery and radiation -clinically N0 or N1 neck
-lymphomas: chemotherapy and radiation -two or more histologically positive nodes
-histologically positive nodes at multiple
-malignant minor salivary gland tumours: sites
-wide local excisions with or without post-op -perineural or vascular invasion
XRT -extracapsular nodal spread
-melanomas and sarcomas: -N2 or N3
-wide local excision and neck dissection
RADIATION
-6000 to 7000 cGy through external-beam shrinking field to primary lesion and necks over 6-7 weeks
872
SURGERY
Primary Tumour
-tumour becomes unresectable after extension into poststyloid parapharyngeal compartment, prevertebral
fascia, or involvement of carotid artery
-resection margins: 1-2 cm
-frozen section required because of submucosal spread
Surgical Approaches
Transoral Approaches:
-Oral:
-no external excisions
-limited exposure
-for small (T1), superficial or exophytic cancers (eg. on soft palate, anterior tonsillar pillar,
posterior wall, uvula)
-Mandibular Lingual Release:

-lesions confined to base of tongue
-outer incision around lower border of mandible; inner incision through lingual mucoperiosteum
-delivers tongue and floor of mouth into neck
Transpharyngeal Approaches:
-Suprahyoid Pharyngotomy
-lesions at base of tongue and pharyngeal walls
-pharynx entered through vallecula
-visualization of superior margin in large tumours is inadequate
-risk of cutting into cancer if extensive involvement of tongue base or vallecula
-Lateral Pharyngotomy
-small lesion of base of tongue and pharyngeal walls
-pharynx entered posterior to thyroid ala on least affected side
-limited superior visualization and risk of damage to hypoglossal and superior laryngeal nerves
Transmandibular Approaches:
-Midline Labiomandibular Glossotomy

-rarely used
-only for small midline posterior pharyngeal wall cancers too low to reach thorough a transoral
approach
-involves splitting lip, gingiva, mandible, anterior tongue in midline
-no access to parapharyngeal space or lateral oropharyngeal sites
-Mandibular Swing Approach

-provides wide exposure to entire oropharynx and allows en bloc resection of cancer and draining
nodes
-osteotomy placed anterior to mental foramen; full thickness of FOM is incised; mandibular
segments are then retracted laterally, allowing good access to oropharyngeal structures and
parapharyngeal space
-main disadvantage is potential sacrifice of whole hemimandible if unsuspected mandibular
873
involvement that is not amenable to marginal resection
-Mandibulectomy
-for advanced cancers with overt bony invasion
-entire mental canal must be resected if there is overt mandibular canal invasion
-disadvantage: functional and cosmetic deficits
NECK
-N0: modified and selective levels II, III, and IV

-N1: modified or radical
-N2 and N3:
-radical neck dissection with post-op XRT if surgery is primary modality
-if XRT used initially then planned RND performed 4-6 weeks later
RECONSTRUCTION
-limited to restoration of integrity, bulk and sensation, but complex motor functions or the oropharynx
cannot be duplicated at present
Soft-Tissue Reconstruction:
-small defects of pharyngeal walls up to 3 cm and those less than 1/3 the volume of tongue base can be
closed, primarily by STSG or left to granulate if not open into neck
-free fasciocutaneous flaps are required for larger defects to prevent tongue tethering or pharyngeal
stenosis
COMPLICATIONS OF TREATMENT
FOLLOW-UP
Radiation
-1st year: 1-3 mo
-mucositis
-2nd year: 2-4 mo -xerostomia
-3rd year: 3-6 mo -taste dysfunction
-4th and 5th: 4-6 mo -dysphagia
-fibrosis
-after 5th: 12 mo
-ulceration and tissue necrosis
-osteoradionecrosis of mandible
-hypoglossal palsy
PROGNOSIS
Surgical
-5-year survival: -approach related:
-stage 1: 67% -damage to teeth
-stage 2: 46% -damage to nerves
-stage 3: 31% -cerebral embolism and carotid artery
thrombosis
-stage 4: 32% -resection and reconstruction related
-haemorrhage
-wound infection and dehiscence
-positive resection margin
-pharyngocutaneous fistula
-aspiration
-dysphagia
-poor speech
-VPI
-ET dysfunction
-nonunion and osteomyelitis of mandible
-malocclusion and TMJ dysfunction
874
-not common: 5-10% of cancers in upper aerodigestive system

-0.5% of all malignancies
-M:F = 8:1
-women with Plummer-Vinson syndrome have high incidence of cancer of post-cricoid region
BASIC SCIENCE
Anatomy
-superior limit: pharyngoepiglottic fold (level of hyoid bone)
-inferior limit: inferior border of cricoid
-three anatomic sites:
-piriform fossa
-postcricoid region
-posterior pharyngeal wall
-innervation:
-sensation: glossopharyngeal nerve and internal
branches of superior laryngeal nerve
-motor: inferior constrictor and cricopharyngeus via
pharyngeal plexus
-upper deep cervical lymph nodes
-retropharyngeal nodes (superior)
-jugulo-omohyoid nodes (lateral)
-paratracheal, paraesophageal, thyroid nodes (inferior)
875
Physiology
-important component of both respiration and deglutition
-obstruction d/t edema secondary to lymphatic invasion or infection
-invasion of arytenoid or RLN a/w obstruction and aspiration
DIAGNOSIS
History
-treated for pharyngitis
-tobacco and ethanol abuse
-weight loss, dehydration
-odynophagia, dysphagia
-hoarseness, dyspnea
-otalgia
-neck mass
-airway obstruction
Physical
-weight loss or cachexia, decreased skin turgor
-hyporesonant voice (“hot potato”), hoarseness, stridor
-status of dentition
-indirect examination with mirror: pooled secretions, vocal cord paralysis, other lesions
-flexible fiberoptic laryngoscopy
-full neck examination
Radiology
-CXR
-barium swallow
-to evaluate swallowing mechanism and dynamic effects of tumour on swallowing
-detect GERD
-CT and/or MRI of neck
Laboratory
-complete chemistries
Staging endoscopy and biopsy

-control of airway
-complete paralysis
-gross characteristics of tumour
-three-dimensional relationships of tumour
-biopsy
-determination of inferior border
-will determine extent of surgical resection and reconstruction
-esophagoscopy
-complete examination to r/o other sites of malignancy
-bronchoscopy if warranted
Pathology
-95% epidermoid carcinomas; 5% adenocarcinomas arising from glandular structures
876
-sites of involvement:
-piriform fossa: 64%
-posterior wall: 30%
-postcricoid: 4%
-submucosal spread common; may have “skip areas”
-adequate margins:
-superior: 2-3 cm of mucosa from gross tumour edge
-inferior: 4-6 cm if tumour involves cervical esophagus
-lymph node metastasis
-palpable nodes present in 75%
-bilateral disease in 10%
-if N0 then risk of occult nodes is high (30-40%) - therefore
must treat all necks
-risk at presentation of distant metastasis: 20%
PROGNOSIS
-overall survival rate ranges form 35-40%

-varies by site: (5-year survival)
-piriform fossa (54-5%; 30% overall)
-posterior wall (100-0%; 56% overall)
-postcricoid (33-0%; 25% overall)
MANAGEMENT
Preoperative Treatment
-nutritional support
-enteral feeds
-improving pulmonary status (ie. antibiotics for COPD)
Treatment Options
-early:
-T1: -XRT to primary and bilateral necks
-surgical salvage
-T2: -XRT to primary and bilateral necks
-consider chemotherapy
-consider hyperfractionated XRT
-late:
-T3: -chemoradiation (organ preservation approach -
induction chemotherapy followed by adjuvant
XRT) with surgical salvage
-surgery and neck dissection with postoperative
XRT
-T4: -surgery (laryngectomy/pharyngectomy) and neck dissection with postoperative XRT
-N0, N1: XRT or neck dissection

-N2, N3: both XRT and neck dissection
877
Surgery TREATMENT OF
-neck dissection performed in most patients - bilateral
recommended in pts with medial wall piriform sinus disease Surgery
-suprahyoid pharyngotomy
-partial laryngopharyngectomy
Posterior Hypopharyngeal Wall Cancer -laryngectomy
-often remain localized and present opportunity for wide excision -pharyngectomy
with uncomplicated reconstruction -partial cervical esophagectomy
-skin graft
-approached via suprahyoid pharyngotomy -free flap
-incision into posterior hypopharyngeal wall carried down to -gastric interposition
prevertebral fascia -feeding tube
-posterior wall defects reconstructed with STSG secured with -neck dissection
-superior mediastinal dissection
bolster Radiotherapy
-bolster removed transorally 5-10 days post-op -T1, some T2
-reconstruction of posterior or posterolateral hypopharyngeal wall -postsurgical
should not extend below level of corniculata cartilages with larynx Chemotherapy
Chemoradiation
in place marked interference with swallowing High-dose Intraarterial chemotherapy and
radiotherapy
Piriform Fossa Cancers Must treat necks even in pts w/o palpable
metastases
T1 Cancers
-indications:
-must be < 2 cm and located in superior aspect of piriform fossa
-no impairment of vocal cord movement
-1.5-cm margin between inferior aspect of tumour and piriform fossa apex
-good pulmonary function
-partial laryngopharyngectomy
Resection of T2 and Larger Piriform Fossa Cancers

-requires total laryngectomy for adequate resection
-may require partial pharyngectomy and reconstruction
-cancers extending into piriform apex:
-aggressive submucosal and lymphatic growth
-inferior resection line must include upper cervical esophagus with paraesophageal and
paratracheal lymphatic and ipsilateral lobe of thyroid gland
Postcricoid Cancer
-total laryngectomy, partial pharyngectomy and cervical esophagectomy
-total esophagectomy if inferior line of resection is below mediastinal inlet
-paraesophageal and paratracheal lymph node resection with hemithyroidectomy also essential - might also
require mediastinal dissection
Reconstruction
-enough pharynx primary closure
-not enough pharynx RFFF, pectoralis major flap
-no pharynx jejunal free flap, RFFF, pectoralis major flap, colonic flap
-laryngopharyngoesophageal defect gastric pull up
Radiation therapy
-primary radiation for curative treatment is preferable for T1 lesions
-debate for T2 lesions: XRT with surgery for salvage
878
Chemotherapy
-currently under investigation
COMPLICATIONS
-wound breakdown with fistula formation, infection, haemorrhage

-aspiration and stenosis
EMERGENCIES (pretreatment)
-Obstruction
-airway
-tracheotomy
-laser debulking
-esophagus
-feeding tube
-fluid resuscitation
-disimpaction
-Hemorrhage
-isolate source
-angiography
-embolization
-surgical ligation
879
CERVICAL ESOPHAGEAL CANCER
ANATOMY
-cervical esophagus:
-superior limit: cricopharyngeus
-inferior limit: suprasternal notch
-layers:
-mucosa: stratified squamous epithelium
-submucosal or areolar layer
-muscular layer (striated muscle)
-outer longitudinal layer
-inner circumferential layer
-blood supply:
-arterial: thyroid branch of thyrocervical trunk
-venous: inferior thyroid vein
-nerve supply:
-vagus
-paratracheal nodes
superiorly to lymphatics of pharynx IJ nodes
OR inferiorly to superior mediastinum
PHYSIOLOGY
-upper esophageal sphincter: cricopharyngeal muscle

-normal resting tone prevents reflux
-dilatation results in initiation of peristalsis
EPIDEMIOLOGY
-80x more common in Middle East, southern and eastern Africa, and northern China
-alcohol and tobacco major risk factor
-other risk factors:
-nitrosamines
-most common malignancy: SCCa
-other tumours:
-adenocarcinoma:
-arises from gastric mucosa near GE junction
-associated with Barrett’s esophagus
-5% with GERD Barrett’s 5% adenocarcinoma
-Tylosis:
-AD trait: marked thickening of palms and soles
-associated with high risk of esophageal carcinoma by age 65
-increased risk of developing second primary in upper aerodigestive tract
F.Ling - Cervical Esophageal Cancer (1)
880
EVALUATION
-solid food dysphagia and weight loss
-most common abnormal finding: neck mass (21%)
-pooling of secretions in hypopharynx
-associated diseases: achalasia, Plummer-Vinson syndrome, prior H+N cancer
Laboratory tests
-barium swallow routinely used to evaluate patients with cervical dysphagia
-probably superior to CT or MRI in delineating cephalocaudal extent of mucosal involvement
-CT/MRI used to define depth of invasion and to identify liver, pulmonary or mediastinal metastasis
DIAGNOSTIC SURGERY
-endoscopic evaluation under general anaesthesia

-assess superior margin of tumour and its relationship to posterior aspect of cricoid cartilage and
arytenoid cartilages
-assess distal extent of mucosal disease; limited by degree of obstruction
-biopsy for histologic conformation
-early gastrostomy or jejunostomy for near total obstruction
-however relative contraindication for gastric pull-up
STAGING
-Tis: -carcinoma in situ

-T1: -5 cm or less esophageal length without obstruction; no transmural or circumferential involvement
-T2: -more than 5 cm esophageal length without extraesophageal spread; any tumour that produces
obstruction or involves entire circumference of esophagus
-T3: -extraesophageal spread
MANAGEMENT
-summary:
-extension to postcricoid area mandates laryngectomy
-involvement of thoracic esophagus mandates total esophagectomy
-gastric pull-up is preferred reconstruction
-chemotherapy and radiation are used for palliation of patients with advanced carcinoma
-complicating factors:
-obstruction aspiration pneumonia
-malnutrition
-intractable aspiration:
-laryngotracheal separation (Lindeman):
-proximal trachea is oversewn - suture line reinforced with muscle flap developed from
adjacent SCM
-esophagectomy or laryngopharyngoesophagectomy for incurable carcinoma rarely indicated
881
Nonoperative Management of Cervical Esophageal Cancer
Advanced Esophageal Carcinoma

-incurable palliation:
-metastatic disease
-transmural involvement of prevertebral fascia, trachea or carotid arteries
-chemoradiation:
-5-FU and cisplatin with radiation
-complete responses in 45-87%
-median survival still dismal: 11-22 months
-early disease (stage I) and about half of advanced disease (stage II-III) can be controlled with
concurrent chemoradiation and esophageal conservation
Operative Cervical Esophageal Carcinoma
-survival rate of patients requiring total cervical esophageal reconstruction for advanced carcinoma of the
hypopharynx and cervical esophagus:
-2 year disease-free survival rates are poor (9-39%)
-reconstructive options:
-tubed pedicle flaps (eg. pectoralis major, latisimus dorsi)
-disadvantages: bulkiness, wound breakdown and fistula common, post-op stenosis
-colonic interposition
-mobilization on superior mesenteric artery
-significant incidence of postoperative infection
-not first-choice reconstructive alternative
-gastric pull-up and pharyngogastric anastomosis

-reasons for esophagectomy:
-pull-up devascularizes esophagus
-skip-lesions possible
-technically cannot do anastomosis midway
-procedure:
-stomach brought through posterior mediastinum
-Kocher manoeuver to mobilize duodenum
-vagotomy and pyloroplasty required
-jejunostomy tube inserted
-advantage:
-one-stage procedure
-total esophagectomy encompasses lesions that extend below sternum; wider
margin of resection
-disadvantage:
-morbidity incurred during mediastinal part of procedure which often results in
PTX or hemothorax
-operative mortality 5-15%
-sequalae:
-early satiety, emesis, dumping
-stricture most commonly associated with anastomotic leakage
-free jejunal autograft

-patients who do not need resection of esophagus distal to thoracic inlet
-however, propensity for submucosal spread may be more extensive than initially realized
882
COMPLICATIONS
-wound separation and fistula formation

-associated with stenosis of pharyngeal lumen
-slower healing in prior irradiated patients might required second reconstructive efforts
EMERGENCIES
-postoperative haematoma: explore and evacuate promptly

-vascular thrombosis of microvascular percutaneous anastomosis:
-monitor with Doppler
-reexplore anastomosis in OR
Important Recent Information

-postoperative anastomotic leakage single most important source of morbidity
-hand sewn anastomoses more reliable
-single layer closure as reliable as two layer closure
883
EARLY GLOTTIC CARCINOMA
Vertical Partial Laryngectomy and Laryngoplasty
-larynx cancer originates on true vocal cord ~ 75% of the time

-early detection and treatment can achieve cure rates of 90% or more
-preservation of life given higher priority than preservation of laryngeal function
-VPL = vertical partial laryngectomy
-LME = laser microscopic excision
DIAGNOSTIC ASSESSMENT
History:
-cigarette smoking, ethanol intake
-occupational exposure to fumes
Physical examination:
-most early glottic tumours arise on membranous portion of true vocal cord
-20% extend to supraglottis
-20% extending 5 mm or more below glottic margin
-25% extending to anterior commissure
-PFTs are controversial for pts being considered for VPL

-ideally FEV1 > 50-60% ok for operation; but this did not reliably predict postop complications
-if pts could climb two flights of stairs preop ok for surgery
-CT scanning used to delineate extent of tumour invasion
-tends to underestimate staging of glottic carcinoma related to its small size (volume effect)
-findings usually unremarkable in early glottic carcinoma
-Nodal involvement:
-T1 and T2: 5% nodal involvement
-T3 disease: (vocal cord fixation) - 30-40% incidence of positive nodes; survival rate of 50%
HISTOLOGICAL CLASSIFICATION
Hyperplasia and hyperkeratosis:

-an increase in number of cells and keratin production
-not a significant risk factor for malignant degeneration
Mild Dysplasia:
-abnormal dyskaryotic squamous cells with mild atypical cytological alteration involving cell size,
shape, colour and organization
-not a significant risk factor for malignant degeneration
Moderate Dysplasia:
-atypical cytological alteration involving cell size, shape, colour and organization
-risk factor for malignant degeneration
Severe Dysplasia and Carcinoma In Situ

-1/6 lesions progress eventually to invasive carcinoma
-cells demonstrate cytological features of malignancy without invasion beyond the basement
membrane
F.Ling - Larynx Cancer (1)
884
-microscopic suspension laryngoscope with stripping of epithelium and a closely monitored
program of follow-up are indicated
-careful assessment q2-3 months for at least 5 years
-repeat biopsy if any changes
-some reports recommend radiation therapy initially and others advise radiation therapy if there is
recurrence after initial stripping
Microinvasive Carcinoma
-malignant cells extend through basement membrane of vocal cord epithelium but do not invade
vocalis muscle
-can be managed by endoscopic excisional biopsy, laser excision, or by radiation therapy
Invasive Carcinoma
-malignant cells that frankly invade through the basement membrane
-can be treated by endoscopic excision, laser excision, thyrotomy with cordectomy,
hemilaryngectomy, VPL with laryngoplasty, or radiation therapy
-traditionally radiation therapy has been offered as the preferred treatment
Ackerman’s Tumour
-aka: verrucous carcinoma
-rough, shaggy surface, a rounded pushing margin and no metastasis
-histopathology:
-benign-appearing (nonmitotic, no infiltration)
-well-differentiated squamous epithelium with papillary projections, extensive hyperkeratosis,
basement membrane intact
-“pushing margins”
-tumour less radiosensitive
-small lesions excised endoscopically; larger tumours managed by partial laryngectomy
TREATMENT OPTIONS FOR EARLY GLOTTIC CANCER
General
-options include for early invasive SCCa of glottis:
-single modality therapy:
-limited-field primary external beam radiation
-surgical management:
-endoscopic surgical excision
-thyrotomy with cordectomy
-hemilaryngectomy
-VPL with laryngoplasty
-elective neck dissections are NOT indicated for early glottic cancer
-microlaryngoscopic surgery is safe and effective management for T1 lesions
-LME is an acceptable alternative:
-anterior commissure involvement
-subglottic extension
-T3 glottic cancer
-posterior commissure involvement
885
Open Partial Laryngectomy
-cordectomy:
-limited excision of true vocal cord
-for early lesions not extending to anterior commissure
or involve region of arytenoid cartilage
-true hemilaryngectomy:
-excision of ~50% of endolarynx with overlying thyroid
cartilage
-for larger lesions T1 and T2
-VPL:
-indications:
-transglottic or very extensive bilateral
glottic carcinoma
-select T1 and T2 glottic carcinoma
-tumour does not extend beyond 1/3 of
opposite cord
-less than 1 cm of anterior subglottic
extension or 5 mm of posterior
subglottic extension
-no posterior commissure involvement
-good pulmonary function
-patient must also give consent for possible
total laryngectomy
-technique:
-removes one vocal fold from anterior
commissure to vocal process
-up to ½ of opposite vocal fold may be
removed (frontolateral VPL)
-removes ipsilateral false vocal fold,
ventricle, paraglottic space, and
overlying thyroid cartilage (3 mm posterior strip of cartilage preserved
-advantages:
-allows decannulation, functional glottic voice
-disadvantages:
-risk of aspiration, requires initial tracheotmy
-extended hemilaryngectomy
-indications:
-select T3 lesions or arytenoid involvement
-removes one vocal fold, arytenoid and overlying thyroid cartilage
-outer thyroid perichondrium lines the laryngeal surface
-strap muscle used for laryngoplasty
-contraindications for above procedures:

-fixed vocal cord
-involvement of posterior commissure
-invasion of both arytenoid cartilages
-bulky transglottic lesions
-lesions invading thyroid cartilage
-subglottic extension
886
-significant oropharyngeal extension
-tumour spread into neck
-anterior commissure involvement:

-overlying thyroid cartilage must be included en block with tumour because of direct insertion of
vocalis tendons into adjacent cartilage (Broyles tendon): a direct pathway for tumour extension
into cartilage
-curability of radiation therapy is hampered, surgical approach preferred
-post-radiation tumour recurrence: indications for partial laryngectomy

-lesion limited to one true vocal cord
-body of arytenoid free of tumour
-subglottic tumour extension no more than 5 mm
-mobile cord is present
-cartilage not invaded
-recurrent cancer correlates closely with original primary lesion
-most recurrent carcinomas do not meet these criteria, therefore total laryngectomy is usually necessary
-persistent edema following radiation therapy strongly suggests possibility of residual cancer
-if greater than 6 months must confirm with biopsy
COMPLICATIONS
Early
-subcutaneous emphysema, haemorrhage, tracheotomy tube obstruction
Late
-persistent aspiration, lingering infection, laryngeal stenosis, severe hoarseness, granulation tissue
formation, tumour recurrence
-two common causes for failure with hemilaryngectomy are inability to recognize inferior margin of
tumour and spread of cancer outward through cricothyroid membrane
EMERGENCIES
-airway obstruction
-aspiration
887
EARLY SUPRAGLOTTIC CARCINOMA
Supraglottic Laryngectomy
-cancers of epiglottis:
-tend to have pushing borders rather than infiltrating ones, which allows for resection with
millimetre tumour-free margins
-tend to remain supraglottic until late in their progression
Combined therapy
-if primary tumour is completely resected, there is no need for radiation (no neck node metastasis)
-a recent study finds no measurable benefit to combined therapy with either preoperative or postoperative
radiation and surgery
Radical radiation with surgery for salvage

-question: whether radiation or supraglottic resection provides greater certainty of primary control
-most often total laryngectomy used for salvage
-estimated that 2/3 will fail radiation and subsequently require total laryngectomy
-difficult to predict who will respond to radiation
Other surgical options

-transoral laser resection:
-curative for T1 and T2 lesions as long as adequate resection techniques are used
-endoscopic treatment:
-for pts with small superficial tumours of the suprahyoid epiglottis
-near-total laryngectomy:
-connection still exists between trachea and pharynx
Nonsurgical options
-unsuccessful in a high percentage of pts with T2 and T3 lesions
-today, virtually all pts who have early supraglottic cancer can expect to have a lung-powered glottis voice
after treatment is completed
-supraglottic resection
-cricohyoidopexy
-near-total laryngectomy
TREATMENT PLANNING
General Treatment Options (Early Supraglottic Carcinoma):

-single-modality therapy:
-primary radiation (external beam) to primary site with surgical salvage for failure
-supraglottic laryngectomy
-N0 neck:
-external radiation therapy to neck
-elective bilateral selective neck dissection
-N1-3 neck:
-radical or modified radical neck dissection for clinical nodes
-postoperative radiation therapy may be considered for:
-positive of close margins
-multiple positive neck nodes
-extracapsular extension
-perineural or intravascular invasion; bone, cartilage or soft tissue invasion
888
Horizontal (Supraglottic) Hemilaryngectomy
-rationale:
-embryological boundary between false and true vocal folds results in independent lymphatic
drainage
-supraglottic cancer tends to have pushing borders rather than infiltrating borders
-patient selection criteria for supraglottic laryngectomy
-T1 or T2 lesion
-cordal mobility
-anterior commissure uninvolved by cancer
-tumour does not involve vocal fold, ventricle, arytenoid, interarytenoid, piriform, base of tongue
-thyroid cartilage uninvolved by cancer
-surmountable nodal metastasis
-general good health
-good pulmonary function (FEV1 > 50-60%)
-technique
-removes epiglottis, AE folds, false vocal cords, pre-epiglottic space, portion of hyoid bone and
thyroid cartilage
Tumour Variables:
-T1, T2 and some T3 are suitable for supraglottic partial operation
-paramount clinical feature is cordal mobility
Absence of thyroid or Arytenoid Cartilage Invasion

-tumours rarely invade cartilage if there is no cord fixation
-usual place for thyroid cartilage invasion is at the anterior commissure
Fixation of a Vocal Cord

-not stage T1 or T2
Involvement of a Significant Part of the Base of Tongue

-closure becomes difficult and aspiration increases
Involvement of the Apex of the Piriform Sinus

-when a significant portion of pharynx is lost, aspiration and dysphagia are inevitable
Patient Variables:
-aspiration a big risk post-surgery
-obvious severe and uncorrectable chronic pulmonary disease will disqualify a patient
-uncorrectable swallowing disorders (ie. Scleroderma or serious stricture) usually disqualify a pt from sx
Clinical Assessment
-voice quality:
-pts with T1 and T2 supraglottic cancers do not have glottic hoarseness
-fiberoptic examination
Radiographic Examination
-supraglottic operation is safe with millimetre margins, but those margins must be identified accurately, and
if the surgeon lacks confidence in the pathology report, a safe operation is less likely
-most important clinical preoperative assessment relates to presence or absence of regional metastasis
-CT can be used to determine presence of metastasis
-failure to manage metastasis in the neck is the major cause of failure in the surgically treated early
supraglottic cancer
889
Extensions of the Supraglottic Operation
Upward extension into Base of Tongue

-generally loss of bulk not a problem pt can adapt
-problem occurs with excision of both hypoglossal nerves and supraglottic larynx almost
impossible to swallow
Downward extension to the Glottis

-downward extension with cordal mobility occurs infrequently
-problem is paraglottic space may be involved when tumour extends to level of vocal cord;
supraglottic operation does not encompass the paraglottic space
Dorsal extension to involve an arytenoid

-if involvement is mucosa, the mucosa can be removed and if margins are safe, the cartilage can
be spared and covered
-increased risk of local recurrence
Endoscopic Laser Supraglottic Laryngectomy

-may be considered for T1 or T2 (limited T3) supraglottic that can be accessed endoscopically:
-suprahyoid epiglottis
-aryepiglottic folds
-vestibular folds
-pharyngoepiglottic folds
COMPLICATIONS
-major:
-airway obstruction
-pneumonia
-aspiration
-speech alteration
-minor:
-delayed feeding tube removal
-wound infection
-fistula
-supraglottic stenosis and redundant arytenoid mucosa (which sucks into the glottis and becomes an
obstruction)
-preserving the false vocal cords contributes to both problems
890
EARLY GLOTTIC AND SUPRAGLOTTIC CARCINOMA
Supracricoid Partial Laryngectomy
SUPRACRICOID PARTIAL LARYNGECTOMY
-SCPL is a horizontal partial laryngectomy technique

-avoids total laryngectomy
-function is maintained by remaining arytenoids that abut tongue base during speech and swallowing
DIAGNOSTIC ASSESSMENT
-history
-physical examination: careful examination of larynx for mobility of vocal cord or arytenoid
-CT scan
-panendoscopy
-CXR
-assessment of pulmonary reserve
-preoperative evaluation by radiation oncologists is recommended to explain the alternatives for treatment
Indications for Supracricoid Partial Laryngectomy with Criochyoidopexy

-T2, T3 supraglottic carcinoma
-floor of ventricle involvement
-anterior commissure involvement
-impaired vocal cord or arytenoid mobility
-preepiglottic invasion
-paraglottic space invasion below the glottis level
-selected T4 supraglottic carcinoma
-transglottic glottic carcinoma
-radiation failure for glottic and supraglottic carcinoma
Contraindications
-hyoid invasion
-massive preepiglottic space or vallecular invasion
-tongue base invasion
-arytenoid fixation
-subglottic extension to cricoid
-pharyngeal or interarytenoid involvement
-extensive thyroid cartilage invasion
-inadequate pulmonary reserve
-resectable by supraglottic laryngectomy
Technique
-remove:
-entire thyroid cartilage
-bilateral true and false vocal folds
-one arytenoid (may spare both arytenoids if not involved)
-paraglottic space
-spares:
-cricoid cartilage
-hyoid bone
891
-cricohyoidopexy:
-used for reconstruction for supraglottic cancer
-cricohyoidoepiglottopexy:
-used for transglottic cancer
-preservation of function requires at least a cricoarytenoid unit and cricoid ring
COMPLICATIONS, EMERGENCIES AND FUNCTIONAL RESULTS
-severe or chronic aspiration/pneumonia - (most important major complication)

-improper alignment of the cricoid and hyoid bone
-ruptured pexy
-immobile arytenoid
-insensate arytenoid (injury to superior laryngeal nerves)
-tongue immobility (injury to hypoglossal nerves)
-inadequate patient selection or postoperative management
-arytenoid dislocation
-delayed decannulation
-edema
-stenosis
-inadequate pexy
-inadequate patient selection
-inadequate voice
-impaired arytenoid mobility and others as noted for aspiration
-wound infection
-salivary fistula
-haemorrhage and other neck dissection complications
-medical complications
SUMMARY
-acceptable functional results can be maintained after SCPL-CHP provided one functional cricoarytenoid
unit and an intact or reconstituted cricoid ring are preserved
-combination chemotherapy with radiotherapy with laryngectomy as salvage treatment have not shown a
significant change in survival rates compared with conventional therapy
-conservation laryngeal surgery does not preserve the entire organ anatomically, but usually maintains a
functional organ
-the most practical use for the SCPL-CHP is for T2 or T3 supraglottic carcinoma extending to the glottic
level
-SCPL can be viewed as the most extensive partial laryngectomy that is compatible with speech and
swallowing without a permanent tracheotomy
892
ADVANCED CANCER OF THE LARYNX
EPIDEMIOLOGY
-second most common H+N malignancy (~25%)

-1-5% of all malignancies
-85% attributed to smoking and alcohol
-highest incidence in 6th and 7th decade
ANATOMY
-supraglottic region: tip of epiglottis apices of both ventricles including false cords
-glottic region: both true cords, floor of ventricle, anterior commissure, interarytenoid area
-subglottic region: extends from 5 mm inferior to free edge of true vocal cords to lower border of cricoid
cartilage
-tissue barriers to cancer spread:

-thyroid and cricoid cartilage
-conus elasticus
-quadrangular membrane
-ventricle
-thyrohyoid membrane
-hyoepiglottic ligament
PATTERNS OF SPREAD
-pre-epiglottic space:
-superior: hyoepiglottic ligament
-anterior: thyroid cartilage and thyrohyoid membrane
-posterior: epiglottis and thyroepiglottic ligament
-spread to preepiglottic space soft tissues of neck via dehiscence in thyrohyoid membrane created by
superior laryngeal vessels and nerves
-paraglottic space:
-lateral to ventricles
-boundaries:
-anterior: continuous with pre-epiglottic space
-superior: aryepiglottic folds
-inferior: gap between thyroid and cricoid cartilage
-lateral: thyroid cartilage
-medial: conus elasticus and quadrangular membrane
-transglottic if inferior and superior to ventricle
-invasion of this space associated with high rate of subglottic or extralaryngeal spread of tumour
-most tumours involving the subglottic region are extensions of large laryngeal cancers rather than primary
tumours of the subglottis
893
-most common sites of cartilage invasion:
-anterior commissure tendon (Broyles’ ligament)
-attachments of cricothyroid membrane to adjacent cartilage
-anterior portion of thyroid lamina near origin of thyroarytenoid muscle
-posterior border of thyroid lamina adjacent to piriform sinus
-capsule of cricoarytenoid joint
-nodal metastasis:
-more common in supraglottic cancers than subglottic or glottic
-supraglottic tumours:
-upper and middle jugular lower jugular
-glottic tumours:
-delphian middle and lower jugular regions
-subglottic tumour:
-pretracheal, paratracheal, middle, and lower jugular lymph nodes
-in absence of tongue invasion, rare metastasis to submandibular/submental regions or to posterior
triangle
-preservation of zone I and V for laryngeal primary tumours with less than N2 disease
STAGING
-fixed vocal cord indicates deep invasion into the laryngeal musculature
-pathologic examinations have shown that the clinical staging of a laryngeal cancer is underestimated at
25% to 40%
-presence of mutant p53 clearly associated with diminished survival, but not included in staging system
Supraglottis
-approximately 30-40% of laryngeal cancer
-subsites:
-suprahyoid epiglottis
-infrahyoid epiglottis
-aryepiglottic folds
-false vocal cords
-arytenoids
-tumour invasion typically occurs superiorly toward base of tongue or pre-epiglottic space
-overall 25-75% risk of regional metastasis, primarily to nodal levels II, III, and IV
-staging:
-T1: primary tumour limited to one subsite
-T2: primary tumour involves mucosa of adjacent subsite or outside region of supraglottis
(glottis, base of tongue, medial wall of piriform sinus)
-T3: vocal cord fixation or primary tumour involves pre-epiglottic space, postcricoid, or deep
base of tongue
-T4: invades thyroid cartilage, soft tissues of neck, thyroid, or esophagus
Glottis
-approximately 50-75% of laryngeal cancer
-staging:
-T1: primary limited to vocal folds (1a = one cord; 1b = both cords) <5% regional metastasis
-T2: primary involves subglottis or supraglottis, impaired vocal fold mobility; 5-10% region
metastasis
894
-T3: vocal fold fixation; 10-20% regional metastasis
-T4: invades thyroid cartilage or beyond larynx; 25-40% regional metastasis
Subglottis
-rare primary site
-poor prognosis
-<20% regional metastasis
-staging:
-T1: primary tumour limited to subglottis
-T2: primary tumour involves vocal folds with normal mobility
-T3: primary tumour limited to larynx with fixed cords
-T4: primary tumour invades thyroid cartilage or beyond larynx
Differential Diagnosis and Pathology

-squamous cell carcinoma:
-most common malignancy (90%)
-granulomatous disease:
-tuberculosis, sarcoidosis, Wegener granulomatosis, blastomycosis, histoplasmosis
-respiratory papilloma
-granular cell tumous: pseuoepitheliomatous hyperplasia
-paragangliomas, plasmacytomas, carcinoid tumours
-tumours of minor salivary gland origin:
-most commonly in supraglottic larynx
-eg. adenoid cystic carcinoma, mucoepidermoid carcinoma
-small cell (oat cell) neuroendocrine carcinoma and adenocarcinoma NOS
-lymphoma
-aggressive thyroid cancers
-sarcoma: fibrosarcoma, chondrosarcoma, malignant fibrous histocytoma, rhabdosarcoma
MANAGEMENT
Natural History Without Treatment

-degree of dysphonia has no correlation to extent of tumour within larynx
-hemoptysis more common with supraglottic tumours
-airway obstruction
-dysphagia
-death
Treatment
-primary goal is to cure pt with preservation of speech and swallowing
-extent of regional involvement determines survival
-involvement of preepiglottic space, cartilages or soft tissues associated with even higher rate of lymphatic
spread to prelaryngeal and deep cervical nodes
895
ADVANCED SUPRAGLOTTIC LESIONS
Supraglottic Laryngectomy:
-indications:
-supraglottic cancers classified as T3 d/t preepiglottic space invasion or minimal medial piriform
sinus involvement above level of true cords
-no extension to vocal cord
-good health and pulmonary reserve
-possibility of converting to total laryngectomy
Supracricoid partial laryngectomy with cricohyoidopexy:

-indications:
-supraglottic tumours classified as T3 due to vocal cord fixation, preepiglottic space invasion,
mobile arytenoid cartilage, T4 carcinomas with only limited invasion of the thyroid ala, patient in
good general health with good pulmonary reserve
Near-total layrngectomy:
-single arytenoid cartilage preserved to produce a lung-powered voice through a trachea esophageal conduit
-contraindications: subglottic extension below cricoid ring or failure of radiation therapy
-indications:
-large T3 or T4 lesions not amenable to supraglottic or supracricoid resection with one uninvolved
arytenoid and ventricle
-pts with lesions amenable to standard supraglottic procedure but with poor cardiopulmonary
function
-unilateral transglottic tumours with cord fixation
-poor pulmonary function and cardiac reserve negate conservation surgery, as does failure of prior full-
course radiation therapy
Total Laryngectomy:
-indications:
-all T3 cancers not amenable to supraglottic or supracricoid laryngectomy
-all T4 cancers not amenable to supracricoid or near-total laryngectomy
-tumours with extensive involvement of thyroid or cricoid cartilage
-invasion of surrounding soft tissue of the neck
-extension beyond posterior third of base of tongue
The Neck
-bilateral selective neck dissection would be treatment of choice of N0 pt
-most common site of recurrence is contralateral undissected neck
-for N0 or N1 regional disease, radiation has been shown to be equivalent to surgery
Adjuvant Radiation
-for patients at higher risk of recurrence:
-positive margins, T4 lesions, N2 neck or evidence of extracapsular lymph node spread, perineural
or vascular invasion, metastasis to inferior tracheoesophageal, lower jugular or mediastinal nodes,
multiple levels of nodal involvement, and subglottic extension
Survival
-rate for stage IV supraglottic cancer no better than 50% even with combined treatment
896
ADVANCED GLOTTIC LESIONS
-limited lymphatic flow fewer regional metastases

-favourable may be candidates for conservation surgery or radiation:
-lesions confined mostly to one side of larynx with minimal airway obstruction
-unfavourable requires near-total or total laryngectomy, combination therapy:
-extensive bilateral disease
-extralaryngeal involvement
-extensive cartilage invasion
-subglottic extension below level of cricoid
-initial choice of therapy has no effect on survival
-preoperative radiation therapy improves survival but increases surgical complications (eg. Fistula);
therefore post-operative radiation is used shown to improve local and regional control compared with
surgery alone without significantly increasing complications
Radiation or Surgery?
-primary radiation limited to pt with favourable T3 lesion
-total laryngectomy is procedure of choice for tumour recurrence if radiation therapy was delivered in
curative doses
The Neck
-most likely regions involved: jugular chain, paratracheal, pretracheal groups
ADVANCED SUBGLOTTIC CANCER
-no feasible partial resections for this region

-regional metastasis frequent and bilateral
-total laryngectomy with postoperative radiation the current standard for treatment
CHEMOTHERAPY AND ORGAN PRESERVATION
-cisplatin and 5-FU commonly used

-concomitant chemoradiation therapy:
-chemotherapy acts as radiation sensitizer while providing systemic antineoplastic effect
-adjuvant chemotherapy has not been shown to improve survival and is rarely added to treatment regimen
-definitive proof does not exist that neoadjuvant chemotherapy is superior to radiation alone as an organ
preservation modality
COMPLICATIONS
Complications of Surgery
-haematoma, hypothyroidism aspiration pneumonia, wound infection, hypocalcemia, fistula
-late complications: structure, stomal stenosis, hypothyroidism
Complications of Radiation
-hoarseness, edema, dysphagia, odynophagia, mucositis, thick secretions, skin breakdown
-late effects chondronecrosis, fibrosis of skin/soft tissue/mucous membranes, severe dryness, stricture,
hypothyroidism, trismus, secondary neoplasm eg. Sarcoma (rare)
897
LARYNGEAL CARCINOMA TREATMENT OVERVIEW
Site T Treatment options Survival Risk of Management

stage occult of N0 neck
nodal
metastasis
Supraglottis T1 -radiation or surgery 70-80% 20% bilateral XRT

or SND II-IV
T2 -radiation or surgery (incl. supraglottic 60-70% 40%
laryngectomy)
T3 -total laryngectomy and postoperative <50% 60%

XRT or
-chemoradiation with surgical salvage
T4 -total laryngectomy and postoperative <50% 80%

XRT
Glottis T1 -radiation or surgery 90-95% ~5% No elective

treatment
T2 -radiation or surgery (incl. VPL) 85-90% ~5-10% required
T3 -radiation alone (66-70 Gy) or <50% ~10-20%
-conservation surgery (SCPL, rarely
used) or
-chemoradiation with surgical salvage or
-total laryngectomy and postoperative
XRT
T4 -total laryngectomy and postoperative <50% ~25-40% bilateral XRT

XRT or or SND II-IV
-chemoradiation with surgical salvage
-N1 neck: treat with radiation or surgery (functional neck dissection)

-N2-3 neck: not entirely controlled by radiation will require combined therapy (eg. XRT and planned
neck dissection)
Induction chemotherapy plus radiation compared with surgery plus radiation in patients with advanced
laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study Group.
BACKGROUND. We performed a prospective, randomized study in patients with previously untreated

advanced (Stage III or IV) laryngeal squamous carcinoma to compare the results of induction
chemotherapy followed by definitive radiation therapy with those of conventional laryngectomy and
postoperative radiation. METHODS. Three hundred thirty-two patients were randomly assigned to receive
either three cycles of chemotherapy (cisplatin and fluorouracil) and radiation therapy or surgery and
radiation therapy. The clinical tumor response was assessed after two cycles of chemotherapy, and patients
with a response received a third cycle followed by definitive radiation therapy (6600 to 7600 cGy). Patients
in whom ther was no tumor response or who had locally recurrent cancers after chemotherapy and radiation
therapy underwent salvage laryngectomy. RESULTS. After two cycles of chemotherapy, the clinical tumor
response was complete in 31 percent of the patients and partial in 54 percent. After a median follow-up of
33 months, the estimated 2-year survival was 68 percent (95 percent confidence interval, 60 to 76 percent)
for both treatment groups (P = 0.9846). Patterns of recurrence differed significantly between the two
groups, with more local recurrences (P = 0.0005) and fewer distant metastases (P = 0.016) in the
898
chemotherapy group than in the surgery group. A total of 59 patients in the chemotherapy group (36
percent) required total laryngectomy. The larynx was preserved in 64 percent of the patients overall and 64
percent of the patients who were alive and free of disease. CONCLUSIONS. These preliminary results
suggest a new role for chemotherapy in patients with advanced laryngeal cancer and indicate that a
treatment strategy involving induction chemotherapy and definitive radiation therapy can be effective in
preserving the larynx in a high percentage of patients, without compromising overall survival.
899
TRACHEAL TUMOURS
RADIOLOGIC EVALUATION
-to determine location and linear extent of lesion, extra-tracheal involvement, and amount of airway not
involved
-standard views
-fluoroscopy functional asymmetry of vocal cords and provides information about extent of lesion
-polytomography gives additional detail, particularly of mediastinal involvement
-barium esophagography define esophageal involvement by extrinsic compression or invasion
-CT/MRI
AIRWAY MANAGEMENT
-may be difficult to maintain airway

-elevate head of pt, administration of cool mist and O2 and careful sedation
-control airway in OR
-paralysing agents not used to prevent lethal combination of a/w obstruction and apnea
-initial evaluation with rigid bronchoscope
-most tumours even near-total obstruction allow a rigid bronchoscope to be passed beyond them
-tumour partially removed with biopsy forceps
-bleeding pass bronchoscope beyond bleeding point; epinephrine soaked pledgets applied
-coring of tumour provides temporary airway
TUMOUR CLASSIFICATION PRIMARY TRACHEAL TUMOURS
-primary tracheal tumours SCCa

ACC
-2/3 are ACC (40%, aka cylindroma) and SCCa (36%)
-other (24%) Other:
-secondary tracheal tumours: Benign:
-invasion or metastasis -squamous papilloma
-pleomorphic adenoma
-papillary and follicular carcinomas of thyroid can invade -granular cell tumour
at level of isthmus -fibrous histiocytoma
-tracheal invasion best managed by resection -leiomyoma, chondroma
and tracheal reconstruction -chondroblastoma
-schwannoma
-paraganglioma
-adenoid cystic carcinoma: -hemangioendothelioma
-prolonged course -vascular malformation
Intermediate:
-submucosal and perineural spread
-carcinoid
-metastasis to lungs common: can be asymptomatic for -mucoepidermoid
many years -plexiform neurofibroma
-SCCa: -pseudosarcoma
Malignant:
-exophytic or ulcerative
-adenocarcinoma
-multiple and scattered over a considerable length of -adenosquamous carcinoma
trachea -small-cell carcinoma
-invades mediastinal structures -atypical carcinoid
-melanoma
-chondrosarcoma
-spindle cell sarcoma
-rhabdomyosarcoma
F.Ling - Tracheal Tumours (1)
900
SIGNS AND SYMPTOMS
-SOBOE (54%)
-hemoptysis (41%) - usually for SCCa earlier diagnosis
-cough (37%)
-wheezing and stridor (35%)
-dysphagia or hoarseness (7%)
-recurrent pneumonitis
-CXR usually normal
DIAGNOSIS
-usually given misdiagnosis of asthma

-flow-volume curves:
-loss of peaks suggestive of UAO
-imaging studies
-careful bronchoscopy
ANESTHESIA
-best administered by inhalation of volatile anesthetic

-requires slow induction rather than paralysis
-surgeon on stand-by with various rigid bronchoscopes
-small ETT placed past obstruction
SURGICAL TECHNIQUE
-cervical collar incision

-vertical midline extension to access upper mediastinum
-preferred approach to tumours of lower trachea and carina is via a high, right, posterolateral thoracotomy
-approach trachea from above and below the lesion
-identification of recurrent laryngeal nerves
-blood supply of trachea
-upper part principally supplied by branches of inferior thyroid artery
-lower portion supplied by branches of bronchial artery with contributions from the subclavian,
supreme intercostal, internal thoracic, and innominate arteries
-blood supply enters segmentally
-these vessels supply branches anteriorly to trachea and posteriorly to esophagus, arriving at
trachea through lateral pedicles of tissue
-transverse intercartilaginous arteries branch ultimately into a submucosal capillary network
-do not dissect around trachea for any great distance if portion is to remain
-do not circumferentially free more than 1-2 cm of tracheal length
-risk of devascularization and necrosis stenosis
-traction sutures placed at 3 and 9 o’clock position
-trachea transected transversely intubation across operative field
-margins taken for frozen section
-if esophageal wall involved then partial- or full-thickness resection of anterior of anterolateral esophageal
wall may be necessary
-~50-60% of trachea can be resected
901
Reconstruction
-neck flexion to provide anastomosis without tension
-options:
-primary anastomosis:
-pedicled strap muscle over anastomosis
-suprahyoid laryngeal release (Montgomery release):
-provides extra 1-2.5 cm of length (up to 5 cm of length)
-infrahyoid release described
-hilar release:
-mobilization of the right pulmonary hilum
-involves making a U-shaped incision in pericardium beneath inferior pulmonary vein
-incising septum, which extends inferiorly from the right inferior pulmonary vein and
joins lateral aspect of atrium and inferior vena cava to pericardium
-left mainstem bronchus divided and reanastomosed end-to-side with bronchus intermedius
-provides extra 2.7 cm length
-Marlex and Silicone grafts
-carinal involvement:
-approach via right posterolateral thoracotomy
-right or left main bronchus sutured to trachea in an end-to-end manner; anastomosis of other
bronchus to lower portion of trachea wall laterally above initial anastomosis is performed
Complications:
-anastomotic stenosis
-air leaks subcutaneous emphysema
-anastomotic separation
-suture line granuloma
-esophageal fistula
-aspiration (after laryngeal release) pneumonia/empyema
-post-obstructive pulmonary edema
-haemorrhage from innominate artery
-operative death
Effect of Tumour at Resection Margins and in Lymph Nodes

-extensive regional lymph node dissection limited as it can destroy the blood supply
-SCCa:
-positive lymph nodes and margins poorer prognosis
-ACC:
-positive margins, lymph nodes or both little difference compared with results among pts who
had negative margins and nodes
Role of Radiation
-SCCa and ACC are radiosensitive
-resection combined with irradiation tripled survival time for both SCCa and ACCa
Recommendations
-benign primary tumours and tumours of intermediate aggressiveness are best managed by means of
surgical resection with reconstruction of airway
-for SCCa and ACC, resection followed by full-dose mediastinal irradiation advocated
902
VASCULAR TUMOURS OF THE HEAD AND NECK
BENIGN TUMOURS
VASCULAR TUMOURS OF THE
Localized Tumours HEAD AND NECK (Batstakis)
Hemangioma Benign Tumours

Localized
-most common localized benign vascular tumour to head and
-hemangioma
neck -lymphangioma
-cutaneous or mucosal -angiofibroma
-subglottic hemangioma Generalized
-angiomatosis
-seen in children -cystic hygroma
-posterolateral position Inflammatory
-50% associated with other cutaneous hemangioma AV fistula, aneurysm
-supraglottic hemangioma usually in adults Telangiectasia, phlebectasia
-medical therapy: Syndromes
-corticosteroids -Osler-Weber-Rendu
-interferon-alpha2a: -Sturge-Weber
-effective -Maffucci
-Von Hippel-Lindau
-risk of spastic diplegia in young children
-not used as often Malignant
-angiosarcoma
Port-wine Stains (Nevus Flammeus) -hemangiopericytoma
-aka: capillary malformation Paragangliomas
-mature endothelial lining and no hypercellularity -carotid
-rarely proliferates -vagus
-association with sensory nerves (trigeminal nerve V1 - -larynx
-jugular
Sturge-Weber syndrome) -tympanic
-tx: surgical excision, cosmetic camouflage, argon laser
therapy
Lymphangioma
-most tend to progress
-commonly occur in neck and mucosal surfaces of oral cavity (tongue)
Angiofibroma
-predominantly among male adolescents
-consists of multiple vascular channels surrounded by tough fibrous connective tissue
-originates in lateral wall of nasopharynx and tends to invade posterior aspect of choana,
pterygopalatine fossa, orbit, and occasionally intracranial cavity
-most common feeding vessels from external carotid system
-IMAX and ascending pharyngeal arteries
-angiography and embolization
-medial maxillectomy
-facial degloving
-combination
-endoscopic approach for small tumours
-radiation reserved for large unresectable tumours
F.Ling - Vascular Tumours (1)
903
Generalized Tumours
-cystic hygroma:
-occurrence in posterior triangle associated with hydrops fetalis, Turner syndrome, chromosomal
aneuploidy, fetal death
-cytogenic analysis of fetuses born with cystic hydroma indicated
-extensive infiltration; CT/MRI to assess
Inflammatory Tumours
Granuloma pyogenicum and gravidarum

-lobular capillary hemangioma
-caused by minor trauma
-treat with local excision
Arteriovenous Fistula or Aneurysm

-pulsatile, painless masses
-may have palpable thrill or audible bruit
-may be associated with high output CHF
-surgical excision may be difficult
-embolization may not be feasible because of high vascular flow
Telangiectasis
-Osler-Weber-Rendu
-familial occurrence
-autosomal dominant
-clinical triad:
-characteristic telangiectatic lesion
-hereditary incidence
-presence of haemorrhagic diathesis
-epistaxis is hallmark; bleeding from oral mucosa
-telangiectasia on facial skin, particularly cheeks
-for septal telangiectasia, treatment is septal dermoplasty
-estrogen and other hormones effective, as is laser treatment
MALIGNANT TUMOURS
Angiosarcoma
-malignant tumour of vascular endothelial cells
-extremely rare
-scalp > neck > mouth > antrum
-rapidly growing neoplasms with insidious onset and minimal symptoms
-50% cured by primary excision or die of disease within 3 years
-XRT for palliation
Hemangiopericytoma
-arise wherever there are capillaries
-tx is wide surgical excision
-XRT for palliation
904
Kaposi Sarcoma
-HIV
-non-pruritic, painless, flat or nodular, pigmented lesion on any skin or mucosa surface of H+N
-treatment geared toward local control, reduction of symptoms, and improvement of appearance
-XRT and chemotherapy effective but have serious side effects
-interferon can be effective, but recurrence common
-intralesional injection of vinblastine, cryotherapy, and laser excision
PARAGANGLIOMA
-derived from neural crest cells

-each composed of two cell types:
-granule-storing chief cells
-Schwann-like satellite cells
-typically related to arterial vasculature and cranial
nerves
-paraganglia of the head and neck
-tympanic p. glomus tympanicum
-intravagal p. glomus vagale
-jugular p. glomus jugulare
-glossopharyngeal p.
-inter-carotid p. carotid body tumour
-superior laryngeal p.
-inferior laryngeal p.
-subclavian p.
-aortico-pulmonary p.
-coronary p.
-distribution:
-aortic arch
-superior and inferior laryngeal paraganglia
-carotid body
-vagal body
-jugulotympanic region
-also: posterior nasal region and in orbit
-most common tumours:
-carotid body
-glomus jugulare
-glomus tympanicum
-glomus vagale
-sporadic cases ~ 90%; familial cases ~10%
-bilaterality and multicentricity:
-sporadic cases 3%
-familial cases 26%
-test for 24h urinary catecholamines:
-vanillyl-mandelic-acid (VMA)
-urinary metanephrine, catacholamines, epinephrine, norepinephrine
-Rule of 10's: (carotid body tumours)
-10% familial
-10% malignant
-10% multicentric
-10% secrete catecholamines
905
Carotid Body Tumours
-asymptomatic, slowly enlarging, nontender neck masses immediately anterior to SCM at level of hyoid
bone
-bruit on auscultation
-widening of carotid bifurcation by well-defined tumour blush splaying of vessel (Goblet/Lyre sign)
-MRI: “salt and pepper” appearance d/t flow voids
-Shamblin classification:
-Group I: -small and easily dissected away from vessels
-Group II: -medium-sized; intimately associated with vessels but separable with dissection
-Group III: -large tumours encasing the carotid necessitating partial or complete vessel
resection and replacement
-treatment:
-approach is similar to that of acoustic neuromas:
-young patient early resection advocated
-older patient, small lesion observation
-surgical treatment is mainstay of therapy - potential vascular replacement surgery considered
-palliative radiation if pt’s high surgical risk
-mortality rate 8%
-early operation desirable: less extensive procedure that is better tolerated
-surgical details:
-potential for vascular replacement
-adventitial plane can be developed tumour removed from bifurcation
Glomus Jugulare and Tympanicum

-paraganglioma most common neoplasm of the middle ear
-pulsatile tinnitus or hearing loss
-typical finding: reddish mass behind tympanic membrane
-Brown's sign: blanching of TM and of the area behind it, seen with pneumatic pressure on the
membrane; it indicates presence of a vascular tumour or other lesion in the middle ear
-high-riding jugular bulb or carotid artery can mimic tumour (if dehiscent)
-CT and angiography
-late growth can give rise to intracranial symptoms and otic and neurologic symptoms
-surgery for treatment; radiation for palliation
-Fisch classification:
-Type A -Tumour limited to the middle ear cleft (glomus tympanicum)
-Type B -Tumour limited to the tympanomastoid area with no infralabyrinthine
compartment involvement
-Type C -Tumour involving the infralabyrinthine compartment of the temporal bone and
extending into the petrous apex
-Type C1 -Tumour with limited involvement of the vertical portion of the carotid canal
-Type C2 -Tumour invading the vertical portion of the carotid canal
-Type C3 -Tumour invasion of the horizontal portion of the carotid canal
-Type D1 -Tumour with an intracranial extension less than 2 cm in diameter
-Type D2 -Tumour with an intracranial extension greater than 2 cm in diameter
906
907
908
909
-surgical approach depends on the localization and extension of the tumour
-Fisch type A tumours:
-excised by a transmeatal or perimeatal approach
-Fisch type B tumours:
-require an extended posterior tympanotomy
-Fisch type C tumours:
-require radical resection via a standard combined transmastoid-infratemporal or
transtemporal-infratemporal approach with or without ICA trapping, preceded by
external carotid artery embolization or superselective embolization
-surgery leads to therapeutic success in about 90% of patients.
-Fisch type D tumours:
-treated with a combined otologic and neurosurgical approach
-infratemporal approach with a skull base resection and a posterior fossa exploration are
the most advisable in the attempt to remove the entire tumour
-partial resection is followed by radiation and follow-up MRI/CT scanning.
-classic fractionated radiation therapy (40-50 gray [Gy]) and stereotactic radiosurgery are successful in
long-term control of tumour growth and in decrease of catecholamine excretion in functional tumours
-radiation treatment is advised as the sole treatment modality for elderly or infirm patients who are
symptomatic, especially those with extensive or growing tumours
Intravagal Paraganglioma
-arises from nests of paraganglionic tissue within perineurium of vagus nerve immediately below or at level
of ganglion nodosum
-lie near skull base
-diagnostic clue:
-anteromedial displacement of internal carotid artery
-cf carotid body tumour splaying of internal and external carotid arteries
-may be “dumbbell” shaped into jugular foramen
-resection may cause laryngeal paralysis requires rehabilitation
SYNDROMES
Osler-Weber-Rendu Syndrome (Hereditary Hemorrhagic Telangiectasia)

-multiple telangiectasia of skin and mucous membranes
-occasional GI and CNS involvement
-AD
Sturge-Weber Syndrome
-capillary malformation over trigeminal distribution
-ipsilateral meningeal vascular malformations
-possible association with seizure disorder and mental retardation
Maffucci Syndrome
-multiple cavernous hemangiomas
-dyschondroplaisa with shortening and deformity of involved bones
-occasional visceral vascular lesions
-25% incidence of chondrosarcoma
Von Hippel-Lindau Disease

-hemangiomas of cerebellum and retina
-cysts of kidney and pancreas
910
CRANIAL-BASE SURGERY
NEUROANATOMIC CONSIDERATIONS
Arterial Supply
1. vertebral artery
2. posterior inferior cerebellar artery (PICA)
3. basilary artery
4. anterior inferior cerebellar artery (AICA)
5. posterior cerebral artery (PCA)
6. posterior communicating artery
7. middle cerebral artery (MCA)
8. internal carotid artery
9. ophthalmic artery
10. anterior cerebral artery
11. anterior communicating artery
12. medial striate artery
13. anterior choroidal artery
Lateral medullary syndrome:

-occlusion of PICA
-loss of ipsilateral P+T on face and contralateral P+T on body
-ipsilateral Horner’s
-nystagmus, cerebellar dysfunction, vertigo, hoarseness, dysphagia, loss of ipsilateral taste
Venous Drainage System

-superior sagittal sinus transverse sinus sigmoid sinus
-inferior petrosal sinus jugular bulb
-petrosal sinuses cavernous sinus
-vein of Labbe drains temporal lobe; enters transverse sinus
at position medial to superior petrosal sinus
Ventricular CSF Drainage System

-CSF production at the choroid plexus within lateral
ventricles third ventricle [foramen of Sylvius] fourth
ventricle subarachnoid space
NEUROPHYSIOLOGY
Intracranial Pressure
-edema usually is caused by prolonged or excessive retraction of brain during tumour resection
-correlates highly with postoperative course complicated by short-term decrease in mental function and
long-term neurologic deficit
-prevention of edema by means of removal of large segments of calvarium and base of skull to obviate
brain retraction
Cerebral Blood Flow

-sensitive to changes on PaCO2 and inhalational anesthetics
-anesthetic technique is critical in preventing increased ICP, minimizing cerebral edema and maintaining
adequate CBF
F.Ling - Cranial-Base Surgery (1)
911
CSF Production
-produced at rate of 20 ml/h (500 ml/d)
-amount of CSF reabsorbed cannot be controlled pharmacologically
-amount produced can be altered with carbonic anhydrase inhibitors (ie. acetazolamide)
EVALUATION
Imaging Studies
Modality Advantages Disadvantages
CT -superior for visualization of bone -dental artifact

-short image acquisition times -unable to obtain sagittal views
-poorer in differentiating soft-tissue
-exposure to radiation
MRI -can differentiate tumours on basis of signal response -longer image acquisition times
-can generate sagittal images -poorer bone evaluation
-can perform angiography (MRA)
-provide detailed images of soft tissue invasion
Appearance of normal tissues with MRI

Sequence Bone Fat Water (CSF) Muscle Brain (white) Brain (grey)
T1- weighted very dark very bright dark intermediate bright dark
T2-weighted very dark dark very bright intermediate dark bright
TUMOURS INVOLVING CRANIAL BASE

Cerebrovascular Evaluation
-temporary balloon occlusion test: Anterior cranial base
-simulates carotid clamping or permanent ligation -benign
-intraarterial balloon catheter inserted during -meningioma
-juvenile angiofibroma
cerebral angiography -fibroosseous lesions
-if neurologic signs develop during 10-20 minutes -malignant
of occlusion considered failure of test -squamous cell carcinoma
-xenon CT: -esthesioneuroblastoma
-inflation of intraarterial balloon within ICA and Middle cranial base
allowing pt to breathe xenon-oxygen mixture -benign
-xenon is radiodense and diffuses into blood -meningioma
stream marker for cerebral perfusion -pituitary adenoma
-chordoma
-compare regions of blood flow before and after -craniopharyngioma
balloon occlusion -malignant
-~2% of pts who pass xenon CT-TBO test have a -nasopharyngeal carcinoma
neurologic deficit after carotid resection -squamous cell carcinoma (PNS
extension)
Posterior cranial base

-benign
-glomus tumours
-meningioma
-chordoma
-schwannoma
-malignant
-squamous cell carcinoma (otogenic)
912
SURGICAL ANATOMY
FORAMINA OF THE BASE OF SKULL
Foramen Structures Transmitted
Cribriform plate -olfactory nerve (CN I)
Foramen cecum -occasional small vein; origin of sagittal sinus
Optic canal -optic nerve

-ophthalmic artery
Superior orbital fissure -oculomotor nerve (III)

-trochlear nerve (IV)
-ophthalmic division of trigeminal (V1)
-abducens nerve (VI)
-superior ophthalmic vein
Inferior orbital fissure -maxillary division of trigeminal (V2)

-zygomatic branch of trigeminal nerve
-filaments from pterygopalatine branch of
maxillary nerve
-infraorbital vessels
-anastomosis between inferior ophthalmic vein
and pterygoid venous plexus
Foramen rotundum -maxillary division of trigeminal (V2)
Foramen ovale -mandibular division of trigeminal (V3)
Foramen spinosus -middle meningeal artery
Sulcus tubae auditive -Eustachian tube
Foramen lacerum -closed inferiorly be fibrocartilaginous plate

that contains auditory tube
-upper part transversed by internal carotid
artery
Carotid canal -internal carotid artery
Stylomastoid foramen -facial nerve (VII)

-stylomastoid artery
Jugular foramen -glossopharyngeal nerve (IX)

-vagus nerve (X)
-accessory nerve (XI)
-jugular vein
Internal acoustic meatus -facial nerve (VII)

-acoustic nerve (VIII)
Hypoglossal canal -hypoglossal nerve (XII)
Foramen magnum -spinal cord

-spinal accessory nerves
-vertebral arteries
-anterior and posterior spinal arteries
-occipitoaxial ligament
913
Anterior Cranial Base
-roof of ethmoidal and sphenoidal sinuses form floor of anterior cranial base between orbits
-portion of ethmoidal sinuses that contributes to anterior floor of base of skull is fovea ethmoidalis
-most common location of iatrogenic defects and CSF leaks through floor of anterior cranial base
after ethmoidal sinus surgery
-extracranial landmarks that identify floor of anterior cranial base:
-anterior and posterior ethmoidal arteries
-optic nerve located 5 mm posterior to posterior ethmoidal artery
Middle Cranial Base

-intracranial surface composed of greater wing and body of sphenoid bone, petrous bone anterior to petrous
ridge, squamous portion of temporal bone
-transsphenoidal approach provides access to middle, not anterior cranial base
-Cavernous sinus:
-contains:
-CN III, IV, V1, V2, and
VI
-drained by paired superior and
inferior petrosal sinuses
-internal carotid artery located by
identifying GSPN
-course of GSPN directly above
and in same direction as
horizontal portion of petrous
portion of ICA
-most reliable intracranial
landmark for petrous portion of
ICA
-superior orbital fissure transmits several
vital structures
-inferior orbital fissure opens into
pterygopalatine fossa
-deep temporal artery provides primary
blood supply for temporalis muscle;
reconstructive flap most commonly used in
cranial-base surgery
Lacrimal (V1)
Frontal (V1)
Trochlear (IV)
Supraorbital vein
Oculomotor (III)
Abducens (VI)
Nasociliary (V1)
Zygomaticofacial (V2)
Zygomaticotemporal (V2)
Inferior ophthalmic vein
Orbital Fissure with annulus of
Zinn
914
Pterygopalatine fossa:
-space between posterior wall of maxillary sinus and pterygoid
plates
-boundaries:
-superior: -posterior part of the inferior orbital
fissure (a)
-orbital process of the palatine bone, body
of the sphenoid bone
-anterior: -posterior maxillary sinus wall (b)
-posterior: -lateral pterygoid plate
-inferior surface of greater wing of
sphenoid
-lateral: -pterygomaxillary fissure (c)
-medial: -vertical lamina of the palatine bone
-inferior: -hard palate
-communicates with:
-anterosuperior: inferior orbital fissure orbit
-posteriorsuperior: foramen rotundum, vidian canal middle cranial fossa
-medial: sphenopalatine foramen nasal cavity
-lateral: pterygomaxillary fissure infratemporal fossa
-inferior: greater and lesser palatine canals oral cavity
-contents:
-internal maxillary artery
-foramen rotundum maxillary division of trigeminal
-sphenopalatine ganglion and nerve
-vidian nerve
-formed by contributions of lesser petrosal and deep petrosal nerves
-passes through pterygoid canal to synapse in pterygopalatine ganglion
-provides autonomic innervation to nasal cavity, nasopharynx and lacrimal glands
915
Infratemporal fossa:
-contains:
-pterygoid muscles
-maxillary artery and its branches
-pterygoid venous plexus
-branches of the mandibular division of the trigeminal
nerve (foramen ovale)
-otic ganglion
-chorda tympani
-middle meningeal artery (foramen spinosum)
-boundaries:
-superior: -base of skull
-anterior: -posterior buttress of malar eminence and maxillary sinus
-posterior: -glenoid fossa, mandibular neck and condyle
-medial: -plane extending from lateral pterygoid plate to spine of sphenoid bone
-lateral: -medial surface of the ramus of mandible
-inferior: -medial pterygoid muscle
-important foramina:
-foramen ovale and spinosum
Infratemporal region - medial surface
916
MANAGEMENT OF CRANIAL BASE TUMOURS
Surgical Approaches
APPROACHES TO CRANIAL BASE
Anterior cranial base:

-basilar subfrontal with or without facial incision (craniofacial
approach)
-transfrontal sinus
Middle cranial base:

-transoral, transseptal, transsphenoidal approaches to sella
-subtemporal-infratemporal fossa (preauricular)
-subtemporal-infratemporal fossa (postauricular)
-facial translocation
-midfacial split
-facial degloving
-mandibular split procedure
-palatal split procedure
-Le Fort I osteotomy with or without transseptal exposure
Posterior cranial base:

-extreme lateral approach
-transoral approach to craniovertebral junction
-palatal split procedure
-translabyrinthine approach
-retrosigmoid approach
-suboccipital approach
Anterior Cranial Base

-tumour involvement usually caused by
contiguous spread from paranasal sinuses, nasal
cavity or nasopharynx
-access usually through bicoronal incision
-preservation of important vessels:
-superficial temporal artery
-supraorbital artery
-supratrochlear artery
-superficial temporal artery preserved to allow use
of temporoparietal fascial flap
-most useful in reconstruction of middle
fossa and sphenoidal sinus defects
-deep tissues of forehead elevated to level of
superior orbital rims in a plane deep to
pericranium
-supraorbital and supratrochlear vessels preserved
to allow use of pericranial flap
-most useful to completely resurface
floor of anterior cranial fossa
-use of both temporoparietal fascial flap and
pericranial flap to manage complex sphenoidal
sinus defects can decrease risk of postop CSF
fistula
917
-bifrontal craniotomy:
-to expose dura over frontal poles
-subfrontal craniotomy:
-Raveh approach
-segment of bone containing glabella and supraorbital rims removed between supraorbital foramen
-provide direct anterior exposure of ethmoidal sinuses and to maximize exposure of subfrontal
base
-may obviate the use of facial incision for selected tumours of paranasal sinus
-frontal poles and overlying dura separated from bony cranial base to allow transection of olfactory nerve
connection through cribriform plate
-exposes planum sphenoidale and optic chiasm
-facial incisions:
-lateral rhinotomy:
-exposes superior limit of nasal cavity and paranasal sinuses for complete tumour
removal
-can be combined with periorbital incisions: subciliary or transconjunctival
-facial degloving and transpalatal approach:
-exposes nasal cavity and nasopharynx without facial incisions
-provide more limited exposure of upper vault and ethmoidal sinuses
-central anterior cranial base usually reconstructed with pericranial flap

-bone grafts considered when substantial portion of bone covering orbits has been removed
-if bony orbital volume and structural integrity are not reestablished exophthalmos d/t posterior-
superior retraction of intraorbital soft tissues within expanded orbital space
Middle Cranial Base

-most concepts embodied by three procedures:
-transsphenoidal approach:
-limited to midline tumours affecting posterior nasal cavity, nasopharynx, sphenoidal
sinus, and sella turcica
-lesions usually benign
-infratemporal fossa approach
-tumours that arise in petroclival portions of middle cranial base and involve petrous
carotid artery
-facial translocation or maxillotomy procedure
-provides superior exposure of infratemporal fossa, nasopharynx and external part of
middle cranial base
Transsphenoidal Approach to Sella Turcica

-through transoral gingivobuccal incision that provides wide exposure of piriform aperture
-mucoperichondrial flap elevated
-osseous septum resected to expose sphenoidal rostrum
-anterior sphenoid sinus wall entered sella identified and bone carefully removed to expose dura over
pituitary gland
-extent of central cranial-base exposure can be increased by combining with LeFort I osteotomy of the
maxilla
-separates superior dental arch from midface at level just superior to roots of teeth
-causes down-fracturing of palate and provides wide exposure of clivus, craniocervical junction
and nasopharynx
918
Infratemporal Fossa Approach
-temporal and infratemporal regions are reached through:
-preauricular or postauricular incision that extends onto the cervical region
-hemicoronal or bicoronal incision
-removal of orbitozygomatic segment of bone allows elevation of temporalis muscle from temporal fossa to
gain access to infratemporal fossa
-+/- removal of mandibular neck and condylar head
-frontotemporal craniotomy can be performed to elevate brain
-internal carotid artery medial to osseous eustachian tube
-uncovered mobilized to allow access to medial petroclival structures
-sphenoid sinus entered between 2nd and 3rd division of CN V
-reconstruction:
-ipsilateral temporalis muscle or temporoparietal fascial flap OR
-temporalis flap obtains blood supply from deep temporal arteries
-free flap reconstruction
Facial Translocation and Maxillotomy Approaches

-for wide exposure of middle cranial base, infratemporal fossa, pterygopalatine fossa and nasopharynx
-disadvantage: need for facial incisions
-(three or four frontal branches of CN VII tagged and transected to allow elevation of facial flaps - then
reanastomosed at end of procedure) - can be avoided in most tumour resections
-infraorbital nerve transected
-lacrimal system transected in preparation for osteotomy
-osteotomy:
-removal of anterior face of maxillary sinus in continuity with zygoma direct access to
infratemporal fossa obtained
-complete en bloc resection of pterygoid plates and nasopharyngeal mucosa can be
achieved
-sphenoid sinus, cavernous sinus, petrous carotid artery and petroclival portions of base
of skull can be reached
-reconstruction:
-temporalis muscle flap
-positioned within infratemporal fossa and below central cranial base
-free flap if no adequate coverage
-zygomaticomaxillary bone segment replaced
-lacrimal system reconstructed with silicone stents
919
920
921
Posterior Cranial Base
-approaches:
-transmastoid-translabyrinthine
-retromastoid-retrosigmoid
-sub-occipital craniotomy
-provide access to jugular bulb and CPA
ADJUVANT THERAPIES
-unresectable or recurrent meningioma treated with external beam or stereotactic radiation

-XRT most frequently considered an adjunctive modality after resection of malignant tumours of cranial
base
-brachytherapy for recurrent disease after full dose XRT and salvage surgery
-gamma knife (stereotactic radiation or radiosurgery) used after cranial-base tumour resection
-computer controlled focussing of many small beams of radiation
-chemotherapy not proved useful
-however pediatric rhabdomyosarcoma is chemosensitive
COMPLICATIONS
CSF Fistula
-most common complication after cranial-base surgery (20%)
-determine type of leak:
-high flow: active flow seen from wound, ear canal, or nasal cavity
-usually managed by direct closure in OR
-CT cisternography used if source of leak not evident
-low flow: CSF on dressings
-lumbar drain placed
-draining too much CSF can cause air entrainment into cranial vault through cranial-base
defects pneumocephalus
-if a low-flow leak has not stopped within 5 days, reoperation usually is necessary
-CSF leak specifically confirmed by means of testing for protein B2-Transferrin
-contained in only three body fluids: CSF, perilymph, vitreous fluid of the eye
Meningitis
-N+V, headache, decreasing mental status
-positive Brudzinski sign (stiff neck) and Kernig sign (pain in hamstring muscles on knee
extension)
-diagnosis by LP and CSF analysis
-postsurgical aseptic meningitis caused by meningeal irritation from surgical manipulations,
blood, and blood breakdown products
-bacterial meningitis:
-posttraumatic: S.aureus, Pneumococcus
-postoperative: S.aureus, Enterococcus
-treatment: IV antibiotics
Surgical Management of Postoperative CSF Fistula

-postoperative leaks almost always necessitate surgical closure
-usually necessitate application of vascularized tissue
-lumbar drainage for longer than 5 days generally contraindicated
922
-any leak, regardless of causation, persists longer than 5 days, operative closure is
pursued
-long-term antibiotics does not prevent meningitis and specifically increases risk of meningitis or
wound infection with resistant microorganisms
-techniques:
-CSF leak in sphenoidal sinus after transsphenoidal hypophysectomy
-endoscopic closure with fibrin glue or hydroxyappatite cement or autografts +/- pre-
operative lumbar drainage
-dural patching: reestablishment of the continuity of dura
Cranial Nerve Deficits

-cavernous sinus syndrome:
-combined paralysis of cranial nerves III, IV, VI total ophthalmoplegia
-unilateral conjunctival injection and edema
-temporary facial nerve paralysis common if nerve transposition performed for access for infratemporal
fossa approach
-lower cranial nerves (IX, X)
-vocal cord and swallowing dysfunction
-may require tracheotomy and feeding gastrostomy
Fluid and Metabolic Disturbances

-two disturbances: diabetes insipidus or SIADH
-Diabetes Insipidus:
-usually occurs after severe head trauma or removal of pituitary or hypothalamic tumours
-decreased secretion of ADH
-polyuria, dehydration, hypovolemia and polydipsia
-tx: fluid and electrolyte replacement; vasopressin can be given to control urine output
(temporary)
-SIADH:
-caused by head trauma or intraoperative manipulation
-can be cause by stroke, systemic metabolic disturbances, or intracranial bleeding
-inability to eliminate free water hyponatremia and hypoosmolality
-tx: fluid restriction to maximum of 1L day
-severe cases may require 3% hypertonic saline solution
Laboratory Value Diabetes Insipidus SIADH
Serum osmolality increased <280 mOsm/kg
Urine osmolality <150 mOsm/kg increased
Serum sodium >150 mEq/L <135 mEq/L
Urine sodium Decreased >25 mEq/L
Urine specific gravity <1.005 >1.015
Circulating free water decreased increased
Volume of urine output >250 mL/h for more than 2 h <30 mL/h
923
POTENTIAL COMPLICATIONS (Summary)
Category Complication Treatment Options
Mass lesions -brain edema -mannitol, diuretics, barbiturate coma, occasionally lobectomy
-haematoma -evacuation
Vascular -carotid or vertebral artery rupture -reexploration and repair or occlusion

-arterial thrombosis -microvascular bypass
-anticoagulation
-arterial dissection -anticoagulation
-cerebral infarction -induced hypertension
-venous thrombosis -volume expansion
-diuretics, heparinization
-air embolism left lateral decubitus position, occlusion of venous defect
Cerebral -seizures -anticonvulsants
CSF -leak -reexploration and repair; spinal fluid drainage; vascularized flap
Infections -meningitis -antibiotics

-wound abscess -drainage
-epidural, subdural, or brain abscess -antibiotics
Wound -flap necrosis -local or distant flap repair
Cranial nerve palsy -cranial nerves I-XII -nerve reconstruction

-compensatory procedures (eg. vocal cord injection)
-rehabilitation
Metabolic -diabetes insipidus -fluid replacement, vasopressin

-SIADH -fluid restriction, hypertonic saline solution
EMERGENCIES
Postoperative Cerebral Edema

-mainly from brain retraction
-treatment options:
-hyperventilation, IV mannitol, corticosteroids, barbiturate coma (for severe edema)
Hematoma and Vascular Emergencies

-haematoma evacuated ASAP
-exposure of petrous carotid:
-arterial wall dissection, pseudo-aneurysm, or thrombosis
Air Embolus
-from open venous sinuses within diploe of skull, sigmoid sinus, jugular bulb or jugular vein
-fairly large amount of air needed but circulatory compromise can occur with volumes as low as 30 ml
-tx: -wound filled with wet packing
-patient turned to head-down, left lateral decubitus position traps air to right side of heart to
minimize embolization to lungs
-position maintained until circulatory stability returns or aspiration of air can be achieved with
transvenous catheter
-source of air-leak sealed
924
Postoperative Seizures
-manipulation or resection of temporal lobe particularly epileptogenic
-prophylactic antiseizure prophylaxis routine
-tx: IV phenytoin, phenobarbital, or diazepam
-search for metabolic or structural cause
925
SURGICAL TECHNIQUES TO ENHANCE PROSTHETIC REHABILITATION
-early dental intervention can decrease inpatient days by reducing sites of oral infection and decreasing risk factors
for oral complications, such as osteoradionecrosis
ORAL AND DENTAL ANATOMY
-universal numbering system of teeth:

-numbered sequentially from 1-32 beginning
with right maxillary 3rd molar left maxillary
3rd molar left mandibular 3rd molar right
mandibular 3rd molar
-important anatomic landmarks for support in prosthetic

rehabilitation:
-maxillary:
-tuberosity
-alveolar ridge
-hard palate
-mandibular:
-alveolar ridge
-retromolar pad
-buccal shelf
ORAL AND DENTAL EVALUATION
-note advanced periodontal disease, gross dental caries, tissue irritation, poor oral hygiene
-dentist’s evaluation:
-confirms existence of acute and chronic oral pathologic conditions such as dental abscess, teeth
with advanced periodontal disease, or dental calculus causing gingivitis
-Panorex obtained to demonstrate overall topographic features of dentition, maxilla, mandible, sinuses,
nasal cavity and TMJ
-teeth with poor or questionable prognosis are identified and extracted before or during primary ablative
surgical procedure
PRINCIPLES AND INFORMATION FOR THE SURGEON
-radiation reduced salivary flow xerostomia dental caries

-fluoride reduces radiation decay of teeth
-reducing risk of dental infection can decrease risk of ORN
-three phases of prosthetic rehabilitation:
-surgical and interim
-may require frequent adjusting while tissues are healing
-used to restore oral contour and function immediately after maxillectomy
-definitive
-oral lavage and rinses immediately postop
-routine oral and dental hygiene can be initiated 2 weeks postop
F.Ling - Prosthetic Rehabilitation (1)
926
SURGICAL TECHNIQUES TO ENHANCE PROSTHETIC REHABILITATION
Maxilla
-alveolar cuts made through socket of an extracted tooth to prevent iatrogenic bone loss and to ensure
longevity of tooth next to this cut
-spare as much premaxilla as possible for support and retention of prosthesis
-STSG placed in maxillary defect to provide scar tissue band for retention of prosthesis, decrease mucous
secretion and crust formation
-palatal mucosa can be wrapped around midline portion of palatal cut
-removal of inferior and middle turbinates allows extension of prosthesis into defect area
-surgical obturator prosthesis placed to restore oral contour for immediate function and good postoperative
appearance
Soft Palate
-it is easier to rehabilitate a pt’s speech and swallowing if soft palate is removed totally
-if remaining soft palate is nonfunction, rehabilitation can be difficult or even impossible
Mandible
-three types of osseous free tissue transfer have been used:
-scapula
-iliac crest
-fibula
-fibular graft supplies length and quality of bone to reconstruct defects of mandible and is an excellent
recipient for dental implants and prostheses
-procedures to aid support of a prosthesis:
-vestibuloplasty with placement of STSG
-placement of dental implants
Tongue
-palatal augmentation prostheses approximated to maxilla to increase linguopalatal contact help normalize
speech and swallowing
-tongue prostheses are available but provide poor function
Extraoral Lesions
-prostheses are retained with adhesives and tissue undercuts or extraoral osseointegrated implants
Orbit
-surgical considerations to improve prosthetic rehabilitation
-eyelid resection while maintenance of brow position
-rough bony margins smoothed
-STSG placed in depth of defect to cover expose bone
Ear
-easier to replace complete ear than partial ear
-recipient area must be flat or concave
-skin devoid of hair provides good adhesive base
-if tissue can be spared, tragus is the first choice allows anterior margin of prosthesis to be hidden
927
GENERAL INFORMATION ABOUT OSSEOINTEGRATED DENTAL IMPLANTS
-implants are made of titanium and are cylindrically designed with threads that anchor them in bone
-stages:
-placement of implant into bony recipient site under local or general anesthesia
-covered by tissue flap and allowed to integrate with bone for 12 or more weeks
osseointegration
-superior portion of implant is uncovered and connector is placed on implant
928
CUTANEOUS MALIGNANCY
Merkel Cell Carcinoma
-aka neuroendocrine carcinoma of the skin

-unusual and highly aggressive skin cancer, similar to malignant melanoma
-high propensity for local recurrence and regional and distant metastases
-1/3-1/2 eventually die of the disease
Epidemiology
-rare neoplasm - just over 600 cases reported
-6th and 7th decades of life (mean age, 67.8 y); M=F
Histology
-small, round, basophilic cells arranged in sheets, rests, or trabeculae
-originates in the dermis
-rounded nuclei, finely divided chromatin, scant cytoplasm, and high rate of mitosis
-three histologic subtypes of MCC:
-solid type (most common)
-trabecular type
-diffuse type (worst prognosis).
-immunohistochemical staining:
-cytokeratin (in the form of a perinuclear dotlike pattern typical of neuroendocrine tumors) and
neuron-specific enolase makes the definitive diagnosis
-absence of S-100 protein and homatropine methylbromide marker (HMB-45) essentially excludes
the diagnosis of malignant melanoma
Prognosis
-aggressive malignancy similar to malignant melanoma
-10-25% of pt with regional nodal involvement at presentation
-local recurrence after primary treatment in 25-45% of pts
-regional nodal involvement develops in 50-70%
-distant metastases occur in more than 30% of patients
-overall 5-year survival rate is 50-70%
Treatment
-surgical excision:
-wide local excision, to include 2-3 cm of normal-appearing skin
-Mohs micrographic surgery effective
-radiation therapy:
-radiosensitive tumor
-adjuvant XRT after excision recommended to reduce local recurrence
-45-60 Gy in standard fractions to surgical site and regional lymphatic bed are used
-N0 neck (Stage I disease):
-controversial: both elective lymph node dissection and radiotherapy are advocated
-N+ neck (Stage II disease):
-complete lymph node dissection
-postoperative XRT to regional site and neck is unknown at this time
-treatment of recurrence:
-reexcision with a 2-cm margin or with Mohs micrographic surgery
-distant metastasis (Stage III):
-lungs, liver, bone, or brain
-mean survival time of 8 months
F.Ling - Cutaneous Malignancy - Merkel Cell (1)
929
-histochemically similar to small cell carcinoma of the lung: similar chemotherapeutic regimens
-carboplatin and etoposide
F.Ling - Cutaneous Malignancy - Merkel Cell (2)
930
NECK CANCER, UNKNOWN PRIMARY
-when clinicians are unable to determine origin of metastatic cervical lymphadenopathy, cancer is said to
originate from an unknown primary site
-when primary site of carcinoma is known, one is able to administer focused therapy to primary site and
cervical lymphadenopathy
-if site is unknown must treat entire pharyngeal axis and larynx to cover possible origins of metastatic
carcinoma
-treatment results in a significant increase in morbidity
-occult primary carcinoma either metastasizes early to cervical lymphatics or develops in an anatomical site
that is not detectable by endoscopy or imaging techniques
-typical presentation is complaint of a painless neck mass
-thorough head and neck exam is performed
-if no primary site is found, one is obligated to perform a panendoscopy of upper aerodigestive tract with
biopsy samples obtained from designated high-yield anatomical sites and any other suspicious areas
-surgical treatment of cervical lymphadenopathy in certain clinical situations may be performed at same
time as panendoscopy.
Relevant Anatomy
Occipital nodes:
-drainage of posterior scalp
Postauricular nodes:
-lymphatic drainage of posterior scalp, mastoid, and posterior auricle
Parotid nodes:
-extraglandular nodes: drainage of anterior scalp (anterior to imaginary anatomical line)
-intraglandular nodes: same anatomical regions as extraglandular nodes as well as parotid gland
itself
Submandibular nodes (level I):

-drain ipsilateral lower and upper lip, cheek, nose, medial canthus, and oral cavity up to anterior
tonsillar pillar
Submental nodes (level I):

-drain mentum, middle two thirds of lower lip, anterior gingiva, and anterior tongue
Retropharyngeal nodes:
-drainage of posterior region of nasal cavity, sphenoid and ethmoid sinuses, hard and soft palate,
nasopharynx, and posterior pharyngeal wall
Anterior cervical nodes (level VI):

-drain anterior cervical skin as well as supraglottis, glottis, subglottis, thyroid, and parathyroid
glands
Lateral cervical nodes (levels II-V):

-located along internal jugular vein in this region, are responsible for lymphatic drainage of all of
above sites, including tonsil, hard and soft palate, larynx, thyroid, parathyroid glands, major
salivary glands, and external and middle ear
-nodes along spinal accessory nerve, which are found in posterior triangle, are responsible for
drainage of nasopharynx and posterior scalp
F.Ling - Unknown Primary (1)
931
-when lymphadenopathy is located in supraclavicular space, lower deep lateral cervical chain, or lower
posterior triangle, primary lesion is often not from upper aerodigestive tract
Treatment:
Radiation therapy:
-Jesse et al demonstrated added advantage of radiation therapy to locoregional control following surgical
removal of cervical metastases
-locoregional failure rate of 13-32% when treated with surgery alone cf 0-18% when patients are treated
with primary surgery (neck dissection) followed by adjuvant external beam radiotherapy.
-field to be covered by radiation therapy is controversial
-pts treated with ipsilateral irradiation had a relative risk of recurrence in head and neck of 1.9
compared to patients treated with bilateral irradiation
-bilateral cervical irradiation with surgical therapy improves locoregional control of cancer and is
accepted as standard of care for patients with advanced cervical disease (>N2)
-mucosal sites that are to be included in radiation field of patients with occult primary lesions are generally
accepted as entire pharyngeal axis
-in theory, this should prevent occurrence of primary lesion
-some argue that, to decrease morbidity of radiation-induced xerostomia, nasopharynx should not
be included in radiation ports when results of endoscopy and findings on imaging studies are
negative
Chemotherapy:
-generally reserved for patients with clinical or pathologic indicators of aggressive disease or primary
nasopharyngeal carcinoma:
-extensive lymphadenopathy (>N2C)
-extracapsular spread of carcinoma
-unresectable local disease
-distant metastatic spread of carcinoma often undergo chemotherapy for possible cure or palliative
treatment
Surgical therapy:
-Panendoscopy:
-generous biopsy samples of nasopharynx are obtained for both frozen sectioning and permanent
sectioning
-inspection and palpation of oral cavity, oropharynx, hypopharynx, and larynx
-rigid cervical esophagoscope is used to examine esophagus
-biopsy samples are obtained by examiner of base of tongue
-unilateral tonsillectomy vs bilateral tonsillectomy
-depending on results of panendoscopy, either newly found primary lesion (other than nasopharynx) is
addressed surgically along with cervical lymphadenopathy or lymphadenopathy is addressed separately
with appropriate neck dissection.
F.Ling - Unknown Primary (2)
932
OSTEORADIONECROSIS AND HYPERBARIC OXYGEN THERAPY
Osteoradionecrosis (ORN)
-condition of nonvital bone in a site of radiation injury
-can be spontaneous, but it most commonly results from tissue injury
-apparently innocuous forms of trauma as denture-related injury, ulcers, or tooth extraction can overwhelm
the reparative capacity of radiation-injured bone
-grades of disease:
-Grade I:
-most common presentation
-exposed alveolar bone is observed
-Grade II:
-ORN that does not respond to hyperbaric oxygen therapy and sequestrectomy/saucerization
-Grade III:
-full thickness involvement and/or pathologic fracture
Frequency:
-rare in patients who receive less than 60 gray (Gy) radiation therapy
-incidence is increased in patients receiving combined chemotherapy-radiation
Etiology:
-ORN can be either spontaneous (39% of cases) or the result of an insult (61%)
-cumulative progressive endarteritis caused by radiotherapy results in insufficient blood supply (tissue
oxygen delivery) to effect wound healing
Pathophysiology:
-irradiated mandible, periosteum, and overlying soft tissue undergo hyperemia, inflammation, and
endarteritis thrombosis, cellular death, progressive hypovascularity, and fibrosis
-radiated bed is hypocellular and devoid of fibroblasts, osteoblasts, and undifferentiated osteocompetent
cells
Work-up:
-rule out recurrence
-determine method of radiation treatment, total dose, and radiation portal
-CT/MRI of mandible
-future: SPECT scan
Treatment:
Medical therapy:
-pretreatment phase:
-dental evaluation for patients with oral cancer who may need radiotherapy
-dentist should perform prophylaxis, periodontal scaling, caries control, and fabrication of
fluoride trays
-teeth that cannot be salvaged with conservative endodontic therapy should be extracted
-fluoride treatment to prevent radiation caries
-posttreatment phase:
-primarily supportive: nutritional support along with superficial debridement and oral saline
irrigation for local wounds
-antibiotics are indicated only for definite secondary infection
F.Ling - ORN and HBO (1)
933
Hyperbaric Oxygen:
-HBO transiently elevates tissue oxygen tension and stimulates fibroblastic proliferation and oxygen-
dependent collagen synthesis
-allows for angiogenesis in radiated bed
Current protocol for treatment of mandibular ORN according to Marx

-Stage I:
-perform 30 HBO dives (1 dive per day, Monday-Friday) to 2.4 atmospheres for 90
minutes
-reassess patient to evaluate decreased bone exposure, granulation tissue covering
exposed bone, resorption of nonviable bone, and absence of inflammation
-patients who respond favorably, continue treatment to a total of 40 dives
-Stage II:
-perform transoral sequestrectomy with primary wound closure followed by continued
HBO to a total of 40 dives
-Stage III:
-perform transcutaneous mandibular resection, wound closure, and mandibular fixation
with an external fixator or maxillomandibular fixation, followed by an additional 10
postoperative HBO dives.
-Stage IIIR:
-perform mandibular reconstruction 10 weeks after successful resolution of mandibular
ORN
-complete 10 additional postoperative HBO dives.
Microvascular reconstruction
-after resection of nonviable bone, vascular free tissue transfer offers immediate reconstruction and
restoration of mandibular continuity
-free tissue transfers offer patients a shorter treatment course without the need for HBO
Postoperative details:
-risk of developing ORN is cumulative in relation to radiation dose, and risk continues throughout pts life
-risk of ORN in patients who must undergo procedures involving the mandible following radiation
treatment increases with time from radiation therapy
-prophylactic use of HBO can decrease morbidity and increase success of dental therapy
-prior to dental extraction/implant placement, consider HBO if surgery will occur in a field of radiation that
is known to have received 60 Gy
-follow the standard HBO regimen of 20 preoperative treatments and 10 postoperative treatments
-perform surgery in as atraumatic a fashion as possible
F.Ling - ORN and HBO (2)
934
Page 1 of 13
TNM STAGING OF HEAD AND NECK TUMOURS
ORAL CAVITY
Anatomical Sites and Subsites
 Lip
 External upper lip (vermilion border)
 External lower lip (vermilion border)
 Commissures
 Oral Cavity
 Buccal mucosa
 mucosa of upper and lower lip
 cheek mucosa
 retromolar areas
 bucco- alveolar sulci, upper and lower (vestibule of mouth)
 Upper alveolus and gingiva (upper gum)
 Lower alveolus and gingiva (lower gum)
 Hard palate
 Tongue
 anterior 2/3
 inferior (ventral) surface
 Floor of mouth
 TX: Primary tumor cannot be assessed

 T0: No evidence of primary tumor
 Tis: Carcinoma in situ
 T1: Tumor 2 cm or less in greatest dimension
 T2: Tumor more than 2 cm hut not more than 4 cm in greatest dimension
935
file:///C:/Users/user/Desktop/Dr%20flings%20Notes/Contents/TNM_Staging.htm 3/22/2013
Page 2 of 13
 T3: Tumor more than 4 cm in greatest dimension

 T4: Tumor invades adjacent structures (e.g., through cortical bone, into
deep [extrinsic] muscle of tongue, maxillary sinus, skin. Superficial erosion
alone of bone/tooth socket by gingival primary is not sufficient to classify as
T4)
Summary of Stage Groupings
 Stage 0:ÇTis N0 M0
 Stage I:ÇT1 N0 M0
 Stage II:ÇT2 N0 M0
 Stage III:ÇT3 N0 M0; T1- 3 N1 M0
 Stage IVA:ÇÇÇT4 N1- 2 M0; Any T N2 M0
 Stage IVB:ÇAny T N3 M0
 Stage IVC:ÇAny T Any N M1
PHARYNX
Nasopharynx
 Postero- superior wall

 extends from the level of the junction of hard and soft palates to base
of skull
 Lateral wall
 including the fossa of Rosenm±ller
 Inferior wall
 consists of the superior surface of the soft palate
 TI: Tumor confined to the nasopharynx

 T2: Tumor extends to soft tissues of oropharynx and/or nasal fossa
936
Page 3 of 13
 T2a Without parapharyngeal extension

 T2b With parapharyngeal extension
 T3: Tumor invades bony structures and/or paranasal sinuses
 T4: Tumor with intracranial extension and/or involvement of cranial nerves,
infratemporall fossa, hypopharynx, or orbit
 Stage 0:Ç
 Tis N0 M0
 Stage I:Ç
 T1 N0 M0
 Stage IIA:Ç
 T2a N0 M0
 Stage IIB:Ç
 T1 N1 M0
 T2 N1 M0
 T2a N1 M0
 T2b N0 M0
 T2b N1 M0
 Stage III:Ç
 TI N2 M0
 T2a N2 M0
 T2b N2 M0
 T3 N0 M0
 T3 N1 M0
 T3 N2 M0
 Stage IVA:Ç
 T4 N0 M0
 T4 N1 M0
 T4 N2 M0
 Stage IVB:Ç
 Any T N3 M0
 Stage IVC:Ç
937
Page 4 of 13
 Any T Any N M1
Oropharynx
 Anterior wall (glossoepiglottic area)

 base of tongue (posterior to the vallate papillae or posterior third)
 vallecula
 Lateral wall
 tonsil
 tonsillar fossa and tonsillar (faucial) pillars
 glossotonsillar sulci (tonsillar pillars)
 Posterior wall
 Superior wall
 inferior surface of soft palate
 uvula
 T1: Tumor 2 cm or less in greatest dimension

 T2: Tumor more than 2 cm but not more than 4 cm in greatest dimension
 T3: Tumor more than 4 cm in greatest dimension
 T4: Tumor invades adjacent structures (e.g., pterygoid muscle[s], mandible,
hard palate, deep muscle of tongue, larynx)
938
Page 5 of 13
Hypopharynx
 Pharyngo- esophageal junction (postcricoid area)

 extends from level of arytenoid cartilages and connecting folds to the
inferior border of the cricoid cartilage thus forming the anterior wall of
the hypopharynx
 Piriform sinus
 from pharyngoepiglottic fold to upper end of esophagus
 bounded laterally by thyroid cartilage and medially by hypopharyngeal
surface of aryepiglottic fold and arytenoid and cricoid cartilages
 Posterior pharyngeal wall
 from superior level of hyoid bone to level of inferior border of cricoid
cartilage and from apex of one piriform sinus to the other
 T1: Tumor limited to one subsite of hypopharynx and 2 cm or less in

greatest dimension
 T2: Tumor involves more than one subsite of hypopharynx or in adjacent
site, or measures more than 2 cm but not more than 4 cm in greatest
diameter without fixation of hemilarynx
 T3: Tumor measures more than 4 cm in greatest dimension or with fixation
of hemilarynx
 T4: Tumor invades adjacent structures (e.g., thyroid/cricoid cartilage,
carotid artery, soft tissues of neck, prevertebral fascia/muscles, thyroid
and/or esophagus)
939
Page 6 of 13
(staging same for oral cavity, oropharynx, hypopharynx)
LARYNX
Supraglottis
 suprahyoid epiglottis (including tip, lingual [anterior], and laryngeal surfaces)

 aryepiglottic folds (laryngeal aspect)
 arytenoids
 infrahyoid epiglottis
 ventricular bands, false cords

 T1: Tumor limited to one subsite of supraglottis with normal vocal cord
mobility
 T2: Tumor invades mucosa of more than one adjacent subsite of
supraglottis or glottis or region outside the supraglottis (e.g., mucosa of
base of tongue, vallecula, medial wall of piriform sinus) without fixation of
the larynx
 T3: Tumor limited to larynx with vocal cord fixation and/or invades any of
the following: postcricoid area, preepiglottic tissues
 T4: Tumor invades through the thyroid cartilage, and/or extends into soft
940
Page 7 of 13
tissues of the neck, thyroid, and/or esophagus
Glottis
 vocal cords
 anterior commissure
 posterior commissure

 T1: Tumor limited to the vocal cord(s) (may involve anterior or posterior
commissure) with normal mobility
 T1a Tumor limited to one vocal cord
 T1 b Tumor involves both vocal cords
 T2: Tumor extends to supraglottis and/or subglottis, and/or with impaired
vocal cord mobility
 T3: Tumor limited to the larynx with vocal cord fixation
 T4: Tumor invades through the thyroid cartilage and/or to other tissues
beyond the larynx (e.g., trachea, soft tissues of the neck, including thyroid,
pharynx
Subglottis

 T1: Tumor limited to the subglottis
 T2: Tumor extends to vocal cord(s) with normal or impaired cord mobility
 T3: Tumor limited to larynx with vocal cord fixation
 T4: Tumor invades through cricoid or thyroid cartilage and/or extends to
other tissues beyond the larynx (e.g., trachea, soft tissues of neck, including
thyroid, esophagus)
941
Page 8 of 13
 Stage 0:Ç
 Tis N0 M0
 Stage I:Ç
 T1 N0 M0
 Stage II:Ç
 T2 N0 M0
 Stage III:Ç
 T3 N0 M0
 TI N1 M0
 T2 N1 M0
 T3 N1 M0
 Stage IVA:Ç
 T4 N0 M0
 T4 N1 M0
 Any T N2 M0
 Stage IVB:Ç
 Any T N3 M0
 Stage IVC:Ç
 Any T Any N Ml
MAXILLARY SINUS

 T1: Tumor limited to the antral mucosa with no erosion or destruction of
bone
 T2: Tumor causing bone erosion or destruction, except for the posterior
antral wall, including extension the hard palate and/or the middle nasal
meatus
942
Page 9 of 13
 T3: Tumor invades any of the following: bone of the posterior wall of the
maxillary sinus, subcutaneous tissues, skin of cheek, floor or medial wall of
orbit, infratemporal fossa, pterygoid plates, ethmoid sinuses
 T4: Tumor invades orbital contents beyond the floor or medial wall including
any of the following: orbital apex, cribriform plate, base of skull,
nasopharynx, sphenoid, frontal sinuses
 Stage 0:Ç
 Tis N0 M0
 Stage I:Ç
 T1 N0 M0
 Stage II:Ç
 T2 N0 M0
 Stage III:Ç
 T3 N0 M0
 T1 N1 M0
 T2 N1 M0
 T3 N1 M0
 Stage IVA:Ç
 T4 N0 M0
 T4 N1 M0
 Stage IVB:Ç
 Any T N2 M0
 Any T N3 M0
 Stage IVC:Ç
 Any T Any N M1
PAROTID GLAND
943
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 T1: Tumor 2 cm or less in greatest dimension without extra- parenchymal
extension
 T2: Tumor 2 cm but not more than 4 cm in greatest dimension without
extra- parenchymal extension
 T3: Tumor having extra parenchymal extension without seventh nerve
involvement and/or more than 4 cm but not more than 6 cm in greatest
dimension
 T4: Tumor invades base of skull, seventh nerve, and/or exceeds 6 cm in
greatest dimension
 All categories are subdivided:

 (a) no local extension
 (b) local extension
(Local extension is clinical/macroscopic invasion of skin, soft tissue, bone, or

nerve. Microscopic evidence alone is not local extension for classification
purposes.)
 Stage I:Ç
 T1 N0 M0
 T2 N0 M0
 Stage II:Ç
 T3 N0 M0
 Stage III:Ç
 T1 N1 M0
 T2 N1 M0
 Stage IV:Ç
 T4 N0 M0
944
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 T3 N1 M0
 T4 N1 M0
 Any T N2 M0
 Any T N3 M0
 Any T Any N M1
THYROID GLAND

 T1: Tumor 1 cm or less in greatest dimension limited to the thyroid
 T2: Tumor more than 1 cm but not more than 4 cm in greatest dimension
limited to the thyroid
 T3: Tumor more than 4 cm in greatest dimension limited to the thyroid
 T4: Tumor of any size extending beyond the thyroid capsule
Papillary or Follicular
Under 45 Years
 Stage I: Any T Any N M0

 Stage II: Any T Any N M1
45 Years and Over
 Stage I:Ç
 T1 N0 M0
 Stage II:Ç
 T2 N0 M0
 T3 N0 M0
 Stage III:Ç
 T4 N0 M0
945
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 Any T N 1 M0
 Stage IV:Ç
 Any T Any N M1
Medullary
 Stage I:Ç
 T1 N0 M0
 Stage II:Ç
 T2 N0 M0
 T3 N0 M0
 T4 N0 M0
 Stage III:Ç
 Any T N 1 M0
 Stage IV:Ç
 Any T Any N M1
Undifferentiated
 All cases are Stage IV

 Stage IV: Any T Any N Any M
CERVICAL NODE CLASSIFICATION
The following regional node classification is applicable to all malignant head and
neck tumors. In clinical evaluation the actual size of the nodal mass should be
measured and allowance made for intervening soft tissues. It is recognized that
most masses over 3 cm in diameter are not single nodes but confluent nodes of
tumor in soft tissues of the neck. There are three stages of clinically positive
nodes: N1, N2, and N3. The use of subgroups a, b, and c is not required but is
recommended. Midline nodes are considered as ipsilateral nodes.
946
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REGIONAL LYMPH NODES (N)
 NX Regional lymph nodes cannot be assessed

 N0 No regional lymph node metastasis
 N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest
dimension
 N2 Metastasis in a single ipsilateral lymph node, more than 3 cm but not
more than 6 cm in greatest dimension; or in multiple ipsilateral lymph
nodes, none more than 6 cm in greatest dimension; or in bilateral or
contralateral lymph nodes, none more than 6 cm in greatest dimension
 N2a Metastasis in single ipsilateral lymph node more than 3 cm but
not more than 6 cm in greatest dimension
 N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6
cm in greatest dimension
 N2c Metastasis in bilateral or contralateral lymph nodes, none more
than 6 cm in greatest dimension
 N3 Metastasis in a lymph node more than 6 cm in greatest dimension
947
TRACHEAL RESECTION WITH PRIMARY ANASTOMOSIS
-“safe” anastomotic tension: 1000g

-upper limit of safe tracheal resection (Grillo et al, 1964):
-6.4 cm, 13.4 rings, or 58.7% of the human trachea
-release manoeuvres:
-hilar release manoeuvres (uncommonly used today)
-division of right pulmonary ligament
-division of left main stem bronchus just distal to carina with end-to-side anastomosis to bronchus
intermedius
-pericardial dissection
-cervical flexion
-suprahyoid release (SHR)
-amount of trachea released:

-cervical flexion (15-30o): 4-5 cm
-suprahyoid release: 2.5 cm
-hilar release:
-division of inferior pulmonary ligament: 3 cm
-intrapericardial dissection: 0.9 cm
948
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Treatment Outcomes - Head and Neck Cancers
ORAL CAVITY
Lip Carcinoma
 Regional metastasis:
 relatively uncommon; ~10%
 Locoregional control:Ç>90%
 5- yr survival:
 Overall:Ç91%
 I- II:Ç>90%
 III- IV:Ç30- 70%
Tongue Carcinoma
 Regional metastasis:Çcommon
 clinically apparent:Ç25- 33%
 occult: 25- 33%
 5- yr locoregional control:Ç91%
 5- yr survival:
 I- II:Ç60- 75%
 III- IV:Ç25- 40%
 Effect of extracapsular spread (ECS) - 5- yr survival and overall
 N0:Ç88% and 75%
 N+/ECS- :Ç65% and 50%
 N+/ECS+:Ç48% and 30%
Floor of Mouth Carcinoma
 Regional metastasis (occult):Ç23- 50%

 Locoregional recurrence:
 primary site:Ç41%
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 neck:Ç18.5%
 5- yr survival:
 I- II:Ç60- 80%
 III:Ç28- 68%
 IV:Ç6- 36%
Retromolar Trigone Carcinoma
 Regional metastasis:Çcommon
 10- 20%
 5- yr survival:
 T1:Ç80%
 T2:Ç57.8%
 T3:Ç46.5%
 T4:Ç65.2%
 Overall survival:Ç26- 55%
Alveolar ridge, Gingival Mucosa, Gums Carcinoma
 Regional metastasis:
 clinically apparent:Ç25- 30%
 occult:Ç15%
 Locoregional control:Ç70- 80%
 Mandibular cortical invasion:Ç5- yr survivalÇ85% - - > 68%
 Cervical metastasis:Ç5- yr survivalÇ86% - - > 59%
Palate Carcinoma
 Local recurrence:Ç53%
 Regional recurrence:Ç30%
 5- yr survival:Ç44- 75%
Buccal Carcinoma
 Locoregional recurrence:Ç43- 80%

 5- yr survival:
950
Page 3 of 5
 I- II:Ç65- 78%
 III- IV:Ç50- 60%
PHARYNX
Nasopharynx
 Nodal metastasis:
 clinically apparent:Ç87%; 20% bilateral
 Locoregional control
 radiation:Ç60%
 chemoradiation:Ç70- 80%
 5yr- survival
 radiation:Ç36- 58%
 chemoradiation:Ç70- 80%
 10- yr survival:
 10- 40%
Oropharynx - Tonsil
 I- II:Ç75- 90%
 III:Ç50%
 IV:Ç20- 50%
 5yr- survival
 I- II:Ç80%
 III:Ç50%
 IV:Ç20- 50%
Oropharynx - Base of Tongue
 I- II:Ç75- 90%
 III:Ç50%
951
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 IV:Ç20%
 5yr- survival
 I- II:Ç85%
 III- IV:Ç20- 50%
Oropharynx - Soft Palate
 I- II:Ç75- 90%
 III:Ç75%
 IV:Ç35%
 5yr- survival
 I- II:Ç70- 80%
 III:Ç64%
 IV:Ç20- 40%
Hypopharynx
 Regional metastasis:Ç60- 75%

 Locoregional control:
 piriform sinus:Ç58- 71%
 pharyngeal wall:ÇT1 91%; T2 73%; T3 61%; T4 37%
 postcricoid:Ç<60%
 5- yr survival:
 piriform sinus:Ç20- 50%
 pharyngeal wall:Ç21%
 postcricoid:Ç35%
LARYNX
Supraglottis
Glottis
Subglottis
952
Page 5 of 5
MAXILLARY SINUS
PAROTID GLAND
THYROID GLAND
Well- differentiated Thyroid Carcinomas
 Mortality:
 low- risk group:Ç1- 2%
 high- risk group:Ç40- 50%
Medullary Carcinoma
Anaplastic Carcinoma
average survival:Ç6 months
953
VELOPHARYNGEAL INSUFFICIENCY
Introduction:
-inadequate velopharyngeal closure (VPC) allows air to escape through nose during generation of
consonants requiring high oral pressure, leading to inappropriate nasal resonance during speech production
Problem:
-VPC is an important part of speech
-all phonemes in English language with the exception of 3 (/m/, /n/, /ng/) are produced with oral airflow
velopharynx closed
-nasal phonemes (/m/, /n/, /ng/) are produced with nasal resonance velopharynx open
-VPI is inadequate closure of velopharyngeal port resulting from a structural problem with the velum
-eg, submucous cleft palate, shorted velum relative to the depth of the posterior pharyngeal wall,
overt cleft palate
Etiology:
-overt cleft palate (most common)
-submucous cleft palate
-bifid or double uvula, muscular diastasis of the soft palate (zona pellucida), and notching of
posterior border of hard palate
-occult submucosal cleft palate
-absence or deficiency of musculus uvulae with a diastasis of levator veli palatini but without
presence of a bifid uvula or grooving of oral surface of soft palate
-best visualized endoscopically as absence of bulge on nasal surface of soft palate during speech.
-transient VPD with hypernasal resonance following adenoidectomy, with or without tonsillectomy
-Down syndrom:
-predisposition to VPD is present
-often have a narrow velopharynx and a shallower skull base, resulting in less distance for palate
to traverse to effect closure
-VCF syndrome
-autosomal dominant entity linked to microdeletions in long arm of chromosome 22
-major findings include cleft palate (overt, submucous, or occult submucous), conotruncal heart
anomalies, mental disabilities, and a characteristic facies
-common in patients with VCF syndrome due to presence of a cleft palate and pharyngeal
hypotonic
-low muscle tone:
-may be a feature of other syndromes (eg, neurofibromatosis, myotonic dystrophy, any syndrome
in which low muscle tone is a feature)
-tonsil hypertrophy that prevents palate from adequately moving superiorly during attempted VPC
-acquired causes include:
-stroke or head injury
-other neurologic diseases (eg, muscular dystrophy, multiple sclerosis, amyotrophic lateral
sclerosis [ALS], Parkinson disease)
Clinical:
-nasal resonance, and nasal emissions (ie, air escape through nasal passage with speech)
-nasal regurgitation
-recurrent and chronic sinus infections
F.Ling - VPI (1)
954
Relevant Anatomy:
Six muscles comprise velopharyngeal sphincter.
-Tensor veli palatini

-Levator veli palatini
-Musculus uvulae
-Palatoglossus
-Palatopharyngeus
-Superior constrictor
When viewed endoscopically, several topical anatomic features of velopharynx (nasopharynx) are important to note.
-Pharyngeal ostium of eustachian (auditory) tube: This opening and its associated structures comprise
lateral wall of nasopharynx
-Pharyngeal tonsil (ie, adenoid): adenoid, which is a closely aggregated collection of lymphoid nodules, is
directly posterior in nasopharynx and overlies basilar portions of sphenoid and occipital bones
-Posterior pharyngeal wall: comprises mainly superior pharyngeal constrictor muscle. Contraction of this
muscle in axial plane at level of VPC constitutes a structure known as Passavant ridge.
-Pharyngeal surface of soft palate
Diagnostic Procedures:
-Voice and resonance evaluation
-articulation assessment
-oral motor assessment
-measurement of nasal airflow:
-MacKay-Kummer sensory nerve action potential (SNAP) test
-assesses ratio of oral airflow to nasal airflow
-nasometer results are compared to normative data
-score 3 standard deviations above mean indicates hypernasal resonance
-Fiberoptic nasoendoscopy
-Videofluoroscopy
-allows more precise localization of level of VPC by measuring level against spine
TREATMENT
Speech therapy
-Speech therapy improves velopharyngeal function when VPD is minimal or due to articulation errors and
in postoperative patients
Nasal continuous positive airway pressure therapy

-patients whose VPD seems related to oral motor issues or velar weakness rather than structural problems
of velum
-palate-strengthening program using CPAP
Prosthetics
-obturators can substitute for tissue deficiency and are attached to teeth by metal wire or bands
-palatal lifts are used when adequate palatal length exists but dynamic motion of palate is poor due to
neuromuscular etiologies
F.Ling - VPI (2)
955
Surgical therapy:
Preoperative details:
Velopharyngeal closure pattern

-determined by relative contribution of palate and lateral pharyngeal walls to closure of
velopharyngeal sphincter.
-four basic types of closure patterns:
1. Coronal:
-most common closure pattern (present in 55% of patients with normal velar function)
-major contribution to closure is from soft palate as it contacts a broad area of posterior
pharyngeal wall
-little medial motion of lateral pharyngeal walls occurs
2. Circular:
-present in approximately 20% of individuals with normal closure
-involves contribution from both soft palate and lateral pharyngeal walls
-closure that resembles a circle getting smaller
3. Circular with Passavant ridge:

-occurs in 15-20% of population and is a circular pattern that involves anterior motion of
posterior pharyngeal wall
4. Sagittal:
-least common pattern (10%)
-palatal motion is minimal
-main contribution from medial motion of lateral pharyngeal walls
-pattern seen most commonly in patients with persistent VPD following repair of cleft
palate.
-type of closure pattern determines type of surgical intervention

-surgical intervention most effective when it targets point of maximal pharyngeal motion
Tonsillectomy and adenoidectomy

-in case of pharyngoplasty, adenoidectomy makes room for placement of lateral pharyngeal wall flaps
-need for tonsillectomy before pharyngoplasty determined by degree of obstruction
-removing both tonsils and adenoid often necessary
Other considerations
-placement of a pharyngeal flap increases degree of nasal airway obstruction and may worsen any
preexisting obstructive sleep apnea consider pharyngoplasty instead
-location of internal carotid arteries as they traverse lateral pharynx is an important consideration,
especially in VCF syndrome preoperative evaluation with contrast-enhanced CT scan or magnetic
resonance angiography
F.Ling - VPI (3)
956
Intraoperative details:
Pharyngoplasty
-advantageous when coronal or circular closure is present and lateral pharyngeal wall motion is deficient
-goal is to develop a more functional sphincter by improving dynamics and bulk of velopharyngeal tissues
and by tightening and reducing size of velopharyngeal sphincter
-two superiorly based flaps comprising posterior tonsillar pillars with underlying palatopharyngeus muscles
-small inferiorly based posterior pharyngeal wall flap then was elevated, and 2 lateral flaps were rotated
90 ° and inserted onto posterior flap
-success rate: 78-100%
-incidence of postoperative hyponasality: 12-17%.
Pharyngeal flap
-preferred method in patients with good lateral pharyngeal wall motion who have a persistent central gap
due to poor palatal motion
-superiorly based posterior wall flap sutured to nasal surface of soft palate
-flap raised down to prevertebral fascia, creating a tissue flap of superior constrictor muscle with
its overlying mucosa
-flap then is sutured to nasal surface of palate by incorporating it into split repair
-normalization or resolution of hypernasality in 90% of patients
Posterior wall augmentation

-for persistent gap in central velopharyngeal port measuring at most 1-3 mm
-also indicated when patient can achieve touch closure that is not tight enough to prevent air escape with
high oral pressure
-autogenous tissue and foreign implants have been used
-superiorly based pharyngeal flap incorporating superior constrictor is raised down to prevertebral fascia
-superior extent of elevation is defined just above point of maximal closure
-it then is buckled onto itself and sutured in place
-implantable materials:
-problems with extrusion, migration, resorption, and infection
Postoperative details:
-immediate postoperative concerns deal mainly with upper airway obstruction
F.Ling - VPI (4)
957
AUDIOLOGICAL TESTS
AUDIOLOGY IN AN ADULT SETTING
Standard Tests Specials Tests

Audiogram PI-PB Roll-over
Tympanogram ECoG
Acoustic Reflexes Fistula Test
Reflex Decay OAEs
Speech Discrimination ABR
Audiogram
-frequencies tested: 250 to 8000 Hz
-interoctave frequencies and ultra-high frequencies on a case-by-case basis (ie. suspected
ototoxicity, hearing aid user, precipitous loss)
-inserts vs phones: 40 vs 60 dB interaural difference
Acoustic Reflex Testing (ART)

-mainly for differential diagnosis of auditory and neurologic disorders, as well as to reconfirm audiogram
results
-findings:
-75 dB - 110 dB
-normal: <100 dB is normal
-Abs: absent (>110 dB)
-CNT/DNT: could not test / did not test
-Neg. Deflc: Negative deflection common in the beginning stages of otosclerosis
-Too noisy: possible vascular interference (ie. high riding jugular bulb) or hypercompliant TM
-89% sensitivity for CPA tumours, low specificity
-low specificity of elevated AR is reasons ARD tested together, since ARD has better specificity
Acoustic Reflex Decay

-persistence of reflex response upon prolonged stimulation
-10 second tone presented at 10 dB supra contralateral reflex threshold for 500 Hz and 1000 Hz
-ie. reflex threshold is 95 dB, decay tested at 105 dB
POSITIVE REFLEX DECAY

NEGATIVE REFLEX DECAY
-combined ART and ARD has sensitivity of 73% and specificity of 90% for prediction of acoustic
neuroma; sensitivity of 80% and specificity of 60% for CPA tumours
-reflex decay phenomenon is specifically associated with eighth-nerve lesions
F.Ling - Tests in Audiology (1)
958
PI-PB Function
-performance intensity (PI) function for phonetically balanced (PB) words
-aka rollover function
-list of one-syllable words presented at a comfortable intensity vs a loud intensity
-word lists are balanced to equally represent all of the speech sounds, therefore different
frequencies
-for a patient with hearing within normal limits, first list would be presented at 50 dB and the
second at 80 dB
-score at comfort level minus score at elevated level
-difference of more than 25% = positive result
-can be suggestive of retrocochlear pathology
Electrocochleography (EcoG)
3 main applications
-neurodiagnostic evaluation of Menière’s disease
-enhancement of ABR wave I
-intraoperative monitoring
-extratympanic, tympanic and transtympanic electrode options
-abnormally large summation potential (SP) is seen in most patients with Menière’s disease
-an elevated SP/AP amplitude ratio is seen in approximately 60% of Menière’s patients
-SP/AP > 0.4 considered abnormal
-sensitivity of 62% and specificity of 95%
Endolymphatic Fistula Test

-performed to confirm the presence of a fistula between the membranous labyrinth and the middle ear
-audiologist + ENG nurse/technician
-done with immittance probe as in standard tympanometry however, negative pressure is rapidly decreased
from +200 to -400 mmH2O
-“positive” fistula test defined by nystagmus and/or a patient report of vertigo or dizziness as negative
pressure was created in the ear canal
-Referral criteria
-requires ABR wave I
-cannot do on a conductive loss or with a perforated TM
-requires no worse than a moderate hearing loss
Otoacoustic Emissions
-2 types: transient evoked (TEOAEs)and distortion product (DPOAEs)
-main applications:
-suspicion of auditory neuropathy
-malingering patients
-patients with tinnitus
-to monitor cochlear status over time
-TEOAE restricted to <5 kHz and cannot test ears with >30 dB loss
-DPOAE can test 1-8KHz range and can test to 55 dB loss
-able to test selected frequencies in detail as opposed to one response curve representing the
frequency range
Auditory Brainstem Response

-main applications
-to verify the integrity of the VIIIth nerve pathway
-to verify hearing thresholds
959
-to verify presence of auditory neuropathy
-uses a 10 millisecond window to record five peaks which represent different areas along the auditory
pathway
-degree of loss
-more hearing = better results
-clear results are usually obtained when threshold at 4000 Hz is 70 dB or better
AUDIOLOGY IN A PEDIATRIC SETTING
Standard Tests Specials Tests

Audiogram Acoustic Reflexes
Tympanogram Central Testing
Otoacoustic Emissions (OAEs) Speech Perception Testing (SPT)
Auditory Brainstem Response (ABR) Ultra-high Frequency Audiometry
Stenger Test (for malingerers)
Central Auditory Processing

-male to female ratio of 2:1
-children with CAPD have been shown to have depressed academic performance
-children with HL tend to have difficulty with auditory processing, especially auditory memory
-a relatively easy adaptation to ask for written homework assignments rather than verbal.
-examples of tests:
Dichotic Listening Tasks

-information to both ears at the same time
-different information to each ear
-patient is asked to either repeat both or just one
-have shown to be sensitive to disruption of interhemispheric transfer (via corpus callosum) as well as to
brainstem and cortical dysfunction
Monaural Low-Redundancy Speech

-presentation of words that have been distorted (i.e. low-pass filtering, time compression)
-evaluates the listener’s ability to achieve closure
-have been shown to be sensitive to brainstem and cortical dysfunction
Temporal Patterning Tests

-pitch pattern (frequency)
-temporal pattern (duration)
-sets of 2 to 3 presentations
-requires efficient interhemispheric transfer of acoustic information
-have been shown to be sensitive to cortical and interhemispheric disruptions
Ultra High Frequency Testing

-includes 9000 – 16000 Hz
-not typically done
-not part of the main speech spectrum
-high intersubject variability
-useful in ototoxicity monitoring and tinnitus cases
960
Stenger Test
-two tones presented in both ears at the same time but at different intensities
-10 dB above threshold in the better ear
-10 dB below threshold in the poorer ear
-when the patient fails to respond, it is a positive Stenger Test which suggests malingering
961
TYMPANOSTOMY TUBES
INDICATIONS
-does not ‘‘cure’’ the underlying conditions

CONDITIONS IN WHICH TYMPANOSTOMY TUBE
leading to OM, and thus these tubes are only PLACEMENT MAY BE INDICATED
effective for as long as they are in place and
patent -Recurrent acute otitis media
-most common indications for TT placement -Chronic otitis media with effusion in healthy children
-Otitis media or eustachian tube dysfunction coexisting with other
are recurrent acute OM and OM with effusion medical conditions:
-Craniofacial anomalies
Recurrent acute otitis media -Down syndrome
-children in group childcare settings are much -Underlying sensorineural hearing losses
-Other (e.g., patients undergoing hyperbaric therapy)
more likely to be otitis-prone -Tympanic membrane abnormalities (e.g., severe retraction,
-rate doubling in groups of six or atelectasis, impending ossicular chain erosion, or cholesteatoma)
more children
-one in four infants or toddlers will have
recurrent acute OM at a rate of six cases per
FACTORS INFLUENCING DECISIONS ABOUT
12-month interval at some point while in a
TYMPANOSTOMY TUBE PLACEMENT IN
group childcare setting ‘‘OTITIS-PRONE’’* CHILDREN
-overall, a reduction in the rate of recurrent
acute OM by about 50% per year, or 3.5 Factors making tympanostomy tube placement desirable:
-Severe pain with most bouts of acute otitis media (OM)
bouts fewer per year in the most severely -Long (weeks or more) periods of OM with effusion following
affected children, can be expected individual bouts of acute OM
-TTs did no better than amoxicillin in -Hearing loss of 25 dB or more with OM with effusion
preventing the onset of new OM, defined as -Attendance in a large-group (six or more children) childcare
setting
either acute OM behind an intact eardrum or -Language or developmental delays
otorrhea through a TT or TM perforation, but -Antibiotic allergies
TTs did significantly reduce the time with -Poor response to medical therapy
OM of any type compared with amoxicillin -First bout of OM prior to 6 months of age
-Older siblings
-both forms of management elicited -Craniofacial or syndromic anomalies predisposing to OM
significantly better results than placebo by -An underlying hearing loss
both measures -Balance disorder with acute OM
-rate of acute OM in the surgical group to be -Pacifier use
-Other medical conditions whose management is complicated
less than half that of the control group by OM
Persistent otitis media with effusion Factors making tympanostomy tube placement less desirable:
-various meta-analyses have reported -Mild symptoms with acute stages of infection
-Good response to medical therapy
short-term resolution rates between 16% and -Little or no hearing loss with OM with effusion
32%
-long-term resolution rates of 65% at 3 * A child with a history of four or more bouts of acute OM in the
months and 85% at 6 months last 6 months, six or more bouts in the last 12 months, three or more
months of bilateral OM with effusion, or 6 or more months of
-losses of 20 dB or more will certainly hinder unilateral OM with effusion.
the child’s understanding and appreciation of
his or her surroundings; whether it will also
lead to delays in short- or long-term speech
and language acquisition or have lasting consequences for cognitive development is debatable
-few small studies that have compared scholastic aptitude in children with unoperated OM with effusion
with those who had TT placement do not show significant differences
-TT placement should be seriously considered in cases of bilateral OM with effusion that has been present
for 3 or more months if the hearing loss in the better ear is 20 dB or greater
F.Ling - Tympanostomy Tubes (1)
962
Frequent otitis media in patients with an underlying sensorineural hearing loss
-the additional 10- to 30-dB hearing loss produced by a middle-ear effusion can significantly complicate
efforts to take advantage of residual hearing in patients with an underlying hearing loss
Cleft palate and other craniofacial abnormalities

-severe eustachian tube dysfunction with longstanding OM with effusion and hearing loss is the norm in
patients with cleft palate
-TT placement should be considered earlier and for a longer term in these patients because a fluctuating
conductive hearing loss can make habilitative efforts in these children more challenging
Suppurative complications of acute otitis media

-placement of at least a short-term TT may be warranted as an adjunctive measure when managing
complications such as mastoiditis, facial nerve paralysis, or intracranial otogenic infections
Severe tympanic membrane retraction with hearing loss, impending cholesteatoma formation, or ossicular
chain erosion
-untreated TM atelectasis is frequently complicated by the difficult problems of cholesteatoma and erosion
of the long process of the incus and eventual ossicular chain discontinuity
-TT retraction/atelectasis can frequently be completely reversed by timely TT placement
Hyperbaric oxygen therapy

-those undergoing hyperbaric oxygen therapy, 45% had middle-ear complications, including severe pain,
hemotympanum, and OM with effusion
-rate increased to 94% of patients who required an artificial airway during therapy and presumably could
not equalize middle-ear pressure during the ‘‘dive.’’
-TT placement effectively prevents these difficulties and should be considered for routine use in these
patients
PERIOPERATIVE CONSIDERATIONS
Tube selection
-most TTs are variations of the grommet or the T-tube
-generally speaking, the larger and stiffer the flange, the longer the tube remains in situ
-T-tubes will remain in situ for extended periods when designed with long, stiff flanges and is one of the
few tubes that is easily removed in the office without an anesthetic
-could potentially serve as either long- or short-term tubes
-disadvantage is the high reported rate of perforation
-perforation rate can be reduced to less than 10% if a short-flanged T-tube of soft
silicone is used
Insertion technique
-myringotomy is performed in the anterior portion of the TM to avoid the acoustically sensitive portion of
the drum
-classic dogma states that a radial incision is less damaging to the TM and that TTs will be retained longer
if placed in the anterosuperior quadrant
-a recent study showed no difference in TM sequelae with radial or circumferential incisions and no
difference in retention time based on location of incision
Antibiotic drops
-ototopic antibiotic drops can be considered in the immediate postoperative period in an effort to reduce
postoperative otorrhea, particularly when a mucoid effusion was evident during TT placement.
963
Swimming
-no consensus as to whether patients with TTs should be permitted to swim, and, if so, whether earplugs
are necessary
Follow-up
-assuming there are no other problems, the ears should be examined at least twice yearly to assess TT and
TM status
Removal of tympanostomy tubes

-indications for removal include chronic otorrhea, granuloma formation, tube blockage, migration of the
tube into the middle ear, and when external ventilation of the middle ear is no longer likely to be necessary
COMPLICATIONS
Anesthetic complications
Otorrhea
-most common complication following TT placement and will occur at some point during the life of the TT
for as many as 50% of patients
-likely to follow an upper-respiratory infection
Myringosclerosis
-tympanosclerotic plaques within the TM in 40% to over 50% of TMs after TT placement—which is much
higher than would be expected from a history of recurrent OM alone without TT placement
-a large series showed that this finding did not significantly affect hearing
Tympanic membrane perforation

-smaller-flanged, briefly retained grommet-style TTs will have a perforation rate of between 1% and 3%,
whereas larger-flanged, longer-lasting TTs such as the large-flanged, stiff T-tube may have perforation
rates as high as 30%
-most perforations caused by TTs are small, produce a hearing loss of less than 10 dB, and are easily
managed with a simple myringoplasty such as a fat patch
Tympanic membrane atrophy, retraction, and atelectasis

-focal thinning or atrophy of the TM is common following extrusion of the TT and healing of the
membrane (occurring in as many as 40% of ears requiring repeated intubations and in less than 15% of the
more general population receiving tubes)
-adhesions may form between the TM and promontory or other structures, and if the segment overlies the
ossicular chain, erosion of the incus may occur
-process may progress to cholesteatoma
Cholesteatoma
-may arise independently of the TTs in patients with longstanding eustachian tube dysfunction and
recurrent OM
-may also arise as a direct complication of TT placement, either in a retraction pocket that progresses to the
point of debris accumulation or as the result of ingrowth or transplantation of keratinized epithelium into
the middle-ear cleft
-longer retention associated with higher rates of cholesteatoma formation
964
DEVELOPMENT OF THE EAR
AURICULAR DEVELOPMENT
-5th week GA
-three hillocks arise from first branchial
(mandibular) arch: hillocks 1, 2, 3
-three hillocks arise from second branchial (hyoid)
arch: hillocks 4, 5, 6
-on either side of first branchial cleft
-8th week GA
-identifiable auricle
-hillock 1: tragus
-hillock 2: crus helices
-hillock 3: ascending helix
-hillock 4: horizontal helix, upper portion of scapha
and antihelix
-hillock 5: descending helix, middle portion of
scapha, antihelix
-hillock 6: antitragus and inferior aspect of helix
-18th week GA: auricle reaches adult form
DEVELOPMENT OF EXTERNAL AND MIDDLE EAR
External Auditory Canal

-begins in 4th week GA
-first branchial cleft widens and ectoderm
proliferates to form a pit forerunner of
cartilaginous external auditory canal
-becomes into apposition with endoderm of 1st
pharyngeal pouch
-8th weeks GA
-deep portion of EAC: a strand of epithelial cells
running down to the disc-shaped precursor of the
TM
-28th week GA
-epithelial core canalized from medial to lateral
aspect to allow communication with TM
-epithelial core is precursor of bony EAC
-Fissures of Santorini:
-lymphatic channels that connect the lateral
cartilaginous EAC to the parotid and glenoid fossa
region, allows for extension of infection and
malignant tumours
-Foramen of Huschke:
-embryological remnant that forms a defect that connects the medial EAC to the parotid and
glenoid fossa region, allows for extension of infection and malignant tumours outside the
temporal bone
F.Ling - Development of the Ear (1)
965
Tympanic Membrane
-trilaminar origin:
-ectoderm from floor of 1st branchial cleft epidermal layer
-endoderm of 1st pharyngeal pouch mucosa layer
-neural crest mesenchyme with cephalic mesoderm fibrous layer
-notch of Rivinus:
-notch of the squamose portion of the temporal bone located superiorly, within lies the pars
flaccida
Middle Ear Cavity

-develops from expanding terminal end of first pharyngeal pouch (tubotympanic recess)
-endodermal pouch surrounds ossicles and their supporting structures
-antrum begins development at 22 weeks
-formation of mastoid air cells late in fetal life
Ossicles
-main source of development of ossicles is neural crest
mesenchyme of first and second branchial arches
-Meckel’s cartilage (first arch)
-head of malleus
-body and short process of incus
-mandibular branch of CN V and tensor
tympani muscle
-Reichert cartilage (second arch)
-long process of incus
-handle of malleus
-stapes superstructure and tympanic surface
of stapes footplate
-facial nerve and stapedius muscle
-mesoderm of otic capsule
-vestibular surface of footplate
-annular ligament
-ossification of malleus and incus by 16th week GA and almost complete by 30th week GA
-ossicles reach their adult size at birth
Maldevelopment
-ossicular abnormalities:
-middle ear deformities without coexisting outer ear defects are unusual
-incudomalleolar fusion or fixation a common defect
-stapedial abnormalities are less common
-footplate may have normal mobility because of its separate development from otic
capsule
-persistent stapedial artery
-usually regresses at 10 weeks
-when the artery persists, a vessel arises from internal cartotid artery in hypotympanum, which
courses through the crura of the stapes to the fallopian canal enters fallopian canal and courses
forward to geniculate ganglion and to dura
-risk of bleeding during middle ear surgery (ie. stapedectomy or cochlear implantation)
-congenital cholesteatoma
-failure of atrophy of epidermoid formation in the anterior mesotympanum
966
DEVELOPMENT OF THE FACIAL NERVE
-facial nerve supplies second arch structures

-facial nerve in children: located higher and more superficial
-maldevelopment:
-congenital defects of outer and middle ear facial nerve lies more anteriorly and superficially in
the lateral temporal bone
-in atretic ears, facial nerve is abnormal in as many as 50% of cases
-dehiscence of fallopian canal common:
-~25% of temporal bones
-most common site is above the oval window
-10% coexistence of inner and middle/outer ear abnormality
DEVELOPMENT OF INNER EAR
Membranous Labyrinth
-develops from otic placode (3rd week GA)
-invaginate to become otocysts
subdivides into vestibular and cochlear
compartments and grows and
dramatically changes shape to achieve
adult form at 10 weeks and adult size
at 20 weeks GA
-sensory epithelium of cochlea develops at 7th
week GA as the duct grows and begins to coil
-hair cells begin to develop from base to
apex
-inner cells develop before outer cells
-afferent nerves develop before efferent
nerves
-endolymphatic duct and sac continue to grow
into the third trimester
-while otocysts is dividing into vestibular and
cochlear portions, the vestibulocochlear ganglion
divided into a superior and inferior division:
-superior:
-superior and lateral ampullae
of SCC
-utricle
-inferior:
-posterior ampulla
-saccule
-periotic duct:
-within cochlear aqueduct
-connects scala tympani to posterior cranial fossa
-ductus reunions:
-narrowest segment between cochlea and saccule
Osseous Labyrinth
-perilymph-filled osseous labyrinth
-derived from the labyrinthin capsule from periosteal and enchondral ossification (susceptible to bony
967
diseases such as Paget’s, osteodystrophies, or otosclerosis)
-most important aspect is resorptive process in mesoderm that separates membranous from developing
bony otic capsule
-cochlear aqueduct:
-begins in inner ear at base of scala tympani subarachnoid space in posterior cranial fossa
-vestibular aqueduct:
-contains endolymphatic duct and veins of vestibular aqueduct
-runs from vestibule to posterior surface of petrous pyramid in posterior cranial fossa (opening is
the operculum)
Otic Capsule
-develops from 14 centers of ossification
-achieves adult size by week 22 GA
-precartilaginous precursor appears in 7th week from cephalic
mesoderm
-oval window formed in the ninth week vestibular surface of
footplate
-rim of footplate and facing rim of window remain
cartilaginous
-round window forms adjacent to basal turn of cochlea
Maldevelopment
-categorization:
-membranous labyrinth anomalies alone (80%)
-osseous and membranous labyrinth anomalies (20%)
-inner ear abnormalities caused by arrested or aberrant
development
-genetically predetermined
-insult can occur before 5th week GA
968
-separate portions of developing system can be variably susceptible to teratogenic insult
Membranous Labyrinth Anomalies:
-Scheibe:
-described the most common histopathologic finding in congenital deafness
-cochleosaccular dysplasia due to incomplete development of caudal portion of the otocysts (pars
inferior)
-organ of Corti typically partially or completely missing
-cochlear duct and saccule are collapsed
-stria vascularis is degenerated
-utricle and SCC are normal
-Bing-Siebemann dysplasia:
-complete membranous labyrinthine dysplasia
-rare
-most severe membranous abnormality
Combined Membranous-Osseous Anomalies:

-most combined membranous-osseous labyrinth abnormalities appear to be caused by arrested development
between fourth and eighth weeks GA
-Michel malformation:
-disruption of development before 4th week
-most severe abnormality of labyrinthine development
-complete aplasia
-failure of otic vesicle to develop
-disruptions at week:
-4 common cavity (can still be implanted)
-5 cochlear aplasia
-early 6 cochlear hypoplasia (severe)
-late 6 cochlear hypoplasia (mild)
-early 7 incomplete partition of cochlea: Mondini
malformation (severe)
-late 7 incomplete partition: Mondini malformation
(mild)
-dysplasia of SCC caused by failure of central epithelial fusion

-lateral SCC most commonly affected
-40% of ears with osseous cochlear abnormalities have
concomitant abnormalities of SCCs
-enlarged vestibular aqueduct

-most common radiologically detectable abnormality of inner ear
-can be acquired by increased CSF pressure
-due to congenital defect of cochlear modiolus at distal end of IAC increased CSF pressure
enlarged VA
-findings on CT:
->2 mm at mid-portion of canal
-larger than width of lateral SCC
-significance: minor head trauma can cause hearing loss; hearing may fluctuate
969
-narrow internal auditory canal
-can indicate failure of development of CN VIII
-if < 3 mm and normal facial function, it is likely that only the facial nerve is present
-this condition is a contraindication to cochlear implantation
970
ANATOMY AND PHYSIOLOGY OF HEARING
EXTERNAL EAR
-EAC ~ 2.5 cm long

-lateral 1/3 of EAC:
-cartilaginous
-cerumen-producing glands and hair follicles
-concha:
-resonance of 5 kHz; irregular surface introduces other resonances and antiresonances
-allows differentiation of sound sources in front and from behind
-acoustic properties of external ear are one of reasons noise-induced hearing losses occur first and most
prominently at the 4-kHz region (boilermaker notch)
-sound localization:
-head shadow effect:
-head is an attenuator at frequencies where width of head > wavelength of sound
-frequencies > 2 kHz interaural intensity differences of 5-15 dB used to localize sound
sources
-at lower frequencies, little attenuation is provided by the head
-also explains hearing loss in hunters - loss is in opposite ear because the opposite ear is
closer to where acoustic energy is greatest while the other is protected by the head
shadow effect
-interaural time differences (0.6 ms for sound to travel across the head)
-resonance of EAC is 8 kHz in infants and decrease to adult values (3.5 kHz) after 2.5 ya
F.Ling - Anatomy and Physiology of Hearing (1)
971
MIDDLE EAR
-impedance matching device: couples low impedance of air to high impedance of fluid filled cochlea
-impedance matching achieved by
1. effective vibratory area of tympanic membrane ~17-20x greater than that of stapes footplate
2. lever action of ossicular chain
-arm of long process of incus shorter by factor of 1.3 than length of manubrium and neck of
malleus
3. shape of tympanic membrane
-transforming ratio:
-22:1 = (17x1.3):1
-results in pressure gain of ~ 25-30 dB
-TM protects round window by allowing a phase difference between sound conducting to the oval
window and sound directly reaching the round window; if sound waves would strike the oval and round
windows simultaneously, the resultant forces would suppress the cochlear fluid wave
-effects of conductive system defects and hearing loss:

-isolated tympanic membrane perforation: 30-45 dB CHL
-tympanic membrane perforation and ossicular chain discontinuity: 40-50 dB CHL
-intact tympanic membrane and ossicular chain discontinuity: 55-60 dB CHL
-other roles of TM:

-protection from FB, maintenance of air cushion that prevents insufflation of FB from
nasopharynx
-middle ear system is highly damped and linear and has a wide frequency response
-less than half of power entering middle ear actually reaches the cochlea
-cannon shot experiments in cats showed:
-low frequency energy is not transmitted to cochlea and frequency region of greatest energy
concentration is 3-4 kHz
-explains ability of intense low-frequency sounds to produce high-frequency HL
-middle ear muscles:
-tensor tympani muscle
-attaches to malleus and innervated by trigeminal nerve
-does not normally respond to intense acoustic stimulation
-stapedius muscle
-attaches to stapes and innervated by stapedial branch of facial nerve
-functions:
-protect cochlea from loud sounds
-sounds > 80 dB SPL results in consensual reflex contraction of stapedius
attenuates sounds less than ~ 2 kHz
-if latency of acoustic reflex > 10 ms, cochlea may be unprotected from short-duration,
unanticipated impulsive sounds
-general functions of middle ear muscles:
-provide strength and rigidity to ossicular chain
-contributing to blood supply of ossicular chain
-reducing physiologic noise caused by chewing and vocalization
-improving signal-to-noise ratio for high-frequency signals by attenuating high-level,
low-frequency background noise
-automatic gain control and increasing dynamic range of ear
-smoothing out irregularities in middle-ear transfer function
972
-resonance frequencies:
-natural frequencies that vibrate a mass with the least amount of force
-concha: 4-6 kHz
-EAC: 2-3 kHz
-TM: 0.8-1.6 kHz
-ossicles: 0.5-2 kHz
-middle ear: 0.8 kHz
COCHLEA
-35 mm coiled bony tube; ~2.5 turns

-divided into:
-scala vestibuli and tympani
-contains perilymph; ECF-like: [Na]140 mM > [K] 10 mM
-production of perilymph:
-unknown
-thought to be an ultrafiltrate of blood
-may also be from CSF
-scala media
-located in between scala vestibuli and tympani
-contains endolymph; ICF-like: [K] > [Na] (15-25 mM)
-bounded by Reissner’s membrane, basilar membrane and osseus spiral lamina and
lateral wall
-stria vascularis in lateral wall:
-highly vascularized
-cells contain Na-K-ATPase to produce endocochlear potential of ~80 mV
973
-production of endolymph:
-marginal cells of stria vascularis
-dark cells of cristae and maculae of vestibule
-sound transmission and transduction:
-stapes footplate oval window perilymph of scala vestibuli helicotrema (opening at apex
of cochlea) perilymph of scala tympani
-basilar membrane
-0.12 mm wide at base and increases to 0.5 mm at apex
-base more stiff than flexible apex
-organ of Corti
-rests on basilar membrane and osseous spiral lamina
-components:
-outer and inner hair cells
-supporting cells: Deiters, Hensen, Claudius
-tectorial membrane
-reticular lamina-cuticular plate complex
-supporting cells provide structural and metabolic support for organ of Corti
-inner and outer hair cells
-differing morphology and innervation
-spiral ganglion: cell body of auditory nerve, axons to cochlear nucleus in brainstem and
dendrites project through osseous spiral lamina
-50,000 neurons innervate cochlea:
-90-95% synapse directly on inner hair cells (Type I neurons)
-predominantly afferent
-15-20 of these neurons innervate each inner hair cells
-5-10% synapse directly on outer hair cells (Type II neurons)
-predominantly efferent
-each type type II neuron branches to innervate ~ 10 outer hair cells
974
-transduction: displacement of basilar membrane
-basilar membrane stiffer at base than apex - travelling wave progresses from base to apex
-peak or maximum amplitude of basilar membrane displacement varies as function of stimulus
frequency:
-high frequency: max displacement at base
-low frequency: max displacement at apex
-cochlear amplifier:
-activity of outer hair cells that enhances motion of basilar membrane at frequencies near
the best frequency of the particular cochlear location
-out hair cells shorten and lengthen when stimulated by sound
-contributes to fine frequency-selective abilities of ear and sensitivity and ability to detect
extremely faint sounds
-produces the “tuning curve” seen when sound intensity is plotted against
frequency
-notion of cochlear amplification supported by phenomenon of otoacoustic emissions
-stereocilia-hair cell complex
-stereocilia of outer hair cells are in direct contact with tectorial membrane
-deflection of sterocilia by travelling wave opens and closes non-specific ion channels
influx of K depolarization of cell intracellular enzyme cascade (Ca++ mediated)
release of chemical transmitters (glutamate) activate afferent neural fibers
-recruitment:
-loudness in abnormal ear that grows abnormally quickly with intensity once threshold is
reached due to loss of outer hair cells (tips of tuning curve missing)
Gross Cochlear Potentials
-four potentials:
-endolymphatic (endocochlear) potential
-cochlear microphonic
-summating potential
-whole-nerve action potential
-endolymphatic potential:
-not generated in response to acoustic stimuli
-DC potential of 80-100 mV recorded in scala media
-arises from stria vascularis
-related to heavy vasculature of stria vascularis and to Na-K-ATPase
-cochlear microphonic:
-alternating AC current
-represents potassium ion current flow though outer hair cells
-waveform mirrors motion of basilar membrane
-summating potential:
-DC potential recorded in response to sound
-largely reflects DC shifts caused by stimulus-driven intracellular potentials of outer hair cells
-represents asymmetry in basilar membrane movement resulting from pressure difference between
scala tympani and scala vestibuli during sound stimulation
-whole-nerve (compound) action potential:
-arises from all-or-none discharge of auditory nerve fibers
975
NONLINEAR PROPERTIES OF THE EAR
Otoacoustic Emissions (OAE)

-cochlea can generate and amplify sound
-several types of OAE:
-spontaneous:
-occurs in absence of acoustic stimulation
-SPLs of 10-30 dB
-cochlear echo or transiently evoked:
-evoked by short-duration or transient acoustic signal
-stimulus-frequency:
-produced by low-level pure tones
-emission has most of its energy at stimulating frequency
-distortion product:
-two primary tones presented to cochlea distortion products produced
-middle ear system must be normal
-provides information about the integrity of the cochlear transducer
-most sensitive measure of hearing loss among children: useful for screening
AUDITORY CENTRAL NERVOUS SYSTEM
-cochlea cochlear nucleus superior olivary complex lateral lemniscus inferior colliculus medial
geniculate body of thalamus auditory cortex (at Sylvian Fissure of Temporal Lobe - Brodmann’s area 41)
-extensive contralateral innervation
-tonotopic organization from basilar membrane to cortex

-high-frequency sounds localized to base
-low-frequency sounds localized to apex
-evoked potentials:
-PI and PII generated by spiral ganglion cells
-PIII generated by spherical cells of cochlear nucleus
-PV generated by cells of medial superior olive which projects to lateral lemniscus
976
VESTIBULAR FUNCTION AND ANATOMY
-detection of angular acceleration: 3 SCC (posterior, lateral, anterior)

-detection of linear acceleration: maculae utriculus and sacculus
-R+L utricles in same plane as R+L lateral SCCs

-R+L saccules are perpendicular to utricles
END ORGAN SENSORS
Hair Cells
-stereocilia and kinocilia extend from cell body and in contact with
gelatinous membrane
-bending of hair cells opens K-channels changes resting potential
-two cell body types:
-type I (chalice cells)
-totally engulfed by one afferent terminal
-efferent innervation is indirect with efferent
nerve synapsing on afferent nerve
-type II (cylindrical)
-may have one or more afferent nerve endings on
body of cell
-direct and indirect efferent innervation of hair
cell body
-kinocilium:
-longest and largest hair cell occurring near periphery of
cell body
-polarization vector of hair cells toward kinocilium
-deflection of hair cells toward excitation
-deflection of hair cells away inhibition
F.Ling - Vestibular Function and Anatomy (1)
977
Semicircular Canals
-torus-shaped; filled with endolymph (density, viscosity of

water)
-cupula completely seals one side of ampulla from the other
-deflection of cupula bends stereocilia within
-each canal exhibits a resting basal discharge rate
-in lateral SCCs:
-both lateral semicircular canals lie in same plane,
tilted 30o from the horizontal and runs parallel to
line between external auditory canal and outer
canthus
-kinocilia are closest to vestibule:
-maximal excitation occurs with
ampullopetal flow of endolymph
-displacement away (ampullofugal) flow
causes decrease in firing rate
-in posterior and anterior SCCs:
-kinocilium is farthest from vestibule:
-ampullofugal flow is excitatory
-ampullopetal flow is inhibitory
Pairing of Canals
-functional canal pairs:
-R+L lateral SCCs
-R anterior SCC and L posterior SCC
-L anterior SCC and R posterior SCC
-angular rotation perpendicular to any of these planes produces maximum response from the two canals in
that plane
-operate in push-pull manner:
-movement directed along maximum excitation of one member of the pair produces maximum
inhibition in the other member
Blood supply
-labyrinthine artery (arises from anterior cerebellar artery, superior cerebellar artery or basilar artery)
anterior vestibular artery utricle, posterior and horizontal ampullae
common cochlear artery
proper cochlear artery
vestibulocochlear artery
cochlear ramus
vestibular ramus posterior ampulla, sacculus, utricle, horizontal and
superior ampullae
Otolith Organs
-inertial mass component: calcium carbonate crystals = otoconia
-hair cells project into gelatinous supporting substrate
-each has sensory hair cells arranged in wide variety of orientations of its polarization vectors
-striola: line of orientation of hair cells in the utricle and saccule around which the polarity of the sensory
cells changes 180o
-orientation of polarization vector:
-away from striola in saccular macula; toward striola in utricular macula
978
Afferent Connections
-afferent nerve fibers are bipolar: one synapse at hair cell, other in
vestibular nucleus
-cross-connections are present between right and left vestibular
nuclei
-superior vestibular nerve innervates:
-anterior SCCs
-horizontal SCCs
-utricle
-inferior vestibular nerve innervates:
-posterior SCCs
-saccule
PHYSIOLOGY OF BALANCE
Vestibulo-Ocular Reflex (VOR)

-head rotation in a plane results in an opposite eye rotation to
allow the eye to maintain fixation on an object
-eg. motion of 10o to left produces eye movement 10o to right
-head turns to left
-left horizontal SCC:
-fluid flows toward ampulla (ampulopetal flow)
-deflection of haircells toward kinocilium
-relative stimulation
-right horizontal SCC:
-fluid flows away from ampulla (ampullofugal
flow)
-deflection of hair cells away from kinocilium
-relative inhibition
-eyes move toward side of inhibition (right)
Vestibulospinal Reflex
-otolithic organs modulate the antigravitational muscles in a similar way as the vestibulo-ocular reflex
modulates the eye to allow for postural control
-eg. simultaneous contraction of the extensor muscles with contralateral flexor muscles to maintain posture
-position and motion of muscles and joints may also modify vestibulospinal reflex via receptors found in
intervertebral joint receptors
Semicircular Canals Activation and Extraocular Muscle Excitation/Inhibition
-anterior SCC:
-excitatory: ipsilateral SR, contralateral IO
-inhibitory: ipsilateral IR, contralateral SO
-horizontal SCC:
-excitatory: ipsilateral MR, contralateral LR
-inhibitory: ipsilateral LR, contralateral MR
-posterior SCC:
-excitatory: ipsilateral SO, contralateral IR
-inhibitory: ipsilateral IO, contralateral SR
979
Caloric Testing
Cold water calorics:

-cool water endolymphatic fluid drops
-causes ampullofugal flow in SCC
-deflection of haircells away from kinocilium
-relative inhibition on involved side
-causes slow drift of eyes towards involved side
-compensatory saccades in the opposite direction (“cold-opposite”)
-note: same response seen in negative pressure fistula test
Warm water calorics:

-warm water endolymphatic fluid rises
-causes ampullopetal flow in SCC
-relative excitation on involved side
-causes slow drift of eyes towards opposite side
-compensatory saccades in the same direction as stimulus (“warm-
same”)
-note: same response seen in positive pressure fistula test
*slow phase of nystagmus is in direction of flow of endolymph fluid
980
BALANCE FUNCTION TESTS
-formal balance function testing indicated when:

-site and side of lesion cannot be identified through history or physical examination
-ascertain who is likely to benefit from vestibular rehabilitation
-assess recovery of vestibular function
-document contralateral function when a destructive procedure is contemplated
ELECTRONYSTAGMOGRAPHY ENG INTERPRETATION
-vestibular subtests: Findings suggestive of central disorder:

-spontaneous nystagmus -spontaneous or positional nystagmus with normal caloric
results
-gaze nystagmus -direction-changing nystagmus independent of stimulus
-positional nystagmus evaluation changes
-positioning nystagmus -failure of fixation suppression
-fistula test -bilateral reduced or absent caloric responses without a history
of labyrinthine or middle ear disease
-bithermal caloric tests -abnormal saccades or pursuit results, especially with normal
-oculomotor subtests: caloric results
-pursuit system evaluation -hyperactive caloric responses (loss of cerebellum-generated
-saccadic system inhibition - “cerebellar clamp”)
-optokinetic system evaluation Findings suggestive of peripheral disorder:
-fixation system evaluation -unilateral caloric weakness
-bilateral caloric weakness with hx of labyrinthine disease or
-tests based on vestibuloocular reflex (VOR) administration of ototoxic drugs
-fatiguing positional nystagmus
-corneal-retinal potential (cornea + -intact fixation suppression response
and retina -) -direction-fixed nystagmus
-electrooculography (EOG)
-nystagmus:
-direction: horizontal, vertical, torsional
-determined by fast component
-velocity: degrees per second
-calculated from slow-phase component
-significant if greater than 6 degrees per second
Type of Nystagmus
-gaze
-induced (eg. calorics)
-positional
-spontaneous
Spontaneous and Gaze Nystagmus

-spontaneous nystagmus: nystagmus recorded with eyes open
-latent nystagmus: nystagmus recorded with eyes closed
-peripheral lesion:
-increasing nystagmus with eyes closed
-unidirectional and unchanging
-central lesions:
-failure of fixation suppression
-direction changing nystagmus irrespective of eye movement
F.Ling - Balance Function Tests (1)
981
Positional and Positioning Tests
-patient moved slowly into series of stationary positions with eyes closed and presence or absence of
nystagmus is assessed
-Dix-Hallpike manoeuver used
-torsional nystagmus cannot be measured by ENG
-head hanging:
-right: counterclockwise torsional nystagmus
-left: clockwise torsional nystagmus
-peripheral lesion:
-direction of nystagmus does not change independently of head movement
-central lesion:
-direction-changing nystagmus without an accompanying change in head position
Bithermal Caloric Tests

-evaluates function of horizontal SCC
->20% difference considered abnormal; reported as left- or right-sided weakness
->30% difference in directional preponderance considered significant
-abnormal directional preponderance without unilateral weakness suggests central pathology
-bilateral weakness is suggested when the total caloric maximum slow phase velocity from each ear is < 12-
24o/second
ENG Fistula Test

-objective nystagmus or clear subjective response to positive or negative middle ear pressure suggests
perilymph fistula or dehiscence of horizontal or superior portion of SCC
Saccadic System
-latency, maximum velocity, duration, gain (overshoot or undershoot), refixation saccades, glissade
(postsaccadic drift, or slip of the eye) measured
-abnormal saccadic response caused by lesions in cerebellum (dorsal cerebellar vermis), brainstem
(paramedian tontine reticular formation and MLF) or ocular muscles and nerves
-cerebellar lesions saccadic overshoot or undershoot dysmetria
-age, fatigue, lack of attention, sedatives, drug intoxication and other factors can cause slow saccades or
increase latency
Pursuit System
-healthy pts can pursue object moving at velocity of 30 degrees per second
-gain, phase lead or lag, symmetry are measured
-anatomic localization usually not possible
-saccadic pursuit suggests cerebellar disease
-reduced bilateral gain can be caused by brainstem lesion
Optokinetic System
-keeping pt stationary and moving environment
-separating smooth pursuit system and optokinetic system can be difficult
-if lights are extinguished, SP system response drops to zero pts continue to have nystagmus for ~25s
(optokinetic afternystagmus OKAN)
-abnormalities are not site specific
-not routinely used
982
ROTARY CHAIR, SINUSOIDAL HARMONIC ACCELERATION
-offers higher frequency conditions than calorics

-stimulus precisely controlled and is repeatable
-both ears tested simultaneously represent integrated function of both ears
-acceleration frequencies: 0.01-1.28 Hz with maximum velocity of 50 degrees/s
-chair rotates right compensatory movement of eye left saccadic eye movement returns eye to central
position
-useful for:
-monitoring changes in vestibular function over time, especially bilateral lesions or lesions due to
vestibular toxicity
-monitoring compensation after acute injury
-identifying residual labyrinthine function for pts with no response during caloric testing or low
frequency rotatory chair testing
-measurements:
-phase
-relations between maximum chair velocity and maximum slow-phase velocity
-phase-lead: eye velocity typically leads chair velocity
-often exaggerated in pts with central or peripheral vestibular disease
-gain
-ratio of maximum eye velocity to maximum chair velocity
-gain of one indicates that slow-phase eye velocity equals chair velocity and is opposite
in direction
-gain of 0 is no eye movement
-depressed gain values under good testing conditions suggest bilateral peripheral lesions
-abnormally high gain can indicated cerebellar lesion that is decreasing vestibular
inhibition
-highly variable
-symmetry of eye movement
-compares peak slow-wave velocity when pt rotated to left and peak slow-wave velocity
with rotation to right
-if acute, uncomplicated unilateral weakness, the symmetry measure shows weakness on
the affected side
VESTIBULAR AUTOROTATION TEST
-evaluates VOR
-pts wired with conventional EOG and fitted with head band with EOG amplifier and rotational velocity
sensor
-pt fixes on stationary target and rotate head in synchrony with auditory cue (max 6 Hz)
-vestibular system evaluated at frequencies more physiologic than ultralow frequencies used in ENG and
rotational chair testing
-clinical value questionable with sensitivity of only 27% and specificity of 85%
DYNAMIC POSTUROGRAPHY
-eliminates visual and somatosensory input and therefore better isolates the vestibular apparatus
-two tests:
-sensory organization test
-movement coordination test
983
-sensory organization test:
-evaluation under six conditions in which sensory and proprioceptive inputs are varied
-anterior and posterior body sway is recorded
1. Eyes open, fixed surface and visual surround.

2. Eyes closed, fixed surface.
3. Eyes open, fixed surface, sway referenced visual surround.
4. Eyes open, sway referenced surface, fixed visual surround.
5. Eyes closed, sway referenced surface.
6. Eyes open, sway referenced surface and visual surround.
-anterior and posterior body sway is recorded

-12o body sway is estimated maximum without falling
-movement coordination test:

-visual surround fixed
-platform undergoes series of translational and rotational movements
-measures:
-latency to onset of active recovery from destabilizing perturbation
-amplitude and symmetry of neuromuscular responses
-assesses patient's ability to quickly and automatically recover from unexpected external
provocations
-adaptation test (ADT):

-assesses the patient's ability to modify motor reactions and minimize sway when support moves
unpredictably in the toes-up or toes-down direction
-for each platform rotation, a sway energy score quantifies the magnitude of the force response
required to overcome induced postural instability
984
985
ASSESSMENT OF PERIPHERAL
AND CENTRAL AUDITORY FUNCTION
PHYSICS OF SOUND
Measurements of Intensity
-decibel (dB):
-unit of measurement of sound pressure or intensity based on a logarithmic ratio
-dB = 10 log (Ioutput/Ireference) = 10 log (Poutput2/Preference2) = 20 log (Poutput/Preference)
-I = P2; P = unit of sound pressure level
-Preference = 2x10-4 dyne/cm2
Reference Levels of the Decibel

-Hearing Level (HL):
-threshold dB based on normative hearing data as a reference
-0 dB hearing loss is the least intensity for the average normal ear to perceive a specific frequency
-biologic reference level, rather than sound pressure level
-audiometric 0:
-mean normal hearing threshold level
-minimal detectable intensity for each test frequency for persons with normal hearing
-Sensation Level (SL):
-level in dB above an individuals threshold
Sound Intensity
-whispered speech ~ 25 dBHL
-conversational speech ~ 40-50 dBHL
-shouting ~80dBHL
Rinne Test and Conductive Hearing Loss

-if Rinne negative then ABG is at least:
-15 dB for 256 Hz
-25 dB for 512 Hz
-35 dB for 1024 Hz
BASIC AUDIOLOGIC TEST BATTERY
Pure-Tone Audiometry
-degree of hearing loss:
-mild: 20-40 dBHL
-moderate: 40-60 dBHL
-moderate-severe: 60-80 dBHL
-severe: 80-100 dBHL
-profound: > 90-100 dBHL
-speech frequencies: 500-4000 Hz
-audiometry uses pure tones at 250, 500, 1000, 4000 and 8000 Hz (octave frequencies); interoctave
frequencies: 3000 and 6000 Hz
-Pure-Tone Average (PTA):
-average hearing thresholds for 500, 1000, and 2000
-typically should be within 10 dB of speech reception threshold
F.Ling - Audiology (1)
986
-crossover:
-occurs with sounds greater than 40 dBHL
-interaural attenuation for air conduction ~ 50dB for lower frequencies and 60 dB for higher
frequencies
-interaural attenuation for bone conduction assumed to be 0 dB
-masking required to prevent crossover phenomenon
-masking:
-uses “white noise” = narrow band noise for pure-tone signals and speech noise for speech signals
-bilateral ABG of 50 dB cannot be masked (masking dilemma)
-configuration:
-hearing loss as a function of test frequency
-low frequency SNHL: characteristic of endolymphatic hydrops
-high frequency SNHL: characteristic of presbycusis
-bilateral down-sloping high frequency SNHL: characteristic of presbycusis
-Carhart’s Notch: falsely depressed bone conduction peaking at 2000 Hz suggestive of
otosclerosis, secondary to a reduction of the inertial component of bone conduction
-4 kHz Notch (Boilermaker Notch): high frequcny SNHL at 4000-5000 Hz that occurs with NIHL
-Cookie Bite (U-shape): associated with hereditary hearing impairment
-Recruitment:
-increasing signal intensity produces an out-of-proportion perception of loudness
-suggests cochlear hearing loss
-recruitment causes discomfort within a shorter range of the SRT (normally 95 dB above SRT
causes discomfort)
Guidelines for Evaluation of Hearing Handicap

-determine loss as a percentage
-sum DHL at 500, 1000, 2000 and 3000 Hz
-determine percentage of monaural hearing impairment from table (AAOCHE)
%hearing handicap = (5x %[better ear] + %[poorer ear])/6
Speech Audiometry
-speech reception threshold (SRT):
-softest intensity level at which pt can correctly repeat words ~50% of the time
-uses spondee words: two syllable words with equal stress on each syllable
-if difference between PTA and SRT exceeds +/- 7 dB - suspect malingering
-speech recognition
-uses phenomes: phonetically balanced words; 25-50 single-syllable words
-phenomes are presented at 30-40 dB above SRT/PTA
-percentage of correct words repeated is recorded
-rollover:
-a paradoxical decrease in discrimination ability with increasing signal intensity
-suggestive of a retrocochlear disorder
Aural Immittance (Impedance) Measurement

-impedance:
-tone delivered toward TM
-middle ear with low impedance more readily accepts acoustic energy of probe tone; abnormally
high impedance (eg. fluid) tends to reject energy flow
987
Tympanometry:
-dynamic recording of middle ear impedance as air pressure in EAC systematically increased or decreased
-classification of middle ear disorders:
-Type A:
-peak in compliance within +50 to -100 mmH2O
-normal
-Type As:
-s = “shallow”: peak compliance less than lower normal limit of compliance
-middle ear impedance abnormally high (stiff):
-otosclerosis, tympanosclerosis
-Type Ad:
-d= “deep”: peak compliance exceeds upper compliance limits
-ossicular disruption, flaccid TM, monomeric TM
-Type B:
-flat
-associated with presence of middle ear fluid
-sometimes seen for perforated TMs
-Type C:
-peak within negative pressure region beyond -100 mmH2O
-eustachian tube dysfunction and inadequate ventilation of middle ear space
Acoustic Stapedial Reflex Measurement

-measurement of contractions of stapedial muscle in response to high sound intensity levels (>80dB)
-usually measured at 500, 1000, and 2000 Hz
-reflex arc:
-afferent portion (8th nerve) cochlear nucleus trapezoid body bilateral superior olive
motor nucleus of CN VII contraction of stapedius
-small change in compliance that follows stapedius muscle contraction within 10 ms is detected
-provides objective information on status of auditory system from middle ear to brainstem
-CHL:
-may not be able to stimulate response initially if > 40 dB CHL in receiving ear or may not be able
to receive signal because ossicles cannot transmit stapes signal to TM in probe ear
-SNHL:
-may not be able to stimulate response initially if >60 dB
988
-absence of reflexes:
-minimal CHL (5-10 dB)
-SNHL (>60 dB)
-mild CN VIII impairment (0-40 dB)
-brainstem lesion
-CN VII dysfunction proximal to stapedial branch
Acoustic Reflex Decay Test

-measures maintenance of stapedial reflex for sustained signal at 10 dB SL for 10 seconds
-decay of < 50% abnormal suggestive of retrocochlear lesions
AUDITORY EVOKED RESPONSES

-electrophysiologic recordings of responses
to sounds
-generated with clicks or tone bursts
-occurs during first 10-20 ms after the
stimulus
-surface electrodes utilize signal averaging
to record specific ABR waves
-SNHL > 85 dB would preclude ABR
-indications:
-asymmetric hearing loss
-unilateral vestibular weakness
-unilateral tinnitus suggestive of
retrocochlear pathology
-high risk children or with failed
auditory screening
-suspected malingerers
-intraoperative monitoring
-diagnosis of peripheral
neuropathies and brainstem lesions
-unaffected by sedation; affected by
phenytoin, lidocaine, diazepam, and
halothane
ABR waves:
-I: compound action potentials from distal
(cochlear end) of eighth CN
-II: proximal end of eighth CN
-III: caudal pons (cochlear nuclei, trapezoid
body, superior olivary complex)
-V: lateral lemniscus as it approaches inferior colliculus
-reproducible absolute latencies for each wave component and relative (interwave) latencies b/n
components are calculated in milliseconds
-latency data assessed for symmetry and compared to appropriate normative data
989
-conductive or mixed hearing loss:
-well-formed and clear wave 1 at a
delayed latency value for
maximum stimulus intensity level
-cochlear hearing loss:
-small and poorly formed wave I
-normal interwave latency values
-wave I-V latency value < 4.60 ms
-retrocochlear auditory dysfunction
1. Abnormal interaural wave V
latency difference (IT5)
- > 0.2 msec
-may be relative to size of
tumour
2. Abnormal interaural wave I-
V latency difference (IT1-5)
3. Abnormal III-V latency
difference (IT3-5)
4. Prolonged interwave latency
between I-V(T1-5) or I-III
(T3-5)
5. Increased absolute latency
measurements:
-5.7 msec for wave V
-compared with normal standard
-may not be as accurate since latency may be affected by CHL
-wave I is the benchmark for peripheral auditory function

-identification of retrocochlear disorders with accuracy > 95%
-false-negative results with small intracanicular
vestibular schwannomas
Electrocochleography (EcoG)
-indications:
-direct measurement of cochlear and auditory
nerve function
-for intraoperative monitoring of cochlear and
8th nerve status
-diagnosis of Menieres
-three major components:
-cochlear microphonic (CM)
-summating potential (SP)
-compound action potential (AP)
-CM and SP reflect cochlear bioelectric activity

-AP generated by synchronous firing of distal afferent
8th nerve fibers and is equivalent to ABR wave I
-ratio of SP/AP calculated:
-abnormal if
-> 50% for ear canal electrode type
-> 40% for tympanic membrane
electrode
990
-> 30% for transtympanic electrode (on promontory)
-Menieres:
-abnormal enlargement of relation b/n component amplitudes of SP and AP; large SP/AP ratio
highly suggestive of endolymphatic hydrops
-tympanic electrode: sensitivity 57%, specificity 94%
Cortical Auditory Evoked Responses

-characterized by longer latencies (100-300 ms) than ECoG waveforms and ABR
-more rostral regions of auditory CNS and depend on multisynaptic pathways
-recording electrodes usually on scalp rather than near ears
Auditory middle latency response (AMLR)

-generated by pathways leading to primary cortex and from temporal-parietal region of temporal lobe
-for electrophysiologic assessment of higher level auditory CNS function of pts at risk of or undergoing
evaluation of neurologic disease or dysfunction involving thalamus or primary auditory cortex
Auditory late responses
P300 response
-oddball paradigm: two stimuli, one frequent predictable stimulus, one rare or deviant stimulus
-pt try to attend to rare stimuli produces large positive peak in 300 ms region
-presumed generators are regions of medial temporal lobe (hippocampus) that are important in auditory
attention
-requires attention to the stimuli
Mismatch negativity response (MMN)

-recorded to frequent and rare stimuli; the distinction between the two types of stimuli are very small
-thought to be generated before conscious perception by neuronal mismatch in the brain
-does not require attention to the stimuli
OTOACOUSTIC EMMISIONS
-low-intensity sounds produced by cochlea in

response to an acoustic stimulus CLINICAL APPLICATIONS OF OTOACOUSTIC
EMISSIONS
-outer hair cell movement affects basilar
membrane biomechanics intracochlear Children
energy amplification and cochlear tuning for -newborn hearing screening
precise frequency resolution -diagnostic pediatric audiology
-monitoring ototoxicity
-outer hair cell motility generates mechanical -assessment of auditory processing disorders
energy within cochlea that is propagated -assessment of suspected functional hearing loss
outward through middle ear to TM
-vibration of TM produces an acoustic signal Adults
-early detection of noise induced cochlear dysfunction
(the OAE) which can be measured by a -monitoring of cochlear status in potential ototoxicity
sensitive microphone -differentiation of cochlear versus retrocochlear auditory
-cochlear disorders > 30 dB hearing loss and dysfunction
-assessment in suspected functional hearing loss
middle ear disease may not have OAE
-confirmation of cochlear dysfunction in patients with
tinnitus
-two classes: spontaneous and evoked
-spontaneous OAE:
-measured in EAC when
there is no external sound stimulation
991
-occur among 60% of persons with normal hearing
-stimulus-frequency OAE:
-least studied of the evoked OAE
-distortion-product OAE:
-two pure-tone stimuli are presented to the ear simultaneously
-determined by the equation: 2f1-f2
-actual cochlear frequency region assessed is closer to f2 stimulus
-ideally ratio of f1/f2 ~ 0.22
-transiently evoked OAE:
-elicited with brief acoustic stimuli such as clicks or tonebursts
-when outer hair cells are structurally damaged or non functional, OAEs cannot be evoked
-OAE provide information about auditory function at far more frequencies than does an audiogram
-advantage: used in pts with tinnitus and normal audiogram (30% of outer hair cells can be
damaged without affected audiogram)
ASSESSMENT OF AUDITORY PROCESSING DISORDERS (CENTRAL AUDITORY DISORDERS)
Risk Factors for Central Auditory Nervous System Dysfunction

-in uteri infection, bacterial infection, asphyxia, hyperbilirubinemia, head trauma, intraventricular
haemorrhage
-in adults: advanced age, stroke, head injury, brain neoplasms, Alzheimer disease
Test Battery
-auditory evoked responses
-behavioural tests
-dichotic word test, dichotic sentence test, speech-in-competition test, binaural stimulation on one
or more nonspeech measure (pitch pattern sequence and duration pattern tests)
-peripheral auditory function is normal
PSEUDOHYPACUSIS
-findings suggestive of malingering

-SRT does not correlate with PTA (>10dB)
-normal stapedial reflexes despite high levels of hearing loss
-poor test-retest reliability (>10dB difference)
-air conduction thresholds better than bone conduction thresholds
-half-word answers on SRT
-inappropriate shadow curve
Shadow curve:
-patient with severe to profound unilateral hearing loss will hear a tone in the opposite or
contralateral ear. The thresholds will mimic those in the better ear but will be reduced by about 50
to 60 dB.
-result is a shadow curve due to cross-over resulting from sound being perceived by the better ear
even through presented to the poorer ear
-failure to show a shadow effect is considered a positive indication of pseudohypoacusis
Stenger test
-based on principle that asymmetry in loudness of only a few decibels will cause any person to
992
hear sound only in the louder side
-two acoustic stimuli identical in every way except intensity
-sound presented at 10 dB above threshold in good ear; 10 dB below threshold in poor ear
-if a sound is heard in good ear and patient acknowledges this negative Stenger; pt has genuine
hearing loss
-if pt does not acknowledge that they heard a sound in good ear positive Stenger; suspect
malingering
993
ANATOMY OF THE SKULL BASE,
TEMPORAL BONE, EXTERNAL EAR, AND MIDDLE EAR
(Cummings Ch 132)
SKULL BASE
-temporal bone articulates with five other cranial bones: frontal, parietal, sphenoid, occipital, and zygomatic.
Fig. 132-1. Skull base and cervical neurovascular anatomy observed from the right side. The right half of the body
of the mandible has been cut through in the parasagittal plane.
Fig. 132-2. Skull base and cervical neurovascular anatomy seen from the medial side after removal of the
pharyngeal wall.
-Jugular foramen:
-internal jugular vein
-spinal accessory (CN XI), glossopharyngeal (CN IX), and vagus (CN X)
-CN XI is the most posterior of the three nerves, and CN X lies between it and CN IX
-nerves are medial to the internal jugular vein and internal carotid artery at the base of the skull,
but CN X shifts to a position between and posterior to the vessels lower in the neck.
-Stylomastoid foramen:
-facial nerve (CNVII): exits the skull anterior to the digastric notch and slightly posterolateral to the styloid
process
-Carotid canal:
-internal carotid artery enters anterior to the jugular fossa and medial to the styloid process
-Hypoglossal canal:
-between the carotid canal and the styloid process
F.Ling - Temporal Bone Anatomy (1)
994
-hypoglossal nerve (CN XII) exits
-Foramen spinosum:
-middle meningeal artery enters the middle cranial fossa
-Foramen ovale:
-transmits the mandibular division of CN Vas it passes from the cranial fossa to the infratemporal fossa
-Meckel’s cave contains the trigeminal ganglion

-abducens nerve (CN VI) passes into the cavernous sinus via Dorello’s canal within the substance of the dura
-nerve involvement within Dorello’s canal is an important clinical sign for the diagnosis of Gradenigo’s
syndrome in cases of petrous apicitis
TEMPORAL BONE
-temporal bone can be divided into four parts:

-squamous
-mastoid
-petrous
-tympanic.
-Fig 132-4. Right temporal bone. A, Lateral view. B,

Medial view. C, Inferior view.
1. Squamous portion
-articulates with: parietal bone, frontal bone, and greater
wing of the sphenoid bone
-lateral surface defines boundary middle cranial fossa
-sulcus of middle meningeal artery scores medial surface
-caudal portion of bone extends medially to join
superior surface of petrous bone in the region of the
tegmen forms petrosquamous fissure
-forms posterosuperior portion of external auditory
meatus
-the hiatus between tympanic bone and squama
corresponds to notch of Rivinus (incisura typanica)
2. Mastoid portion
-squama forms anterosuperior portion of the mastoid
process
-petrous bone forms posteroinferior parts
-posterosuperior portion of external auditory meatus, is
the (suprameatal) spine of Henle
-pneumatization within the mastoid process varies
-squama of temporal bone forms a lateral wall of the
central air-containing space, the antrum, which
communicates with the middle ear by the aditus
-suprameatal spine and cribriform area provide
important landmarks for surgical access to the antrum -
from the region of the antrum, pneumatization may
extend inferiorly into the tip of the mastoid process,
995
where the remnant of the petrosquamous suture may persist as a thin plate of bone, Körner’s septum
3. Petrous portion
-petrous portion of the temporal bone approximately assumes
the configuration of a four-sided pyramid
-within the body of petrous bone is the labyrinth; the internal carotid artery, CN VII, and CN VIII (acoustic and
vestibular portions)
-lateral dimension defines the medial limit of the middle ear cavity
-contains the first turn of the cochlea, or promontory; the dome of the lateral semicircular canal; and the
medial wall of the antrum.
Superoanterior surface
-forms part of the middle cranial fossa
-laterally the bone is fused with the squama and anteriorly it articulates with the sphenoid bone
-foramen lacerum is found between the apex of the petrous bone and the sphenoid bone and contains but
does not transmit the internal carotid artery
-at the bone’s anterior margin, the large wing of the sphenoid bone forms musculotubal canal
-contains the semicanal for tensor tympani and the semicanal of the eustachian tube
Posterior or cerebellar surface

-forms the anterolateral wall of the cerebellar or posterior fossa
-sulcus for the superior petrosal sinus defines its superior border
-posteriorly the bone articulates with occipital bone
-midway between the apex and the anterior border of the sigmoid sulcus is the internal auditory meatus
-meatus is a short canal that begins medially at the internal acoustic pore
-trancsverse crest: horizontal ridge of bone divides the pore into upper and lower areas
-anterior portion of the superior division contains the facial nerve, which is separated from the
superior vestibular nerve in the posterior portion of the upper division by a small, vertical crest of
bone (Bill’s bar)
-cochlear nerve perforates the anterior portion of the lower division
-posterior portion of the lower division accommodates the inferior vestibular nerve
-internal auditory canal also contains the internal auditory artery, a branch of the anterior inferior cerebellar
artery that supplies the entire membranous labyrinth
4. Tympanic portion
-forms anterior and inferior walls and part of the posterior wall of the external auditory meatus
MIDDLE EAR
The middle ear consists of the tympanic cavity and the osseous
eustachian tube.
Confines of tympanic cavity
The tympanic cavity (Figure 132-6, Figure 132-7, Figure 132-8)

contains the sound-pressure transformer mechanism, the tympanic
segment of the facial nerve, and a complex of vessels and nerves.
The tympanic cavity is a cleft within the temporal bone between the
tympanic membrane laterally and the osseous labyrinth medially. The
roof of the tympanic cavity is the tegmen, a thin plate of bone
996
separating the space from the middle cranial fossa. The floor of the
tympanic cavity is a thin layer of bone over the bulb of the internal
jugular vein and an irregular collection of air cells. The posterior
boundary is more complex and contains many important anatomic
landmarks. The posterior wall is close to the mastoid air cell system;
the pyramidal eminence, a bony elevation that transmits the tendon
of the stapedius muscle, is attached to the superior aspect of this
wall. Part of the muscle is contained within the pyramidal process
itself. The chorda tympani nerve enters the tympanic cavity lateral to
the pyramidal process through its foramen, the tympanic opening of
the canal for the chorda tympani. The posterior sinus, or facial
recess, is between the pyramidal process and the chorda tympani
nerve (see Figure 132-6). The incudal fossa, where the posterior
ligament of the incus is attached, is cephalad to the facial recess. The
anterior boundary of the tympanic cavity partly consists of the wall
of the carotid canal, which may be very thin. The tensor tympani
muscle and its semicanal are found superiorly, and the eustachian
tube orifice is found more inferiorly along the anterior wall. The
medial wall consists of the promontory, or basal turn of the cochlea;
the oval and round windows; and the fallopian canal. A ridge of
bone found superiorly—the ponticulus—and a ridge of bone found
inferiorly—the subiculum—divide the medial wall into three main
depressions. The round window niche is inferior to the subiculum,
the oval window niche is superior to the ponticulus, and the
tympanic sinus is medial to the facial nerve between the subiculum
and ponticulus (see Figure 132-7). Inferior to the subiculum in the
round window niche, or fossula of the cochlear window, is the
cochlear window or round window orifice, which is closed by a
fibrous mucosa-covered membrane. Superior to the ponticulus is the
oval window niche, or fossula of the vestibular window, which leads
to the vestibular or oval window. The footplate of the stapes closes
the window. The prominent ridge of bone posterosuperior to the
fossulae contains the facial nerve, and posterosuperior to this
structure is the prominence of the lateral semicircular canal. The
lateral boundary of the tympanic cavity is the membranous wall
formed by the tympanic membrane and its annulus, the bony
tympanic sulcus, and the lateral wall of the epitympanic recess, the
tympanic scutum. The epitympanic recess is a space defined
superiorly by the tegmen tympani, medially by the prominence of the
facial cranial and semicircular canal, laterally by the scutum, and
posteriorly by the incudal fossa.
Click to enlarge
Fig. 132-6. Scanning electron
micrograph of posterior and superior
middle ear taken from a primate shows
the relationship of the facial canal to
the intact ossicular chain, stapedius
tendon, tensor tympani tendon, and
cochleariform process. The facial
997
recess is caudal to the incudal fossa,
and the tympanic sinus extends a
variable distance medial to the facial
nerve (cranial nerve VII) in its vertical
segment. The chorda tympani nerve is
shown as it passes between the neck
of the malleus and the long process of
incus to the petrotympanic fissure. The
relationship between the facial recess,
the short process of the incus (outlined
in white), and the facial canal is clearly
shown. (´40.)
Click to enlarge
Fig. 132-7. A, Tympanic cavity,
showing the relationship of the
tympanic sinus to the ponticulus and
subiculum. B, Observation of a
pathologically altered left human
middle ear with a 25° 1.9-mm rigid
endoscope showing the relationship
between the facial nerve (FN) and
recess, round window (RW),
ponticulus (P), sinus tympani
(asterisk), subiculum (S), round
window (RW), and promontory (PR).
The incus and stapedial crura are
absent.
Click to enlarge
Fig. 132-8. Scanning electron
micrograph of mucosa overlying the
center of the promontory in a human.
Many nonciliated cells with surface
microvilli and few ciliated cells are
shown. (´1950.)
The tympanic cavity is lined with a mucous membrane that also

invests the contents of the cavity. The epithelium consists of flat,
cuboidal, and columnar cell types. Each type may bear cilia (see
Figure 132-8). The epithelium extends from the eustachian tube
orifice over the promontory to invest the muscles and tendons within
the middle ear cleft and form several pouches in the superior aspect
of the cavity. One such space is the superior recess of the tympanic
membrane, or Prussak’s space, which is found between the pars
flaccida of the tympanic membrane and the neck of the malleus.
Two other blind pouches, the anterior and the posterior recesses of
998
the tympanic membrane, or the pouches of von Troltsch, are formed
from reflections of the anterior and posterior mallear folds among
the ossicles, their ligaments, and the tympanic membrane.
The middle ear cleft communicates with the tympanic antrum via the
aditus ad antrum in the posterosuperior wall of the epitympanic
recess. It is by this route that cholesteatoma extends from the middle
ear cleft into the mastoid cavity. The membranous folds and
pouches may influence the direction and location of spread.
Vascular system of tympanic cavity and ossicles
The blood supply of the middle ear and mastoid cavity originates
from the internal and external carotid arteries. The anterior tympanic
artery is a terminal branch of the internal maxillary artery. Two of its
branches supply the bone and mucosa of the superior and lateral
walls of the epitympanic cavity, and a third branch provides the main
blood supply for the malleus and incus (Figure 132-9). Another
branch of the internal maxillary artery, the deep auricular artery,
provides two branches to the vascular ring of the tympanic
membrane. A posterior branch supplies most of the tympanic
membrane, whereas the anterior branch supplies a lesser portion of
the anterior and inferior region.
Click to enlarge
Fig. 132-9. Lateral views of the incus
and malleus show their blood supply
based on the anterior tympanic artery.
Portion of the posterior branch
(between cut ends) has been omitted.
Two arteries originate from the middle meningeal artery: the superior
petrosal and the superior tympanic. The superficial petrosal artery
enters the facial hiatus and divides into two main branches. Both
branches pass within the fallopian canal to provide a major blood
supply to the geniculate ganglion and the facial nerve. The blood
supply to the incudostapedial joint area derives from the superior
and inferior arteries of the stapedius tendon and posterior crural
artery (Figure 132-10). These arteries originate from the arterial
plexus, supplied by the superficial petrosal artery within the fallopian
canal and its anastomosis with a stylomastoid artery. The superior
tympanic artery enters the middle ear adjacent to the lesser petrosal
nerve. The artery supplies the tensor tympani and a portion of the
epitympanic space. It also forms an anastomotic plexus with the
inferior tympanic artery, giving rise to the anterior stapedial artery
and the anterior crural (femoral) artery (see Figure 132-10).
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Click to enlarge
Fig. 132-10. Normal blood supply to
the lenticular process of incus,
incudostapedial joint, and stapes.
The caroticotympanic arteries are branches of the internal carotid

artery that pass through the bony partition between the carotid canal
and middle ear cleft and eventually anastomose with branches of the
inferior tympanic and tubal arteries. The inferior tympanic artery is a
branch of the ascending pharyngeal artery that enters the middle ear
cleft with the tympanic (Jacobson’s) nerve. This artery, along with
the caroticotympanic arteries, provides the major blood supply to
the mucosa of the promontory and the lower tympanic cavity
(hypotympanum).
The venous drainage from the middle ear cleft is principally via the
lateral sinus, jugular bulb, the petrosal sinuses, the pterygoid plexus
of veins, and the middle meningeal veins.
Sensory nerves of tympanic cavity
The sensory root of the facial nerve is the intermediate nerve. Fibers
from this nerve pass anteriorly from the geniculate ganglion as the
greater petrosal nerve or posteriorly within the facial nerve to exit as
the chorda tympani nerve. After exiting the facial hiatus, the greater
petrosal nerve enters the foramen lacerum, where it joins the deep
petrosal nerve to form the nerve of pterygoid canal (vidian nerve).
This nerve traverses the pterygoid (vidian) canal and then the
sphenopalatine ganglion, where the sensory fibers have their cell
bodies. These fibers are distributed to the soft palate and tongue.
Preganglionic secretory fibers from the cell bodies in the superior
salivatory nucleus also end in the sphenopalatine ganglion. Their
corresponding postganglionic fibers innervate the lacrimal gland and
provide secretory innervation to the nasal cavity. Sensory fibers of
the chorda tympani nerve have their cell bodies in the geniculate
ganglion and provide taste sensation to the anterior two thirds of the
tongue. The chorda tympani nerve also carries preganglionic
secretory fibers from cell bodies within the superior salivatory
nucleus, which synapse within the submaxillary ganglion, and then it
provides secretory motor impulses to the submaxillary and
sublingual glands.
The tympanic (Jacobson’s) nerve provides sensory innervation to

the mucosa of the middle ear cleft and eustachian tube region. This
nerve originates from the inferior ganglion of the glossopharyngeal
nerve, and after entering the tympanic cavity through the inferior
tympanic canaliculus, branches repeatedly within shallow bony
channels overlying the promontory. Branches of the tympanic nerve
join branches of the caroticotympanic nerve at the level of the
cochleariform process to form the lesser petrosal nerve. The lesser
petrosal nerve provides preganglionic secretory motor fibers to the
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parotid gland via the otic ganglion. Small branches from the
tympanic nerve and lesser petrosal nerve appear to anastomose with
the facial nerve and greater petrosal nerve, respectively, as they
course close to each other within the middle ear cleft and substance
of the petrous bone.
A branch of the vagus nerve and a smaller branch from the inferior
ganglion of the glossopharyngeal nerve join to form Arnold’s nerve
(auricular ramus of the vagus). This nerve and branches of the facial
nerve provide cutaneous innervation to the posterior surface of the
external auditory canal.
Tympanic membrane
The tympanic membrane (Figure 132-11) is found at the end of the

osseous external auditory meatus and forms the lateral wall of the
tympanic cavity. The membrane is elliptic in shape, approximately 8
mm wide, 9 to 10 mm high, and about 0.1 mm thick. The inferior
pole of the membrane lies further medially than the superior pole, at
an inclination of about 40° relative to the inferior wall of the auditory
meatus. The drum is funnel-shaped, with the umbo corresponding to
the tip of the manubrium at its apex. The handle of the malleus shines
through the tympanic membrane, and in the upper anterior part of
this bony process is a protuberance, the short process of the malleus
or mallear prominence. The anterior and posterior mallear folds
extend from this process to the tympanic sulcus and define the
inferior extent of the flaccid portion of the membrane, or Shrapnell’s
membrane. Shrapnell’s membrane appears thinner than the inferior
larger portion of the tympanic membrane, the pars tensa. The pars
tensa inserts into a small bony groove in the tympanic bone, the
tympanic sulcus, and is attached by a fibrocartilaginous ring.
Shrapnell’s membrane is attached directly to the squama of the
temporal bone at the notch of Rivinus.
Click to enlarge
Fig. 132-11. A, Scanning electron
micrograph of radial fiber distribution
over the umbo viewed from the canal
side after removing the epidermal
layer. (´30.) B, Higher-magnification
electron micrograph of radial fibers.
(´4500.)
Both the pars tensa and pars flaccida consist of three layers: a lateral
epidermis continuous with the skin of the external auditory meatus, a
middle layer or lamina propria, and a medial mucosal layer
continuous with the mucosa of the tympanic cavity. Originally, it was
believed that Shrapnell’s membrane possessed no lamina propria
layer because it appears thinner and more distensible than the pars
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tensa. This is, however, not the case, and the appearance of this
membrane more likely is caused by the organization and content of
the connective tissue within the lamina propria. The lamina propria
of the pars tensa consists of connective tissue fibers arranged in two
basic layers. Outer radial fibers originate from the inferior four fifths
of the handle of the malleus and the umbo and insert into the
tympanic sulcus (see Figure 132-11, A). An inner layer of circular
fibers originates primarily from the short process of the malleus.
Transversely and parabolically oriented fibers intertwine these two
layers. The exact nature of the fibers is unknown; they are probably
neither pure collagen nor elastin (see Figure 132-11, B).
Vessels within the mucosal and epidermal surfaces that

communicate through anastomoses within the lamina propria provide
the blood supply to the tympanic membrane. The epidermal vessels
originate from the deep auricular branch of the internal maxillary
artery (the mucosal vessels originate from the anterior tympanic
branch of the internal maxillary artery) and from the stylomastoid
branch of the posterior auricular artery.
The tympanic nerve and the auricular branch of the vagus nerve
provide part of the nerve supply to the tympanic membrane. The
auriculotemporal branch of the mandibular nerve provides additional
sensory innervation.
Auditory ossicles
The three major auditory ossicles (Figure 132-12) are the malleus,
incus, and stapes. Together with the tympanic membrane and the
ligamentous attachments, the ossicular chain forms the
sound-pressure transformer mechanism of the middle ear. The
malleus is the most lateral of the three ossicles and is attached to the
tympanic membrane, whereas the stapes is attached to the vestibular
window.
Click to enlarge
Fig. 132-12. Articulated ossicles and
dimensions and form of the stapes.
The malleus bones consist of two main parts: the head and the
handle, or manubrium. The head of the malleus occupies a portion
of the upper tympanic space and has a tooth-like process that
articulates with the body of the incus. Between the head and the
elongated handle is the neck of the malleus. The anterior process
projects from the anterior surface of the neck. Opposite and just
inferior to the short process is a roughened area on the handle of the
malleus for the attachment of the tendon of the tensor tympani
muscle. The handle of the malleus is firmly attached to the tympanic
membrane on its lateral surface, giving rise to the mallear stripe (stria
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mallearis). Medially the handle is covered with middle ear mucosa.
The incus resembles a molar tooth. The crown of the tooth, or the
body, articulates with the head of the malleus. The short and long
processes of the incus correspond to the roots of the tooth. The
short process rests in the incudal fossa and is attached by a
ligament. The long process is thinner and more tapered than the
short process and articulates with the head of the stapes. A flattened
bony platform, the lenticular process, sits at the end of the long
process at the point of articulation.
The stapes bone is shaped like a stirrup and consists of two legs, the
anterior and posterior crura, and a footplate, which is attached by
an annular ligament to the margins of the vestibular window. The
two crura are joined superiorly at the head, which articulates with
the lenticular process of the incus. Each leg resembles a trough, with
the concave surfaces facing each other. Of the two legs, the anterior
crus is more delicate and less curved. On the posterior crus is a
roughened area in the region of the head for the attachment of the
tendon of the stapedius muscle. Cartilage covers the articulating
surface of the head.
Six ligaments support the ossicles within the tympanic cavity. The
anterior ligament of the malleus extends from the angular spine of the
sphenoid bone through the petrotympanic fissure to insert on the
neck of the malleus. The superior mallear ligament extends from the
upper tegmen tympani to insert on the head of the malleus. The
lateral mallear ligament extends from the neck of the malleus to the
upper edge of the notch of Rivinus. The superior incudal ligament
passes from the tegmen tympani to the body of the incus, whereas
the ligament of the short process passes from the incudal fossa to
the floor of the antrum. The annular ligament of the stapes attaches
the footplate to the margins of the vestibular window.
The stapedius muscle lies within the pyramidal process and

originates along the ascending part of the fallopian canal.
Contraction of this muscle drives the anterior aspect of the stapes
base laterally. The stapedial branch of the facial nerve innervates the
muscle. The tensor tympani muscle is about four times as long as the
stapedius muscle, or 2 cm, and originates from the cartilaginous
portion of the eustachian tube, the adjacent part of the cartilaginous
portion of the eustachian tube, the adjacent part of the sphenoid
bone, and the bony semicanal of the petrous pyramid. The tensor
tympani tendon exits the bone from the cochleariform process, a
bony prominence overlying the first genu of the facial nerve. From
here, the tendon extends laterally to attach to the handle of the
malleus. The motor supply to the tensor tympani muscle is the
trigeminal nerve.
The ossicles obtain their blood supply from submucosal vessels

within the tympanic cavity. Blood vessels passing through the
mucosal folds that invest the ossicles provide the blood supply to the
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malleus and incus. Many vessels pass through the ossicular complex
along the tendon of the stapedius muscle, first to the stapes and then
laterally to the incus and malleus. Other vessels pass directly from
the facial canal to the stapes.
Eustachian tube
Anatomy of the eustachian tube is discussed in Chapter 153.
Facial nerve
The facial nerve (CN VII) (Figure 132-13) occupies an anterior

cephalad position within the internal auditory canal and remains
anterior to the superior vestibular nerve and cephalad to the
cochlear nerve. As the nerve leaves the internal acoustic meatus, it
separates from the statoacoustic nerves and passes cephalad to the
transverse crest and anterior to a vertical crest of bone known to
surgeons as Bill’s bar. In the region of Bill’s bar, the nerve leaves
the longitudinal axis of the temporal bone and curves anteriorly
around the basal turn of the cochlea between the basal turn and the
vestibule in its labyrinthine segment. The nerve expands at the
geniculate ganglion and proceeds in a posterior direction. At the
acute right angle bend (external genu), the greater petrosal nerve
leaves the facial nerve at the anterior edge of the geniculate ganglion
and proceeds anteriorly through the hiatus of the facial canal. At the
hiatus, the facial nerve proceeds posteriorly and enters the tympanic
cavity, where it runs transverse to the longitudinal axis of the
temporal bone in the horizontal or tympanic segment. This segment
extends from the geniculate ganglion to just anterior and caudal to
the lateral semicircular canal. The cochleariform process overlaps
the beginning of the tympanic segment of the nerve. For most of its
length, the horizontal segment of the fallopian canal defines the
superior boundary of the entrance to the oval window niche.
Click to enlarge
Fig. 132-13. A, Scanning electron
micrograph of the facial nerve in the
region of the fissula of the vestibular
window taken from a primate. The
facial nerve sheath is composed of
fibrous epineurium, vascular connective
tissue, and periosteum, which has been
removed with bony facial canal.
NF-nerve fibers. (´255.) B,
Higher-magnification electron
micrograph shows individual nerve
fibers invested by connected tissue
fibers making up the endoneurium.
Fibers appear to be hollow tubes
formed by the Schwann cell myelin
1004
sheath. Axoplasmic remnants (A) are
seen within some tubules. An
occasional Schwann cell nucleus
(asterisk) is seen bulging from within
the myelin sheath. (´3375.)
As it curves around the oval window niche, the nerve begins its
vertical segment anterior and inferior to the lateral semicircular canal.
In the region of the oval window niche, the facial nerve lies within
the medial wall of the tympanic cavity, where the bone of the facial
canal is very thin. The nerve may be in direct contact with the
mucosa of the tympanic cavity by dehiscences in the facial canal in
50% to 60% of healthy petrous bones. As the nerve begins its
vertical segment, it passes lateral to the tympanic sinus, which
extends a variable distance medial to the nerve.
As the facial nerve enters its vertical portion, it is medial to the short
process of the incus and lateral to the stapedius muscle. Inferior to
the short process of the incus, the facial sinus cells are delineated
superiorly by the incudal fossa, medially by the facial canal, and
laterally by the chorda tympani nerve. The facial recess within the
posterior wall of the tympanic cavity also may be called the
suprapyramidal process because of its relationship to the
pyramidal eminence.
A complex relationship exists within the vertical segment of the facial

canal between the nerve and its perineural investments, the stapedius
muscle and nerve, and the tympanic vascular plexus. The stapedius
muscle is medial to the facial nerve in its vertical course, where it
may or may not occupy compartments separate from the facial
canal. The nerve to the stapedius muscle branches from the adjacent
facial nerve, where it is juxtaposed to the muscle. In addition to the
stapedius muscle, the facial canal also is occupied partly by a
circumneural investment of vessels and connective tissue, which may
occupy more than 50% of the bony canal.
In addition to the vascular plexus, two other connective tissue

investments make up the circumneural sheath. Within the facial
canal, just peripheral to the vascular plexus, is the periosteum. The
periosteal layer is less well developed than a second connective
tissue investment, the epineurium, which lies deep to the vascular
plexus and is the chief component of the perineural sheath (see
Figure 132-13, A). No well-defined perineum exists. Individual
connective tissue fibers course through the nerve fibers and make up
the endoneurium (see Figure 132-13, B). The facial nerve sheath
therefore consists of three layers: the periosteum, the vascular
plexus, and the epineurium.
1005
NEUROPHYSIOLOGIC INTRAOPERATIVE MONITORING
MONITORING OF THE AUDITORY SYSTEM
Injury to the Auditory System

-microvascular decompression of CN V, VII, and VIII 10-15% incidence of HL
-risks of penetration of cochlea, damage to labyrinthine artery causing cochlear ischemia
-stretching, compression, transection, or heating of auditory nerve
-auditory nerve more fragile than other cranial nerves, rendering it particularly susceptible to stretch or
thermal injury
-goals of intraoperative monitoring:
-warn surgeon when surgical manipulation is causing injury
-predict postoperative hearing function
Auditory System Monitoring Techniques

-three types: ABR, EcoG, auditory nerve compound action potential [aka. direct eighth nerve monitoring
(DENM) or cochlear nerve action potential (CNAP) monitoring]

-five peaks seen
-I and II: distal and proximal cochlear nerve
-III: cochlear nucleus
-IV: superior olive
-V: lateral leminiscus
-intraoperative changes observed:
-desynchronization of wave V, diminished amplitude or elimination of waves I, III, or V and
lengthening of I through V latency
-stretching the nerve elicits increase in wave V latency and the wave I through wave V latency
interval
-severe injury such as contusion or complete transection, eliminates wave V
-disadvantages:
-far-field technique
-several minutes can lapse b/n manipulation and presence of changes in baseline recording
-does not provided immediate, real-time information
-affected by hypothermia, some volatile anesthetics, blood in middle ear, tumour or pathologic
condition itself, and surgical manipulations away from the cochlear nerve
Electrocochleography
-near field technique
-wide-band click composed of many frequencies that stimulate the entire cochlea
-monitors cochlear microphonic and summating potential and eighth-nerve action potentials arising from a
stimulus
-cochlear microphonic:
-alternating current response generated by hair cells of organ of Corti
-summating potential:
-can represent asymmetry in basilar membrane caused by pressure differences between
the scala media and scala vestibuli that indicate changes in the endolymphatic fluid
-compound action potential:
-representative of responses from basal turn of the cochlea
-N1 latency is inversely related to stimulus rate; amplitude is directly related to stimulus rate
-EcoG can best sense changes in cochlear blood supply
-reduced amplitude or loss of ECochG action potential indicates injury to labyrinthine (internal
F.Ling - Neurophysiologic Intraop Monitoring (1)
1006
auditory) artery
-decreased amplitude, or prolonged latency, of N1 or the cochlear microphonic has been associated with
postoperative hearing loss
-disadvantages:
-transtympanic needle placement
-may not be sensitive to medial intraoperative changes within the CPA
-may not be useful in detection of intraoperative damage or manipulation of the cochlear nerve
Direct Eighth-Nerve Monitoring

-monopolar or bipolar electrode is placed directly on or near the cochlear nerve
-information received almost instantaneously; most sensitive eighth-nerve monitoring modality
-requires adequate exposure of nerve
-stretching of nerve increases N1 latency, and diminishes N1 amplitude
Applications and Benefits

-monitoring associated with improved outcomes of some otologic and neurotologic procedures
-ABR associated with increased likelihood of hearing preservation during resection of acoustic neuroma,
vestibular nerve section, endolymphatic sac surgery, cochlear implantation, and microvascular
decompression of cranial nerves
-persistence of waves I and V at conclusion of procedure indicates hearing preservation
-when intermural latency of wave V is < 0.4 ms, more than 75% of pts have serviceable
postoperative hearing
-loss of waves or presence of waves does not necessarily mean hearing loss or hearing
preservation
-EcochG has been useful in surgical therapy for Meniere’s disease
-sac decompression precipitates a decrease in previously elevated summating potentials in several
pts
-loss of CAP strongly correlated with postoperative hearing impairment
-DENM most useful technique in surgical dissection and providing a reasonably accurate gauge of
postoperative hearing
-preservation of N1 peak associated with serviceable hearing among as many as 54% pts
-lack of AP response at completion of procedure never associated with postoperative hearing
preservation
-postoperative hearing changes can be predicted by analysing click threshold shift:
-all pts with shift between 30 and 60 dB had no serviceable hearing
Combined Approaches and Horizons

-combinations of near and far-field techniques can provide complete information about auditory system
from cochlea and distal part of eighth nerve to brainstem and higher centers
-OAEs may be new way of monitoring cochlear blood flow
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INTRAOPERATIVE FACIAL NERVE MONITORING
-procedures that risk injury to facial nerve:

-excision of acoustic neuroma
-revision mastoid surgery
-repair of congenital malformations
Facial Nerve Injury TYPES OF FACIAL NERVE INJURY

-most facial nerve injuries during resection of acoustic
neuroma occur medially to porus acousticus at -transection
midcerebellopontine angle, where nerve can be injured -direct trauma from surgical dissection
-direct trauma from surgical drill
through surgical dissection or compression by mass -stretch
-excluding operations for acoustic neuroma, most -compression
common site of iatrogenic injury is lower tympanic -thermal damage from drilling, cautery, laser, irrigation
segment, followed by mastoid segment -vascular compromise
-direct or indirect injury from ultrasonic aspiration
-edema to nerve in fallopian canal from surgical
Facial Nerve Monitoring Systems dissection
-electromyography and evoked electromyography
-changes in neural activity can occur during
operative dissection near facial nerve and during manipulation of the nerve, altering baseline
neural activity and propagating compound action potentials that appear as deflections on the
oscilloscope
-no reliable correlation has been established between magnitude or duration of EMG response and
presence, if any, of facial nerve injury
Anesthesia and Facial Nerve Monitoring

-paralysis of muscles by muscle endplate blocking agents interferes with recording of EMG potentials
-nondepolarizing agents typically are contraindicated when facial monitoring is planned
-succinylcholine usually used because of short duration
-local anaesthesia can impair use of facial nerve monitoring
Indications for Intraoperative Facial nerve Monitoring

-decision to use facial nerve monitoring remains at the discretion of the surgeon
-potential indications for facial nerve monitoring
-acoustic neuroma and tumours of the CPA
-vestibular nerve section
-repair of congenital aural atresia
-skull base surgery
-microvascular decompression of cranial nerves V, VII, VIII
-cochlear implantation
-labyrinthectomy
-endolymphatic sac surgery
-facial nerve decompression
-mastoidectomy
-tympanoplasty
-canalplasty
-stapedectomy
1008
IMAGING STUDIES OF THE TEMPORAL BONE
Parameters Tissue Signal Characteristics
TR TE Fat or Bone Marrow CSF Nasal mucosa Air and Bone
T1 short short High Low Low Low
T2 long long Low to intermediate High High Low
Enhanced T1 short short High Low High Low
F.Ling - Imaging Studies of the Temporal Bone (1)
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EXTERNAL AUDITORY CANAL
Congenital Anomalies of External Ear Canal

-result from developmental defect of 1st
and 2nd branchial arches
-congenital aural atresia 1/10000 births
-important CT findings in pts with aural
atresia include:
-presence of stapes in oval
window
-extent of mastoid
pneumatization and size of
middle ear cavity
-course of facial nerve
-development of incudomalleus
complex
-type of atresia
-presence of normal inner ear
with patent oval and round
windows
-an inner ear malformation excludes the pt
from atresia repair
Benign Neoplasms
-EAC cholesteatomas usually present with focal bony erosion of bony ear canal
-CT will show soft tissue filling EAC with adjacent smooth bony erosion
-Keratosis obturans:
-abnormal epithelial migration of TM though to be responsible
-most pts present with otalgia, CHL and otorrhea
-CT demonstrates significantly diffuse widening of EAC
-exostoses and osteomas:

-most common benign bony tumours of EAC
-exostoses: broad-base lesions that arise from medial aspect of bony EAC near tympanic annulus,
along tympanomastoid and tympanosquamous suture lines
-osteomas: solitary and unilateral found in lateral bony canal
Malignant Neoplasms
-primary EAC tumours are rare

-include SCC, BCC and ceruminous gland tumours
-SCC:
-associated with irregular bony erosion or destruction of bony canal wall
-tumours involving cartilaginous lateral third of EAC can easily extend anteriorly through fissure
of Santorini to the parotid gland
1010
Infectious and Inflammatory Diseases
-necrotizing otitis externa

-“malignant external otitis”
-usually occurs in elderly
diabetics or
immunocompromised
-CT can demonstrate subtle
bony erosion and
involvement of mastoid and
middle ear cavity
-findings are nonspecific and
can be confused with
malignancy
MIDDLE EAR AND MASTOID
Inflammatory Disease
-because all pneumatized spaces of temporal bone are contiguous, OM involves inflammation in other
three regions of pneumatization (mastoid, perilabyrinthine and petrous apex)
-pneumatized areas in temporal bone pacified but integrity of mastoid bony septae, ossicular chain
and mastoid cortex would be intact
-coalescent mastoiditis:
-mastoid cavity filled with granulation tissue
and bony septae undergo enzymatic bony
resorption
-subperiosteal abscess can develop as a
result of direct inflammatory extension
through thin trabecular bone in lateral
mastoid cortex
-Bezold abscess:
-inflammatory debris erodes
mastoid tip medial to insertion of
SCM abscess in upper neck
-can spread via direct extension,
hematogenous spread or by retrograde
thrombophlebitis
sigmoid dural venous sinus
thrombosis, abscesses and
meningitis (most common
intracranial complication of AOM)
-otogenic brain abscess:

-usually involves either temporal lobe or cerebellum
-MRI: -T1 with contrast: hypointense center with enhancing capsule
-T2: high signal intensity
-sigmoid dural venous sinus thrombosis:
-MRI: -T1: isointense (acute clot); many enhance on contrast if chronic
-T2: hypointense
1011
-petrositis:
-Gradenigo triad: retroorbital pain, sixth nerve
palsy, chronic otorrhea
-CT: opacified petrous apex cells with lysis of bony
septae
-MRI: peripheral meningeal enhancement at petrous
apex as adjacent dura becomes thickened and covered
with granulation tissue
-cholesterol granulomas:
-caused by trapped chronic inflammatory mucosal
secretions within pneumatized petrous apex
-encapsulated cystic lesion filled with brownish liquid
containing cholesterol clefts
-clinical presentation: hearing loss, tinnitus,
hemifacial spasm and cranial nerve deficits
-MRI: high signal intensity in both T1 and T2
-cholesteatoma:
-MRI: -T1: isointense with brain
-T2: hyperintense
Cholesteatoma
-sac lined by keratinizing stratified squamous epithelium that gradually enlarges in air spaces inside middle
and mastoid cavity
-pars flaccida cholesteatomas:
-begin in Prussak space, between lateral attic wall and head of malleus
-usually erode lateral attic wall (scutum)
-extend posteriorly to involve posterolateral attic and antrum
-pars tensa cholestatomas:
-originate form postero-superior retraction and progress posteriorly to involve facial recess and
sinus tympani
-bony erosion:
1012
-ossicular chain destruction:
-long process of incus > body of incus > head of malleus
-labyrinthine fistula
-most common site is lateral semicircular canal
-cochlear fistula at promontory area
-facial paresis
-imaging:
-MRI: -T1: nonspecific signal intensity with some rim enhancement after contrast
-granulation tissue will enhance whereas cholesteatoma will not
-T2: moderately hyperinse
Tumours of Middle Ear
-glomus tympanicum:
-most common primary tumour of middle ear
-originates from glomus bodies along Jacobson’s
nerve (a branch of glossopharyngeal nerve) and
rarely from Arnold’s branch (vagus nerve)
-will enhance intensively after administration of
contrast in both CT and MRI
-congenital cholesteatoma:
-rare tumour
-arises from aberrant epithelial embryonic rests
left behind in middle ear
-propensity of its occurrence in anterosuperior
middle ear near eustachian tube opening
INNER EAR
Congenital Anomalies
-membranous labyrinth originates from neuroectodermal-derived otic placode starting in 4th GA
-formation of entire membranous labyrinth with 2.5-2.75 cochlear tumours is complete by 8th week
-otic capsule grows and ossifies to its full adult size by 24th week
-majority of congenital SNHL are limited to membranous labyrinth (80%) majority of pts have normal
CTs
-bony labyrinthine deformities (20%) believed to be d/t developmental defect between 4th and 8th weeks of
gestation
-Michel aplasia:
-absence of entire inner
ear including
vestibulocochlear nerve
-d/t arrested development
of otic placode during 3rd
GA
-common cavity deformity:
-d/t arrested development
in 4th and 5th GA
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-cochlear aplasia arrest in 5th week
-cochlear hyperplasia arrest in 6th week
-Mondini deformity:
-developmental arrest during 7th GA
-only 1.5 turns of cochlea with absence of interscalal septum between apical and middle
turns
-SCCs develop between 6th and 8th GA

-superior and posterior SCC develop before horizontal SCC
-horizontal SCC deformities are the most common vestibular organ deformity discovered
-most common imaging finding in individuals with

congenital SNHL is enlarged vestibular aqueduct
-vestibular aqueduct measures greater than
1.5 mm at midpoint between common curs
and external aperture
-best diagnosed with axial CT or a
corresponding T2 image
-clinical presentation:
-moderate hearing loss in early
childhood that gradually
deteriorates especially after
minor head trauma
-associated with Pendred
syndrome (congenital SNHL and
euthyroid goiter)
-absence of bony partition between a widened IAC
and vestibule pts predisposed to devlop CSF
“gusher” upon a manipulation of stapes
1014
Inflammation of Inner Ear
-labyrinthitis:
-postcontrast T1 MRI demonstrates diffuse abnormal enhancement of the normally nonenhancing
labyrinth
-in haemorrhagic labyrinthitis, T1 images show increased signal intensity within labyrinth
-chronic labyrinthitis fibrous tissue fills membranous labyrinth (seen on T2)
-abnormal bone formation within membranous labyrinthine space labyrinthitis ossificans
Neoplasms
-intralabyrinthine schwannoma
-rare
-Meniere-like symptoms of recurrent vertigo and hearing loss
-endolymphatic sac tumour

-associated with von Hippel-Lindau disease
-arises from epithelial cells of endolymphatic duct or sac and can erode posterior bony cortex into
CPA
-MRI: -T1: high signal intensity (precontrast); solid part of tumour enhances
OTODYSTROPHIES
-otosclerosis:
-otospongiosis
-enchondral bone around otic capsule is replaced by multiple foci of spongy vascular irregular
bone spongy bone later becomes calcified and sclerotic
-commonly involved site is anterior oval window region (fistula ante fenestrum)
-“double ring sign”: CT appearance of otic capsule along basilar turn of cochlea
1015
-obliterative otosclerosis new bone formation
limited to round window and basilar turn of cochlea
-osteogenesis imperfecta:
-all or part of otic capsule can be demineralized,
similar to cochlear otosclerosis, but is more severe
TEMPORAL BONE TRAUMA
-longitudinal type more common (80% cases)

-ossicular chain and gerigeniculate ganglion region
of facial nerve commonly involved
-otic capsule injury rare
-facial nerve injury 10-20%
-subluxations of incudostapedial joint most common
posttraumatic ossicular injury
-transverse type:
-commonly begin near jugular foramen or foramen magnum and extend to middle cranial fossa
-profound SNHL and vertigo
-facial nerve injury up to 50%; at labyrinthine segment or perigeniculate ganglion region
-CSF otorrhea or rhinorrhea usually associated with longitudinal fractures involving tegmen tympani
FACIAL NERVE DISORDERS
-CT to demonstrate facial nerve in bony canal

-MRI for evaluating inflammatory and neoplastic processes of facial nerve
-geniculate ganglion and anterior tympanic segment often enhance d/t rich perineural venous
plexus
Neoplasms
-facial nerve schwannoma:

-rare; <1% of all temporal bone tumours
-gradual or recurrent facial palsy, hearing loss, tinnitus, vertigo, hemifacial spasm, or otalgia
-MRI: enhances homogenously on postcontrast T1
-facial nerve hemangioma:

-CT findings: soft tissue mass in perigeniculate area with irregular, poorly defined, bony margins
-MRI: -T1: hypointense or isointense to brain; will enhance with contrast
-T2: hyperintense
Inflammation
-Bell’s palsy caused by HSV I infection
-MRI demonstrates a linear uniformly enhancing facial nerve from distal IAC to mastoid segment
on contrast
-MR evaluation indicated in pts with facial paralysis persisting beyond 2 months, recurrent palsy
or slowly progressive palsy
1016
VASCULAR ANOMALIES AND DISEASES
Normal Vascular Variants

-venous lesions:
-asymmetrically enlarged jugular bulb
-high-riding jugular bulb
-“high riding” if superior limit above floor of IAC
-if bone is dehiscent may present as vascular mass behind posteroinferior quadrant of
TM
-jugular bulb diverticulum
-superior part of jugular bulb bulges outward form lumen
-arterial anomalies:
-aberrant internal carotid artery
-on CT, vertical segment of carotid canal is
absent and normal bony covering over
posterolateral aspect of horizontal portion of
carotid artery is absent
-aberrant stapedial artery
-associated with enlargement of anterior
tympanic segment of facial nerve
-rare
-occurs when second branchial artery fails to
regress by third month of gestation
-courses through stapedial obturator foramen
and anterior tympanic segment of facial nerve
canal to form middle meningeal artery
-on CT, foramen spinosum is absent and
anterior tympanic segment of facial canal is
enlarged
Vascular Neoplasms
-paraganglioma:
-most common cause for objective pulsatile
tinnitus and a vascular hypotympanic mass
-MRI: enhances on T1 “salt and pepper”
appearance d/t flow voids
-glomus jugulare:
-supplied mostly by ascending pharyngeal
artery
-some contributions from posterior
auricular and occipital arteries
Other Vascular-related Conditions

-dural AVF
-direct anterior venous connection between
meningeal branches of external carotid artery and
dural venous sinus
-pulsatile tinnitus
-detected by selective angiography of external
carotid artery
-tx: intra-arterial embolization
1017
-benign intracranial hypertension (pseudotumour cerebri)
-can also cause subjective pulsatile tinnitus
-MRI to r/o significant intracranial mass (none)
-LP to confirm and relieve elevated CSF pressure
-other causes of pulsatile tinnitus:
-arteriosclerosis, fibromuscular dysplasia, arterial dissection, arteritis
INTERNAL AUDITORY CANAL AND CEREBELLOPONTINE ANGLE LESIONS
-IAC contents: vestibulocochlear nerve, facial nerve, nervus intermedius, labyrinthine artery, sometimes a
loop of AICA
Neoplasms
-vestibular schwannomas (acoustic neuromas)

-5-10% of all intracranial tumours
-85% of all CPA tumours
-MRI: T1: hypointense/isointense to brain; enhance on contrast
T2: hyperintense
-meningioma
-second most common CPA tumour
-trigeminal neuropathy more common
-MRI: T1: isointense to brain; enhance intensely and homogeneously post-contrast
T2: isointense or hyperintense
1018
Congenital Lesions
-epidermoid cyst:
-third most common lesion of CPA
-MRI: T1: hypointense; no enhancement
T2: hyperintense
-arachnoid cysts:
-MRI: T1: low intensity
T2: high intensity
-lipoma:
-presumed to arise as a result of maldifferentiation of meningeal precursor tissues
-CT and MRI show fat-containing lesion in CPA
-CT: -dark
-MRI: T1: bright
T2: dark
Inflammatory
-granulomatous processes such as sarcoidosis can involve IAC and CPA
-postcontrast T1 images abnormal leptomeningeal thickening and enhancement
Vascular Lesions
-microvascular loop compression syndrome

-may cause trigeminal neuralgia and hemifacial spasm
-caused by vascular loop compressing trigeminal and facial nerve
-associated with atherosclerotic and tortuous vertebrobasilar vessels
-best seen on T2 and MRA images:
-dolicoectasia of basilar artery toward affected side when a prominent loop of the AICA
is seen near the vestibulocochlear nerve complex
1019
IMAGING STUDIES OF THE TEMPORAL BONE
Parameters Tissue Signal Characteristics
TR TE Fat or Bone Marrow CSF Nasal mucosa Air and Bone
T1 short short High Low Low Low

(<1000) (<30)
T2 long long Low to intermediate High High Low

(>1000) (>30)
Enhanced T1 short short High Low High Low
1020
EXTERNAL AUDITORY CANAL
Congenital Anomalies of External Ear Canal

-result from developmental defect of 1st
and 2nd branchial arches
-congenital aural atresia 1/10000 births
-important CT findings in pts with aural
atresia include:
-presence of stapes in oval
window
-extent of mastoid
pneumatization and size of
middle ear cavity
-course of facial nerve
-development of incudomalleus
complex
-type of atresia
-presence of normal inner ear
with patent oval and round
windows
-an inner ear malformation excludes the pt
from atresia repair
Benign Neoplasms
-EAC cholesteatomas usually present with focal bony erosion of bony ear canal
-CT will show soft tissue filling EAC with adjacent smooth bony erosion
-Keratosis obturans:
-abnormal epithelial migration of TM though to be responsible
-most pts present with otalgia, CHL and otorrhea
-CT demonstrates significantly diffuse widening of EAC
-exostoses and osteomas:

-most common benign bony tumours of EAC
-exostoses: broad-base lesions that arise from medial aspect of bony EAC near tympanic annulus,
along tympanomastoid and tympanosquamous suture lines
-osteomas: solitary and unilateral found in lateral bony canal
Malignant Neoplasms
-primary EAC tumours are rare

-include SCC, BCC and ceruminous gland tumours
-SCC:
-associated with irregular bony erosion or destruction of bony canal wall
-tumours involving cartilaginous lateral third of EAC can easily extend anteriorly through fissure
of Santorini to the parotid gland
1021
Infectious and Inflammatory Diseases

-“malignant external otitis”
-usually occurs in elderly
diabetics or
immunocompromised
-CT can demonstrate subtle
bony erosion and
involvement of mastoid and
middle ear cavity
-findings are nonspecific and
can be confused with
malignancy
MIDDLE EAR AND MASTOID
Inflammatory Disease
-because all pneumatized spaces of temporal bone are contiguous, OM involves inflammation in other
three regions of pneumatization (mastoid, perilabyrinthine and petrous apex)
-pneumatized areas in temporal bone opacified but integrity of mastoid bony septae, ossicular
chain and mastoid cortex would be intact
-coalescent mastoiditis:
-mastoid cavity filled with granulation tissue
and bony septae undergo enzymatic bony
resorption
-subperiosteal abscess can develop as a
result of direct inflammatory extension
through thin trabecular bone in lateral
mastoid cortex
-Bezold abscess:
-inflammatory debris erodes
mastoid tip medial to insertion of
SCM abscess in upper neck
-can spread via direct extension,
hematogenous spread or by retrograde
thrombophlebitis
sigmoid dural venous sinus
thrombosis, abscesses and
meningitis (most common
intracranial complication of AOM)
-otogenic brain abscess:

-usually involves either temporal lobe or cerebellum
-MRI: -T1 with contrast: hypointense center with enhancing capsule
-sigmoid dural venous sinus thrombosis:
-MRI: -T1: isointense (acute clot); many enhance on contrast if chronic
-T2: hypointense
1022
-petrositis:
-Gradenigo triad: retroorbital pain, sixth nerve
palsy, chronic otorrhea
-CT: opacified petrous apex cells with lysis of bony
septae
-MRI: peripheral meningeal enhancement at petrous
apex as adjacent dura becomes thickened and covered
with granulation tissue
-cholesterol granulomas:
-caused by trapped chronic inflammatory mucosal
secretions within pneumatized petrous apex
-encapsulated cystic lesion filled with brownish liquid
containing cholesterol clefts
-clinical presentation: hearing loss, tinnitus,
hemifacial spasm and cranial nerve deficits
-MRI: high signal intensity in both T1 and T2
-cholesteatoma:
-MRI: -T1: isointense with brain - non-enhancing
-T2: hyperintense
Cholesteatoma
-sac lined by keratinizing stratified squamous epithelium that gradually enlarges in air spaces inside middle
and mastoid cavity
-pars flaccida cholesteatomas:
-begin in Prussak space, between lateral attic wall and head of malleus
-usually erode lateral attic wall (scutum)
-extend posteriorly to involve posterolateral attic and antrum
-pars tensa cholestatomas:
-originate from postero-superior retraction and progress posteriorly to involve facial recess and
sinus tympani
1023
-bony erosion:
-ossicular chain destruction:
-long process of incus > body of incus > head of malleus
-labyrinthine fistula
-most common site is lateral semicircular canal
-cochlear fistula at promontory area
-facial paresis
-imaging:
-MRI: -T1: nonspecific signal intensity with some rim enhancement after contrast
-granulation tissue will enhance whereas cholesteatoma will not
-T2: moderately hyperintense
Tumours of Middle Ear
-glomus tympanicum:
-most common primary tumour of middle ear
-originates from glomus bodies along Jacobson’s
nerve (a branch of glossopharyngeal nerve) and
rarely from Arnold’s branch (vagus nerve)
-will enhance intensively after administration of
contrast in both CT and MRI
-congenital cholesteatoma:
-rare tumour
-arises from aberrant epithelial embryonic rests
left behind in middle ear
-propensity of its occurrence in anterosuperior
middle ear near eustachian tube opening
-ddx: -neuroma, fluid (OME), schwannoma, adenoma
INNER EAR
Congenital Anomalies
-membranous labyrinth originates from neuroectodermal-derived otic placode starting in 4th GA
-formation of entire membranous labyrinth with 2.5-2.75 cochlear turns is complete by 8th week
-otic capsule grows and ossifies to its full adult size by 24th week
-majority of congenital SNHL are limited to membranous labyrinth (80%) majority of pts have normal
CTs
-bony labyrinthine deformities (20%)
believed to be d/t developmental defect
between 4th and 8th weeks of gestation
-Michel aplasia:
-absence of entire
inner ear including
vestibulocochlear
nerve
-d/t arrested
development of otic
placode during 3rd
GA
1024
-common cavity deformity:
-d/t arrested development in 4th and 5th GA
-cochlear aplasia arrest in 5th week
-cochlear hypoplasia arrest in 6th week
-Mondini deformity:
-developmental arrest during 7th GA
-only 1.5 turns of cochlea with absence of interscalal septum between apical and middle
turns
-SCCs develop between 6th and 8th GA

-superior and posterior SCC develop before horizontal SCC
-horizontal SCC deformities are the most common vestibular organ deformity discovered
-most common imaging finding in individuals with

congenital SNHL is enlarged vestibular aqueduct
-vestibular aqueduct measures greater than
1.5 mm at midpoint between common crus
and external aperture (operculum)
-best diagnosed with axial CT or a
corresponding T2 image
-clinical presentation:
-moderate hearing loss in early
childhood that gradually
deteriorates especially after minor
head trauma
-associated with Pendred
syndrome (congenital SNHL and
euthyroid goiter)
-absence of bony partition between a widened IAC
and vestibule pts predisposed to develop CSF
“gusher” upon a manipulation of stapes
1025
Inflammation of Inner Ear
-labyrinthitis:
-postcontrast T1 MRI demonstrates diffuse abnormal enhancement of the normally nonenhancing
labyrinth
-in haemorrhagic labyrinthitis, T1 images show increased signal intensity within labyrinth
-chronic labyrinthitis fibrous tissue fills membranous labyrinth (seen on T2)
-abnormal bone formation within membranous labyrinthine space labyrinthitis ossificans
Neoplasms
-intralabyrinthine schwannoma
-rare
-Meniere-like symptoms of recurrent vertigo and hearing loss
-endolymphatic sac tumour

-very rare
-associated with von Hippel-Lindau disease
-arises from epithelial cells of endolymphatic duct or sac and can erode posterior bony cortex into
CPA
-MRI: -T1: high signal intensity (precontrast); solid part of tumour enhances
OTODYSTROPHIES
-otosclerosis:
-otospongiosis
-enchondral bone around otic capsule is replaced by multiple foci of spongy vascular irregular
bone spongy bone later becomes calcified and sclerotic
-commonly involved site is anterior oval window region (fistula ante fenestrum)
-“double ring sign”: CT appearance of demineralization of otic capsule along basilar turn of
cochlea
1026
-obliterative otosclerosis new bone formation
limited to round window and basilar turn of cochlea
-osteogenesis imperfecta:
-all or part of otic capsule can be demineralized,
similar to cochlear otosclerosis, but is more severe
TEMPORAL BONE TRAUMA
-longitudinal type more common (80% cases)

-ossicular chain and perigeniculate ganglion region
of facial nerve commonly involved
-otic capsule injury rare
-facial nerve injury 10-20%
-subluxations of incudostapedial joint most common
posttraumatic ossicular injury
-transverse type:
-commonly begin near jugular foramen or foramen magnum and extend to middle cranial fossa
-profound SNHL and vertigo
-facial nerve injury up to 50%; at labyrinthine segment or perigeniculate ganglion region
-CSF otorrhea or rhinorrhea usually associated with longitudinal fractures involving tegmen tympani
-if considering facial nerve decompression
-if patient has transverse fracture with no hearing and total facial nerve paralysis
-translabyrinthine approach to repair facial nerve
FACIAL NERVE DISORDERS
-CT to demonstrate facial nerve in bony canal

-MRI for evaluating inflammatory and neoplastic processes of facial nerve
-geniculate ganglion and anterior tympanic segment often enhance d/t rich perineural venous
plexus
Neoplasms
-facial nerve schwannoma:

-rare; <1% of all temporal bone tumours
-gradual or recurrent facial palsy, hearing loss, tinnitus, vertigo, hemifacial spasm, or otalgia
-MRI: enhances homogenously on postcontrast T1
-facial nerve hemangioma:

-CT findings: soft tissue mass in perigeniculate area with irregular, poorly defined, bony margins
-MRI: -T1: hypointense or isointense to brain; will enhance with contrast
-T2: hyperintense
Inflammation
-Bell’s palsy caused by HSV I infection
-MRI demonstrates a linear uniformly enhancing facial nerve from distal IAC to mastoid segment
on contrast
-MR evaluation indicated in pts with facial paralysis persisting beyond 2 months, recurrent palsy
or slowly progressive palsy
1027
VASCULAR ANOMALIES AND DISEASES
Normal Vascular Variants

-venous lesions:
-asymmetrically enlarged jugular bulb
-high-riding jugular bulb
-“high riding” if superior limit above floor of IAC
-if bone is dehiscent may present as vascular mass behind posteroinferior quadrant of
TM
-jugular bulb diverticulum
-superior part of jugular bulb bulges outward from lumen
-arterial anomalies:
-aberrant internal carotid artery
-on CT, vertical segment of carotid canal is
absent and normal bony covering over
posterolateral aspect of horizontal portion of
carotid artery is absent
-aberrant stapedial artery
-associated with enlargement of anterior
tympanic segment of facial nerve
-rare
-occurs when second branchial artery fails to
regress by third month of gestation
-courses through stapedial obturator foramen
and anterior tympanic segment of facial nerve
canal to form middle meningeal artery
-on CT, foramen spinosum is absent and
anterior tympanic segment of facial canal is
enlarged
Vascular Neoplasms
-paraganglioma:
-most common cause for objective pulsatile
tinnitus and a vascular hypotympanic mass
-MRI: enhances on T1 “salt and pepper”
appearance d/t flow voids
-glomus jugulare:
-supplied mostly by ascending pharyngeal
artery
-some contributions from posterior
auricular and occipital arteries
Other Vascular-related Conditions

-dural AVF
-direct anterior venous connection between
meningeal branches of external carotid artery and
dural venous sinus
-pulsatile tinnitus
-detected by selective angiography of external
carotid artery
-tx: intra-arterial embolization
1028
-benign intracranial hypertension (pseudotumour cerebri)
-can also cause subjective pulsatile tinnitus
-MRI to r/o significant intracranial mass (none)
-LP to confirm and relieve elevated CSF pressure
-other causes of pulsatile tinnitus:
-arteriosclerosis, fibromuscular dysplasia, arterial dissection, arteritis
INTERNAL AUDITORY CANAL AND CEREBELLOPONTINE ANGLE LESIONS
-IAC contents: vestibulocochlear nerve, facial nerve, nervus intermedius, labyrinthine artery, sometimes a
loop of AICA
Neoplasms
-vestibular schwannomas (acoustic neuromas)

-5-10% of all intracranial tumours
-MRI: T1: hypointense/isointense to brain; enhances hetergeneously on contrast
T2: hyperintense
-meningioma
-second most common CPA tumour
-trigeminal neuropathy more common
-MRI: T1: isointense to brain; enhance intensely and homogeneously post-contrast
T2: isointense or hyperintense
1029
Congenital Lesions
-epidermoid cyst:
-third most common lesion of CPA
-MRI: T1: hypointense; no enhancement
T2: hyperintense
-arachnoid cysts:
-MRI: T1: low intensity
T2: high intensity
-lipoma:
-presumed to arise as a result of maldifferentiation of meningeal precursor tissues
-CT and MRI show fat-containing lesion in CPA
-CT: -dark
-MRI: T1: bright
T2: dark
Inflammatory
-granulomatous processes such as sarcoidosis can involve IAC and CPA
-postcontrast T1 images abnormal leptomeningeal thickening and enhancement
Vascular Lesions
-microvascular loop compression syndrome

-may cause trigeminal neuralgia and hemifacial spasm
-caused by vascular loop compressing trigeminal and facial nerve
-associated with atherosclerotic and tortuous vertebrobasilar vessels
-best seen on T2 and MRA images:
-dolicoectasia of basilar artery toward affected side when a prominent loop of the AICA
is seen near the vestibulocochlear nerve complex
1030
INFECTIONS OF THE EXTERNAL EAR
-lymphatic drainage of EAC:

-anterior and superiorly preauricular lymphatic in parotid gland and superior deep cervical
nodes
-inferior infra-auricular nodes near angle of mandible
-posteriorly postauricular nodes and superior deep cervical nodes
-venous and arterial supply:
-superficial temporal and posterior auricular branches of external carotid artery and veins
-innervation:
-from cutaneous and cranial nerves:
-auriculotemporal branches of CN V
-CN VII, IX, and X
-greater auricular nerve from cervical plexus (C2-3)
-human cerumen is hydrophobic and acidic; contains lysozyme and immunoglobulin
OTITIS EXTERNA
-acute OE:
-usually begins with itching instrumentation with Q-tip or fingernail
-removal of protective lipid film allows proliferation of bacteria “itch-scratch cycle”
-rapid bacterial growth purulent discharge
-may progress to subacute to chronic forms
History
-pain, fullness, itching, hearing loss
Bacteriology
-Pseudomonas aeruginaosa, Proteus mirabilis, staphylococci, streptococci, and various gram-negative
bacilli
-swabs usually taken for recalcitrant infections
Staging
-Senturia et al:
-preinflammatory
-acute inflammatory: mild, moderate or severe
-chronic inflammatory
-preinflammatory:
-stratum corneum becomes edematous d/t removal of protective lipid layer
-plugging of apopilosebaceous unit
-pt feels sense of fullness or itching
-acute inflammatory:
-pain and tenderness of auricle
-mild: mild erythema and minimal edema with small amount of cloudy secretion
-moderate: thicker more profuse exudate
-severe: increased pain and obliteration of lumen with profuse greenish-grey purulent exudate
F.Ling - External Ear Infections (1)
1031
-chronic inflammatory:
-less pain but more profound itching for a longer period
-mild edema of canal skin may extend to skin of concha secondary changes:
-eczematization, lichenification and superficial ulceration
-bullous external otitis
-granular external otitis
-perichondritis
-chondritis
-relapsing polychondritis
-furunculosis
-carbunculosis
-other dermatomes: eg. psoriasis and seborrheic dermatitis
Natural History
-acute: spread of infection to adjacent preauricular tissues, face and neck
-may progress to perichondritis, chondritis, cellulitis, erysipelas
-chronic: excoriation canal skin becomes lichenified complete obliteration of canal
Medical Treatment
-fundamentals:
-frequent and thorough cleaning
-judicious use of appropriate antibiotics
-treatment of associated inflammation and pain
-recommendations regarding prevention of future infections
-in absence of purulence - brief course of acidifying drop efficacious in discouraging bacterial or fungal
growth
-antibiotic drops:
-Cortisporin: neomycin-hydrocortisone
-Cipro HC
-Moderate Stage:
-insert wick and instill drops on it expands and presses soft tissues and periosteum toward
nondistracted position may also relieve pain
-antibiotic drops continues for 2-3 days after cessation of pain
-oral antibiotics in mild and moderate stages is of no proven value
-Severe Stage:
-add oral antibiotics with broad-spectrum coverage for 10-14 days
-antistaphylococcal penicillins, 1o cephalosporins, antipseudamonal fluoroquinolones
(ciprofloxacin, levofloxacin, gatifloxacin)
-fluoroquinolones contraindicated in pts under age 18
-warm compresses and local wound care
-Chronic Stage:
-repeated cleaning and instillation of antibiotics and steroids
-triamcinolone acetonide 0.25% cream or ointment (Kenalog)
-dexamethasone sodium phosphate 0.1% (Decadron, Pred Forte 1%) ophthalmic drops
-avoid placing FB in ear canal
-may try acidifying drops: 1:1 vinegar:water or ethyl alcohol:water
1032
Surgical Management of Hypertrophic Chronic Otitis Externa
-when local measures are insufficient to eradicate infection must remove involved canal skin and any
adjacent involved cutaneous or cartilaginous tissue
-rarely required but performed through postauricular incision
-wide meatoplasty
-canal resurfaced with STSG
NECROTIZING (MALIGNANT) EXTERNAL OTITIS
-progressive osteomyelitis of temporal bone

-mainly in diabetics, immunocompromised and elderly
Diagnosis
-four salient features:
-persistent severe otalgia for longer than 1 month
-persistent purulent otorrhea with granulation tissue for several weeks
-diabetes mellitus, another immunocompromised state or advanced age
-cranial nerve involvement
Clinical and Radiographic Findings

-granulations in external canal
-rare to see granulation tissue in patients with routine otitis externa; however granulations
common in an acute exacerbation of chronic otitis media with perforation of TM
-organism:
-almost always P. aeruginosa
-P. mirabilis, Aspergillus fumigatus, Proteus sp. Klebsiella sp., Staphylococcus sp
-natural hx:
-relentless progression to involve cranial nerves (VII 75%, X 70%, XI 56%)
-progression of disease (Naldol):
1. EAC with invasion of fissures of Santorini or tympanomastoid suture to
retromandibular fossa
2. Involvement of stylomastoid an jugular foramen
3. Septic thrombosis of lateral venous sinus
4. Spread to petrous apex through vascular and fascial planes and not air cells
-CT findings:
-erosion of anterior canal wall with involvement of TMJ
-erosion of tympanic ring and base of skull
-soft tissue thickening and mastoid clouding
-other tests:
-MRI - define medial extent of disease at skull base
-detect presence of infection
-Tc-99m bone scanning:
-evaluates osteoblastic activity, excellent for localization
-documents present of osteomyelitis
-Ga-67 scanning :
-indicator of active inflammation
-use this scan to follow resolution of disease
-stages:
-I: limited to soft tissue and cartilage
-II: soft tissue and bony erosion of temporal bones
-III: intracranial extension
1033
Medical Treatment
-control underlying medical condition if possible (eg. diabetic control)
-obtain cultures
-otic drops
-anti-Pseudomonas antibiotics for 6 weeks or more
-eg. 3rd generation cephalosporin (ceftazidime) + quinolone (ciprofloxacin)
-eg. pip/tazo +gentamycin or tobramycin or amikacin
-eg. imipenem or meropenem
-eg. gentamicin or tobramycin +/- ticarcillin or piperacillin
-eg. mezlocillin or azlocillin
-eg. ceftazidime, imipenem, aztreonam, amikacin, norfloxacin, ciprofloxacin
-must continue on antibiotics despite improvement of symptoms
-regular debridement
-other:
-HBO: thought to facilitate osteoneogenesis and promote repair of diseased bone; value
questionable
-indications of improvement:
-resolved otalgia
-resolution of granulation tissue
-improved gallium scan
Surgical Treatment
-controversial
-reserved for pts who do not respond to conventional therapy
-excision of underlying necrosis and replace it with vascularized tissue
-wide local excision of infected cartilage and soft tissues
-middle ear exploration
-mastoidectomy
-facial nerve decompression
-temporal bone resection if no response
Complications
-cranial neuropathy
-meningitis, brain abscess and death
-overall mortality:
-37% before introduction of Abx; 23% afterward
-60% if multiple cranial nerve involvement
CONDITIONS RELATED TO EXTERNAL OTITIS
Radiation-induced Otitis Externa

-XRT weakens local defence mechanisms and allow resident bacteria to flourish
-osteoradionecrosis sequestra of devitalized tissue must be removed and replaced with vascularized
tissue
Bullous External Otitis

-vesicles or bullae noted in bony portion of EAC
-pathogens: H. influenzae, S. pneumoniae, M. catarrhalis, parainfluenzae, mycobacteria, mycoplasma
-do not rupture
-otic drops against Pseudomonas
1034
Granular External Otitis
-resembles earliest stage of NEO
-loss of TM for more than 1 month without middle ear disease
-pathogens: S. aureus, S. epidermidis, P. aeruginosa
-usually resolve with conventional treatment
-oral antibiotics if infection extends beyond canal
Perichondritis and Chondritis

-ear is indurated and erythematous
-causative organisms: P. aeruginosa > S. aureus > Enterobacter > Proteus mirabilis
-debridement, topical and oral antibiotics
-may need surgical debridement in OR
-excise necrotic cartilage
-intermittently progressive disease marked by inflammatory destruction of cartilage
-cartilage of external ear, larynx, trachea, bronchi, nose may be involved
-fever, anemia, erythema, swelling, pain and elevated ESR
-diagnosis based on hx and p/e supported by elevated ESR
-tx: oral corticosteroids
Furunculosis and Carbunculosis

-gram-positive infections (staph) of hair follicles
-usually at junction of concha and canal skin
-warm compresses, topical and oral antibiotics, +/- I+D
Infectious Eczematoid Dermatitis

-from drainage of contaminated material from middle ear into floor of EAC
-causes secondary infection or autosensitization phenomenon
-tx: controlling underlying middle ear infection; conventional treatment
Otomycosis
-fungal infection of skin of EAC
-Aspergillus sp. most common (A. niger, A. flavum, A. fumigatus, A. albicans; C. albicans)
-pruritus
-white, black or dotted gray membrane
-treatment:
-acidifying solutions:
-aluminum sulfate-calcium acetate (Domeboro)
-boric acid
-Castellani’s paint (acetone, alcohol, phenol, fuschin, resorcinol)
-clotrimazole cream or solution (Lotrimin)
-powders (in TM perforations):
-Metacresyl acetate (Cresylate) painted on margin of perforation
-nystatin powder
-gentian violet
-fungizone powder (amphotericin B)
-chloromycetin-sulfanilamide-tinactin (tolnaftate)
Herpes Zoster and Herpes Simplex

-burning pain, vesicles rupture and form crusts
-supportive treatment with topical application of H2O2 for crusts
1035
-?surgical decompression if facial nerve affected
-acyclovir, famcyclovir, valacyclovir ameliorate herpetic infections
-famcyclovir reduces duration of postherpetic neuralgia
Dermatoses
-allergic and irritant contact dermatomes
-erythema, weeping and vesiculation accompanied by itching
-tx: removal of causative agent and use of topical steroids and astringents
Psychocutaneous Diseases
-primary essential pruritus, neurodermatitis, delusions of parasitosis, factitial dermatitis
Keratitis Obturans
-cholesteatoma of EAC
-bony erosion of external auditory canal
-frequently associated with COPD, bronchiectasis, sinusitis
-tx: debridement
1036
NEOPLASMS OF THE EAR AND LATERAL SKULL BASE
NEOPLASMS OF CELL-SPECIFIC ORIGIN
Paraganglioma
-most common true neoplasm of middle ear

-most common pathologic condition involving jugular foramen
Origins
-arise from glomus bodies that occur in:
-adventitia of jugular bulb
-along tympanic branch of CN IX (Jacobson nerve)
-along auricular branch of vagus nerve (Arnold nerve)
Histology
-clusters (zellballen) of chief cells containing norepinephrine and dopamine
-arise from neural crest cells
-lack affinity for chromium salts “nonchromaffin paraganglia”
-only 1-3% actually secrete norepeinephrine
Epidemiology
-whites
-L>R
-F:M = 6:1
-peak incidence: 5th decade
-multicentric in 5%; if secondary to AD disorder 50% multicentricity
-metastases uncommon (3-4%): lymph nodes, lungs, liver, spleen and bone
-glomus tympanicum
-originate on promontory of cochlea
-conductive hearing loss and pulsatile tinnitus most common
-otalgia or bloody otorrhea
-multiple cranial neuropathies
-reddish pulsatile mass medial to inferior TM:
-Brown Sign: positive pressure during pneumatic otoscopy causes blanching of mass
-Aquino Sign: diminished pulsations with ipsilateral carotid artery compression
-objective tinnitus with auscultation
-glomus jugulare
-arise in jugular fossae
-jugular foramen syndrome (Vernet syndrome); + Horner’s = Villaret syndrome
-erosion of jugular fossa anteriorly and superiorly exposes petrous carotid artery and allows
tumour to invade middle ear CHL and pulsatile tinnitus
-intracranial extension can occur
Investigations
-24h urine vanillylmandellic acid and metanephrine if symptomatic (flushing, diarrhea, palpitations,
headaches, orthostasis, perspiration)
-CT temporal bones (high resolution)
-erosion of caroticojugular spine usually indicates glomus jugulare tumour
-MRI to evaluate intracranial extension
F.Ling - Temporal Bone Tumours (1)
1037
-vascular flow voids: salt and pepper appearance
-four vessel angiography
-for pre-operative planning
-pre-operative embolization to decrease intraoperative blood loss
Treatment
-complete surgical excision
-secreting tumours treated with adjunctive alpha- and beta-blockade
-glomus tympanicum:
-transcanal or hypotympanotomy approach
-extended facial recess approach
-glomus jugulare:
-transmastoid-transcervical exposure +/- facial nerve rerouting (Fisch A) or formal infratemporal
fossa dissection
-(see Vascular Tumours in Head and Neck Oncology section)
-XRT available but has little effect on primary tumour cells
-causes obliterative endarteritis in the vessels and controls rate of tumour growth
Epidermoid (Cholesteatoma)
-see Cholesteatoma notes
-most lesion of petrous apex and CPA are thought to be of congenital origin
-squamous metaplasia within temporal bone or intradural space proposed histogenesis
-developmental entrapment of ectodermal rests is more likely the cause
-slow infiltrative growth
-manifestations usually facial weakness, diminished facial sensation or facial pain
-histology:
-cyst lined with benign keratinizing squamous epithelium
-three components: sac or epithelial matrix, perimatrix, contents of cyst
-diagnosis:
-CT: well-defined homogeneous mass that contains areas of calcification
-MRI: low-signal intensity on T1; high signal intensity on T2; non-enhancing
-treatment:
-complete surgical excision by posterior fossa craniotomy
-complete excision difficult; 30% recurrence
Hemangioma and Hemangiopericytoma

-haemangioma:
-benign vascular proliferation arising from capillaries, arterioles or venules
-may be confused with paraganglioma, AN
-geniculate haemangiomas most common temporal bone haemangioma
-arise from superior aspect of geniculate ganglion and extend into floor of middle fossa
-localized inflammatory response frequently associated with facial nerve dysfunction
-treatment: observation surgical excision when severe facial nerve dysfunction occurs
-hemangiopericytoma:
-rare vascular tumour derived from pericytes
-metastatic spread in 50% lungs and bone
-treatment: wide excision; XRT and chemotx for extensive, recurrent or inoperable tumours
1038
Lymphoma, Plasmacytoma and Leukemia
-lymphoma:
-primary or metastatic
-conductive hearing loss, otalgia, otorrhea, fevers, facial nerve weakness, sensorineural hearing
loss
-treatment: chemotherapy and/or XRT
-extramedullary plasmacytoma:
-rare in temporal bone
-histology: sheets of monotonous round cells typical of plasma cells
-serum and urine analysis with monoclonal antibodies r/o multiple myeloma
-chemotherapy or XRT
-leukemia:
-marrow spaces in temporal bone infiltrated by leukemic cells
NEOPLASMS OF PINNA AND EXTERNAL AUDITORY CANAL
Cutaneous Carcinoma
-basal cell carcinoma:

-usually 6th decade of life; M>F
-more common on pinna and preauricular area than SCC
-locally infiltrating nodular growth with rolled border and central crusting ulcer
-metastasis rare
-histology: rim of palisading basaloid cells at tumour margin with central necrosis and ulceration
-treatment:
-complete surgical excision
-XRT as palliative therapy or adjunct therapy for extensive or recurrent tumours
-squamous cell:
-more common in EAC than BCC
-most SCC originate on pinna from sun exposure
-average age at diagnosis 7th decade
-SCC of EAC:
-chronic bloody drainage and sudden onset of deep ear pain suggest an invasive
malignancy
-ipsilateral facial nerve deficit
-metastasis:
-30% if temporal bone invasion
-15% if limited to pinna or membranous portion of EAC
-treatment:
-complete resection of lesions
-temporal bone invasion requires radiation therapy in addition to temporal bone resection
Melanoma (see Melanoma notes)
1039
Glandular Tumours
-rare tumours of EAC
-ceruminous adenoma:
-arise from ceruminous glands
-well-differentiated proliferating ceruminous glands that form solid, cystic, and papillary patterns
-ceruminous adenocarcinoma:
-invasive; metastasis to regional lymph nodes
-adenoid cystic carcinoma:

-most common glandular neoplasm of EAC
-lack capsule and consist of small hyperchromatic cells arranged in cribriform, tubular, or solid
patterns
-distant metastasis not uncommon
-more common in females
-invasive malignant tumours can extend radially through auricular cartilage and the fissures of Santorini
into the parotid gland or into surrounding periauricular tissue
-treatment:
-benign tumours: wide local excision
-malignant tumours:
-lateral temporal bone resection with parotidectomy and postoperative radiation +/-
cervical lymph node dissection for larger lesions
Osteomata and Exostoses
-osteoma:
-solitary pedunculate osseous lesions that originate on tympanosquamous and tympanomastoid
suture lines inside bony EAC
-if large CHL +/- OE
-removed with drill +/- STSG
-exostoses:
-broad-based osseous lesions that occur around circumference of medial aspect of bony EAC
-occurrence strongly associated with exposure to cold water
-postauricular approach; facial nerve at risk during drilling of posteroinferior aspect of bony canal
Miscellaneous Neoplasms of Pinna and EAC
-Merkel cell carcinoma

-rare but highly malignant neuroendocrine tumour
-treated with wide local excision, neck dissection, radiotherapy +/- chemotherapy
-squamous cell papilloma
-benign epithelial neoplasm
-HPV type 6 infection
-pilomatrixoma
-solitary cystic lesions originating from primitive hair matrix cells
-common in children
1040
-auricular endochondrial pseudocysts
-cyst-like degenerations of auricular cartilage
-from recurrent minor trauma
NEOPLASMS OF THE MIDDLE EAR, MASTOID AND TEMPORAL BONE
Adenomatous Tumours
-benign adenomas of middle ear

-rare nonaggressive neoplasms found in adolescents and young adults
-histology: benign glandular proliferation
-middle ear mass with intact TM
-excisional biopsy recommended
-endolymphatic sac tumours (EST)

-rare aggressive papillary tumours of middle ear
-association with von Hippel-Lindau disease:
-AD
-hemangioblastomas of retina and CNS along with renal cysts, renal carcinoma,
pheochromocytoma, pancreatic cysts, papillary cystadenomas of epididymis,
endolymphatic sac tumour
-60% of pts who also have hearing loss may eventually develop EST
-EST extend along endolymphatic duct in direction of bony labyrinth unilateral SNHL, tinnitus,
vertigo
-may have extensive spread into mastoid cavity, middle ear, middle fossa, EAC, Meckel’s cave,
IAC, cerebellum, posterior fossa, jugular foramen
-CT scans:
-soft tissue mass on posterior petrous face with erosion of adjacent regions of temporal
bone
-stippled, reticular or speculated areas of calcification
-“expansile” appearance
-MRI scans:
-T1: tumours less than 3 cm show circumferential rim of increased signal intensity
characteristic for only ESTs
-T2: scattered areas of increased signal intensity
-treatment:
-ideally total excision
-often extensive at presentation subtotal excision with regular follow-up and revision
surgery
Langerhans Cell Histiocytoses
-characterized by idiopathic histiocytic and eosinophilic proliferation

-histiocytes: mobile macrophages that originate in bone marrow
-eosinophilic granuloma
-unifocal bony lesion - frontal and temporal bones, mandible
-histology: localized collection of histiocytes and polygonal and sheet formation
-dx: bone scan and open biopsy
-tx: surgical excision with XRT for recurrence
1041
-Hand-Schueller-Christian disease
-chronic disseminated form of LCH
-classic symptoms:
-chronic otorrhea
-diabetes insipidus
-exophthalmos
-polyostotic lesions: “punched-out” or “moth-eaten” appearance
-involvement of abdominal viscera and cutaneous lesions
-tx: vinblastine and corticosteroids or XRT
-Letterer-Siwe disease
-HSM, lymphadenopathy, bleeding diathesis, anemia, cutaneous lesions, generalized hyperplasia
of macrophages
-acute disseminated form of LCH
-highly fatal
-tx: chemotherapy
Sarcoma and Chordoma
Sarcomas:
-exceptionally rare; in children however: most common primary malignancy of temporal bone
-rhabdomyosarcoma:
-30% of sarcomatous lesions (most common)
-80% pts <12 ya
-originate from pleuripotential mesenchymal cells in middle ear and eustachian tube
-histological subtypes:
-embryonal
-most common
-small round and spindle-shaped primitive mesenchymal cells in loose myxoid
or compact pattern
-botryoid
-alveolar
-sheets of round, oval, or straplike cells arranged in trabecular pattern
surrounding empty alveolar compartments
-pleomorphic
-anaplastic multinucleated spindle cells that form whorls and fascicles with
longitudinal striations
-dx: biopsy
-tx: limited surgical intervention, XRT and chemotherapy
-survival rarely exceeds 50%
-chondrosarcoma:
-petroclival region near foramen lacerum and petrous apex most common location of origin
-present with multiple CN neuropathies
-surgical excision primary therapy; recurrences common - resistant to XRT and chemotx
-other rare tumours:

-Ewing sarcoma
-osteogenic sarcoma
-fibrosarcoma
1042
Chordomas
-low- to intermediate-grade malignancies that result from defective embryonic remnants of notochord
-occurs in clivus but also as primary intracranial or nasopharyngeal soft tissue tumour
-histology:
-stellate, intermediate and vacuolated physaliphorus or soap-bubble cells in mucoid matrix
growing in nests, cords, or trabeculae
-stains positive for cytokeratin
-slow growing; metastasis unusual
-headache, diplopia and visual deficits common
-imaging:
-CT scan:
-bony erosion of clivus or basiocciput in midline
-MRI:
-high signal on T1; low signal on T2
-tx: -surgical excision via transoral-transpalatal or infratemporal fossa approach
-recurrence common
Dermoid, Teratoma, Choristoma

-mass lesions resulting from errors in fetal development
-dermoids:
-rare cystic lesions in temporal bones
-thought to originate at point where 1st branchial cleft (anlage of EAC) lies adjacent to 1st
branchial pouch (anlage of middle ear and ET)
-suggests histogenesis related to incomplete closure at lines of fusion b/n branchial
elements
-have both mesodermal and ectodermal components
-lined by keratinizing stratified squamous epithelium that contains hair follicles, sebaceous glands,
smooth muscle and adipose tissue
-teratomas:
-rare in temporal bone
-arise from pluripotential stem cells near notochord
-contain all three embryonic germinal layers
-symptoms include facial paralysis, hearing loss and airway obstruction
-tx: surgical resection
-choristoma
-normal tissue that occurs in nonnative location
-eg. salivary tissue (most common), sebaceous glands and neural tissue in middle ear
-only require incisional or excisional biopsy
Cholesterol Granuloma
-mass lesion that results from reactive process within temporal bone
-hypothesis of pathogenesis:
-interference with drainage of middle ear
-haemorrhage
-obstruction of ventilation
-foreign body reaction to cholesterol crystals derived from haemoglobin catabolism
-thought to be start secondary to temporal bone trauma, ETD or mucosal edema
1043
-histology:
-cholesterol crystals surrounded by multinucleated giant cells, round cell infiltration, hemosiderin-
laden macrophages
-imaging: MRI: nonenhancing lesion bright on BOTH T1 and T2 weighted images
-treatment: drainage
NEOPLASMS OF INTERNAL AUDITORY CANAL AND CPA
-see CPA tumour notes
Schwannoma
Meningioma
Lipoma
-rare
-imaging:
-T1 MRI: bright
-T2 MRI: dark
-nonenhancing
-confirmed with MRI fat suppression
-usually expectant management
-surgery for progressive or disabling symptoms
METASTATIC DISEASE
-infrequent but not insignificant

-breast > lung > kidney > GI > larynx > prostate > thyroid
-may cause hearing loss, facial paralysis or dysequilibrium
1044
CONGENITAL AURAL ATRESIA
-incidence 1/10 000 to 1/20 000

-bilateral in approximately 1/3 of cases
-most significant difference between major and minor malformations of the ear involves status of the EAC
EMBRYOLOGY
External Auditory Canal

-EAC derived from 1st branchial groove and initially represented by a solid core of epithelial cells that
extends down to area of tympanic ring and first pharyngeal pouch
-in middle trimester, absorption of epithelial cells begins, progressing in medial to lateral direction
-malformation of tympanic bone produces atretic bone at level of tympanic membrane and results in atresia
of ear canal
Mastoid and Middle Ear

-eustachian tube, middle ear, and mastoid air cells are derived from 1st pharyngeal pouch
-a well-pneumatized mastoid usually indicates good middle ear development, including size of tympanum
and formation of ossicles
-ossicles, except for vestibular portion of stapes footplate, are formed from 1st and 2nd branchial arches
-EAC and TM derived from first branchial cleft
Facial Nerve
-abnormalities of facial nerve common in cases of aural atresia
-bony dehiscence frequently occurs and nerve may take an anomalous course
-typically, facial nerve makes an acute angle at second genu crossing middle ear in a more anterior
and lateral direction
-a correlation b/n degree of microtia and extent of facial nerve abnormality has been observed
PATIENT EVALUATION
-two principal objectives:
-assess overall hearing status and need for immediate amplification
-formulate a treatment plan that provides for consultation with members of other specialties
PHYSICAL EXAMINATION
-focus on overall craniofacial development
-look for abnormalities or syndromes involving first or second branchial arch
-evaluate facial nerve function:
-most common anomaly of facial function is congenital absence of depressor anguli oris muscle
Audiometric Evaluation
-essential to determine level of cochlear function in each ear to prevent operating on an only-hearing ear or
on an ear with little or no potential for hearing improvement
-bone conduction ABR can provide valuable information
Computed Tomography
-necessary in all pts being considered for surgery
-used to examine for possible cholesteatoma formation
-decision to operate depends primarily on degree of middle ear development, as reflected by size of
tympanum and status of ossicles
F.Ling - Congenital Aural Atresia (1)
1045
MEDICAL MANAGEMENT
Unilateral Atresia
-no immediate intervention needed if contralateral hearing is normal
-bone conduction hearing aids for adults who want them
Bilateral Atresia
-early amplification essential in infants with bilateral atresia
SURGICAL MANAGEMENT
Unilateral and Bilateral Atresia Repair

-many surgeons reluctant to repair unilateral atresia:
-uncertain degree and predictability of hearing improvement
-potential lifetime care of mastoid cavity
-risk to facial nerve in atresia surgery
-many recommend delaying surgery in unilateral cases until adulthood, when pts can make their own
decisions based on risks and benefits
-for pts with bilateral atresia, goal is to restore sufficient hearing so that amplification is no longer needed
-“best” ear is selected for initial surgical procedure
Selection Criteria
-risk of surgical complications will be minimized and chances for successful hearing result are increased if
middle ear and mastoid size are at least 2/3 of normal size and if all three ossicles, although deformed, can
be identified
-relationship of the facial nerve to the oval window is noted
-anterior displacement reduces the chance for successful hearing and increases the chance of
facial nerve injury
-unilateral cases: only ideal candidates are selected
-minimal criteria in bilateral cases:
-middle ear of at least ½ normal size and presence of an ossicular mass
Timing of Surgery
-can be performed as early as 5-6 years
-pneumatization of temporal bone is well advanced
-children old enough to cooperate with postop care
-permits microtia repair
Cholesteatoma
-pts with cholesteatoma should undergo surgery to eradicate disease process and if possible improve
hearing
-an average canal diameter of 4 mm or less 50% will develop cholesteatoma
-preponderance of cholesteatomas developed in canals 2 mm or less in diameter
-usually no cholesteatoma seen for child < 3 years of age
-therefore can wait far CT at age 6-8 years of age
1046
SURGICAL TECHNIQUE
-two basic approaches:

-mastoid approach
-essentially via a wall-down mastoidectomy
-sinodural angle first identified and followed to antrum
-facial recess opened and incudostapedial joint separated
-atretic bone then removed
-anterior approach
-drilling confined to area defined by TMJ anteriorly, middle cranial fossa dura superiorly,
and mastoid air cells posteriorly
-avoids creation of mastoid cavity
-anterior/posterior approach
-wall-up mastoidectomy to identify the lateral SCC
-gives approximate level of ossicles
Anterior Approach
Incision
-postauricular incision used to expose mastoid bone
-elevated anteriorly until a depression that represents the TMJ is encountered
Drilling a Canal
-middle cranial fossa dura is superior landmark
-TMJ is anterior landmark
-epitympanum will be entered and fused heads of malleus and incus identified
-facial nerve always lies medial to ossicular mass in epitympanum
-vulnerable to injury as external canal is enlarged in the posteroinferior direction
-in this area, may lie lateral to middle ear cavity in addition to being anteriorly displaced
Exposure of Ossicular Chain

-malleus neck or deformed manubrium typically fused to atretic bone
-to free ossicular chain, overlying bone is thinned carefully and then completely removed with
incudostapedial joint knife or hook
-bone should be completely removed around the ossicles
Middle Ear Surgery

-in most cases, ossicular chain, although deformed is mobile and hearing results may be better when chain
is left intact instead of interpositioning a prosthesis or autograft material
Tympanic Membrane Grafting

-fascia graft placed
Meatoplasty
-auricle undermined and soft tissue debulked from approximate area of meatus
-circular meatal opening about twice normal size is made
Skin Grafting
-STSG positioned in bony canal to overlap fascia graft
-packing used to maintain graft position
1047
SURGICAL FINDINGS
Ossicles
-expected finding is a fused and deformed malleus-incus complex
-malleus is typically more deformed than incus and has a short manubrium
-stapes is usually small and delicate with misshapen crura
Facial Nerve
-abnormalities common in major atresia pts
-anterior and lateral displacement of mastoid segment (most common)
-complete dehiscence of tympanic segment
-inferior displacement of tympanic segment
-higher incidence of facial nerve anomalies occur in pts with more severe microtia
HEARING RESULTS
-various results
-with carefully selected patients, hearing level of 20-30 dB in only 40-60% of patients
-near-normal hearing is not universally achieved even in carefully selected atresia pts
COMPLICATIONS
-revision surgery often required for:

-canal stenosis (most common)
-TM lateralization
-due to complications, must include option of BAHA as surgical option
Labyrinthine Injury
-high frequency SNHL has been noted in some pts postop (2-4%)
-drilling on bone may be transmitted to inner ear
Facial Nerve Injury

-facial nerve monitoring should be used in all cases
-anomalous nerves common
-to avoid injury, drilling should be concentrated superiorly along middle cranial fossa dural plate
-avoid drilling in posteroinferior direction because of the more anterior and lateral course of mastoid
segment
Canal Stenosis
-may develop in as many as 25% of pts
-secondary meatoplasty may be needed if significant stenosis causes trapping of debris leading to infection
-coverage of all bone by STSG needed to reduce granulation tissue formation
-stenosis may be due to displacement of pinna permanent suspension sutures to mastoid periosteum can
be used for proper realignment
Chronic Infection
-lack of normal migration of keratin debris and sebaceous and apocrine glands
-incidence of canal infections is higher
-may require regular cleaning
1048
Conductive Hearing Loss
-persistent CHL d/t:
-inadequate mobilization of ossicular mass from atretic bone
-unrecognized incudostapedial joint discontinuity
-fixed stapes footplate
-recurrence of CHL d/t:
-refixation of ossicular chain
-TM lateralization
1049
INTRATEMPORAL AND INTRACRANIAL
COMPLICATIONS OF OTITIS MEDIA

COMPLICATIONS OF OTITIS MEDIA
Precursors to Complications 1. Intratemporal:

A. Mastoiditis
-associated with subperiosteal abscess
EARLY SIGNS OF COMPLICATION -lateral mastoid abscess
-medial tip abscess (Bezold)
Impending complication -“masked”
-persistence of acute infections for 2 weeks B. Petrositis
-recurrence of symptoms within 2 weeks C. Labyrinthitis
-acute exacerbation of chronic infection, especially if fetid -serous
-fetid discharge during treatment -suppurative
-Haemophilus influenzae, type B or anaerobes -otogenic
-meningogenic
Early or obvious signs/symptoms of complications -chronic
-fever associated with chronic perforation (intracranial) D. Facial paralysis
-pinna displaced inferolaterally and/or edema of the
posterosuperior canal wall skin (mastoiditis associated with 2. Intracranial:
lateral mastoid abscess) A. Extradural granulation tissue and/or abscess
-retroorbital pain on side of infected ear (petrositis) B. Sigmoid sinus thrombophlebitis
-vertigo and nystagmus (labyrinthitis) -nonoccluding
-facial paralysis on side of infected ear -occluding
-headache and/or lethargy (intracranial) C. Brain abscess
-papilledema (intracranial) -cerebritis
-meningismus (meningitis) -latent period
-focal neurologic signs and/or seizure (brain abscess) -abscess
-catastrophic neurologic signs (intracranial) -termination
D. Otitis hydrocephalus
E. Meningitis
F. Subdural abscess
-high risk pathogens:

-Type III pneumococcus (intracranial predilection)
-H. influenzae type B (higher risk of meningitis)
-presence of coexisting anaerobes
-routes of spread into the intracranium:

-direct extension from bone erosion
-lymphatic or hematogenous spread
-invasion through normal anatomic structures (labyrinth)
-spread through iatrogenic or traumatic defects
-extension through Hyrtle’s Fissure (embryologic remnant that connects hypotympanum to
subarachnoid space)
SYSTEMATIC APPROACH
Mastoiditis
-acute coalescent mastoiditis with subperiosteal abscess lateral to mastoid cortex and medial to concha
characteristically occurring 2 weeks after onset of acute suppurative otitis media
-pathogens:
- S. pneumoniae (most common)
-group A streptococcus (S. pyogenes)
-Staphylococcus epidermidis, Haemophilus influenzae, anaerobes
F.Ling - Complications of Otitis Media (1)
1050
-acute suppurative otitis media should respond within 3-5 days to appropriate antibiotic therapy
-if no response to Abx within first week, mastoiditis considered possible
-postauricular edema, subperiosteal abscess, or recurrence of pain within 2-3 weeks after onset of
acute suppurative otitis media, mastoiditis should be considered imminent
-tx: -from acute OM: ceftriaxone alone +/- flagyl

-from chronic OM: aztreonam + clindamycin or ceftazidime + nafcillin + flagyl
- early surgical intervention recommended
-acute or subacute: large myringotomy removal of ear granulations, mastoidectomy for recalcitrant
disease
-chronic: modified radical mastoidectomy
-conditions for surgical treatment:
-coalescence
-failure to respond to antibiotics
-significant abscess
-intracranial complications
-coalescence surgery
-non-coalescence medical management, myringotomy
Subperiosteal Abscess
-mastoiditis that results in spread of infection to involve outer mastoid cortex elevating the periosteum
-SSx: edema, erythema, and tenderness over site of abscess; associated suppurative otitis media; fever
-postauricular abscess:
-most common site, spread through emissary veins or through bone
-may present with a pinna protruding outward from mass effect
-Bezold’s abscess:
-spread through a perforation in the mastoid cortex, tracts into SCM
-presents as a mass in the posterior triangle of the neck
-tx: parenteral antibiotics, mastoidectomy with drainage of the abscess
Petrositis
-Gradenigo syndrome:
-retroorbital pain, abducens palsy, ipsilateral acute or chronic otitis media
-tx: -parenteral antibiotics
-consider modified radical mastoidectomy extending toward petrous apex (if coalescent)
-approaches to the petrous apex:
-through the superior semicircular canal
-behind superior canal and above the horizontal canal
-infralabyrinthine
-through a triangle defined by the anterior border of the cochlea, the internal carotid
artery, and the middle fossa dura
-infracochlear
-through the root of the zygomatic arch
-anterior to the labyrinth
-treatment similar to treatment of acute mastoiditis
Labyrinthitis
-can be fatal if suppurative labyrinthitis (extremely rare) and meningitis occur
-serous labyrinthitis:
-toxic or metabolic products of bacteria or host inflammatory response enter inner ear through
round window membrane or cholesteatoma-induced fistula SNHL and vertigo with nystagmus
-hearing is recoverable
1051
-suppurative labyrinthitis:
-entrance of bacteria into labyrinth extensive inner ear and spiral ganglia cell loss
-profound HL that never resolves
-tx: clear up middle ear infection with Abx and myringotomy
-chronic infection surgical intervention
-removal of cholesteatoma
Labyrinthine Fistula
-chronic suppurative otitis media from a cholesteatoma erodes the bone of the labyrinth (most commonly at
the arch of the horizontal canal)
-dx: CT scan, fistula test (high false negative rate)
-tx: surgical exploration via a mastoidectomy with exteriorization of cholesteatoma
-matrix should be left intact over lateral SCC
-graft site if fistula is exposed; parenteral antibiotics if infected
Facial Paralysis
-facial paralysis in presence of subacute infection, acute coalescent mastoiditis, mask mastoiditis, petrositis,
or chronic suppurative otitis media may be destructive particularly in the tympanic segment
-cholesteatoma the most common cause of facial paralysis
-tx:
-clearing middle ear infection as rapidly as possible with Abx and myringotomy
-surgical intervention for subacute or chronic infection with evidence of neural degeneration
-do not open nerve sheath - perineurium is a barrier to infection; neural tissue lacks resistance to
infection
Extradural Granulation Tissue or Abscess

-careful inspection of dura of tegmen tympani, tegmen mastoideus, and sigmoid sinus
-bone does not need to be removed to identify normal or abnormal dura
-if dura appears abnormal, bone should be removed over abnormal dura until normal dura is encountered
-granulation tissue removed without perforating dura; some tissue will be left
Sigmoid Sinus Thrombophlebitis

-SSx:
-may show signs of toxaemia (“picket fence” spiking fevers, torticollis and septic embolization
-papilledema
-Griesinger’s sign: pain over mastoid from occlusion of mastoid emmisary vein
-jugular foramen syndrome
-dx:
-diagnosed by MRI with and without gadolinium: increased signal intensity in both T1 and T2
-MRA may reveal total/partial occlusion
-Tobey-Ayer or Queckensteadt’s test
-normally external compression of jugular vein results in a rapid increase in CSF
pressure of 50-100 mmHg
-compression on the side of sinus thrombosis results in a slow rise or no rise in CSF
pressure secondary to obstruction
-tx:
-parenteral antibiotics
-expose diseased dura and remove excess granulation tissue
-controversial:
-expose sigmoid sinus insert 22 gauge needle if no blood, then insert 18 gauge needle
to aspirate sinus
-if frank pus is present carefully open sinus and evacuate thrombus if infected and
1052
septic emboli
-aspirate clot if suspect abscess
-anticoagulant therapy
-ligation of IJV if continued septic emboli despite initial surgery and postoperative antibiotics
Otitic Hydrocephalus (Pseudotumour Cerebri)

-increase ICP 2o acute or chronic middle ear infection w/o evidence of meningitis or subdural or brain
abscess
-occlusion of sigmoid sinus causing intracranial hypertension
-theory: condition arises as a result of arachnoid villi obstruction secondary to retrograde
thrombophlebitis extension from lateral sinus to sagittal sinus
-SSx: chronic course (weeks), papilledema, diplopia nausea, headache and lethargy, abducens palsy
-tx: -requires mastoidectomy appropriate for disease
-exposure of all diseased dura to normal dura
-removal of excess extradural granulation tissue
-not advisable to do thrombectomy
-medical: furosemide and mannitol; consider corticosteroids, lumbar puncture and shunting
lower intracranial pressure
Brain Abscess
-most common sites: temporal lobe or cerebellum
-four clinical stages:
-invasion (initial encephalitis)
-low-grade fever, drowsiness, headache, malaise
-localization (latent or quiescent abscess)
-silent, no symptoms usually
-enlargement (manifest abscess)
-abscess produces focal symptoms
-termination (abscess rupture) rapid death
-tx:
-surgical aspiration of abscess (intracranial and/or via ear)
-IV antibiotics
-surgical excision if gas within the abscess cavity
Meningitis
-most common intracranial complication of otitis media
-three pathways of spread:
-direct extension
-thrombophlebitis
-hematogenous dissemination
-severe Mondini malformation suspected if:
-rapid onset of meningitis within hours of acute suppurative OM in which organism is S.
pneumoniae or nontypable H. influenzae and unilateral or bilateral congenital profound SNHL
and vestibular deficit
-allow unusual connections b/n CSF through IAC, vestibule and stapes footplate
-communicating meningoencephalocele if above symptoms in adults
-pathogens:
-H. influenzae type B, Pneumococcus, hemolytic streptococcus
-dx:
-lumbar puncture for cells and culture
-elevated CSF pressure, decreased CSF glucose, presence of inflammatory cells and bacteria,
increase in protein content
1053
-tx:
-IV antibiotics and myringotomy
-33% of meningitis survivors suffer neurologic sequelae:
-behavioural disorders, mental retardation, deafness
-dexamethasone shown to reduce inflammatory sequelae and not interfere with antibiotic
treatment
-for subacute or chronic mastoiditis:
-ceftazidime for meningitis caused by P. aeruginosa
-metronidazole for anaerobic infection
-surgical debridement
Subdural Abscess
-pus collection between dura and arachnoid membrane
-three mechanisms:
-direct spread through dura
-retrograde venous thrombosis
-brain abscess rupture into subdural space
-dx: CT/MRI reveals crescent shaped enhancement (less resistance to spread) that does not cross midline
-tx: -clearing ear infection with IV antibiotics and myringotomy
-treating subdural abscess: mastoidectomy, careful exploration of dura with removal of excess
granulation tissue; neurosurgery consult
Epidural Abscess
-epidural abscess second most common of all intracranial complications arising from middle ear infections
-pus collection between skull and dura
-most commonly from direct extension via bone erosion
-tx: high-dose parenteral antibiotics and surgical drainage
COMPLICATIONS OF TREATMENT
Complications of Inadequate Antibiotics or Drainage

-undertreated complications more likely to extend medially into intracranial cavity than externally
Complications of Surgery
-excessive blood loss
-blood can be lost rapidly during course of mastoidectomy
-brain herniation
-pulmonary emboli
-air embolism
-tx: HBO and helium treatment
EMERGENCIES
Emergent Presentation of Disease

-vertigo and nystagmus with ear infection
-immediate potential for suppurative labyrinthitis followed by meningitis within minutes to hours
-requires admission to hospital, antibiotics and local ear care
-facial paralysis with ear infection
-mastoidectomy and additional surgical interventions best delayed until appropriate levels of
antibiotics are reached
1054
-headache lethargy/coma
-brain abscess
-otitis hydrocephalus
-meningitis
-subdural abscess
-seizure
-brain abscess
-focal neurologic deficits
-brain abscess
-subdural abscess
-meningismus
-meningitis
-ventriculitis
-subdural abscess
-carotid rupture
-reduction of visual fields or acuity
1055
MIDDLE EAR AND TEMPORAL BONE TRAUMA
History
Chief Symptoms of Temporal Bone Fractures

Symptom Differential Diagnosis Time of Onset Treatment Priority
Hearing Loss Conductive or sensorineural and degree Early Not urgent
Dizziness Peripheral or central Variable Not urgent
Facial weakness Central or peripheral Important to determine Early intervention
Facial hypesthesia Intratemporal cranial nerve V deficit or Usually late onset if intracranial Spontaneous recovery is the
facial injuries general rule
Diplopia Cranial nerve VI deficit or eye injury Usually late Spontaneous recovery is the
general rule
Hearing Loss
-up to 40% HI pts suffer hearing loss
-transverse fractures have greatest propensity for severe SNHL
-longitudinal fractures more frequently with conductive and mixed hearing loss
-labyrinthine or cochlear concussions high frequency SNHL with associated vertigo
-mechanisms of SNHL:
-disruption of otic capsule
-concussion injury
-NIHL
-perilymphatic fistula
-injury to auditory CNS
Dizziness
-often late complaints
-notice once becoming ambulatory
-causes of vertigo with trauma:
-post concussion syndrome (most common)
-concessive injury to membranous labyrinth
-cupulolithiasis
-disruptive injury to labyrinth
-traumatic perilymphatic fistula
-trauma-induced endolymphatic hydrops
Facial Weakness
-easily overlooked
-determination of time of onset important
-late-onset paresis or paralysis common after temporal bone trauma and may be delayed for days or weeks
-areas of facial nerve injury:
-longitudinal fractures: perigeniculate area
-transverse fractures: labyrinthine segment
-penetrating injuries: extra-temporal, stylomastoid portion, vertical segment of nerve
F.Ling - Temporal Bone Trauma (1)
1056
-mechanisms of injury:
-bony spicules
-perineural hematoma
-transection
-edema/swelling
Otorrhea and Rhinorrhea

-CSF leakage from temporal bone disruption
Facial Hypesthesia and Diplopia

-fractures involving Meckel’s cave and the superior surface of the temporal bone or Dorello’s canal
beneath the petrosphenoidal ligament
-prognosis usually very good
-three commonly seen findings for temporal bone trauma
-hemotympanum
-postauricular ecchymosis (Battle sign)
-periorbital ecchymosis (Raccoon eyes)
-facial nerve weakness requires careful evaluation
-CSF leakage: -diagnostic tests: chemical analysis, electrolyte determination, intrathecal dye injection,
and -2 transferrin protein identification
Radiologic Evaluation
-high-resolution CT scanning with bone algorithms
Temporal bone fracture type Longitudinal Transverse
Location -through petrosquamous suture line and continues -involve otic capsule or internal auditory canal
anterior to otic capsule
-through superior EAC, middle ear, long axis of
petrous pyramid
Frequency 70-80% 20-30%
Hearing loss -conductive -sensorineural (usually severe)

-frequently hemotympanum and ossicular
disruption
-incudostapedial joint separation most
common
Facial nerve paralysis -15-20% -50%

-injury at the geniculate ganglion or in horizontal
portion of nerve
Degree of trauma -low to high -usually high

-lateral blunt trauma -occipital or frontal trauma
Complications -ossicular damage common -otic capsule and IAC rupture

-CHL -SNHL
-vertigo rare -vertigo common
-bleeding in EAC -CSF leak common (rhinorrhea)
-CSF leak occasionally (otorrhea)
1057
-gunshot wounds or other penetrating trauma requires evaluation with angiography or MRA greater
possibility of internal carotid artery injury
-options for carotid injury:
-embolization
-surgical revascularization
-ligation
Other Tests
Hearing Tests
-if early surgery is not a consideration, preliminary test is not critical; conductive losses may be repaired at
any time and sensorineural losses have poor prognosis that are not influenced by treatment
Facial Nerve Testing

-if normal facial function exists in the early post-traumatic period, a delayed paralysis is always resolved
with the return of function
-patients who benefit from early surgery:
-immediate paralysis, no clinical evidence of return of function, no electrical responses after 1
week
-immediate paralysis and progressive decline of electrical responses to less than 10% of the
normal side (evaluated with EnoG)
-those with immediate paralysis and CT evidence of significant temporal bone disruption,
indicating severe nerve laceration or sectioning, and injuries often accompanied by CSF otorrhea
-neurotemesis evidenced by no return of function after 1 year
Vestibular Testing: no role
MANAGEMENT
Symptom or Sign No Treatment Non-surgical Treatment Surgical Treatment
Hearing loss May resolve if secondary to Amplification, conventional or Tympanoplasty with or without
hemotympanum CROS aid middle ear reconstruction
Dizziness Spontaneous resolution expected, Pharmacologic vestibular Labyrinthine ablation or vestibular

unless bilateral or central vestibular suppression for acute stage nerve section for long-term
lesion is incurred problems
Facial Paralysis Complete recovery expected in Supportive eye care Decompression or repair of facial
cases of delayed onset -physical therapy if long-term nerve
paralysis expected Measures necessary for eye care
-structured rehabilitation with (gold weight, or tarsorrhaphy)
biofeedback techniques helpful to
improve function and avoid
synkinesis
CSF otorrhea or Spontaneous resolution in > 90% of Elevation of HOB; lumbar drainage Resorted to only after 2 weeks and
rhinorrhea cases failure of conservative measures
-persistent leak
-recurrent meningitis
-persistent pneumocephalus
1058
FACIAL NERVE EXPLORATION AND REPAIR
-determine if fracture is otic sparing versus otic non-sparing

-will determine type of approach
-eg. longitudinal fracture with normal hearing: transmastoid approach
-eg. transverse fracture with no hearing: translabyrinthine approach
-eg. transverse fracture with normal hearing: middle fossa approach
Transmastoid Approach
-suitable only for lesions peripheral to geniculate ganglion
-not appropriate for transverse fractures
-lateral fracture defect involving mastoid cortex fracture line followed medially to facial nerve injury
-bone chips removed from nerve: examined for stretching, compression, laceration, or transection
-if intact decompression of epineural sheath in proximal and distal fashion until normal nerve
encountered
-partial transection repaired with onlay nerve graft
-if > 50% axon separation interpositioning graft
Transmastoid-Translabyrinthine Approach
-used if hearing is not useful and site of facial nerve injury proximal to geniculate ganglion
-usually for transverse fractures with involvement of otic capsule severe SNHL that will never recover
-makes visible the entire intratemporal course of the nerve and brainstem origin
-primary repair, grafting, or short-circuiting techniques are used from the posterior fossa to the parotid
portion of the nerve
Middle Cranial Fossa Approach

-used to expose portion of facial nerve medial to geniculate ganglion if hearing remains intact
Transmastoid Epitympanic Approach

-fractures involving labyrinthine portion of the internal auditory canal with preservation of hearing
REPAIR OF CEREBROSPINAL FLUID FISTULA
-consideration of hearing necessary in planning approach

-same procedures already described for nerve repair used for exposure of posterior or middle fossa
-large bony defects reinforced with Silastic sheeting in addition to fascial grafting, or muscle plugs sutured
to surrounding dura from the temporal side for small defects
POSTOPERATIVE CARE
-eye care essential for pts with facial paralysis

-routine antibiotic coverage not instituted unless dura has been opened surgically
-head elevation; steroids used in moderate doses if dura has been opened
1059
COMPLICATIONS
-failure of return of facial function

-facial function should return within 6-12 months after repair, depending on the site of injury
-if not returned EMG testing to identify early action potentials; CT scan to determine if any
sites missed
-meningitis
-brain herniation
-massive bleeding
-cholesteatoma
EMERGENCIES
-obvious brain herniation into middle ear, mastoid or external auditory canal
-massive bleeding from intratemporal carotid artery laceration
1060
CHOLESTEATOMA
CONGENITAL CHOLESTEATOMA
-embryonic rest of epithelial tissue in the ear without tympanic membrane perforation and without hx of ear
infection
-2/3 seen in anterior-superior quadrant
-mean age of presentation 4.5 years
-M:F = 3: 1
-usually dumbbell shaped
-pathogenesis unclear:
-failure of involution of ectodermal epithelial thickening in proximity to geniculate ganglion
-failure of “epidermoid formation” to involute development of cholesteatoma in anterior
mesotympanum
-other theory: metaplasia of middle ear mucosa
ACQUIRED CHOLESTEATOMA
Theories of Pathogenesis:
Primary acquired:
1. Invagination theory:
-blocked attic and localized negative pressure with retraction of pars flaccida
-pouch invagination occurs and eventually develops into an attic cholesteatoma as it accumulates
keratin
2. Otitis media with effusion theory:

-long-standing otitis media with effusion causing negative middle ear pressure by eustachian tube
dysfunction pouch invagination
3. Basal cell hyperplasia theory:
4. Epithelial invasion theory:

-invasion of middle ear skin from meatal wall of outer drum surface through a marginal
perforation or an attic perforation
-generally accepted theory for formation of secondary acquired cholesteatomas of posterior-
superior tympanic membrane
Secondary acquired:
1. Implantation theory:
-formation by iatrogenic implantation of skin into middle ear as result of surgery, FB or blast injury
2. Metaplasia theory:
-transformation of desquamated epithelium to keratinized stratified squamous epithelium secondary to
chronic or recurrent otitis media
3. Epithelial invasion theory:
F.Ling - Cholesteatoma (1)
1061
Factors involved in bone resorption
-mechanical
-pressure generated by expansion of cholesteatoma as it accumulates keratin debris
-biochemical
-bacterial elements (endotoxins)
-products of host granulation (collagenases, acid hydrolases)
-growth factors, cytokines
-cellular
-osteoclastic activity within subepithelial matrix of cholesteatoma
-release acid phosphatase, collagenase, and other proteolytic enzymes
SURGICAL ANATOMY
-most common locations of origin of cholesteatomas:

-posterior epitympanum
-posterior mesotympanum
-anterior epitympanum
-Prussak’s Space:
-origin of epitympanic cholesteatomas
-floor: lateral process of malleus and its
associated mucosal folds lying in the horizontal
plane
-boundaries:
-anterior/superior/posterior: lateral
malleolar fold
-inferior: lateral process of malleus
-medial: neck of malleus
-lateral: pars flaccida
-most common site of ossicular damage: long process of

incus
1062
-upper boundary defined by 3 well defined routes:
1. Posterior route:
-most common
-penetrates superior incudal space
lateral to body of incus then traverses
aditus ad antrum to enter mastoid
-AND/OR descends through floor of
Prussak space into posterior space of
von Troeltsch (pouch lying between
tympanic membrane and posterior
mallear fold) may involve stapes,
round window, sinus tympani, and
facial recess
2. Posterior mesotympanum route:

-pars tensa retracts into mesotympanum to form
cholesteatoma
-invade sinus tympani and facial recess
-difficult to remove
3. Anterior epitympanic route:

-develop as retraction pocket anterior
to malleus head
-epitympanic space limited:
-anterior: middle cranial
fossa, petrous tip, root of
zygoma
-posteriorly: bony ridge
(cog) extending to
cochleariform process
-superiorly: middle cranial
fossa
-laterally: tympanic bone
and chorda tympani
-associated with horizontal portion of
facial nerve may cause facial
paralysis
1063
PREVENTION
-tympanostomy tube for retraction pockets

-pockets may be adherent even after tube placement surgery may be necessary
-conductive deficit in excess of 35 dB indicates ossicular discontinuity:

-destruction of long process of incus or capitulum of stapes
-microscopic examination:
-erosion of bony canal in posterior-superior region
-granulation tissue may arise from diseased bone polyp may be seen
-pneumatic otoscopy:
-positive fistula response (vertigo and nystagmus) suggestive of erosion into inner ear (horizontal
SCC)
-ear must be carefully debrided
-topical antibiotic applied to “dry ear out”
-surgical goals*:
-1. treating complications (extradural abscess, brain abscess, facial nerve palsy, labyrinthitis)
-2. removing diseased bone
-3. obtain a dry ear
-4. preserve normal anatomy
-5. preserving or improving hearing
-CT scan (not diagnostic but suggestive):

-erosion of scutum and expansion of antrum within areas of air cell breakdown and soft tissue
density
-ossicular destruction and erosion of otic capsule
SURGICAL MANAGEMENT
Canal Wall-Up Procedure:

-preservation of posterior canal wall with or without a posterior tympanotomy (facial recess)
-posterior tympanotomy performed through triangle bounded by fossa incudis, facial nerve and chorda
tympani (facial recess)
-indicated in patients with well-pneumatized mastoid and middle ear space
-increased risk of undetected recurrence or residual cholesteatoma
-may require a “second look” procedure
-faster healing rate
-sclerotic mastoid, labyrinthine fistula, only hearing ear, poor eustachian tube function
Canal Wall-Down Procedure:

-taking down posterior canal wall to vertical facial nerve and marsupializing mastoid into external ear canal
-epitympanum obliterated with removal of scutum, head of malleus, and incus
-divided into:
-modified radical mastoidectomy: middle ear space is preserved
-radical mastoidectomy: middle ear space eliminated and eustachian tube plugged
-indicated for advanced disease, noncompliant patients, only hearing ear
1064
-provides good exposure and easier recognition of recurrent disease
-disadvantages:
-required cleaning of mastoid cavity, difficulty with hearing aid fitting, increased risk of infection
with water exposure
Bondy Procedure:
-removal of scutum and posterior canal wall with preservation of ossicles and middle ear space
EMERGENCIES AND COMPLICATIONS
Hearing Loss
-ossicular chain erosion in 30% of cases
Labyrinthine Fistula
-found in up to 10% of patients
-chronic ear disease, SNHL and /or vertigo induced by noise or pressure changes in middle ear
-fistulae of horizontal SCC most common
-tx: modified radical mastoidectomy
-leave matrix over fistula (1.5-2 mm) to prevent SNHL
Facial Paralysis
-due to infection or chronic expansion
-common site of nerve involvement is geniculate ganglion
Infections
-periosteal abscess: from blockage of aditus ad antrum or extensive erosion through mastoid cortex
-lateral sinus thrombosis
-intracranial abscess
Brain Hernia
-usually seen during revision surgery
-temporalis fascia graft to fix herniation
-large defect: repair from above via middle fossa approach
-small defect: repair from below with fascia patch
-defects larger than a few millimeters require conchal cartilage for support to prevent herniation
-area of brain in mastoid is necrotic and functionless remove it at the level of dural defect
1065
SURGERY OF THE MASTOID AND PETROSA
SURGICAL TECHNIQUE: MASTOIDECTOMY
Incisions
Postauricular Incisions
-Wilde
-afford best exposure
-generally made 8-10 mm behind postauricular crease
-in infants and children under 2 ya, inferior portion placed more posteriorly to prevent injury to facial nerve
-exposure of temporalis fascia; horizontal incision created along temporal line which is inferior margin of
temporalis muscle
-mastoid emissary vein may be encountered in making incision to mastoid cortex should be occluded d/t
possibility of introducing air embolism
-periosteum elevated off mastoid cortex, exposing posterior wall of external auditory canal
Endaural Incisions
-Lempert I: -canal incision medial to bony cartilaginous junction extending along entire posterior half
of canal
-Lempert II: -superior incision extending from Lempert I incision laterally between tragus and root of
helix at meatus of ear canal
-small relaxing incision made at inferior margin of Lempert I incision to allow mobilization of posterior
skin
-endaural incision for access to mastoid have become less commonly used d/t limitations of exposure
Surface Landmarks
-temporal line:
-indicates level of floor of middle cranial
fossa
-root of zygoma:
-extends anteriorly along temporal line
-spine of Henle:
-suprameatal spine
-eminence located near the posterosuperior
wall of the EAC
-Macewen Triangle (cribriform fossa):
-depression in area just posterosuperior to
suprameatal spine with an irregular bony
surface
-the apex, the most lateral extent of
petrosquamous suture line, signifies
location of underlying mastoid antrum
-tympanomastoid suture line:
-located posteriorly in EAC, reliable
landmark for the exit of the facial nerve
-tympanosquamous suture line:
embryonic fusion plane located posteriorly and inferiorly in the EAC, divides tympanic and mastoid
portions of the temporal bone
-vascular strip:
-thickened vascular skin of superior canal between tympanosquamous and tympanomastoid suture line
F.Ling - Surgery of the Mastoid and Petrosa (1)
1066
Simple Mastoidectomy
-used for: CLINICAL INDICATORS FOR MASTOIDECTOMY
-drainage of coalescent mastoiditis
-exposure of antrum, attic, labyrinth Indicators (one of the following)
-persistent or recurrent otorrhea
and endolymphatic sac -persistent or recurrent ear pain
-mastoid antrum generally located beneath -conductive hearing loss
point at intersection between a horizontal and -tympanic membrane perforation and/or cholesteatoma
vertical line drawn tangential to superior and -acute mastoiditis with osteitis
-neoplasm of temporal bone
posterior margins of external auditory canal -fracture of temporal bone with CSF leak
-cortex removed -facial nerve paralysis requiring decompression of facial nerve
-superior limit of dissection: temporal
line/tegmen
-Korner septum:
-bony plate lateral to actual antrum and is remnant of petrosquamous suture line
-divides mastoid air cells into medial and lateral regions
-posterior limit: sigmoid sinus
-in anterior protympanum, a projection of bone extending inferiorly from tegmen tympani, the “cog” can
obscure occult disease in anterior epitympanum and supratubal recess
Facial Recess Approach

-facial recess is an aerated extension of posterior-superior middle ear medial to tympanic annulus and
lateral to fallopian canal that may allow access to middle ear through mastoid cavity
-boundaries of facial recess:

-facial nerve
-chorda tympani
-incus buttress (near tip of short process)
-exposure will aid in complete removal of cholesteatoma involving facial recess

-excessive thinning of posterior wall may result in delayed breakdown of canal wall and recurrent
cholesteatoma
-landmarks of the facial nerve:

-cochleariform process
-facial nerve directly medial to process
-to find cochleariform process, find Jacobson’s nerve and follow it superiorly until you
reach the process
-tip short process of incus
-facial nerve lies medial and inferior
-lateral semicircular canal
-posterior semicircular canal
-chorda tympani nerve
-digastric ridge
-inferiorly, facial nerve may be encountered lateral to tympanic annulus in 65% of cases
-dehiscence of facial nerve in 55-57%
-most common area of dehiscence:
-tympanic portion, superior to oval window
-accounting over 50% of dehiscent nerves
-other areas:
-geniculate ganglion
-facial recess
1067
-tympanic sinus
-mastoid retrofacial air cell region
-most common site of injury to facial nerve: inferior to lateral semicircular canal after second genu
-other anomalies of the facial nerve:
-bifid nerve
-course inferior to oval window
-extended facial recess approach:

-chorda tympani removed
-bone between bony annulus and tympanic membrane and fallopian canal removed inferiorly
-exposes round window and hypotympanic area
-transmission of high-frequency sound from vibration of drill bit through incus and stapes could result in
SNHL d/t transmitted acoustic energy
-regions at risk for residual disease:
-most lateral part of facial recess approach at medial part of posterior ear canal wall
-sinus tympani:
-medial and anterior to mastoid portion of fallopian canal
Open Versus Closed Techniques
Advantages Disadvantages
Canal-wall-up -physiologic tympanic membrane position -residual cholesteatoma may be occult

-deep middle ear -recurrent cholesteatoma may occur in attic
-no mastoid bowl -delayed canal breakdown
-incomplete exteriorization of facial recess
-second stage often required
Canal-wall-down -residual cholesteatoma visible on follow-up -mastoid bowl maintenance can be a lifelong problem
-recurrent cholesteatoma is rare -middle ear is shallow and difficult to reconstruct
-total exteriorization of facial recess -position of pinna may be altered
-second stage sometimes required
Canal-Wall-Up (CWU):
-allows excellent view of facial recess and incus region while maintaining intact posterior ear canal
-may allow more physiologic ossicular reconstruction techniques with a deeper an better aerated middle ear
-increased risk of residual (20-35%) and recurrent disease (5-20%)
-most common site: mesotympanum
-increased likelihood of leaving cholesteatoma in lateral portion of facial recess
-“second-look” operation recommended at 6-12 months to reassess ear for residual disease and perform
planned reconstruction of sound-conducting system
Canal-Wall-Down (CWD):
-decreased risk of residual (2-17%) and recurrent disease (0-10%) cf CWU procedures
-equal or better hearing results reported
-lack of need for two surgeries
-indicated for advanced disease, noncompliant patients, only hearing ear
Radical mastoidectomy
-classic radical mastoidectomy:
-CWD mastoidectomy
-complete removal of TM, annulus, malleus, incus and middle ear mucosa
-eustachian tube plugged with fascia plug
1068
-goal: establish dry open cavity devoid of secretory epithelium
-precludes reconstruction of middle ear
-rarely performed today
-indications:
-unresectable cholesteatoma secondary to extension down ET, into cochlea, or into
perilabyrinthine region
-multiple failed prior modified radical mastoidectomies
Modified Radical Mastoidectomy

-modification of radical surgery to construct a TM and ossicular chain +/- mastoid obliteration
-removal of posterior and superior external auditory canal wall
-scutum (medial portion of superior ear canal) is removed flush with anterior canal wall
-facial ridge:
-posterior and inferior portions of remaining ear canal wall
-must be removed down to level of fallopian canal to have a well-aerated dry mastoid cavity
-cortex completely surrounding mastoid should be well saucerized to a smooth contour
-mastoid tip must be removed if aerated or filled with diseased tissue
-failure to remove mastoid tip may lead to dependent pocket within mastoid defect which will
accumulate debris and harbor infection
-air cells over sigmoid sinus should be removed completely
-extensive saucerization of mastoid and removal of mastoid tip may lead to alteration in position of pinna
after closure
-lower floor of ear canal to same level as digastric ridge to create a smooth easily cleansed mastoid bowl
-most important factors in avoiding a chronic draining cavity and recurrent mastoid bowl infections are size
and shape of meatus and mastoid cavity
Mastoid Obliteration
-mastoid bowl generally needs to be cleansed q6-12 months
-*techniques to minimize potential complications after CWD:
-wide saucerization
-avoidance of dependent pocket in mastoid tip lower floor of ear canal to same level as digastric
ridge
-lowering facial ridge
-generous meatoplasty
-exteriorize sinodural angle
-further modifications:
-Palva flap:
-postauricular musculoperiosteal flap
-temporalis muscle pedicled anteriorly or temporalis fascia pedicled on superficial
temporal artery
-using bone paté and bone chips placed deep to postauricular musculoperiosteal flap
Meatoplasty
-large meatus necessary for effective postoperative care and subsequent cleansing of mastoid bowl
-facilitate epithelialization and reduction of size of mastoid bowl
-crescent of conchal cartilage removed
-most important aspects of meatoplasty are adequate resection of cartilage and positioning of posterior
canal after cartilage removal
1069
Bondy Procedure
-variation of modified radical mastoidectomy performed through either endaural or postauricular incisions
-used in cases of large attic cholesteatomas in which middle ear is functioning well
-ossicular chain and middle ear are free of disease
-posterior ear canal wall removed down to annulus superiorly and facial ridge inferiorly
-scutum removed exposing epitympanum
-cholesteatoma marsupialized and keratin content debrided
-medial wall of cholesteatoma matrix left in place over body of incus and malleus and seals middle ear
space
-if cholesteatoma seen extending around ossicles standard MRM performed
-same principles as outlined apply to mastoid saucerization and reconstruction except middle ear is not
entered
Endoscopy
-to provide visualization of facial recess and sinus tympani
ENDOLYMPHATIC SHUNT
-procedures designed to “shunt” endolymph from lumen of endolymphatic sac into extracellular space in
treatment of intractable Meniere disease
-shunts established with Silastic strips or specially manufactured valves
-exposure of endolymphatic sac attained through complete mastoidectomy
-Donaldson’s Line:
-imaginary line drawn from lateral SCC that bisects perpendicularly the posterior SCC
-region where line crosses the sigmoid sinus marks the superior edge of the
endolymphatic sac
-bone over sigmoid sinus thinned
-bone overlying dura between inferior portion of posterior SCC and sigmoid sinus removed
-endolymphatic sac located between inferior portion of posterior semicircular canal and sigmoid
sinus
-bone over this region of dura is thinned and removed, exposing endolymphatic sac
-appears as a thickened whiter area of dura
-incision made with microscalpel, exposing luminal endothelium
-shunt inserted
1070
PETROUS APICECTOMY
-suppurative processes of petrous apex cause chronic infection and sometimes deep pain, abducens
paralysis, and facial paralysis
-divided into anterior and posterior portion by a coronal plane through internal auditory canal
-anterior portion: pneumatized in 9% pts
-posterior portion: pneumatized in 30% pts
-infection or cholesteatoma spread only to pneumatized apices
-via middle cranial fossa
-via mastoid and middle ear
-surgeon can usually follow infected tracts:
-tracts into posterior apex:
-retrofacial tract
-subarcuate tract
-tracts along sinodural angle (retrolabyrinthine approach)
-tracts into anterior apex:
-infralabyrinthine tract:
-below posterior SCC and posterior to fallopian canal
-high jugular bulb may block entry through this route
-infracochlear tract:
-below cochlea
-carotid artery identified in anterior protympanum
-tensor tympani muscle in superior protympanum removed
-triangle made up of: carotid artery, cochlea and tegmen tympani
-triangle forms a direct opening into anterior petrous apex
-glenoid fossa approach:
-glenoid fossa exposed and contents displaced anterior
-medial wall of glenoid fossa then dissected
-location of carotid artery monitored
-all bone removed between carotid artery and dura of middle cranial fossa
-complete exenteration of anterior petrous apex is impossible without labyrinthectomy, but in most cases,
drainage of infected cells is sufficient to reverse suppurative process
1071
1072
COMPLICATIONS
Facial Nerve Injury Perioperative complications

-heat generated by diamond burr may injure nerve -facial nerve injury
-SNHL
-revision surgery: sclerotic new bone can distort anatomy
-postoperative infection
-if trauma suspected: -dysgeusia
-stimulate (0.5 mA) nerve proximal and distal to site of -brain herniation
injury -CSF leakage
-if no contractions on proximal stimulation, then
Delayed complications
exposure of nerve over lateral 180 degrees performed -posterior canal breakdown
-repair: -perichondritis
-reanastomosis for severely injured or severed nerve -blue-domed cyst
-mucosalization of mastoid bowl
-cable grafting with greater auricular nerve
-stenosis of external canal
-paralysis in post-operative period
-observe for a few hours until effects of local
anaesthetic are gone
-if total paralysis persists early re-exploration indicated
-if facial palsy is delayed or paretic conservative management with steroids
Sensorineural Hearing Loss

-greatest risk to hearing is in treatment of chronic otitis media with cholesteatoma
-removal of cholesteatoma matrix from stapedial footplate or round window or over labyrinthine
fistula
-usually cholesteatoma in a vital area should be left for the second look procedure
-inadvertent contact of drill burr with ossicular chain hf SNHL
Vestibular Injury
-from trauma or subsequent infection
-results in acute vertigo with slow resolution over weeks to months
-chronic disequilibrium or vertigo may occur
Postoperative Infection
-perioperative oral antibiotics administered if infection occurs
Dysgeusia
-injury to chorda tympani
Brain Herniation
-if larger areas of dura are exposed, brain herniation into mastoid cavity and epitympanum can occur
-may result in cerebritis, meningitis and CSF leak
CSF Leak
-lacerated dura sutured and covered by fat, fascia or muscle graft to prevent CSF fistula
Bleeding
-laceration of sigmoid sinus or jugular bulb
-can be controlled by placing Gelfoam
-large lacerations secondary complications such as air embolism, sigmoid thrombosis
-early signs of air embolism:
-increases end-expiratory CO2, hypotension and abnormal cardiac sounds
-injury to carotid artery requires proximal and distal occlusion
1073
RECONSTRUCTION OF THE TYMPANIC
MEMBRANE AND OSSICULAR CHAIN
PREOPERATIVE ASSESSMENT
-important historical information:

-status of contralateral ear
-age at onset
-drainage
-eustachian tube function
-previous surgery
-staging operation based on extent of mucosal disease and destruction by cholesteatoma
-clean up ear during first stage if extensive disease
-reconstruct ossicular chain at second stage
-goals of surgery:
-safe dry ear
-intact tympanic membrane
-improved hearing
-single operation if possible
TECHNICAL CONSIDERATIONS
Tympanic Membrane Reconstruction
-pathologic TM abnormalities
-attic retraction cholesteatoma under
an eroded lateral attic wall
-sinus tympani retraction
cholesteatoma
-central perforation
Central Perforation
-Simple Closure (Paper Patch) Technique:

-may be considered for small
perforations
-requires “rimming” the perforation
to stimulate regrowth with placement
of a cotton disc, cigarette paper,
silastic film or gelfilm to act as a
scaffolding for cellular migration
-Medial Graft Technique (Underlay)

-inspection of heads of ossicles,
epitympanum and aditus ad antrum
-graft placed medial to tympanic
membrane
-advantages:
-technically easier
-fewer complications
F.Ling - Tympanoplasty and Ossiculoplasty (1)
1074
-disadvantage:
-increased incidence of failure
-Lateral Graft Technique (Overlay)

-canal wall skin removed for later placement
-anterior canal wall bony overhang removed
-important that every bit of squamous epithelium is removed from TM remnant
-most crucial area is anterior sulcus at annulus
-graft brought up medial to malleus
-canal skin replaced
-advantages:
-greater chance of success
-disadvantages:
-technically more challenging
-lateralization of graft
-anterior blunting of TM
-inclusion cholesteatoma
-longer operating time
-requires longer healing process
Sinus Tympani Retraction Cholesteatoma

-posterior auricular approach
-posterior fibrous annulus elevated from superiorly to inferiorly
-area of retraction freed and separated from TM anteriorly
-monomeric adhesion elevated toward sinus tympani
-intact canal wall mastoidectomy and facial recess approach to
middle ear are accomplished
-cholesteatoma removed
-tragal cartilage shaped into ovoid rectangle
-placed in middle ear, convexity toward promontory to
block entrance into sinus tympani
-grafting of TM
1075
Lateral Attic Wall Erosion Cholesteatoma
-most common type of cholesteatoma problem requiring TM reconstruction
-key is to reconstruct lateral attic wall with cartilage
-postauricular approach
-superior elevation of fibrous annulus anteriorly and inferiorly
-pulls TM off short process of malleus onto the long process TM flap developed down to but not off the
umbo
-cholesteatoma removed from epitympanum
-lateral attic wall reconstructed with tragal cartilage; cartilage fixed against malleus neck
-saddle blanket graft placed over superior bony external canal and lateral attic walls
Five types of tympanoplasty:

-Type I: all three ossicles to be present and mobile; OCR not needed
-Type II: grafts TM to intact incus and stapes
-Type III: exists when intact mobile stapes superstructure present and TM or graft remains directly on
stapes superstructure
-Type IV: absent or eroded superstrucure with graft or TM overlying a mobile stapes footplate
-Type V: tympanoplasty refers to a fenestration created in the horizontal semicircular canal.
Ossicular Chain Reconstruction
-prostheses:
-PORP = partial ossicular replacement prosthesis
-TORP = total ossicular replacement prosthesis
-plastic prostheses high extrusion rate; reduced with cartilage interposed over prosthesis platform
-hydroxyapatite prostheses tissue integration properties
Incus Replacement Techniques:

-transposed or sculptured incus autograft
-incus is removed, resculptured and placed between malleus and stapes suprastructure or footplate
-homograft
-well tolerated, provides excellend sound conduction
-may be presculpted, requires storage, risk of disease transfer
1076
-synthetic incus strut
-constructed from a variety of materials
-eg. hydroxyapatite, titanium, porous polyethylene
-recreates connection from malleus to stapes suprastructure or footplate
-PORP/TORP
Double Cartilage Block

-advantage:
-can be used for reconstruction
during primary surgery for
draining ear or with
tympanotomy for conductive
hearing loss
-no fear of extrusion
-results in air-bone closure to within 5-15
dB
Total Ossicular Replacement Prosthesis

-Plasti-Pore TORP
-highly erosive therefore use oversewn
platform cartilage
1077
OTOSCLEROSIS
EMBRYOLOGY
-4 weeks: otic capsule development

-8 weeks: cartilaginous framework begun
-16 weeks: endochondral bony replacement begins
-fissula ante fenestram located anterior to oval window usually last area of endochondral bone
formation in the labyrinth
-region affected in 80-90% of pts with otosclerosis
-other areas for predilection for otosclerotic lesions:
-border of round window niche (second most common site)
-apical medial wall of cochlea
-area posterior to cochlear aqueduct
-region adjacent to semicircular canals
-stapes footplate
HISTOLOGY
-early lesions
-active otosclerosis (otospongiotic phase)
-numerous fibrovascular spaces and increased osteoblasts and osteoclasts
-bone resorption begins around existing vessels by osteocytes enlargement of vascular channels
-dilation of these vessels seen clinically as a reddish hue on the promontory as
Schwartze’s sign
-ground substance is deposited in areas of resorption formation of new spongy bone "blue
mantles of Manasse" on H+E staining
-late lesions
-inactive phase (otosclerotic phase)
-osteoclasts are slowly replaced by osteoblasts
-fibrovascular spaces look less active, less vascular, and may resemble the normal adjacent bone
of the cochlear capsule.
-formation of dense sclerotic bone in areas of previous bony resorption
-begins in endochondral bone, eventually endosteal and periosteal layers become involved as well
PHYSIOLOGY
-conductive loss d/t fixation of stapedial footplate to otic capsule

-obliterative otosclerosis: thick stapes that fills oval window niche
-biscuit footplate: involvement of footplate but sparing of annular ligament; minimally fixed
-sensorineural loss
-liberation of toxic metabolites into inner ear with resultant injury to neuroepithelium
-vascular compromise from sclerosis and narrowing of vascular channels
-direct extension of otosclerotic lesions into inner ear disruption of electrolyte concentrations
and subtle changes in basilar membrane biomechanics
-cochlear otosclerosis: isolated pure SNHL
-positive Schwartze sign
-positive family history of otosclerosis
-unilateral conductive hearing loss consistent with otosclerosis and bilateral symmetric
sensorineural hearing loss
F.Ling - Otosclerosis (1)
1078
-audiogram with flat or “cookie-bite” curve with excellent discrimination
-progressive pure cochlear loss beginning at usual age at onset for otosclerosis
-CT revealing demineralization of cochlea typical of otosclerosis (“double ring” sign)
-stapedial reflex demonstrating “on-off effect” seen before stapedial fixation
EPIDEMIOLOGY
-primary disease of otic capsule and ossicles; etiology unknown

-abnormal resorption and deposition of bone in labyrinthine capsule and middle ear
-affects 1% of white population
-autosomal dominant with incomplete penetrance (40%)
-F:M = 2:1
-hearing loss usually begins b/n ages 15-45 years
-hormonal factors may be relevant: some female pts appear to worsen with onset of pregnancy
HISTORY AND PHYSICAL EXAMINATION
-slowly progressive hearing loss over a period of years

-positive family history in 60%
-tinnitus in 75%; vestibular symptoms in 25%
-Schwartze’s sign
-seen in 10% of otosclerotic ears
-increased vascularity of cochlear promontory in active otosclerotic lesions
LABORATORY FINDINGS
-audiogram
-air-bone gap
-Carhart notch:
-loss of 20-30 dB in bone conduction at 2 kHz
-thought to be secondary to the mass effect and loss of resonance of ossicles/stapes
-typically improves after stapedectomy causing overclosure of the air-bone gap
suggesting that the cause of this audiological phenomenon is artefactual
-speech discrimination excellent
-tympanometry may show AS pattern
-on-off effect:
-early stapes fixation characteristic abnormal decrease in impedance noted at onset and
offset of eliciting signal
-absent stapedial reflexes towards late stages of disease
-ossicular discontinuity
-incus necrosis from recurrent chronic OM
-fibrous union of incudostapedial joint
-congenital stapedial footplate fixation
-malleus head fixation
1079
-Paget disease
-begins in periosteal layer and involved endochondral bone last
-excessive absorption of bone with fibrovascular replacement forming weak haphazard trabecular
bone
-usually diffuse involvement of the skull
-stapes involvement or fixation seldom occurs
-tx: hearing amplification, medical management to inhibit bone resorption (eg. mithramycin,
calcitonin)
-Osteogenesis imperfecta
-AD defect of osteoblast activity resulting in multiple fractures
-increased bone resorption and abnormal remodelling
-stapes fixation and blue sclera in 40-60% of affected pts
-Osteopetrosis (Albers-Schonberg Disease)
-rare dominant or recessive forms
-results in ossicular anomalies (otic capsule is resistant to the disease)
-thickened bones of the skull base, blindness (optic nerve atrophy), absent paranasal sinuses,
choanal atresia, facial paralysis, hepatosplenomegaly, brittle bones
MANAGEMENT
Natural History
-90% with only histologic evidence are asymptomatic - active lesions mature w/o stapedial fixation
-in symptomatic pt; slowly progressive conductive and sensorineural hearing loss begins by age 20
-maximum conductive loss of 50-60 dB
Amplification
-effective and safe alternative to surgery
-patient satisfaction an issue however
Medical Management
-sodium fluoride
-replaces hydroxyl ions fluorapatite complex more stable and theoretically resists osteoclastic
action
-20-120 mg/day
-vitamin D and calcium
-in conjunction with NaF
-may accelerate maturation of bony lesions
-with above treatment regimen, 50% pts show no worsening of symptoms, 30% improve, 20% continue to
worsen
Surgical Management
Patient Selection
-contraindications:
-only hearing ear
-active infection
-suspected active endolymphatic hydrops
-other considerations:
-age: -very young pts has higher incidence of oval window reclosure after a successful initial
procedure
-second operation greater risk of cochlear deafness
1080
-occupation:
-divers, pilots, flight attendants, frequent travellers are at greater risk for postoperative
fistula and prosthesis dislocation
-pts whose work or hobbies dictate excellent balance questionable candidates
-tympanic membrane perforations should be repaired before attempted stapedectomy
-history of cholesteatoma or severe ET dysfunction not good candidates
-middle ear effusion a strong relative contraindication
-worst hearing ear approached first
-minimum of 3-12 months before surgery attempted on second ear
Patient counselling, risks, and postoperative complications

-postoperative cochlear deafness (<2%)
-stretching of chorda tympani altered taste
-facial nerve injury facial paralysis
-tympanic membrane perforation (2-3%) d/t trauma or vascular injury to tympanomeatal flap
-acute balance disturbance common; usually resolves in 3-7 days
Procedure
-stapes mobilization
-anterior crurotomy
-stapedectomy: entire stapes and footplate is removed
-stapedotomy:
-creation of fenestra in midportion of stapes - piston prosthesis is then positioned and connective
tissue placed at base of prosthesis to prevent fistula
-some reports suggest a decrease in postoperative cochlear deafness and improvement in air-bone
gap closure above 2kHz
Prosthesis
-connective tissue oval window graft
-wire or piston prosthesis
Intraoperative Complications
-high and dehiscent jugular bulb
-courses b/n stapes crura
-some authors will attempt to cauterize; many will abort procedure
-note: artery may be only source to middle meningeal artery
-dehiscent and abnormally low facial nerve
-can obscure oval window
-may consider gently retracting nerve superiorly (controversial)
-abort procedure if surgeon believes nerve is in jeopardy
-profuse perilymph gusher
-patent cochlear aqueduct
-removal of footplate in presence of gusher increases risk of postoperative cochlear deafness
-risk of permanent SNHL
-tx: seal vestibular opening with a graft, place prosthesis, pack and close, manage for perilymph
fistula, may require lumbar drain
-fracture of long process of incus
-place prosthesis to remaining incus or use malleus to oval window prosthesis
-“floating footplate”
-might be pushed into vestibule and attempts to remove it can result in significant neurosensory
hearing loss
1081
Postoperative period
-no lifting or straining for 6 weeks
-postoperative audiogram at 4-6 weeks
-closure of air-bone gap to within 10 dB in ~ 90% of patients
-10% experience no improvement
-1-2% suffer persistent profound sensorineural loss
Postoperative Complications
-immediate:
-vertigo:
-usually self limited
-if persists > 1 week, corticosteroids may be of some benefit
-acute otitis media
-rare
-may lead to meningitis
-weeks postop:
-reparative granuloma
-1-2%
-progressive SNHL after earlier postoperative hearing improvement
-discrimination scores lower than expected
-requires immediate surgery
-findings: significant granulation tissue around oval window graft
-historically seen with Gelfoam graft
-weeks to years postop:
-oval window fistulae
-fluctuating or progressive hearing loss
-high clinical suspicion
-requires exploratory surgery
-postop expectations usually stabilization of SNHL and resolution of vertigo
-failure of stapedectomy:
-prosthesis displacement (most common)
-footplate refixation
-perilymph fistula
-otosclerotic regrowth
-lateralization of oval window membrane
-revision surgery
-provides improvement in symptoms in less than 65% of cases
-seven times higher risk of postoperative cochlear deafness
1082
ACUTE PARALYSIS OF THE FACIAL NERVE
STRUCTURAL ANATOMY OF THE FACIAL NERVE
Intracranial Segment
-23-24 mm
-segment from brainstem to internal auditory canal
-Nervus Intermedius: parasympathetic and sensory
root of facial nerve
-motor root joins with nervus intermedius in
CPA/IAC to form common facial nerve
Intratemporal Segments
-meatal
-labyrinthine
-tympanic (horizontal segment)
-mastoid (vertical segment)
1. Meatal
-8-10 mm
-from porus acousticus (fundus) to meatal foramen
-traverses in anterior superior quadrant of IAC
separated by falciform crest inferiorly and Bill’s
bar posteriorly
2. Labyrinthine
-3-5 mm
-from meatal foramen to geniculate ganglion
-narrowest segment of fallopian canal (0.68 mm
diameter)
-geniculate ganglion:
-located at first genu Middle fossa approach - GSPN (5); geniculate ganglion (7); facial nerve
-cells bodies of sensory cells and taste meatal segment (10), labyrinthine segment (9), tympanic segment (12)
cells from anterior 2/3 of tongue and
palate
-greater superficial petrosal nerve:
-first branch of facial nerve
-carries preganglionic parasympathetic
fibers to lacrimal gland
3. Tympanic
-8-11 mm
-from geniculate ganglion to pyramidal eminence
(at second genu)
-courses above cochleariform process, oval
window and stapes; below lateral semicircular
canal
-most common site of dehiscence (40-50%)
Lateral approach - facial nerve mastoid segment (1), tympanic segment (2),
labyrinthine segment (3), meatal segment (4); GSPN (5); cochleariform
process (6)
F.Ling - Facial Nerve (1)
1083
4. Mastoid
-10-14 mm
-from pyramidal process to stylomastoid foramen
-nerve to stapedius
-chorda tympani:
-preganglionic fibers to submandibular and sublingual glands
-special sensory taste fibers
Extratemporal Segments
-postauricular nerve
-branch to external auricular and occipitofrontalis muscles
-nerve to stylohyoid
-nerve to posterior digastric muscle
-nerves to muscles of facial expression
-pes anserinus
-branching point of extratemporal segments in parotid gland
-two divisions:
-superior - temporozygomatic
-inferior - cervicofacial
-temporal branch:
-frontalis
-corrugator supercillii
-procerus
-upper orbicularis oculi
-zygomatic branch:
-lower orbicularis oculi
-abundant anastomotic supply with
buccal branch
-buccal branch:
-zygomaticus major and minor
-levator anguli oris
-buccinator
-upper orbicularis oris
-marginal mandibular branch:
-lower orbicularis oris
-depressor anguli oris
-depressor labia inferioris
-mentalis
-cervical branch:
-platysma
Blood Supply of Facial Nerve

-anterior inferior cerebellar artery labyrinthine
artery
-supplies nerve within IAC
-middle meningeal artery petrosal artery
-supplies perigeniculate area
-supplies tympanic and mastoid segments
-rich anastomoses except in the labyrinthine segment at junction between carotid and vertebrobasilar
systems
1084
FUNCTIONAL ANATOMY
Branchial Motor (Special Visceral Efferent)

-motor nucleus
-motor function to:
-stapedius
-stylohyoid muscle
-muscles of facial expression
Parasympathetic (General Visceral Efferent)

-preganglionic fibers in superior salivatory
nucleus (3 subsets):
a) superior salivatory nucleus nervus

intermedius greater superficial
petrosal nerve vidian nerve [in
pterygoid canal] [pterygopalatine
fossa] (sphenopalatine ganglion)
postganglionic fibers to lacrimal
and palatine glands
b) superior salivatory nucleus nervus

intermedius chorda tympani and
lingual nerve (submandibular
ganglion) postganglionic fibers to
submandibular and sublingual glands
c) superior salivatory nucleus nervus

intermedius tympanic plexus
lesser petrosal nerve (otic
ganglion) post ganglionic fibers
to parotid gland*
*parasympathetic innervation from

CN IX, but some describe
contribution from CN VII
Sensory (General Sensory Afferent)

-supplies sensation to auricular concha,
postauricular skin, wall of EAC and part of
tympanic membrane
-cell bodies housed in geniculate ganglion
Taste (Special Sensory Afferent)

-anterior 2/3 of tongue lingual nerve
chorda tympani geniculate ganglion (houses
cell bodies) nervus intermedius tractus
and nucleus solitarius
1085
SURGICAL ANATOMY
1. Middle Cranial Fossa Approach:

-preserves hearing and allows access to IAC and/or geniculate ganglion
-location of internal canal and meatal segment:
-bisection of angle formed between plane of superior SCC (arcuate eminence) and greater
superficial petrosal nerve
-tympanic segment located superior to cochleariform process and oval window; inferior to horizontal SCC
-upper mastoid segment lies posterior and medial to chorda tympani and medial to facial recess air cell tract
-stapedius muscle and posterior SCC are medial to facial nerve
2. Translabyrinthine Approach:
-used when hearing preservation not an issue
-nerve usually found along a line drawn between the horizontal SCC and digastric ridge
Anomalies of the Facial Nerve

-dehiscent facial nerve:
-most common anomaly
-tympanic segment over oval window > geniculate ganglion > mastoid segment adjacent to
retrofacial air cells
-anomalies of fallopian canal are suspect in congenital atresia of middle ear and anomalies of otic capsule
EVALUATION
Symptoms and Signs: Differential Diagnosis of Acute Facial Palsies

-onset: sudden versus delayed
-state: incomplete versus complete Infection: -Bell’s palsy (herpes simplex mononeuritis)
-Herpes zoster oticus (Ramsay Hunt syndrome)
-any palsy progressing > 3 weeks should be
-Otitis media with effusion
investigated for neoplasm -Acute suppurative otitis media
-associated symptoms: -Coalescent mastoiditis
-paresthesias, otalgia, hyperacusis, -Chronic otitis media
-Malignant otitis externa (Skull base osteomyelitis)
diminished tearing, alteration in taste,
-Tuberculosis
hearing loss, vertigo -Lyme disease
-evidence of trauma -AIDS
-Infectious mononucleosis
Trauma: -Temporal bone fractures
Physical Examination: -Birth trauma
-paresis (incomplete) versus paralysis (complete) -Facial contusions/lacerations
-palpate parotid gland for tumours -Penetrating wounds, face and temporal bone
-bilateral nerve involvement in less than 1%: -iatrogenic injury
Neoplasia: -Cholesteatoma
-Guillain-Barre syndrome (most -Glomus jugulare or tympanicum
common cause in adults) -Carcinoma (primary or metastatic)
-Lyme disease (most common cause in -Facial neuroma
children) -Schwannoma of lower cranial nerves
-Meningioma
-brainstem tumours -Leukemia
-intracranial infection -Histiocytoses
-sarcoidosis -Rhabdomyosarcoma
-leukemia/lymphoma Idiopathic: -Recurrent facial palsy
-Melkersson-Rosenthal syndrome
Metabolic and systemic:
-over 50% of facial paresis due to Bell’s palsy; -Sarcoidosis
trauma 20% -Guillain-Barre syndrome
-Autoimmune disorders
1086
Adjunctive Testing:
-CT and MRI
-electrophysiologic testing
-topognostic tests:
-generally not useful and have been replaced with electrophysiological testing
-Schirmer test:
-quantitate amount of tearing in involved eye
-significant if > 30% reduction in tears or < 25 mm tear in 5 mins
-audiometry: should be done in all cases of facial palsy
-treponemal studies: Lyme titers and VDRL/FTA-ABS
-CBC: may suggest inflammatory process
-ACE level: may suggest active sarcoidosis
PATHOPHYSIOLOGY OF NERVE INJURY
Nerve Fiber Components

-Endoneurium:
-surrounds each nerve fiber (axons)
-tightly adherent to the Schwann cell layer, provides the endoneural tube for regeneration
-Perineurium:
-surrounds endoneural tubules
-provides tensile strength, maintains intrafunicular pressure, and protects from infection
-Epineurium:
-outer nerve sheath layer
-contains the vasa nervorum for nutrition
Definitions:
Neurapraxia:
-lesion compresses flow of axoplasm
-nerve is viable and recovers normal function when blockade is removed
-NET, MST and ENOG normal; EMG abnormal
Axonotmesis:
-state of Wallerian degeneration distal to lesion characterized by preservation of endoneural
sheaths of motor axons
-NET, MST and ENOG will indicate rapid and complete degeneration
Neurotmesis:
-Wallerian degeneration and loss of endoneural tubules
-eletrophysiologic tests similar to axonotmesis
Sunderland Classification of Nerve Injury

-Class I:
-neuropraxia
-loss of axoplasmic flow from compression of the axon results in only a conduction block
-complete recovery anticipated
-Class II:
-axonotmesis
-axon disrupted, endoneurium preserved, Wallerian degeneration occurs distal to site of injury
-complete recovery anticipated
-axon regenerates through an intact neural tube at 1mm/day
1087
-Class III:
-neurotmesis
-neural tube (axons, myelin sheath, and endoneurium) disruption
-Wallerian degeneration occurs distal to site of injury
-unpredictable outcome (loss of endoneural tubules results in high risk for synkinesis)
-Class IV:
-neurotmesis
-violates perineurium greater chance of incomplete and aberrant regeneration
-Class V:
-neurotmesis
-complete transection no regeneration without surgical reapproximation
-risk of a neuroma from nerve sprouts outside nerve sheath
Electrophysiologic Tests:
Test Indication Interpretation Limitation
Nerve excitability test (NET) Complete paralysis < 3 wks < 3.5 mamp threshold Not useful in first 3 days after
duration difference: prognosis good onset or during recovery
Maximal stimulation test (MST) same as NET Marked weakness or no muscle Not objective
contraction: advanced
degeneration with guarded
prognosis
Electroneurography (ENOG) Same as NET and MST < 90% degeneration: prognosis False positive results in
good; > 90%: prognosis in deblocking phase
question
Electromyography Acute paralysis less than 1 wk Active mu: intact motor axons Cannot assess degree of
duration degeneration or prognosis for
recovery
Chronic paralysis greater than 2 mu + fibrillation potentials:

wk duration partial degeneration
Polyphasic mu: regenerating
nerve
-within first 3 days after onset of complete paralysis, results of NET, MST, and ENOG yield little useful
information, as Wallerian degeneration distal to the stimulation areas has not occurred; the results always
indicate incomplete degeneration and good prognosis
-prognosis cannot be established until the sixth or seventh day after onset of paralysis
-NET:
-current thresholds required to elicit just-visible muscle contraction on the normal side of the face are
compared with those values required over corresponding sites on the side of paralysis
-side-to-side threshold difference is calculated
-3.0 to 3.5 mA difference compatible with advanced degeneration
-MST:
-modification of NET that uses a level of current sufficient to depolarize all motor axons underlying the
stimulating probe
-muscular responses graded subjectively; markedly decreased or absent facial movement signifies advanced
degeneration
1088
-ENOG:
-supramaximal level of current applied with bipolar electrodes percutaneously over main trunk of facial
nerve
-compound myogenic action potential
-peak-to-peak amplitude directly proportional to number of intact motor axons
-ratio of abnormal side to normal side measured
-> 90% degeneration indicates a poor prognosis for immediate or complete restoration of facial function
-in Bell’s palsy, patients exceeding 95% degeneration within the first 2 weeks of onset fall into the guarded
prognostic category
-limitations: testing error: standard lead placement versus optimal lead placement
-EMG:
-electrodes inserted into muscle, measures muscle response to voluntary contraction
-useful to demonstrate the existence of functional motor units
-fibrillations from deinnervated nerve appear after 1-2 weeks
-polysynaptic signals indicate reinnervation
-presence of voluntary action potentials indicates at least partial continuity of nerve
The Goddamn House-Brackmann Classification of Facial Paralysis
Grade Degree of Gross Appearance Motion

dysfunction
Description Synkinesis Tone and Forehead Eye Mouth
Symmetry
at rest
I Normal Normal facial function in No Normal Normal Normal Normal

all areas
II Mild Slight weakness noticed Very slight Normal Moderate-to- Complete Slight
on close inspection good function closure with asymmetry
minimal
effort
III Moderate Obvious, but not Noticeable Normal Slight-to- Complete Slightly weak
disfiguring difference but not moderate closure with with
between the two sides severe movement effort maximum
effort
IV Moderate-severe Obvious weakness Present Normal None Incomplete Asymmetric

and/or disfiguring closure with
asymmetry maximum
effort
V Severe Only barely perceptible Present None None Incomplete Slight

motion closure movement
VI Total Paralysis No movement None None No movement No movement No movement
CONGENITAL FACIAL PALSY
Birth Trauma
-most common cause of unilateral facial paralysis in the neonate
-facial nerve is at risk for injury during delivery as ti courses the underdeveloped mastoid process
-nerve compression due to molding of head in birth canal
-risks: forceps delivery, prolonged delivery, large infant
-SSx: asymmetric crying facies, hemotympanum, periauricular ecchymosis
1089
-diagnosis:
-if complete paralysis within first 3 days of life EMG to provide conclusive evidence of
neuromuscular integrity
-later presentations, NET, MST and ENOG used initially followed by EMG if myogenic
responses are absent
-treatment: observation
-prognosis for spontaneous regeneration is excellent and surgical exploration not recommended unless
nerve has had an opportunity for recovery
Congenital or Development Causes
-Mobius Syndrome:
-CN VI, VII palsy
-deformity of extremities: club foot (talipes equiovarus)
-tongue weakness
-mixed hearing loss
-mental retardation
-external ear deformities
-tx: treated later in life with muscle transfers and fascial slings
-thalidomide embryopathy:
-limb and ear anomalies and abducens nerve palsy
-Albers-Scheoenberg Disease:
-autosomal recessive inheritance
-disorder of bone metabolism resulting in osteopetrosis of bony IAC causing compression of
nerves (CN III, VII and VIII)
INFECTIOUS AND IDIOPATHIC CAUSES OF FACIAL PALSY
Bell’s Palsy
-most common cause of facial paralysis
-risks: diabetes mellitus, pregnancy, past history (7-12% recur)
-facial paralysis of acute onset (<48 hours) and limited duration, etiology idiopathic
-prognosis:
-1/3 paresis; > 95% recover without sequelae
-2/3 paralysis; > 85% some return of facial tone within 3 weeks; may not have return for 3 to 6
months
-70-85% will have full recovery by 6 months; 15-30% will have incomplete recovery
-longer the delay, the greater likelihood of adverse sequelae
-inflammatory infiltrates throughout course of facial nerve
-infecting agent: HSV in geniculate ganglion
-interventions:
-steroid treatment:
-thought to prevent denervation, speed recovery, lessen synkinesis and prevent
progression of paralysis
-some studies do not show any statistical difference between steroids and placebo
-prednisone 1 mg/kg/day in divided doses and tapered over 7 to 10 days
-acyclovir:
-added to steroid regimen at 2000 mg/day in five doses for 7 days
-delay > 3 days before beginning antiviral therapy likely precludes any additional
efficacy
1090
-surgical:
-still controversial
-considered only for > 90% degeneration on ENOG in first 2 weeks of paralysis
-postulated the maximal nerve injury occurs at the meatal foramen
-unroofing labyrinthine segment via middle fossa approach
-decompression performed within 14 days of onset significantly improves
outcome in patients with poor prognosis; after 14 days no additional benefit
-decompression of mastoid and tympanic segments has no effect on recovery
Herpes Zoster Oticus

-VZV: latent infection in many cranial nerve ganglia
-aka: Ramsay Hunt syndrome
-SSx:
-facial paralysis and severe ear pain and vesicular eruption of external auditory canal and concha
-SNHL and vestibular dysfunction in >20%
-pain and decreased lacrimation
-increased susceptibility of labyrinthine segment to inflammation-induced degeneration
-prognosis:
-spontaneous recovery poorer than in cases of Bell’s palsy
-50% satisfactory return; 50% left with weakness, synkinesis, contractures, and spasm
-degeneration may evolve more slowly over course of 3 weeks; may take 3-6 months for return
-treatment:
-Acyclovir proven benefit: reduces pain and shortening time to resolution of skin lesions
-higher doses needed: Valacyclovir (1000 mg tid x 7d) metabolized to acyclovir
-steroids usually given
-role of surgical decompression remains investigational
Otitis Media
-complication of acute suppurative otitis media, otitis media with effusion, chronic otitis media, and
mastoiditis
-incidence ~ 1:20,000
-prognosis excellent; rapid resolution after resolution of infection
-tx: M+T
Malignant Otitis Externa

-facial nerve injury form the effect of temporal bone osteomyelitis
Melkersson-Rosenthal Syndrome
-unknown familial condition
-symptoms usually begin in childhood and early adolescence
-SSx:
-chronic or recurrent facial edema of upper lip
-recurrent unilateral or bilateral facial motor dysfunction
-fissured tongue
-migraine headaches
-dx:
-clinical history and exam, lip biopsy reveals dilated lymphatics and granulomatous changes with
giant cells, may have elevated ACE levels during attacks
-tx:
-empiric management with corticosteroids
1091
Lyme Disease
-Borrelia burgdorferi transmitted by a deer tick
-SSx:
-10% of patients have ipsilateral or bilateral facial nerve involvement after 1-4 weeks incubation
period
-initial erythema migrans (bull’s eye rash), flu-like symptoms, meningitis, multiple neuropathies,
cardiac conduction disorders, meningoencephalitis, swollen joints
-facial paralysis resolves in 6-12 months (full recovery anticipated)
-tx:
-parenteral penicillin, ceftriaxone, or cefotaxime for severe cases
-for rash only consider oral therapy
TRAUMA
Temporal bone fractures

-most common cause of traumatic injury to facial nerve
-< 5% temporal bone fractures have otic capsule involvement
-otic capsule involvement: 50% will have facial nerve injury
-otic sparing fractures associated with paralysis < 10% of cases
-most injuries occur in perigeniculate region
-approach based on hearing:
-transmastoid/translabyrinthine approach when profound SNHL present
1092
-middle fossa approach in patients with good hearing
-transection rare requires end-to-end anastomosis or interpositional grafting
-edema and contusion more common requires incision of epineural sheath to evacuate hematomas
Gunshot injuries
-paralysis > 50% cases
-d/t direct transection, bony fragments, or secondary kinetic energy
-most common sites of injury are mastoid and tympanic segments and stylomastoid foramen area
-outcome of facial function is poorer
Iatrogenic causes
-less than 1%
-delayed onset paresis more common but usually due to viral reactivation
-common sites of injury:
-tympanic segment adjacent to oval window (d/t dehiscence)(1st)
-mastoid segment (2nd)
-management:
-partial injuries (< 50%) are best treated by decompression proximal and distal to injury
-injuries > 50% require primary anastomosis or cable grafting
-postoperative weakness:
-wait for local anesthetics to wear off
-may consider corticosteroids and follow progression
-consider re-exploration for complete paralysis in select cases
Soft-tissue injuries to face

-lesions of main trunk or larger temporofacial and cervicofacial branches require direct end-to-end
anastomosis or interpositional grafting
-branches medial to lateral canthus rarely need repair because of rich cross-anastomotic connections
spontaneous recovery anticipated
-Interpositional grafts:
-donor sites: greater auricular, median antebrachial cutaneous, sural nerves
TUMOURS OF THE SKULL BASE AND FACIAL NERVE
-circumstances that increase the probability of discovering a neoplastic process:

-slow evolution of paralysis exceeding 3 weeks
-coexistence of facial twitching with an evolving paresis
-chronic eustachian tube dysfunction with no prior history of chronic middle ear disease
-multiple cranial-nerve deficits
-no return of facial function when the process has had an opportunity for regeneration
-recurrent palsy on same side
-presence of neck or parotid mass
-history of cancer
-most common tumour of nerve: Facial Schwannoma

-geniculate and labyrinthine segments most commonly involved
-excision usually requires interpositional grafting
-management depends on timing: old patient watch; young patient surgery
-grade III return of facial function after surgery is best result anticipated from grafting
1093
-skull base tumours:
Anterior transposition:
-spares greater superficial petrosal nerve and preserves normal tearing
-preferred for benign tumours of infralabyrinthine compartment
Posterior transposition:
-provides access to petrous apex
Division and reanastomosis:
-may aid exposure to parapharyngeal space
-avoid this approach because of complications
-when tumour is benign, continuity of nerve is preserved using mobilization techniques EXCEPT
for:
-facial nerve schwannomas
-benign tumour invading the nerve
-recurrent tumour adherent to the nerve
-malignant tumours:
-require tumour-free excision
-exceptions:
-lymphomatous and leukemic invasion of nerve
-low-grade malignancies of parotid
-Parotid Tumours:
-mucoepidermoid carcinoma most common parotid tumour to cause paralysis
-adenoid cystic carcinoma has higher rate of neural involvement
-other neoplasms:
-cholesteatomas
-hemangiomas
-glomus jugulare or tympanicum
-meningioma
-metastatic carcinoma
NEUROLOGICAL CAUSES OF FACIAL PARALYSIS
Stroke
-presents with an acute, forehead sparing facial paralysis associated with other lateralizing neurological
signs
Guillain-Barre Syndrome
-common cause of acute bilateral facial nerve palsy
-associated with generalized weakness, central nervous and autonomic dysfunction
Myasthenia Gravis
-autoimmune disease with antibodies against the acetylcholine receptor at the neuromuscular junction
which causes progressive motor weakness with repetitive function
-associated with ptosis, difficulty chewing, talking, weakness, and thymic tumours
EYE CARE
-most common complication is corneal desiccation
-precautions: ophthalmic lubricants, closure of eye with tape at night, moisture chambers or shielded
glasses, avoidance of wind/fans/vents
-surgical options: gold weight implants, canthoplasty, tarsorrhaphy, and upper eyelid springs
1094
OTOLOGIC MANIFESTATIONS OF SYSTEMIC DISEASE
INFECTIOUS DISEASES
SYSTEMIC DISEASES
Herpes Simplex Infectious

-herpetic external otitis -HSV
-self-limiting -VZV
-mumps
-symptomatic treatment with analgesics and topical or systemic -measles
antibiotics for secondary infection -syphilis
-acyclovir 400 mg tid x 7-10 days -Lyme disease
-leprosy
-tuberculosis
Varicella Zoster -HIV
-chickenpox: maculopapular exanthem involves skin of auricle Immunologic
-self-limited; symptomatic treatment -Wegener’s granulomatosis
-hearing loss usually d/t secondary bacterial infection -relapsing polychondritis
-discoid lupus erythematosus
causing CHL -systemic lupus erythematosus
-Ramsay-Hunt Syndrome -polyarteritis nodosa
-reactivation of latent herpes zoster virus within geniculate -rheumatoid arthritis
-autoimmune inner ear disease
ganglion
Metabolic
-hearing loss 2o nerve inflammation -gout
-vesicular eruption on auricle and external auditory canal -ochronosis
-facial nerve paresis: manifests 1-2 days after vesicular -mucopolysaccharidoses
Diseases of bone
eruption
-osteogenesis imperfecta
-treatment of immunocompetent host is typically not -osteopetrosis
necessary -Paget’s disease
-role of antivirals and corticosteroids (to prevent post- -fibrous dysplasia
Idiopathic
herpetic neuralgia) controversial
-Histiocytosis X
-acyclovir 800 mg po 5x/d x 7-10d
-valcyclovir 1000 mg po tid x 7d
Mumps
-RNA paramyxovirus transmitted by salivary secretions
-salivary adenitis, epididymo-orchitis, pancreatitis, thyroiditis, polyarthritis, myocarditis
-hearing loss in 5/10000
-80% unilateral, high-frequency hearing loss
-usually permanent
-no specific treatment
-corticosteroids reported to help diminish fever and pain resulting from parotid and testicular
swelling
Measles
-caused by highly contagious RNA virus
-pre-vaccination era, was common cause of acquired SNHL
-HL occurs in fewer than 0.1% of all measles infections
-bilateral SNHL and occurs at same time as macular rash
-45% with profound hearing loss
-permanent hearing loss
-asymmetric hearing loss maximal at higher frequencies
F.Ling - Ear Manifestations of Systemic Dz (1)
1095
Syphilis
-middle ear and mastoid affected by both congenital and acquired syphilis
-Treponema pallidum
-tertiary syphilis:
-gumma: granulomatous lesion with central necrosis and obliterative arteritis
-may affect middle ear with TM perforation
-labyrinthine involvement in secondary or tertiary stages
-secondary stage:
-abrupt, bilateral and rapidly progressive hearing loss
-vestibular symptoms unusual
-rash
-CSF: lymphocytosis with elevated total protein and normal glucose levels
-tertiary stage:
-asymmetric and fluctuating hearing loss
-progressive tinnitus and vertigo may occur
-positive fistula test (Hennebert’s sign) may be seen
-loss of speech discrimination out of proportion to pure-tone thresholds
-diagnosis:
-positive serum fluorescent treponemal antibody absorption test (FTA-ABS)
-microhemagglutination assay-Treponema pallidum (MHA-TP)
-treatment:
-penicillin 2.4 MU IM weekly for 6-12 weeks
-penicillin 0.6 MU IM daily for 6-12 weeks
-prednisone 30-60 mg per day on alternate days for 3-6 months with slow taper
Lyme Disease
-Borrelia burgdorferi
-transmitted by ticks
-early symptoms: rash, severe headache, neck stiffness, fever, chills, myalgia, profound fatigue
-late symptoms: multiple neuropathies, arthritis, meningitis, myocarditis
-ENT symptoms: facial paralysis, TMJ pain, tinnitus, SNHL, sudden hearing loss, otalgia, facial pain,
cervical adenopathy, vertigo
-common cause of facial paralysis (bilateral)
-usually resolves slowly over 6-12 months
-antibiotics often used to hasten resolution and prevent disease progression
-responds well to doxycycline, amoxicillin, penicillin, tetracycline, or cefuroxime axetil
Leprosy
-Hansen’s disease
-endemic in tropical countries
-Mycobacterium leprae
-nasal mucosa thought to be primary site of transmission from infected persons
-nervous, cutaneous and ocular involvement can lead to extremity mutilation, leonine features, and
keratoconjunctivitis
-bacillus infects nerves and immune response to infection causes nerves to thicken considerably
-greater auricular nerve, ulnar nerve, peroneal nerve and radial nerve commonly affected
-lesions of external ear in 70%: infiltrating nodules, loss of cartilage, ulceration
-dx: biopsy
-tx: dapsone and rifampin; clofazimine
1096
Tuberculosis
-Mycobacterium tuberculosis
-most infected people are asymptomatic carriers with 5-10% lifetime risk of developing clinical disease
-aural tuberculosis may present as facial paralysis, persistent aural discharge, refractory chronic otitis
media, profuse granulation tissue, bone sequestra or necrosis, perichondritis, or failed otologic surgery
-otitis media:
-may result from hematogenous and lymphatic spread
-generally painless, with multiple small perforations that may quickly coalesce to total tympanic
membrane perforation
-CHL from ossicular destruction
-dx:
-AFB in exudate or tissue preparations
-definite diagnosis made by isolation and identification of M. tuberculosis in culture from
diagnostic specimen
-culture of exudate negative in 60% of cases
-tx:
-antituberculous chemotherapy
-may require surgery to remove intractably pathologic tissue and sequestrated bone
Human Immunodeficiency Virus

-positive patients more susceptible to opportunistic infections
-otitis externa
-common
-Pseudomonas aeruginosa most common causative agent
-Proteus and Aspergillus less common
-Pneumocystis and tuberculous infections polyps of EAC
-recurrent AOM and SOM common otologic problems
-SNHL in 21-41%: d/t otosyphilis, cryptococcal infection, ototoxic medication, CMV, HSV, primary or
metastatic CNS neoplasms, direct infection by HIV
IMMUNOLOGIC DISEASES
Wegener’s Granulomatosis
-otologic involvement seen in ~35% of cases
-most common otologic manifestation are facial or postauricular pain, otitis media with effusion, acute
otitis media, hearing loss, and vertigo
-OM may result from obstruction of ET
-CSOM may resolve with treatment of WG and may be used as an indicator of remission or
recurrence
-SNHL may be d/t immune complex deposits in cochlea, vasculitis of vasa vasorum of cochlea, or
pressure on acoustic nerve by a granulomatous lesion
-dx:
-c-ANCA found in 90% of pts with active WG and in 60% with limited disease
-tx:
-corticosteroids and cyclophosphamide
-episodic inflammation of cartilaginous structures
-over time, recurrent inflammation leads to atrophy, scarring and distortion of involved cartilage
-otologic manifestations:
-red, tender, edematous pinna with sparing of external ear canal
1097
-diagnosis is clinical; biopsy of acutely inflamed pinna avoided because of risk of infection
-lab findings: elevated ESR, anemia and positive RF
-tx: corticosteroids; dapsone, indomethacin and salicylates; MTX has been described
Chronic Discoid Lupus Erythematosus

-causes raised erythematous lesions on skin of head, neck, and chest
-raised lesion on ear, face, neck or chest that slowly enlarges and is pruritic
-necrotizing vasculitis of small- and medium-diameter arteries
-diagnosis based on biopsy:
-PMN infiltrating all layers of vessel wall and perivascular areas intimal proliferation and
degradation of vessel wall
-lesions are segmental and tend to affect areas of arterial bifurcation
-hepatitis B surface antigen can be demonstrated in serum of 30-40% of patients
-predominant otologic symptom is usually hearing loss (conductive or sensorineural)
-tx: systemic corticosteroids combined with cyclophosphamide
Rheumatoid Arthritis
-persistent inflammatory synovitis causing progressive cartilage and bone destruction within joints
-affects 1% of population; F>M
-association with expression of HLA-DR4
-rheumatoid nodules are both cutaneous and subcutaneous and may involve external ear
-conductive and sensorineural hearing loss can occur
-significantly higher incidence of SNHL than normal persons, possibly d/t autoimmune inner-ear
disease
-CHL thought to be d/t abnormal middle-ear stiffness
Autoimmune Inner-Ear Disease

-diagnosis based on rapidly progressive bilateral, often fluctuating hearing loss, unresponsive to
conventional therapy but improved with immunosuppressive drugs
-frequently associated with systemic autoimmune disorders (ie positive ESR, ANA)
METABOLIC DISORDERS
Gout
-disorder of purine metabolisms that causes abnormally high levels of uric acid
-overproducers treated with allopurinol, underexcreters are treated with uricosuric drugs such as
probenecid
-tophus found on auricle no treatment necessary
Ochronosis
-form of alkaptonuria
-AR disorder of homogentisic acid metabolism
-affected persons accumulate homogentisic acid oxidized to black compound that adheres to cartilage
and discolours ear, fingers, buccal mucosa and nose
-tx: low-protein diet
1098
Mucopolysaccharidoses
-inherited deficiencies of enzymes needed of degradation of mucopolysaccharides
-Hunter syndrome:
-deficiency of alpha-iduronidase
-X-linked inheritance
-Hurler syndrome:
-deficiency of alpha-iduronidase but inherited as AR
-Morquio syndrome:
-deficiency of N-acetylgalactosamine-6-sulfatase or of beta-galactosidae
-hearing loss is usually mixed with conductive component d/t ETD and SOM
-SNHL may be d/t abnormal lipid metabolism within nerve cells
DISEASES OF BONE
Osteogenesis Imperfecta
-AD disorder of connective tissue
-mutations in either of two chains that form type I procollagen
-both conductive and sensorineural hearing loss found in 90% pts over age of 30
-CHL associated with blue sclera
-caused by involvement of ossicles with pathologic fractures of long process of incus or stapes
crura
-SNHL associated with gray or white sclera
Osteopetrosis
-inherited disorder causing faulty remodelling of bone
-AD or AR
-dominant form
-progressive enlargement of head and mandible and long-bone clubbing
-progressive cranial neuropathies caused by nerve compression at foramina optic atrophy,
trigeminal hypoesthesia, recurrent facial paralysis, SNHL
-CHL d/t involvement of ossicles and bone of epitympanum
Paget’s Disease
-chronic, often progressive disorder of bone metabolism
-characterized by bony hypertrophy and remodelling d/t increased activity of both osteoclasts and
osteoblasts
-affects 3% of population over 40 years of age and up to 11% of those over 80
-temporal bone involvement can cause SNHL and CHL
-otologic symptoms:
-hearing loss, tinnitus, mild vestibular complaints
-facial nerve not affected
-other signs:
-calvarial enlargement, enlargement of superficial temporal artery, elevated ALP and typical
findings of radiographic studies
-radiographic findings:
-thickening of calvarium
-mixture of dense and radiolucent areas of fibrosis
-areas of cortical erosion
-characteristic coarse bony trabeculae
-treatment:
-calcitonins and etidronate disodium to decrease osteoclast activity
1099
Fibrous Dysplasia
-replacement of normal cancellous bone by spicules of woven bone in a fibrous stroma
-most common presenting symptoms of temporal bone fibrous dysplasia are CHL (80%), progressive
occlusion of EAC (85%), and canal cholesteatoma (40%)
-facial nerve paralysis or paresis and SNHL are other possible complications
-indications for surgical treatment:
-CHL and cholesteatoma secondary to EAC stenosis
IDIOPATHIC DISEASES
Histiocytosis X
-characterized by an accumulation of histiocytes, lymphocytes, and eosinophil in skin, bone marrow, lymph
nodes, lung, liver, thymus, spleen, and CNS
-most pts have deficiency of suppressor lymphocytes and an elevated amount of helper lymphocytes
-definitive diagnosis made by showing presence of Birbeck granules on EM or immunohistochemical
testing showing presence of CD1 antigen
-head and neck involvement seen in 73%
-cranial vault, EAC, temporal bone, lymph nodes, maxilla, mandible
-otologic symptoms:
-otorrhea, aural granulation tissue, mastoid swelling, deafness, collapse of external
auditory canal and swelling of mandible or maxilla
-tx:
-systemic disease: steroids etoposide, vincristine, vinblastine if no response
-topical or intralesional steroids for localized lesions
-eosinophilic granuloma:
-unifocal process affected children and young adults
-osteolytic lesion in temporal bone pain, swelling, purulent otorrhea, CHL
-destructive lesion within temporal bone seen on CT
-tx: XRT is curative and prognosis is excellent
-Hand-Schuller-Christian disease
-multifocal process
-occurs in children under 5 years
-prognosis less favourable than EG
-low-dose chemotherapy may be needed
-Letterer-Siwe disease
-rapidly progressive fulminant form of histiocytosis X
-occurs in children under 3 ya
-rapid fatal course
-death occurs from bleeding or infection caused by bone marrow failure from replacement by
immature histiocytes
1100
INFECTIONS OF THE LABYRINTH
LABYRINTHINE FORM AND FUNCTION
Anatomy
-permeability of round window is implicated in spread of middle-ear infections to labyrinth
-patency of cochlear aqueduct diminishes with age:
-age < 16y 82% have patent aqueducts
-age > 60y 30% have patent aqueducts
-passage of particulate matter from CSF to inner ear possible
-8th nerve termini penetrate to their end organs through cribrose areas and provide potential route
for passage of infectious organisms from CSF
-stria vascularis has rich vascular supply: vestibulocochlear and spiral modiolar arteries
-organisms infect spiral ganglion cells after gaining access by cochlear vasculature
Physiology
-hyperactivity or hypoactivity in one labyrinth produces an imbalance that is perceived as vertigo
-compensation occurs - intervestibular commissural fibers undergo reorganization that is thought to be
important in functional recovery
MENINGITIS
Bacterial Meningitis
Etiology:
-Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae account for 71% of cases
-incidence of partial or complete SNHL after meningitis ranges from 10-20%
-same three organisms were related to 83% of cases of hearing loss
-S. pneumoniae most detriment to hearing: associated with hearing loss in nearly 25% of cases
-initial bacteremia precipitates eventual hearing loss before any symptoms or signs develop
Pathology:
-acute toxic labyrinthitis
-acute suppurative labyrinthitis
-chronic labyrinthitis
-labyrinthine sclerosis
Evaluation and Management:

-Otoacoustic emisisons with tympanometry recommended for children in acute stage
-ABR performed if OAEs are abnormal
-normal ABR in first few days of hospitalization unlikely to develop SNHL
-but only reflects hearing in 2000-4000 Hz range must obtain behavioral audiometry ASAP
-pathophysiology:
-cytokines (IL 1b and TNF-alpha) meningeal inflammation
-modulated by steroids
-dexamethasone is effective in diminishing neurologic deficits in pediatric H. influenzae
meningitis; effectiveness with other meningitis not yet demonstrated
Viral Meningitis
-it has been difficult to link viral meningitis to hearing loss and imbalance
F.Ling - Labyrinthine Infections (1)
1101
Fungal Meningitis
-Rare: Cryptococcus neoformans, Aspergillus, Candida albicans, Coccidiodes immitis causative agents in
only 1.3% of meningitis cases
-neural involvement: granulomas in IAC and Rosenthal’s canal
-associated with retrocochlear lesions rather than cochlear hearing losses seen with bacterial meningitis
VIRAL LABYRINTHITIS
-difficult to prove
-only two viruses: CMV and mumps virus have been isolated and cultured from inner ear of affected humans
Perinatal Viral Labyrinthitis

-congenital CMV and rubella hearing loss
Cytomegalovirus
-DNA-containing virus
-cochlear alterations, most severe in basal turn, include hydrops or collapse of Reissner membrane and
inclusion bodies in cells of stria vascularis and endolymphatic surface of Reissner membrane
-most common cause of viral congenital deafness
-symptomatic disease (cytomegalic inclusion disease)
-only 1-2% of all congenital CMV infections
-hemolytic anemia, hepatosplenomegaly, jaundice, purpura
-30-60% develop severe, symmetric SNHL
-asymptomatic disease:
-majority of congenital CMV infections
-8-15% have mild to moderate SNHL
-diagnosis:
-suggested by radiographic demonstration of intracerebral calcium deposits in a
microcephalic child
-isolation of CMV from fresh urine during first 3 weeks of life can clinch dx in
symptomatic and asymptomatic cases
-identification of anti-CMV IgM in infant’s serum
-may be a role for ganciclovir for improvement and stabilization of hearing
Rubella
-produces multiple malformations including those of the temporal bone:
-cochleosaccular degeneration and strial atrophy
-symptomatic disease:
-implies infection in first trimester
-produces hearing loss in ~50%
-congenital cardiac malformations, visual loss, motor deficits, thrombocytopenic purpura,
hepatosplenomegaly, icterus, anemia, low birth weight, mental retardation
-asymptomatic disease:
-implies infection during second or third trimesters
-associated with hearing loss in 10-20%
-although rubella vaccine, if given to a nonimmune pregnant woman, can cross the placental barrier to
infect the fetus, the risk of subsequent hearing loss is small
-laboratory testing: isolating rubella virus from urine
-SNHL:
-most commonly profound
-in some pts hearing loss may progress
1102
-generally, all frequencies are affected equally; speech discrimination may be poor
-hypoactive vestibular response or frank unilateral or bilateral canal paresis may occur
Neurolabyrinthitis
-acute viral labyrinthitis: involvement of auditory or vestibular end organs
-acute neuritis: disruption of cochlear or vestibular peripheral nerve function
-therapy is not altered by the distinction
Acute Cochlear Labyrinthitis and Neuritis

-afflicts ~ 10/100,000 persons annually
-Acute cochlear labyrinthitis = idiopathic sudden SNHL (ISSNHL)
-loss of > 30 dB hearing in at least three contiguous frequencies in fewer than 3 days in an
otherwise healthy person
-viruses: influenza B, mumps, rubeola, CMV, VZV
-loss of cochlear hair cells, most severe at the basal turn, with relative preservation of other
elements of cochlear duct and spiral ganglion neurons
-true emergency in otology: prompt initiation of appropriate therapy may improve or totally
reverse the hearing loss
-ENG has prognostic value: normal ENG statistically greater likelihood of hearing recovery
-if patient seen within the first 10 days after hearing loss:
-high-dose corticosteroid therapy is begun and tapered over next 12 days
-shown to enhance likelihood of hearing recovery in the intermediate hearing
loss range
-valacyclovir in conjunction with steroids still under investigation
-pts seen long after onset of ISSNHL or in whose hearing does not recover hearing aid
evaluation
Acute Vestibular Labyrinthitis or Neuritis

-sudden, unilateral loss of vestibular function w/o associated auditory or CNS symptoms in an otherwise
healthy adult
-isolated atrophy of vestibular nerve the rule; atrophy of end organs rare
-closely mimic alterations seen with herpes zoster infection of the vestibular system
-recurrent (chronic) forms of disease exist
-acute phase generally lasts several days to few weeks, complete recovery is expected within 6 months
-positional vertigo may appear in recovery phase of acute attack
-tx: vestibular suppressants (Gravol, Valium, Antivert etc..), hydration, antiemetics
-gradual recovery through compensation
MUMPS, MEASLES, AND VARICELLA-ZOSTER INFECTIONS
Mumps
-paramyxovirus
-symptom complex of parotitis, orchitis, meningoencephalitis, and in 0.05% of cases, hearing loss
-hearing loss usually occurs at end of first week of parotitis
-unilateral in 80%
-ranges from mild, high frequence SNHL to profound SNHL
-evidence supports hypothesis that a subclinical mumps infection can cause ISSNHL in an
otherwise healthy person
-vestibular involvement uncommon
-histopathology:
-alterations of cochlear duct structures
1103
-atrophy of organ of Corti and stria vascularis with collapse of Reissner membrane
-deformation and detachment of tectorial membrane and moderate loss of spiral ganglion cells in
basal turn
-no data exist to support steroid therapy - studies are still needed to evaluate steroid and antiviral therapies
Measles
-rubeola virus: RNA myxovirus
-rash, conjunctivitis and buccal mucosal lesions known as Koplik spots
-permanent SNHL in < 0.1%
-usually bilateral, worst in high frequencies
-mild to moderate (55%) or profound (45%)
-loss of vestibular function, manifested by reduced or absent caloric responses in as many as 72%
-vaccine has markedly decreased incidence of measles-related hearing loss
-temporal bone findings:
-atrophy of organ of Corti, which is worst at basal aspect of cochlea
-degenerative changes in spiral ganglion, stria vascularis, and tectorial membrane
-collapse of Reissner membrane
-alterations consist of multinucleated giant cells known as Warthin-Finkelday cells
-acute phase:
-xanthematous rash
-Koplik spots (small white foci representing necrotic lesions of buccal mucosa)
-mild conjunctivitis
-acute otitis media (rarely)
-diagnosis:
-isolating rubeola virus from throat cultures, documenting a fourfold increase in titers of antibody
to rubeola virus between acute and convalescent sera, or immunofluorescent staining of exfoliated
epithelium from oropharynx or conjunctiva, which can demonstrate rubeola antigen
-no clear documentation that steroid or antiviral therapy can benefit acute disease by preventing or
ameliorating SNHL
Varicella-Zoster
-herpesvirus VZV
-primary infection manifested clinically as chickenpox
-pustular rash
-Ramsay-Hunt syndrome:
-develops when latent virus is reactivated and consists of variable severity of facial nerve
paralysis, SNHL, and vertigo in associated with a painful vesicular rash of external auditory canal
and concha
-inflammatory neuritis of facial, cochlear, and vestibular nerves
-histopathology:
-atrophy of cochlear neurons and sensorineural elements of vestibular labyrinth
-collapse of Reissner membrane and fibrous tissue and neoossification in perilymphatic
compartment of lateral semicircular canal
-pts may be immunocompromised
-SNHL worse in high frequencies
-ENG may reveal a reduced or absent vestibular response in involved ear
-treatment:
-corticosteroids and acyclovir
-severe SNHL rarely recovers completely
1104
DELAYED ENDOLYMPHATIC HYDROPS
-Schuknecht proposes that ipsilateral, contralateral or bilateral endolymphatic hydrops is a delayed

manifestation of some viral labyrinthine infections, because a subclinical viral injury to the resorptive
mechanisms of the endolymphatic sac eventually becomes evident clinically by fluctuating sensorineural
hearing loss or episodic vertigo
-history usually of early childhood loss of cochlear or vestibular function - many years later, symptoms of
progressive endolymphatic hydrops appear
-therapy is same as in Menieres
HUMAN IMMUNODEFICIENCY VIRUS LABYRINTHITIS
Etiology
-light microscopy variably reveals:
-cryptococcosis of inner ear and IAC
-CMV-associated inclusion bodies in IAC and inner ear
-no alterations
LUETIC LABYRINTHITIS
Etiology
-T. pallidum
-SNHL develops in congenital and acquired forms with variable frequency
-congenital:
-early: generally fatal
-late: sudden SNHL in childhood generally symmetric and profound with vestibular symptoms
-in 51% SNHL appears suddenly and asymmetrically between ages of 25 and 35 years
-acquired:
-SNHL can occur in primary, secondary, and tertiary forms
-histopathology:
-mononuclear leukocytic infiltrates and obliterative endarteritis
-inflammatory fibrosis with round cell infiltration can obliterate endolymphatic sac and duct
hydrops
-gummas, central necrosis, and lymphocytic infiltrates are most frequent in vestibular otic capsule
and can result in degeneration of sensory and neural structures of labyrinth and eighth cranial
nerve
-gummatous involvement of ossicles CHL
Evaluation and Management

-any unexplained SNHL or vertigo should be evaluated for the possibility of a syphilitic infection
-physical examination generally unremarkable
-Hennebert sign (positive fistula test with an intact tympanic membrane) and Tullio sign (vertigo and
nystagmus precipitated by loud noise exposure) are associated with congenital syphilis
-audiology:
-bilateral hearing loss which may fluctuate and progress to profound hearing loss
-abnormal elevated SP:AP ratio on ECoG
-ENG: decreased vestibular response
1105
-serologic testing:
-VDRL
-FTA-ABS
-false positives in connective tissue diseases, leprosy, infectious mononucleosis,
pregnancy
-treatment:
-at least 3 months
-penicillin G 2.4 MU IM for early stage
-procaine penicillin 1.8 MU IM daily for 3 weeks with 500 mg of probenecid po q6h, then 2.4
MU of benzathine penicillin G IM weekly to total of 3 months for late-stage disease
1106
NOISE-INDUCED HEARING LOSS
PATHOGENESIS
Pure-Tone Threshold Shifts
Temporary Threshold Shifts

-exposure to loud noise for seconds to hours may cause temporary SNHL that recovers almost completely
within 24h
-magnitude of loss dependent on:
-intensity:
-more intense sounds larger shifts
-spectrum (frequency content):
-high-frequency sounds > low frequency sounds
-measurements made on dBA scale
-give greater weight to those frequencies most hazardous to human hearing (1-5
kHz) and lesser weight to lower frequencies
-pure tones cause TTS that are greatest at and slightly above the frequencies of exposure
of the sounds
-time pattern of sound:
-longer exposures increased TTS
-interrupted exposures < continuous exposures
Permanent Threshold Shift

-noise-induced permanent threshold shift (NIPTS)
-does not progress after cessation of offending exposure
-reasons for 4-kHz notch:
-greater sensitivity of human ear to frequencies b/n 1 and 5 kHz
-acoustic reflex protective against NIPTS at least for frequencies below 2 kHz
-if facial nerve paralysis PTS and TTS increase dramatically for lower frequencies
-intermittency most protective for low frequencies
-outer hair cells at base of cochlea more susceptible to oxidative stress
-“conditioning of ear”: amount of threshold shift cause by a particular exposure can be reduced by adding
prior exposure at lower levels
Pathology
-primary site if injury = rootlets of sterocilia
-TTS: outer hair cells’ stereocilia become less stiff respond poorly to stimulation
-stereocilia are able to recover
-PTS: fusion of adjacent stereocilia and loss of stereocilia
Acoustic Trauma
-single exposure to intense short-duration sound can cause permanent HL not preceded by TTS
-sound mechanically damages organ of Corti, tearing membranes, rupturing cells, allowing perilymph and
endolymph to mix
-impulse noise:
-range in 0.2 ms duration with peak energy at 2-3 kHz
-most hazardous (eg. small arms gunfire): above critical level of 140 dB
-impact noise:
-caused by collision of metal objects
-can cause acoustic trauma, but less likely than impulse noise to reach critical levels
F.Ling - NIHL (1)
1107
Interactions
-Aging: additivity: net hearing loss is the decibel sum of threshold shifts from aging and from noise
-Vibration: interacts with noise to damage ear (seen in “vibration induced white finger”)
-Drugs and Chemicals: no definite interactions
-Susceptibility: not well studied
Epidemiology
Damage Risk Criteria

-levels below 80 dBA pose negligible risk to human hearing over a working lifetime
-levels above 85 dBA risk grows rapidly for high frequencies and more slowly for low frequencies
-at 4 kHz, NIPTS grows rapidly over first 10 years and then reaches a plateau
-compared to age-related changes which is an accelerating process
Nonoccupational Exposures
-gunfire
-most important non-occupational cause of NIHL
-impulses can range up to 170 dB
-exposures to leaf blowers, chain saws, and rock concerts can reach the 110-120 dBA range but few
persons accrue significant time in these exposures except in an occupational setting
Diagnosis of NIHL (occupational)

-always sensorineural affecting hair cells of inner ear
-almost always bilateral
-almost never produces profound hearing loss:
-low frequency limits ~ 40 dB
-high frequency limits ~ 75 dB
-once exposure discontinued, no further progression of HL as result of noise exposure
-as hearing threshold increases, rate of loss decreases (plateaus)
-earliest damage reflects loss in 3, 4 and 6 kHz range
-losses at 3, 4 and 6 kHz usually reach maximal level in about 10-15 years
-continuous exposure over years is more damaging than interrupted exposure to noise
Handicap and Compensation

-most of the acoustic power of speech is concentrated below 1000 Hz
-most of the information content of speech is in the high frequencies
-NIHL causes difficulty discriminating among consonants which are high frequency, low intensity
sounds
-AAO-HNS determination of hearing handicap:
-HL does not begin to be handicapping until PTL HL exceeds 25 dB
-handicap grows at rate of 1.5% per decibel of hearing loss beyond 25 dB
-unilateral hearing deafness is only mild handicap: 5 to 1 weighting favouring the better ear is
used
-monaural impairment (MI) for ear calculated: MI = 1.5 (PTA - 25)
-overall hearing handicap (HH) = [5(MIb) + (MIw)]/6
F.Ling - NIHL (2)
1108
MANAGEMENT
Hearing Conservation
-OSHA requires hearing protection for workers exposed to 85 dBA
-prevent exposures exceeding 90 dBA for an 8-hour day
-5 dB “trading rule”:
-exposure time cut in half for each 5 dB increment exposure level
-eg. 8-h exposure to 90 dBA = 4-h exposure to 95 dBA = 2-h exposure to 100 dBA
-maximum permissible exposure (without hearing protection) is 90 dB TWA (time weighted average =
constant exposure for 8 hours)
-impulse noise exposure is limited to 140 dB peak level
-In Canada:
-workplace regulations vary from province to province
-it has been proposed that 85 dB(A) be used as the level for mandatory hearing testing and the
implementation of a hearing conservation program
-Canadian standards restrict noise levels in the workplace to 87 decibels for an eight-hour daily
exposure
-for each increase of 3 decibels, the duration of the worker'
s exposure to noise must be
reduced by half
F.Ling - NIHL (3)
1109
OTOTOXICITY
Aminoglycosides
-act on bacterial ribosomes to stop synthesis of bacterial cell protein
-bactericidal against gram-negative aerobic bacilli
-mechanism of ototoxicity (theory):
-aminoglycosides form complexes with iron free radicals damage to outer hair cells and
vestibular receptors
-histopathology (order of progression):
1. early damage to first row of outer hair cells beginning at basal turn of cochlea high
frequency SNHL
2. progression to apex
3. second and third rows of outer hair cells
4. inner hair cells
-may be genetic predisposition
-damage is permanent if symptoms persist beyond 2-3 months
-vestibulotoxic:
-streptomycin and gentamicin
-manifested by vertigo or disequilibrium
-overall incidence of 15% for gentamicin
-cochleotoxic:
-amikacin, neomycin, kanamycin, tobramycin
-onset heralded by tinnitus
-agents that potentiate or synergise with aminoglycosides to cause ototoxicity:
-ethacrynic acid (facilitates gentamicin diffusion into endolymph)
-furosemide
-cisplatin
-flagyl
Macrolides
-ototoxicity reported mainly in pts receiving long-term, high-dose therapy such as for HIV-related
infections
-MOA for ototoxicity unknown
-most common manifestation is hearing loss in conversational frequencies
-hearing loss is reversible
Vancomycin
-rare reports of cochleotoxicity
-tinnitus and high-frequency hearing loss
Antineoplastic Agents
Cisplatin
-usually permanent hearing loss, bilateral and symmetric
-high-frequency hearing loss:
-histopathology: outer hair cell damage and cell loss most extensive in basal turn
-MOA for ototoxicity thought to be d/t generation of oxygen free radicals within inner ear and
depletion of glutathione in auditory hair cells
->50% receiving > 400 mg/m2 permanent ototoxicity
F.Ling - Ototoxicity (1)
1110
-risk factors:
-high cumulative dose of cisplatin
-hx of noise exposure
-high dose of vincristine
-high dose of individual cycle than total dose
-elderly or young children
Carboplatin
-79% of patients experience hearing loss
-inner rather than outer hair cells are damaged
Diuretics
-furosemide and ethacrynic acid
-SNHL, tinnitus and vertigo
-transient and permanent loss reported
-incidence of ototoxicity ~ 6%
-MOA: injury to stria vascularis
-disturbance of K-ion transport with subsequent reduction of endocochlear potential
-keeping the rate of continuous infusion at rates less than 15 mg/min
Salicylates
-typically from high-dose aspirin therapy for arthritis
-limited to cochlea flat, bilateral, SNHL and tinnitus
-serum salicylate levels > 30 mg/100L
-threshold shifts of 30-40 dB
-complete reversibility within 2-3 days after cessation
Ototopicals
-human studies estimate incidence ~1/10 000
-avoid prolonged use especially when a tympanic membrane perforation present
-avoid use in a healthy ear
-studies in guinea pigs failed to show evidence of ototoxity with topical quinolones
MONITORING
-conventional audiometry often used

-limited by several factors (eg. patient participation, logistical impracticalities)
-ENG and other vestibular testing also impractical
-OAEs currently being studied for monitoring ototoxicity
F.Ling - Ototoxicity (2)
1111
CEREBELLOPONTINE ANGLE TUMOURS
-10% of intracranial tumours

-78% are acoustic neuromas (mostly on vestibular branch)
ANATOMY
-CPA boundaries: -anterior: posterior surface of temporal bone

-posterior: anterior surface of cerebellum
-medial: inferior olive
-superior: inferior border of pons and cerebellar peduncle
-inferior: cerebellar tonsil
-cranial nerves: -VII and VIII
-V
-IX, X, XI
-other important structures: flocculus, lateral aperture of fourth ventricle, AICA
F.Ling - CPA Tumours (1)
1112
VESTIBULAR SCHWANNOMAS
Epidemiology
-incidence: 1/100 000 per year
Tumour Biology
-arise from vestibular segment of eighth cranial nerve (superior = inferior nerves)
-most commonly occur at Scarpa ganglion
-sporadic (98%)
-bilateral in type 2 neurofibromatosis
-genetic defect on long arm of chromosome 22
-autosomal-dominant
-tumours tend to occur in younger patients
-more adherent to facial nerve greater chance of losing hearing with surgical treatment
-symptoms:
-unilateral auditory or vestibular symptoms (true vertigo in 19%)
-hearing loss (85%), tinnitus (56%) and vestibular dysfunction
-disequilibrium (50%)
-fifth cranial nerve compression mid-facial hypesthesia (maxillary division)
-brainstem compression hydrocephalus headache and visual loss
-loss of speech discrimination out of proportion to hearing loss
-SSNHL presenting symptom in 26%
-cause of sudden loss from vestibular schwannoma in 1-2.5% of pts with SSNHL
-d/t sudden vascular occlusion of labyrinthine artery
-others: ocular symptoms (CN VI), dysphagia, hoarseness, aspiration, cerebellar dysfunction
-signs:
-Hitselberger sign: decreased sensation in EAC - sensory branch of seventh nerve affected
-decreased cranial nerve function: eg. decreased corneal reflex
Histology
-Antoni Type A:
-histologically parallel nuclei (palisading Verocay bodies)
-uniform spindle cells
-compact cells
-Antoni Type B:
-histologically less uniform
-may have fatty or hyaline degeneration
-less cellular
-more cystic
Diagnostic Tests
-audiometric testing:
-pure-tone testing: SNHL - most commonly unilateral high frequency (65%)
-speech discrimination: scores out of proportion with pure-tone thresholds
-rollover phenomenon: performance decreases significantly when the intensity of
speech signal is raised
-reflex thresholds typically elevated or absent
-if present reflex then reflex decay measured:
-signal presented 10 dB above reflex threshold for 10s if contraction of
1113
stapedius cannot be maintained for at least half strength for the 10s positive
retrocochlear finding
-electrophysiologic testing:
-ABR most sensitive and specific audiologic test
-electrical potentials measured in response to broad-band clicks of short duration
-abnormalities seen:
-interaural difference in latency of wave V with delay of more than 0.2 msec (40-60%)
-no identifiable waveforms in pt without significant hearing loss in higher frequencies (20-
30%)
-presence of wave I but absence of other waves (10-20%)
-normal in 10-15% of patients: sensitivity is 85-90%
-summary of ABR findings suggestive of retrocochlear lesion:
1. Abnormal interaural wave V latency difference (IT5)

- > 0.2 msec
-may be relative to size of tumour
2. Abnormal interaural wave I-V latency difference (IT1-5)
3. Abnormal III-V latency difference (IT3-5)
4. Prolonged interwave latency between I-V(T1-5) or I-III (T3-5)
5. Increased absolute latency measurements:
-5.7 msec for wave V
-compared with normal standard
-may not be as accurate since latency may be affected by CHL
-vestibular testing:
-ENG: unilateral weakness of involved side on caloric testing
-tumours originating form inferior vestibular nerve may be missed (ENG only tests
superior nerve)
-no abnormality for smaller tumours
-hypoactive response on ENG indicates tumour probably on SVN favourable
prognosis for hearing
-hearing preservation more difficult with tumour in IVN b/c of proximity to
cochlear nerve and possible shared blood supply
-imaging studies:
-CT scan:
-90% of AN are enhanced
-intracanalicular tumours often missed
-CT only 63% accurate in diagnosing AN (may miss tumours smaller than 1 cm)
-intrathecal contrast or air CT cisternography improves diagnostic yield (historical)
-gadolinium enhanced MRI
-sensitive
-differentiation between AN and meningioma:
-AN: centered on IAC and has globular appearance causing acute angle formed
between posterior face of temporal bone and tumour surface; generally extends
into IAC “ice cream cone” appearance
-usually more non-homogenous than meningiomas
1114
Management
-goals: preserve life > avoid serious neurologic sequelae > complete tumour removal > preserve facial
nerve function preserve hearing
-observation:
-growth potential (3 groups):
-no growth or very limited growth (0.2 mm/y) (40%)
-limited growth (2 mm/y)
-rapid growth (10 mm/y)
-observation reserved for elderly pt or those with serious medical disorders who have small slow-
growing tumours
-younger pt better served by having tumour removed
-surgery:
-Translabyrinthine Approach
-indications:
-approach of choice for non-serviceable hearing
-advantages:
-most direct route to CPA
-requires minimal cerebellar retraction
-widely exposes fundus of IAC for better tumour removal
-offers best opportunity for immediate repair of CN VII if it is injured
-disadvantages:
-hearing is sacrificed
-approach used for tumours of all sizes
-results:
-mortality rate low (0.4%) and directly proportional to tumour size
-recurrence rate low (0.3-0.5%)
-complications:
-facial nerve paralysis (usually temporary) - most common
-CSF leak (4-14%)
-meningitis
-Retrosigmoid-Suboccipital Approach
-indications:
-for good preoperative hearing and tumour medially located within IAC and
protrudes >2cm into CPA
-large tumours, tumours of the medial IAC
-advantage:
-potential for hearing preservation
-ability to remove tumours of all sizes
-good visualization of brainstem and lower cranial nerves
-lower risk of facial nerve injury than middle cranial fossa approach
-disadvantage:
-potential for air embolism
-higher incidence of postoperative headaches
-limited exposure to lateral IAC
-higher risk of facial nerve injury than translabyrinthine approach
-requires cerebellar retraction
1115
-results:
-complete resection in 95%
-hearing preservation: 17-63%
-complications:
-CSF leak: 11-15%
-meningitis: 1-7%
-recurrence: <1%-3%
-Middle Fossa Approach

-indications:
-limited to pts with intracanalicular tumours to tumours extending <1 cm into
CPA
-advantages:
-potential for hearing preservation
-disadvantages:
-must work around facial nerve during tumour removal
-technically more difficult
-landmarks sometimes absent on floor of middle cranial fossa
-requires retraction of temporal lobe (risk of aphasia or seizure)
-poor exposure to posterior fossa
-higher risk of facial nerve injury
-technique:
-temporal craniotomy performed
-middle meningeal artery is anterior limit of elevation
-identification of GSPN and arcuate eminence - IAC bisects angle formed by
these two structures
-drilling to expose IAC
-identification of Bill’s bar marks lateral limit of dissection
-proximal labyrinthine portion of facial nerve is decompressed to allow for any
swelling
-dissection of facial nerve and cochlear nerve from tumour
-results:
-preservation of hearing in 71%
-normal facial nerve function 92%
-complications:
-seizures, epidural haematoma, meningitis, CSF fistula
-ABR latency difference < 0.4 msec associated with higher rate of hearing
preservation
-Stereotactic Radiosurgery
-controversial
-radiation doses six times more than clinical maximum failed to eradicate
schwannoma cells in vitro
-no long term results
-significant hearing loss, facial nerve dysfunction
-multisource cobalt 60 gamma unit or linear accelerator
-usually for small tumours (< 1 cm)
-usually used for elderly or otherwise poor surgical candidates
1116
OTHER TUMOURS OF THE CEREBELLOPONTINE ANGLE
Meningiomas
-second most common tumour originating within CPA (3% of tumours in this region)
-arise from cap cells (endothelial cells)- collect in clusters around tips of arachnoid villi
-two types:
-globular
-en plaque (flat and sessile)
-histologic subtypes:
-meningotheliomatous meningiomas (55%)
-fibrous meningiomas (15%)
-transitional meningiomas (30%)
-angioblastic meningiomas (5%)
-generally larger than AN before causing hearing loss or vestibular symptoms
-ABR may be normal in 25% of pts
-CT scans:
-meningiomas:
-more dense appearance and generally are homogenous in taking up contrast medium
-evidence of hyperostosis and calcification within tumour
-sessile and broad based (“dural tail”) - no widening of IAC
-AN usually non-homogeneous because of areas of central necrosis
-MRI scans:
-“washed out” appearance because of vascularity less bright image than that of AN
-surgical resection for treatment:
-translabyrinthine approach:
-poor hearing and tumour at CPA
-transcochlear approach:
-medial extension of tumour to IAC and onto clivus
-GSPN section, facial nerve removed and transposed posteriorly, cochlea drilled away
-other combined approaches: middle fossa, retrosigmoid
Facial Nerve Schwannomas

-facial nerve function generally not impaired until tumour is quite large
-clinical presentation similar to AN
-ipsilateral acoustic reflex may be absent
-MRI method of choice in diagnosing facial nerve schwannoma
-treatment: surgical resection with insertion of cable nerve graft
Epidermoids
-may arise either within temporal bone or CPA
-hemifacial spasm is common early distinguishing feature and progressive facial paralysis frequently noted
-thought to arise from epithelial rests within temporal bone
-identical to cholesteatomas of middle ear
-MRI: dark on T1, extremely bright T2 signal; non-enhancing
-complete surgical resection usually difficult because of propensity of tumour to infiltrate between cranial
nerves and blood vessels
Other Cranial Nerve Schwannomas

-CN V: unilateral facial hypesthesia
-CN IX, X, XI: jugular foramen syndrome
-CN XII: hemiatrophy of tongue
1117
Vascular Tumours
-glomus jugulare tumours
-non-chromaffin paragangliomas that arise from chemoreceptor cells along ninth and tenth cranial
nerves in jugular bulb
-pulsatile tinnitus
-CT: irregular destruction of jugular foramen
-tx: surgical resection through infratemporal fossa approach
-haemangiomas, hemangioblastomas
-often arise from geniculate ganglion
-slowly progressive facial paralysis
-tx: surgical excision by middle fossa approach
Miscellaneous CPA Tumours

-arachnoid cysts
-cholesterol granuloma (of petrous apex)
-results from occlusion of air cells in petrous apex and haemorrhage into air cells causes foreign
body reaction and granuloma formation
-MRI: bright T1 and T2
-tx: drainage through infralabyrinthine or infracochlear approach
-dermoid tumours, teratomas, chordomas
-lipoma
-malignant tumours rare: chondrosarcomas, malignant choroid plexus papillomas, metastatic tumours
CT and MRI characteristics for selective CPA tumours:
Tumour CT MRI T1 MRI T2 T1 with gado
acoustic neuroma -isodense -hypointense -hyperintense -enhances

-heterogeneous
enhancement
meningioma -hypodense -hypointense -variable -enhances

-homogeneous
enhancement
epidermoid -hypointense -hypointense -hyperintense -non-enhancing
cholesterol granuloma -isodense -hyperintense -hyperintense -non-enhancing
mucocele -hypodense -hypointense -hyperintense -rim-enhancing
lipoma -hyperdense -hyperintense -hypointense -non-enhancing
arachnoid cyst -hypodense -hypointense -hyperintense -non-enhancing
1118
1119
SUDDEN SENSORY HEARING LOSS
DEFINITION
-any noticeable and measurable loss of hearing function - pitch or speech perception - occurring over a
matter of minutes to days
-loss of significant hearing (>30 dB) in at least 3 adjacent frequencies that occurs over less then 3 days
EPIDEMIOLOGY
-5-20 per 100 000
-M=F
-bilateral in 1-2% of cases
-median age at presentation: 40-54 years
-defined vs. idiopathic (ISSHL) DDx IN SUDDEN HEARING LOSS
-most cases idiopathic (85-90%); four theories: (defined)
-viral infection Infection Bacterial
-vascular compromise Meningitis
-intracochlear membrane rupture Labyrinthitis
-immune inner ear disease Syphilis
Viral
Mumps
Viral Infection CMV
-high prevalence of recent viral type illness, recent viral
seroconversion, temporal bone histopathology Inflammation Autoimmune
Cogan syndrome
-rates of seroconversion for herpesvirus family significantly SLE
higher in SHL population MS
-viral cause implicated but cannot be proved
Trauma Temporal bone fracture
Acoustic Trauma
Vascular Compromise Perilymphatic fistula
-cochlea: labyrinthine artery - no collaterals
-cochlear function sensitive to changes in blood supply Tumour CPA tumour
Temporal bone metastasis
-reduced O2 tension to stria vascularis
Toxins Aminoglycosides
Intracochlear Membrane Rupture ASA
-a leak of perilymph fluid into middle ear via round window
Vascular Thromoembolism
or oval window postulated to produce hearing loss by creating
Macroglobulinemia
a state of relative endolymphatic hydrops by producing Sickle cell disease
intracochlear membrane breaks Coronary bypass graft surgery
-break in membrane mixing of endolymph and perilymph
alters endocochlear potential
Immune Inner Ear Disease

-progressive SNHL
-Cogan syndrome, SLE, other autoimmune rheumatologic disorders well documented
F.Ling - Sudden Sensory Hearing Loss (1)
1120
EVALUATION
-history, physical
LABORATORY TESTS
-pneumotoscopy search for fistula sign
-audiogram CBC polycythemia, leukemia,
-ABR, OAEs, +/- ENG thrombocytosis
-laboratory tests (see table)
ESR nonspecific screen for autoimmune or
-CT/MRI of CPA eventually inflammatory disease, follow with ANA
-1-2% of pts with ISSHL have IAC or
CPA tumours FTA-ABs/MHA-TP syphilis
-also looking for cochlear dysplasia,
Coagulation studies if indicated, by history
Mondini malformation, or enlarged Thyroid function if indicated by history
vestibular aqueduct
TREATMENT
Empiric Therapy
-corticosteroids
-presumed reduction of cochlea and auditory nerve inflammation
-Prednisone 1 mg/kg po qd x 7-14 days then recheck hearing
-antivirals
-acyclovir: no real benefit if started after 5-7 days
-others: amantadine, famciclovir, valaciclovir
-effects of treatment not yet reported
Other Therapies
Vasodilators
-improve cochlear blood supply
-histamine, nicotinic acid, papaverine, procaine, niacin, carbogen have been used
-few data support vasodilator therapy
Rheologic agents
-alters viscosity of blood to improve blood flow
-LMW dextrans, anticoagulants, pentoxifylline (Trental)
Diuretics
-presumed cochlear endolymphatic hydrops
-mechanism of action for diuretics in SHL not understood
Triiodobenzoic Acid Derivatives

-thought to affect stria vascularis and assist in maintaining endocochlear potential
Surgery
-repair of oval and round window perilymph fistulae
1121
PROGNOSIS
-recovery rates of SSHL generally good (50-60%)

-majority (60%) have spontaneous recovery without treatment
-no definitive treatment; most studies show no significant differences in treatment vs placebo
Poor Prognostic Factors

-associated symptoms of vertigo or imbalance lower recovery rate
-severe vertigo associated with high-frequency or profound hearing loss
-patient age: youngest and oldest pts may have lower recovery rates
-presentation with total deafness
-longer duration of hearing loss
-down-sloping audiogram (high-frequency loss)
-associated vascular risk factors
-delayed treatment
Good Prognostic Factors

-no associated vertigo
-no extremes of age
-no high frequency loss (low frequency hearing loss)
-mild to moderate hearing loss
-early treatment
1122
TINNITUS
DEFINITION
Objective Tinnitus
-perception of sound caused by an internal body sound or vibration
Subjective Tinnitus
-perception of sound in the absence of any acoustic, electrical or external stimulation
-more common than objective tinnitus
-typically associated with high frequency hearing loss
-prevalent b/n ages 40-70
-M > F
CAUSES OF OBJECTIVE TINNITUS ETIOLOGIC FACTORS IN SUBJECTIVE TINNITUS
Vascular abnormalities Otologic factors Presbycusis (most common)

Noise-induced hearing loss
Benign intracranial hypertension Menieres disease
syndrome Otosclerosis
AV shunts
-congential AVM Metabolic function Hypo/Hyperthyroidism (d/t CO)
-acquired AV shunt Hyperlipidemia
-glomus jugulare Zinc deficiency
-glomus tympanicum Vitamin deficiency (A or B)
Arterial bruits
-high-riding carotid artery Neurologic function Skull fracture or closed head trauma
-vascular loop Whiplash injury
-persistent stapedial artery MS
Venous hum Meningitic effects
-dehiscent jugular bulb
-hypertension Medications ASA (most common drug causing
-transverse sinus obstruction symptoms)
Patulous eustachian tube NSAIDs
Palatal myoclonus Aminoglycosides
Idiopathic stapedial muscle spasm Heavy metals
Dental factors TMJ syndrome
Psychological Depression (cause or effect)

Anxiety
WORK-UP
-similar work-up as hearing loss
-special attention to retrotympanic masses, audible bruits, history of trauma, medications, presence of TMJ
and psychological factors
-character of tinnitus:
-high-pitched or low-pitched (roaring, buzzing)
-pulsatile
-clicking
-progression and frequency
-loudness, pure or multiple tones
-level of discomfort
F.Ling - Tinnitus (1)
1123
OBJECTIVE TINNITUS
Vascular Causes
-pulsatile; synchronous with heartbeat
Benign Intracranial Hypertension Syndrome

-most common cause of pulsatile tinnitus; seen especially in overweight females 20-30 years old
-increased intracranial pressure without focal neurological signs (may present with isolated abducens palsy)
-caused by systolic pulsations of CSF
-diagnosis by lumbar puncture to measure CSF pressure
-tx: weight loss and diurectics
AV shunts
-congenital
-interconnections between occipital artery and transverse sinus, internal carotid and vertebral
vessels, or middle meningeal artery and greater superficial petrosal artery have been reported
-acquired
-most common cause: glomus tympanicum or glomus jugulare
-dx: CT of middle ear showing erosion of caroticojugular spine or lesion lying within middle-ear
space
Arterial Bruits
-carotid stenosis (most common cause of objective tinnitus)
Venous Hums
-hypertension or abnormal high placement of jugular bulb
-partial occlusion or narrowing of transverse sinus
-near transverse sinus/sigmoid sinus junction; result of ingrowth of arachnoid granulation
turbulence
-no specific management
Mechanical Causes
Patulous Eustachian Tube

-associated with significant weight loss; ocean roaring sound synchronous with nasal respiration
-placing head in dependent position may relieve symptoms
-might see fluttering motion of TM with respiration on otoscopy
-possible treatments: caustics to nasopharynx, mucosal irritants, saturated solution of KI, and Teflon or
gelfoam injections around torus tubarius
Palatomyoclonus
-sxs: irregular clicking sound, ear fullness, distortion of hearing
-muscle spasm postoccipital headache and TMJ pain
-tx: muscle relaxants, Botox injections into active muscle
Idiopathic Stapedial Muscle Spasm

-may be accentuated by external sound
-dx: history, TM movement synchronous with noise
-tx: division of stapedius muscle and tensor tympani muscle (rarely required); muscle relaxants; avoid
nicotine, coffee, and decongestants
Spontaneous Otoacoustic Emissions

-rare cause of objective tinnitus
1124
SUBJECTIVE TINNITUS
-more common than objective tinnitus (35-45% population experience tinnitus)
-major sleep difficulty in 8%
Examination and Tests

-history, physical
-audiogram
-see SHL chapter for laboratory testing
-unilateral tinnitus: MUST RULE OUT CPA TUMOURS
Treatment
-treat any reversible otologic or medical disorder
-majority of tinnitus cases resolve spontaneously:
-75% improve; 25% remain unchanged
-avoid: chocolate, coffee, tea, cola (caffeine)
-stop smoking
-re-evaluate medications
-radio on at night
-treat depression/anxiety
Specific Treatment Regimens
Masking
-minimal masking level provides some indication as to whether masking can be used successfully
-if level required is greater than 10-15 dB sensation level success is doubtful
-usually ~60% of those with severe tinnitus benefit from masking
-approximately 80% of patients will have their tinnitus masked with 6 dB or less of sound pressure
Hearing Aid
-can be a first-trial device
-only 25% are relieved by this method alone
Tinnitus Instrument
-combination hearing aid and masking device
-produces sound from 1.5 to 8 kHz with volume potential from 45-90 dB
-ability to modify input of hearing aid and masking device independently
Masker
-limited to patients with normal or near normal hearing
-only 1/3 find this device useful
Habituation therapy
-patient stimulated with broad-band noise up to 16 hours a day
-over period of months (10-18) patient may become unaware of or untroubled by the tinnitus
Cognitive Behavioural Therapy

-for stress or depression management
-counselling, biofeedback etc..
Medications
-only medications that have proved useful have been drugs that affect emotional status of patients through
anxiety reduction, improved sleep pattern, and antidepressant effect
-consider benzodiazepines, tricyclics antidepressants, and carbamazepine
1125
Electrical Stimulation
-investigational
-initial results not encouraging
Surgery
-currently rarely has a role in treating tinnitus
1126
AUTOIMMUNE INNER-EAR DISEASE
THE INNER-EAR IMMUNE RESPONSE
-inner ear as well as CNS is capable of mounting an immune response

-inner ear contains immunoglobulin and endolymphatic sac contains immunocompetent cells
-immunoglobulin crosses blood-labyrinthine barrier and is present in perilymph at level of 1/1000 the
concentration found in serum
-cochlea: no cells
-endolymphatic sac: helper and suppressor T-cells, macrophages, B-cells
-IgM > IgG >> IgA
-nonchallenged inner ear derives protection from:
-diffusion of immunoglobulin from systemic circulation and CNS
-immunocompetent cells in endolymphatic sac - which appears to be the originating site for a local
immune response
-antigen does gain access to endolymphatic sac and this appears to be the initial site of the immune
response
-appears to be crucial in antigen processing and appears to be the site from which perilymph
antibody emanates
-cytokines involved:
-IL-2:
-early mediator and is released by T-helper cells on stimulation from IL-1 a lymphokine
released by activated macrophages
-activates T-helper, T-cytotoxic, and T-suppressor cells
-activates B-cells
-enhances natural killer cell activity
-chemoattraction for PMN, monocytes, lymphocytes
-immunoregulation for prevention of autoimmune disease
-TGF-B
-chemoattractant for monocytes, T-cells, and neutrophils
-increases levels of IL-1, IL-6 and PDGF
-interferes with IL-2 response
-deactivates macrophages
-inhibits production of IF-gamma and TNF-alpha
-inner ear also receives systemic immune cells for protection against viral and bacterial antigens
-egress of lymphocytes thought to be from spiral modiolar vein (SMV)
-timing of cells that enter cochlea:
-macrophages and granulocytes observed early (6 hours, and rapidly increase thereafter)
-T-helper cells gradually increase in endolymphatic sac, peaking at 2-3 weeks
-T-suppressor cells not detected until 3 weeks postchallenge
-IgG cells seen in endolymphatic sac by day 1, IgM follows shortly after with and increase on day
2; IgA cells do not appear until 3 weeks
-both suppurative and sterile labyrinthitis are known to result in formation of a dense extracellular matrix
and eventual ossification in the cochlea
-inner ear appears to have difficulty in clearing this matrix
-ossification of normally fluid-filled cochlear scalae is a common result of inner-ear inflammation
-a more robust immune response appears to result in greater damage to inner ear
-inner ear seems particularly sensitive and incapable of controlling the deleterious effects of an
inflammatory response
-results in degeneration of organ of Corti, stria vascularis, and spiral ganglion
F.Ling - Autoimmune Inner-Ear Disease (1)
1127
AUTOIMMUNE IMMUNOPATHOLOGY
-three primary mechanisms:

-autoantibodies against tissue antigens
-deposition of antigen-antibody immune complexes in tissue
-infiltration and destruction of tissue by specific cytotoxic T-cells
-autoimmune disorders associated with cochlear injury:

-Polyarteritis nodosa
-Wegener’s granulomatosis
-SLE
-Cogan syndrome:
-interstitial keratitis and vestibuloauditory dysfunction
-thought to be a hypersensitivity response to one or more infectious agents associated
with vasculitis
-Western-blot analysis positive for 68 kD protein

-found in 89% of pts who had active and progressive bilateral SNHL
TREATMENT
-high dose prednisone mainstay treatment

-early institution of 60 mg daily for 1 month
-short-term or lower dose long-term therapy either ineffective or fraught with risk of relapse
-tapered if hearing loss occurs, then reinstitute high-dose therapy again
-immunosuppressive used if pts relapse on high-dose prednisone
-methotrexate 7.5-20 mg weekly with folic acid
-monitor for CBC, platelets, BUN, Cr, LFTs and U/A
-prednisone-sparing effects may take 1-2 months to achieve
-cyclophosphamide 1-2 mg/kg/day
-for pts with severe hearing losses, positive 68-kD Western blots and nonresponsiveness
to prednisone or MTX
-risks: haemorrhagic cystitis, sterility
F.Ling - Autoimmune Inner-Ear Disease (2)
1128
AGING AND THE AUDITORY AND VESTIBULAR SYSTEM
-hearing loss is a common accompaniment of aging

-dizziness most common presenting complaint in patients over 75 years of age
-28% cardiovascular cause
-18% peripheral vestibular disorder
-14% central neurologic disorder
-18% more than one diagnosis
-22% no attributable cause
AGE-RELATED CHANGES IN AUDITORY AND VESTIBULAR SYSTEM
-anatomic changes due to physiologic aging:

-cerumen:
-desquamated epithelium mixed with sebum produced form sebaceous glands and watery
secretions of modified apocrine sweat glands
-atrophy of sweat glands with age drier, harder cerumen
-EAC hair becomes coarser can cause cerumen impaction
-arthritic changes in diarthrodial joints of ossicles universal after age 70 although not shown to
have any effect on hearing
-age-related changes within human cochlea (Schuknecht):
1. Cochlear
-epithelial atrophy with loss of sensory cells and supporting cells of organ of Corti
-progressive hair cell reduction begins at age 40
-high-frequency hearing loss with speech discrimination preserved in initial phases
2. Neuronal
-reduction of number of functioning cochlear neurons
-when reduction has reached 50% or more, hearing loss develops
-nonprecipitous, generalized loss of pure tone thresholds with speech discrimination
impaired out of proportion to the threshold shift
3. Metabolic
-atrophy of stria vascularis
-loss of 30% or more of strial tissue can result in clinical hearing loss
-flat hearing loss with good preservation of speech discrimination
4. Mechanical (cochlear conductive)

-alterations of basilar membrane that produce stiffening
-gradually sloping high frequency hearing loss with speech discrimination impaired
proportionate to pure tone threshold shift
-age-related anatomic and physiologic changes to vestibular system:

-reduction in sensory receptors located in SCC, saccule and utricle
-degeneration of neural elements in Scarpa ganglia and vestibular nerve
-decreased number of vestibular neurons
-decrease in caliber of peripheral myelinated fibers
-degeneration of otoconia within saccule and utricle
-degeneration of connections in central vestibular pathways
F.Ling - Aging and Otology (1)
1129
CAUSES OF BILATERALLY SYMMETRIC SNHL
Disorder Characteristics Diagnosis Treatment
Meniere disease -episodic attacks of fluctuant SNHL, -hx of typical attacks with medical: diuretics and low-salt diet
vertigo, tinnitus, aural fullness or symptom-free intervals; hearing surgical: decompression or shunt
pressure; bilateral in 20-30% of cases loss involves low tones initially of endolymphatic sac; section of
and later all frequencies; rule out vestibular nerve
neurosyphilis
Luetic hearing -often bilateral SNHL with no -positive FTA-ABS test, with or -penicillin and oral steroids
loss (late acquired characteristic audiometric pattern without clinical history of syphilis
syphilis) -speech discrimination score often worse
than would be predicted on basis of pure
tone thresholds
-often associated with vestibular
symptom
-may mimic Meniere disease
Paget disease -slowly progressive SNHL and CHL -skeletal deformities of skull and -calcitonins
-SNHL worse in high frequencies long bones of extremities, elevated
-maximum CHL of 20-30 dB at 500 Hz serum alkaline phosphatase and
urinary hydroxyproline
Hypothyroidism -slowly progressive SNHL affecting all -usual clinical stigmata of -thyroid replacement
frequencies daily hypothyroidism
-decreased serum T4
Ototoxic drugs -hearing loss with or without vestibular -history -none

dysfunction following treatment with
known ototoxic drug
Hereditary -progressive SNHL beginning at earlier -family history -none

progressive SNHL age than expected for presbycusis
-possible positive family history
Noise-induced -history of prolonged exposure to loud -history -none

hearing loss continuous noise or brief exposure to -characteristic audiogram with -use of ear protectors may prevent
loud impulse noise max hearing loss at 400 Hz further loss from noise exposure
Head Trauma -severe head injury often resulting in -history -none

loss of consciousness and bilateral
temporal bone fractures
Cochlear -far-advanced clinical otosclerosis -history is suggestive but surgical -stapedectomy

otosclerosis and (stapedial fixation) and cochlear exploration of stapes footplate is -sodium fluoride
far-advanced otosclerosis (SNHL) may appear on diagnostic and therapeutic
clinical audiogram as severe to profound SNHL -post-stapedectomy pt may be able
otosclerosis -pt will have good speech modulation to wear ear-level hearing aid with
and will be wearing bone conduction good results
hearing aid
-possibly a family history for
otosclerosis
PRESBYCUSIS
-factors contributing to age-related hearing loss

-microvascular disease resulting in diminished perfusion and hypoxia of labyrinthine hair cells
and neurons
-effects of diet
-noise exposure
-drug effects
-cigarette smoking
1130
-tests of central auditory function suggest that older pts have poorer speech discrimination than younger pts
because of changes in central auditory processing
VESTIBULAR DYSFUNCTIONS
TYPES OF DIZZINESS
Category Sensation Diagnosis
Vertigo -illusion of motion, either linear or rotating -vestibular disturbance d/t peripheral or central disease
Presyncope -impending faint -diffuse cerebral ischemic d/t vasovagal response, cardiac disease, or
metabolic disorders
Dysequilibrium -impaired balance and gaze -impaired motor control d/t neuromuscular disease, severe bilateral
vestibular disease, stroke, multisensory deficits, or medications
Nonspecific -light-headeness, “confusion”, “wooziness”, -often psychological disorders (anxiety, depression, panic),
“foggy-headed” hyperventilation
HISTORY AND PHYSICAL EXAMINATION
-dizziness stimulation battery

-assessment of hyperventilation
-orthostatic hypotension
-carotid sinus stimulation
-potentiated valsalva manoeuver
-Dix-Hallpike
-Barany rotation
-walk and turn
-seated head turn
NONSPECIFIC THERAPY
-drugs:
-five main classes of drugs used to control acute vestibular and autonomic symptoms:
-antihistamines (eg. meclizine - 12.5-25 mg po tid)
-phenothiazine (eg. promethazine)
-anticholinergics (eg. scopolamine)
-5HT3 antagonists (eg. ondansetron)
-benzodiazepines (eg. diazepam - 2.5-7.5 mg po daily)
-should be used sparingly and for short durations because they can cause reduction in CNS compensation
-vestibular rehabilitation
-involves specific habituation exercises designed to enhance normal adaptive mechanisms in CNS
-components: gaze stabilization, balance retraining, desensitization
ABLATIVE THERAPY
-for pts who continue to suffer from incapacitating, lifestyle limiting vertigo despite maximum medical
therapy
1131
COCHLEAR IMPLANTS AND OTHER
IMPLANTABLE AUDITORY PROSTHESES
-essential components of cochlear implants:

1. Microphone: picks up acoustic information and converts it to electrical signals
2. Externally worn speech processor that processes the signal according to a predefined strategy
3. Receiver stimulator
4. Surgically implanted electrode array that is in the cochlea near the auditory nerve
-typical response range of a deaf ear to electrical stimulation is on the order of only 10-20 dB
-cochlear implants convert sound into an electric signal and stimulate the cochlear nerve directly
-strategies of encoding sounds:
-tonotopic organization:
-providing improved sense of pitch by delivering signals to different locations in the
cochlea
-temporal/rate coding:
-recognition from rate of presenting stimulus
-slow rate low pitch sound perceived
-fast rate high pitched sound perceived
-intensity coding:
-varying the intensity of the stimulus
COCHLEAR IMPLANT SYSTEMS
-takes advantage of tonotopic arrangement: incoming speech signal is filtered into a number of frequency
band, each corresponding to a given electrode in the array
Nucleus Cochlear Implant Systems

-Nucleus 22-channel
-Nucleus CI24M
Clarion Cochlear Implant Systems
Medical Electronic (Med-El) Cochlear Implant Systems

-Combi 40+
PATIENT SELECTION
Considerations
-age
-duration of deafness
-language
-mode of communication (auditory, speech cues, sign language etc..)
-other handicaps
-motivation
F.Ling - Cochlear Implants (1)
1132
Adults
-implantation of ear with any residual, Adult criteria:
aidable hearing carries risk that the implanted -> 18 years of age
ear could be made worse than the ear with a -bilateral severe-to-profound hearing loss (> 70 dB)
hearing aid -minimal benefit from conventional hearing aids (SRS
-adults with prelingual hearing loss generally < 30-50% in best aided condition)
are not considered good candidates for -HINT < 50% in best aided condition
cochlear implantation -no medical contraindications
Children
Pediatric Candidacy Criteria for Cochlear Implantation
Children 12-24 months of age Children 25 months to 17 years

-bilateral profound hearing loss (> 90 dB) -bilateral severe-to-profound hearing loss (> 70
-lack of auditory skills development and minimal dB)
hearing aid benefit -lack of auditory skills development and minimal
-no medical contraindications hearing aid benefit (word recognition < 30%)
-enrollment in a therapy of education program -no medical contraindications
emphasizing auditory development -enrollment in a therapy of education program
-HINT (equivalent) < 20% emphasizing auditory development
-both pre- and postlingually deafened children are candidates for cochlear implantation
-trend towards earlier implantation; electrical stimulation appears to be capable of preventing some of the
degenerative changes in the central auditory pathways
-age limit currently 12 months
-early implantation important in meningitis because progressive intracochlear ossification can occur and
precludes standard electrode insertion
-high incidence of OM in children < 2 y might compromise biosafety of cochlear implants
-cochlea is adult size at birth
-by 1 year, facial recess and mastoid antrum are adequately developed
Classification of Cochlear Implant Recipients
1. Postlingually deafened adults and children

-those deaf after 5ya
-rapid deterioration of intelligibility of speech once auditory input and feedback is lost
-implantation soon after loss can ameliorate this rapid deterioration
-this category tends to be the best candidates for implantation
-adults: best if shorter duration of deafness
-children: best if younger age of implantation
2. Congenitally or early (prelingually) deafened children

-most frequently encountered type in children
-acquisition of oral communication skills difficult
3. Congenitally or early (prelingually) deafened adolescents and adults

-this group has not demonstrated high levels of success with electrical stimulation of the auditory system
-generally worse candidates for implantation
1133
AUDIOLOGIC ASSESSMENT
-all potential candidates must have completed a period of experience with a properly fitted hearing aid
-parent questionnaires are used to determine hearing aid benefit
-various tests:
-HINT: hearing in noise test
-ESP: early speech perception test
-MAIS: meaningful auditory integration scale
-LNT: lexical neighbourhood test
-MLNT: multisyllabic lexical neighbourhood test
-PBK: phonetically balanced kindergarten
MEDICAL ASSESSMENT
-high-resolution, thin-section CT: determine presence and patency of cochlea

-T2-weighted MRI: to evaluate soft-tissue obliteration following sclerosing labyrinthitis
-cochlear malformations not a contraindication:
-cochlear dysplasia: 20% children with congenital SNHL
-absolute contraindications to cochlear implants:
-stimulable auditory neural elements NOT present in:
-Michel deformity: congenital agenesis of cochlea
-Small Internal Auditory Canal syndrome: cochlear nerve may be congenitally absent
-stable, infection-free ear required
-chronic OM must be resolved before implantation
-vaccinations:
-pneumococcal vaccine
-HiB vaccine
-note:
-for SNHL secondary to far-advanced cochlear otosclerosis, attempt stapedectomy first to see if
any improvement in hearing results may be able to use hearing aids instead of cochlear implant
PSYCHOLOGICAL ASSESSMENT
-exclusion: organic brain dysfunction, mental retardation, undetected psychosis, or unrealistic expectations
SURGICAL IMPLANTATION
-facial recess bounded by:

-fossa incudis superiorly
-chorda tympani laterally and anteriorly
-facial nerve medially and posteriorly
Special Surgical Considerations

-CSF gusher may be encountered in cases of cochlear dysplasia and Mondini deformity
-pts with severe malformations of the labyrinth, the facial nerve may follow an aberrant course
-ossified cochlea:
-may use double electrode array
1134
Complications
-most commonly encountered:
-postauricular flap problems
-facial nerve injury
-others:
-CSF gushers
-infected implant
-meningitis
-device failure
-device migration or extrusion
-residual hearing will be lost
-temporary dizziness, tinnitus or taste disturbance
CLINICAL RESULTS
-initial stimulation at 4-6 weeks post-op
Adult Outcomes
-many adults now demonstrate substantial speech understanding as early as 3 months following cochlear
implantation
-great deal of variability in performance
-factors affecting success:
-age at implantation and duration of deafness:
-younger age - shorter period of auditory deprivation more likely to achieve good
outcomes
-others:
-IQ associated with good speech perception skills
-lip-reading ability
-degree of residual hearing
Pediatric Outcomes
-assessment of performance in prelingually acquired hearing loss can be challenging
-battery of tests are required for assessment:
Speech Perception Outcomes

-many children with current cochlear implant devices achieve at least moderate levels of open-set
word recognition
-better speech perception performance in children deafened at an older age with corresponding
shorter period of deafness
-however in prelingual deafness, earlier implantation yield superior cochlear implant performance
in children
-implantation prior to 3 ya may yield improved results
-oral children, and those who have more residual hearing prior to implantation, typically
demonstrate superior speech understanding
Speech Intelligibility and Language

-improve significantly over time and on average exceed those of their age- and hearing-matched
peers with hearing aids
1135
MIDDLE EAR IMPLANTS
Principles
-vibrate ossicular chain by electromagnetic or piezoelectric means
-direct transmission of mechanical energy of amplified sound vibrations to ossicular chain
-MEI is coupled to ossicular chain or OW, eliminating acoustic coupling via EAC
-conversion of electric mechanical energy by 2 mechanisms
-electromagnetic (em): max output 140 dBSPL
-piezoelectric (PZ): max output 110 dBSPL
-impedance of electromagnetic implant is 1/5 that of piezoelectric crystal
Mei Products Available

-EM implants: semi-implantable
-VSB (Vibrant Soundbridge, Symphonix) sold by Siemens
-MET (Middle Ear Transducer) sold by Otologics
-DDHS (Direct Drive Hearing System) sold by Soundtec
-PZ implants: fully implantable
-TICA (Totally Implantable Communication Assistance)
-ENVOY, made by St. Croix Medical
-Symphonix Vibrant Soundbridge: the only FDA-approved MEI in US
Components
-external audio processor (battery, digital signal processor, microphone):
-mic picks up acoustic input & transmits electromagnetic signal to implanted receiver
-surgically implanted internal receiver (magnet):
-also incl a floating mass transducer crimped onto long process of incus
-coupling to ossicular chain driven by conductor link / induction coil
-placed via mastoid-facial recess approach
Advantages
-eliminate acoustic feedback
-wider frequency response
-eliminate tight-fitting EAC mold
-improve perception of auditory signal
-usable in professions eg musicians, athletes, headsets
-usable in enviro of heat, moisture, dust
Disadvantages
-for limited range of mod SNHL only
-SD must be > 50%
-not for CHL or retrocochlear HL
-need stable middle ear system
-need intact TM
-need good earmold fit
-very costly!
-risks of surgery: facial nerve injury, dysgeusia, bleed / infection / anesthesia
Indications for MEIs

-stable SNHL
-bilateral & symmetrical
-w/o fluctuation in HL
-mild (41 to 70 dB) to severe range (71 to 90 dB)
1136
-normal tympanometry
-normal middle ear anatomy
-no previous history of chronic middle ear disease or middle ear surgery
-no inner ear disorder
-dissatisfied with or unable to wear HA
1137
HEARING AIDS AND ASSISTIVE LISTENING DEVICES
HEARING AID FUNCTION
-increases output magnitude of acoustic signals presented at instruments’s input

-hearing aid composed of microphone, amplifier, receiver, battery and volume control
-input signal
-microphone stage: acoustic to mechanical mechanical to electrical
-amplifier stage: boosts electrical signal
-receiver stage: electrical to acoustic
- output to EAC
-amplification (gain):
-linear:
-direct relationship maintained b/n signal input and output
-input/output slope = 1.0
-nonlinear:
-vary gain via amplitude compression or expansion
-input/output slope < 1.0; slope reduced by a constant
-sound level at output remains audible and comfortable over broad range of input
intensity
-compression most useful for those with reduced dynamic range (threshold of hearing
and discomfort)
-as hearing input increases, the amount of gain is automatically reduced to avoid
reaching an uncomfortable level
-saturation sound pressure level:
-maximum amount of sound pressure output that a hearing aid can produce
-venting:
-reduced the “occlusion effect” (relative increase in low-frequency sounds muffled sounds)
-categories of hearing aids:

-analogue:
-constantly modifies input stimulus
-digitally programmable:
-analogue/digital hybrid
-program hearing aid response characteristics into digital memory and control the
analogue circuit digitally
-offers variety of memories and different channels of signal processing
-more precision in electro acoustic adjustments, and flexibility in adjusting gain and
output as changes in hearing sensitivity occurs
-true digital devices:
-digital signal processing
-increased programming flexibility
-acoustic signal first converted to string of digits after which a DSP scheme is applied
-improved speech recognition, sound quality and comfort
-eg. complex, frequency-specific amplitude compression amplification schemes
-digital noise reduction
-digital feedback control
-spectral enhancement
F.Ling - Hearing Aids (1)
1138
-Signal to Noise Ratio (SNR)
-quantifies degree to which signal of interest is audible above the interfering noise at any given
moment in time
-directional microphone HA allow for improved SNR based on spatial location of signal of
interest
-offers improved speech intelligibility in noisy environments
-effectiveness is reduced when:
-signal of interest is located at great distance
-increased level of reflected (as opposed to direct) sound energy
TYPES OF HEARING AIDS
ADVANTAGES AND DISADVANTAGES OF HEARING AIDS BY TYPE

Type of Advantages Disadvantages
Hearing Aid
BTE -range of power sufficient to reach severe and profound -earmold must fit snugly in EAC to eliminate feedback
hearing loss -may be difficult to hold in place for those with small
-allows adequate space to accommodate gain, output, and pinna or children
frequency response controls on analogue instruments for -cosmesis
adjustment by dispenser
-allow for placement of directional microphone
ITE -cosmetically appealing -amount of real ear gain may be limited because of
-placement of microphone takes advantage of pinna and feedback problems secondary to close proximity of
concha effects enhancing amplification in high frequencies microphone and receiver especially in cases of severe-
-microphone placement improves sound source profound high-frequency hearing loss
localization as head is moved
-may be easier to insert because only one component is
involved
-allows for placement of directional microphone
ITC -more cosmetically appealing -amount of gain sufficient for no more than moderate
-microphone placement takes advantage of pinna and hearing loss
concha effects boosting gain in high frequencies -requires good dexterity to insert
-microphone placement improves localization to sound -small size limits number of output/response controls in
source as head is moved analogue instruments
-venting options limited
-deep placement precludes use of directional microphone
CIC -most cosmetically appealing -amount of gain is sufficient for no more than moderate
-not visible in ear hearing loss
-takes full advantage of pinna and concha effects and -requires good dexterity to insert/change batteries
reduces occlusion effect -limits number of output/response controls in analogue
instruments
-deep placement precludes use of directional microphone
-venting options very limited
-deep tight fit requires precision and not possible on all pts
d/t ear geometry
1. Body hearing Aids:

-advantage: allows high level output with low feedback, easy to manage
-disadvantage: conspicuous, clothes and body may rub against microphone, poor localization of sound
2. Behind the Ear (BTE)
3. In the Ear (ITE)

-allows gain for moderate to severe hearing loss
1139
4. In the Canal (ITC)
-allows for normal acoustics provided by pinna
-increases gain in high frequencies
-helps with localization of sound
5. Completely in the Canal (CIC)

-maximizes pinna and concha effects greater high-frequency gain
-requires certain fitting criteria
6. Contralateral routing of signal (CROS)

-for no useable hearing in one ear and normal hearing in the other
-microphone on impaired side and transmitted to good ear
-wearer can use good ear to hear signals from impaired side
-BiCROS hearing aids also amplify sound to the better hearing ear
7. Bone conduction aid

-for pts in which a hearing aid or earmold may exacerbate an existing ear problem or result in the
recurrence of a pathologic condition
-bone oscillator placed on mastoid
-can be used only with milder hearing losses
-frequency response not as good as more traditional systems
8. Bone-anchored hearing aids (BAHA)

-for those who cannot use air conduction devices
-eg. congenital atresia and chronic middle-ear disorders
-effective in treating patients with bone conduction puretone averages (500, 1000, and 3000 Hz) up to 45
dB HL
9. Middle-ear Implants (MEIs)

-use piezoelectric or electromagnetic principles to drive an output transducer mounted on the ossicular
chain
-fitted for those with pure SNHL
-claims of improved fidelity as well as elimination of feedback and occlusion effects
-maximum output limits ~ 110 to 140 dB SPL
-claims to provide greater gain for high frequencies and less distortion for mild and moderate SNHL
HEARING AID CANDIDACY
-patients who demonstrate the greatest improvements in speech intelligibility from amplification are those
who demonstrate a moderate to moderately severe hearing loss
-because they use hearing aids all the time
-hearing aid satisfaction, perceived hearing aid benefit and performance are not significantly correlated
with hearing loss
-important factors are motivation and acceptance of hearing loss
MONAURAL OR BINAURAL AMPLIFICATION
-subjectively, individuals who wear two hearing aids often indicate that they find speech easier to
understand even in noisier listening conditions
1140
-advantages of binaural amplification:
-better speech discrimination
-binaural squelch:
-release from masking
-improved speech intelligibility in noise when listening binaurally d/t phase
differences of the signal and noise
-improved sound localization with binaural hearing
-eliminates head shadow effects which reduce high-frequency cues necessary for hearing many
consonants
-binaural summation
-minimizes “auditory deprivation effect” of the unaided ear.
-failure to fit hearing aids on both ears of patients with binaural hearing loss can result in
temporary and perhaps permanent decrease in the auditory function in the unaided ear
-more natural and less stressful listening
-improved speech clarity
SELECTING AND EVALUATING HEARING AIDS
-traditional fitting procedures:

-use “half-gain” rule:
-patient’s hearing threshold at each frequency should be multiplied by a factor of 0.5
-the resultant value represents the recommended gain of the hearing aid at that specific
frequency
-nonlinear fitting procedures:
-provide multiple frequency- and intensity-specific gain targets for different input levels of speech
-“restoration of normal loudness impression”
-“making speech equally loud and comfortable across frequency bands, while attempting to
maximize intelligibility”
ASSISTIVE LISTENING DEVICES
-three types of communication needs:

-interpersonal communication and enjoyment of media
-telecommunications
-signals (ie. wake-up alarms, fire alarms, telephones)
-developed to enhance listening developed for a specific listening situation
FM Wireless System
-affords acceptable SNR for speech understanding
-improves SNR in noisy environments
-improve speech perception in noise, reading/spelling ability, behaviour, psychosocial function, on-task
behaviours, and psychoeducational achievement in children
-talker has microphone FM broadcast to receiver unit worn by listener
Soundfield System
-deliver speech signal through a loudspeaker placed strategically in classroom environments
-proved improved SNR in classroom, which is beneficial for children with minimal hearing loss as well as
for those whose hearing loss has not been identified
1141
Infrared Systems
-signals transmitted via infrared light
-for public facilities
-speaker uses FM microphone/transmitter FM receiver/IR transmitter several light-emitting radiators
placed throughout room for uniform distribution
Other ALDS
-telephone, TV, radio and signalling devices
1142
PERIPHERAL VESTIBULAR DISORDERS
CAUSES OF PERIPHERAL VESTIBULAR DISORDERS
-sudden-onset unilateral vestibular dysfunction:

-labyrinthitis
-neuronitis
-labyrinthine or 8th nerve trauma
-iatrogenic injury (labyrinthectomy, vestibular nerve section)
-unilateral ototoxicity
-vascular labyrinthine lesion
-perilymph fistula
-cholesteatoma
-sudden-onset bilateral disorders:
-ototoxicity
-meningitic labyrinthitis
-bilateral trauma
-gradual-onset unilateral disorders:
-8th nerve neoplasia
-degenerative
-autoimmune disease
-gradual onset bilateral disorders:
-aging
-ototoxicity
-autoimmune disease
-syphilis
-degenerative disorders
-unilateral intermittent disorders:
-hydrops
-BPV
-dehiscence of superior semicircular canal
SIGNS AND SYMPTOMS
Unilateral Disorders of Sudden Onset

-reduced afferent activity from affected side to ipsilateral vestibular nucleus
-asymmetry from labyrinth is interpreted centrally as movement
-reduction in tonic activity to oculomotor nuclei causes nystagmus
-altered vestibulospinal and cerebellar activity causes sensation of falling
-right labyrinth affected slow eye movements to right fast-phase nystagmus to left sensation of
falling right
-altered vestibulospinal activity: past-pointing, Romberg sign
-changes in vestibular nucleus activity affect other brainstem nuclei n/v, sweating, bradycardia
-nystagmus:
-suppressed by visual fixation
-gaze away from lesion increases
-gaze towards lesion decreases
-rate of recovery directly related to activity level and is decreased with advanced age
F.Ling - Peripheral Vestibular Disorders (1)
1143
Bilateral Vestibular Lesions
-symptoms caused by reduction in vestibular sensitivity and inaccuracy of VOR
-rapid head movement requires intact VOR
-without an intact VOR, quick head movements cause a slip of the visual field on the retina, and visual
acuity degrades
-patients report visual disturbance and light-headedness
-cerebellar compensation occurs; but cannot accommodate total or near total loss of bilateral vestibular
function results in oscillopsia (severe visual disturbances with head movement)
Unilateral Lesions of Gradual Onset

-eg. acoustic neuroma
-may not produce severe symptoms because VOR has time to adjust
-gain of VOR adjusted by lateral cerebellum (nodulus and flocculus)
-may see decreased response on ENG if acoustic neuroma affects the superior vestibular nerve
Bilateral Lesions of Gradual Onset

-cause few symptoms because of cerebellar compensatory mechanisms within nodulus and flocculus
-oscilliopsia if total or near total bilateral loss
Fluctuating or Recurrent Symptoms

-eg. Ménières
-no time for CNS to compensate
-recurrent episodes eventually causes loss of vestibular sensitivity cessation of vestibular symptoms
DIAGNOSIS
-history:
-describe dizziness:
-vertigo: illusion of rotational, linear, or tilting movement
-disequilibrium: sensation of instability of body positions, walking, or standing
-oscillopsia: inability to focus on objects with motion
-lightheadedness: sense of impending faint, presyncope
-physiologic dizziness: motion sickness, height vertigo
-multisensory dizziness: diabetes, aging resulting in partial los of multisensory systems
-onset and duration
-seconds to minutes: BPPV, VBI, epilepsy, arrhythmia
-hours: Ménière’s migraine
-days: vestibular neuritis, labyrinthitis
-constant: central causes
-severity, frequency
-auditory (hearing loss, aural fullness, tinnitus, phonophobia)
-visual (blurred vision, diplopia, scotoma, photophobia)
-vegetative (nausea, vomiting)
-neurologic (dysphagia, dysarthria, hemipareisis, paraesthesia, etc..)
-precipitating factors (head movement or motion, stress, diet)
-medications
-PMHx:
-hypertension, cardiac arrhythmia, diabetes, thyroid disorders, vascular disease, otologic
problems, depression, neurologic disease, migraine, PMS
-recent head trauma, loud noise exposure, flying, diving, or heavy lifting
1144
-head and neck examination, cranial nerve examination, eye movement examination, gait and
posture
-otologic testing
-penumatoscopy (induce nystagmus or dizziness) - fistula test
-inspection of TM and middle ear
-tuning forks
-vestibular testing:
-eye motility (check pursuit with convergence and divergence) test using Frenzel lenses
-spontaneous and gaze-evoked nystagmus
-Dix-Hallpike manoeuver
-head-shake nystagmus
-head motion in horizontal plane for 20-30 seconds, then suddenly stop to
evaluate for nystagmus
-head thrust test:
-examiner briskly moves pt’s head to one side while pt is directed to maintain
visual fixation on examiner’s face
-if unilateral vestibular weakness and inadequate VOR in one direction, pt
performs a refixation saccade after the head thrust to maintain visual fixation on
the target
-dynamic visual acuity test:
-pt asked to read lowest line on Snellen chart with head stationary and then
again during 2-Hz head oscillation
-for bilateral vestibular loss visual blurring during head oscillation
-neurologic exam:
-cranial nerve testing, Romberg’s test, gait
-investigations:
-audiogram
-ENG
-CT scan or MRI
1145
TREATMENT
-relief of acute vestibular and autonomic symptoms

-diazepam 5-10 mg IV
-reduces vertigo, nausea/vomiting
-vestibular neuronitis, post-traumatic loss of vestibular function, labyrinthitis or severe
episodic vertigo
-meclizine 12 or 25 mg tid
-vestibular rehabilitation:
-promotes compensation for peripheral vestibular injury by altering the gain of VOR and
developing substitution strategies to maintain balance
-both visual and neck reflexes can be used to compensate for loss of vestibular function
-episodic vertigo (eg. Ménières)
-as soon as severe vertigo ends, vestibular suppressants are discontinued and rehabilitation
exercises are instituted
-decreased dietary salt intake and administration of diuretics: reduce endolymph pressure
-incapacitating vertigo surgical options:
-shunting operations:
-puncture of sacculus through oval window relieve endolymphatic pressure by producing
a decompressive leak between endolymph and perilymph
-cochleosacculotomy:
-disruption of bone b/n scala media and scala tympani of basal turn
-used to decompress endolymph to perilymph
-decompression of endolymphatic sac to mastoid or to CSF
-ablation of labyrinthine function
-drugs or surgery
-endanger auditory function of ear
-systemic streptomycin:
-bilateral Ménière’s disease, who have disease in an only hearing ear, or who
cannot undergo surgical treatment
-IM administration bid ENG tests done when caloric responses decrease,
treatment is stopped
-transtympanic administration of gentamicin for Ménière’s disease
-labyrinthectomy:
-causes loss of vestibular function and destroys remaining hearing
Vestibular Rehabilitation
-most effective for rehabilitation of pts with sudden loss of vestibular function or positional vertigo
-also used in the management of vertigo of unknown causation
-head movements that produce the greatest symptoms of disequilibrium often are most useful in
rehabilitation
Psychogenic Disorders
-pts with dizziness frequently have history of chronic pain syndromes or panic attacks
-difficulty coping with disagreeable life situations
-dizziness disproportionate to objective findings often is part of a mechanism to manipulate family
members or to seek compensation for injury
1146
CENTRAL VESTIBULOPATHY
-central vestibular disorder implies abnormal processing of normal peripheral vestibular sensory inputs by
the CNS
-estimates of incidence among dizzy pts: 10-20%
-central compensation:
-ability of vestibular system to recover much of its overall effectiveness despite permanent
damage to some parts of the central processor
-hastened by repeated stimulation
DIAGNOSIS
-most pts have disequilibrium not vertigo, longer duration of symptoms with gradual onset, minimal
vegetative symptoms
-characteristics of nystagmus usually associated with central causes:
-direction: vertical, horizontal or torsional
-direction changing
-minimal nausea and suppression with visual fixation
-no latency or fatigue
-ENG: -abnormal smooth pursuit, saccadic, optokinetic nystagmus
Summary of Central Disorders:
Degenerative:
-age-related degenerative disease
Infectious:
-otitis meningitis, encephalitis, epidural abscess
-epidemic vertigo (antecedent viral infection)
-congenital syphilis
Circulatory:
-vertebrobasilar insufficiency
-Wallenberg syndrome (lateral medullary infarction)
-cerebellar haemorrhage
Autoimmune:
-Cogan syndrome: interstitial keratitis, fluctuating unilateral or bilateral hearing loss, episodic
vertigo
-acute cerebellar syndrome
Structural:
-Arnold-Chiari malformation: oscillopsia, hydrocephalus or tonsillar herniation
-hydrocephalus
Systemic:
-multiple sclerosis
-Parkinson disease
Primary or secondary neoplasms
Inherited:
-Waardenburg syndrome
-Huntington disease
-Familial periodic vertigo
Other:
-toxin exposure
-motion sickness
-vestibular epilepsy
F.Ling - Central Vestibulopathy (1)
1147
Migraine
-vascular syndrome caused by serial constriction and dilatation of intracranial blood vessels
-vestibular symptoms:
-motion intolerance, episodic vertigo, disequilibrium
-usually precede headache, during aura phase
-migraine-related vestibulopathy suspected when pt has personal or family history of migraine headache,
even if pt does not currently have headaches
-migraine-related vestibulopathy not associated with specific findings at ENG:
-most have no ENG findings
-abnormal findings include: unilateral or bilateral caloric weakness, spontaneous nystagmus,
positional nystagmus
-most common auditory symptom is phonophobia
-variants:
-Basilar migraine:
-headache preceded by symptoms of scotoma, transient blindness, vertigo, paresthesia,
slurred speech, ataxia, tinnitus, diplopia, loss of consciousness, motor weakness, hearing
loss
-Benign Paroxysmal Vertigo of Childhood:
-may represent early manifestations of migraine
-an episodic disorder in children under the age of 4 years
-completely normal child suddenly becomes frightened, cries out, clings to the parent or
staggers as though drunk, and exhibits pallor, diaphoresis, and often vomiting
-symptoms are accentuated by head movements and sometimes nystagmus and torticollis
are observed
-spells typically last for several minutes
-afterward the child is immediately normal and can resume playing as though nothing had
happened
-spells typically begin before age of 4 and occur up to several times a month
-after a period of 2 to 3 years, they decrease in number and gradually disappear
-most have no further spells after age of 7 or 8
-cause might be due to a vascular disturbance affecting the posterior circulation
-most eventually develop migraine
-look for dietary triggers: tyramine, alcohol, caffeine
-treatment:
-symptomatic: promethazine, diazepam, meclizine
-prophylaxis: B-blockers, CCBs, antidepressants
-medications to control headaches are not useful in controlling vertigo (eg. sumatriptan, NSAIDs)
Vertebrobasilar Insufficiency
-compression of vertebral artery compromises flow to posterior and anterior inferior cerebellar arteries
-SSx:
-transient vertigo with neck hyperextension or excessive rotation
-“4 D’s”: dizziness, diplopia, dysphagia, drop attacks
-dysarthria, headaches, hallucinations, ataxia, hemiparesis
-Wallenberg Syndrome:
-aka: lateral medullary syndrome
-infarction of PICA results in infarction of lateral medullary region of brainstem, spares
cochlear nucleus
1148
-SSx:
-acute vertigo (spontaneous nystagmus, nausea and vomiting)
-ataxia from incoordination of the ipsilateral limbs
-ipsilateral Horner Syndrome (anhydrosis, ptosis, miosis) from damage to sympathetic
fibers
-ipsilateral palatal paresis (dysphagia) and vocal fold paralysis (dysphonia) from
destruction of nucleus ambiguus
-ipsilateral numbness of face from involvement of spinal tract of trigeminal nerve
-ipsilateral lateral pulsion, diplopia from damage to CN VI
-ipsilateral loss of P+T sensation on face, contralateral loss of P+T on body, ipsilateral
paralysis of palate, pharynx and larynx
-Infarction of AICA:
-similar findings as above without Horner syndrome and abducens palsy
-hearing loss and tinnitus present (involves cochlear nucleus)
Craniovertebral Junction Disorders
-Chiari Malformation:
-Classification:
-Type I: Protrusion of cerebellar tonsils
-Type II:Protrusion of cerebellar vermis, lower pons, and medulla (Arnold-Chiari
malformation) most common
-Type III: Herniation of cerebellum, forming a high cervical meningocele
-Type IV: Cerebellar hypoplasia, (variant of Dandy-Walker syndrome)
-symptoms:
-dissociated sensory loss:
-loss of P+T with relative sparing of vibratory sense and proprioception
-lower cranial nerve dysfunction:
-bilateral vocal cord paralysis, weakness, ataxia
-treatment:
-extensive surgical procedure consisting of surgical decompression of foramen magnum
with or without cervical laminectomy
-Other Anomalies:
-Basilar impression:
-occipital bone around foramen magnum deforms to cause posterior and superior
displacement of odontoid process
-Assimilation of the atlas
-bony union between atlas and skull base
-associated with posterior displacement of odontoid process
-Atlantoaxial dislocation:
-Down syndrome, Hurler syndrome, Morquio syndrome, achondroplastic dwarfism
Multiple Sclerosis
-multifocal demyelinating disease affecting the nervous system
-clinical course consists of multiple exacerbations followed by remissions
-although dizziness is not a common initial symptom of multiple sclerosis, as many as 50% of pts
eventually have some type of vestibular symptoms
-management of vestibular symptoms is supportive
1149
Miscellaneous Central Vestibular Disorders
-vestibular schwannoma:
-vestibulopathy present before surgical treatment may still be present after surgery
-vascular loop compression of eighth cranial nerve:
-controversial
-limited amount of histopathologic evidence suggests that this syndrome exists
-treatment would require intracranial procedure
1150
MEDICAL MANAGEMENT OF VESTIBULAR DISORDERS
AND VESTIBULAR REHABILITATION
MÉNIÈRE DISEASE
-low sodium diet

-1-1.5 g of sodium per day
-diuretic:
-thiazide diuretics:
-excretion of Na, Cl, H2O, K, Mg, PO4, Ca
-can cause metabolic alkalosis with hypokalemia and hypochloremia
-carbonic anhydrase inhibitors: acetazolamide
-vasodilators:
-hypothesis that pathogenesis of endolymphatic hydrops caused by ischemia of stria vascularis
-agents: isosorbide dinitrate, niacin, papaverine, nylidrin, histamine, betahistine
-betahistine exerts direct inhibitory effect on polysynaptic neurons within vestibular nuclei
-chemical labyrinthectomy:
-10% will have severe symptoms requiring labyrinthine ablation
-goals are to control episodic vertigo and to avoid or minimize treatment-associated disequilibrium
and hearing loss
-20% will have persistent disequilibrium after treatment
-symptoms of disequilibrium usually begin 4 days after beginning of treatment and improve
spontaneously by weeks 6-8
-vertigo can be relieved in 90% of cases
-preparation of gentamicin solution:
~2 mL of 30 mg/mL (pH 6.4) - diluted from 40 mg/mL
-administration protocols:
-Nedzelski: tid x 4 days
-Beck and Schmidt: daily until earliest sign of ototoxicity observed (mean of 4-6 doses)
-other: based on monitoring of patient’s symptoms
-intratympanic dexamethasone:
-conservative use appropriate - some patients benefit from this technique before a more aggressive
surgical option is undertaken
OTOSYPHILIS
-presumptive diagnosis of otosyphilis made when pt has unexplained cochleovestibular dysfunction and
positive results of FTAB absorption test
-penicillin and steroid therapy has been reported to improve vertigo among 58-86% of patients with
symptoms of otosyphilis
MIGRAINE
-migraine abortive therapy
-ergotamine tartrate
-sumatriptan
-migraine prophylaxis
-propranolol, flunarizine, nortriptyline, methysergide, verapamil
-TCA used for prophylaxis of vestibular migraine
-amitriptyline and imipramine have been used but have anti-cholinergic effects
-secondary amines (desipramine or nortiptyline) have fewer side effects and are the TCAs of
choice
F.Ling - Medical Treatment of Vertigo (1)
1151
FAMILIAL ATAXIA SYNDROME
-autosomal dominant inheritance
-recurrent episodes of vertigo and ataxia among several members of a family
-acetazolamide effectively prevents episodic vertigo and ataxia
SYMPTOMATIC PHARMACOTHERAPY
-four general classes of drugs:

-anticholinergic agents
-monoaminergic agents
-antihistaminic agents
-antidopaminergic agents
-theorized mechanism of action: depression of activity within vestibular nuclei
-combined sedative and antivertigo properties of medications for symptomatic relief require a therapeutic
trade-off of acute relief at the expense of attenuating compensation
Prevention of Motion Sickness

-transdermal scopolamine effective and has minimal side effects
-combination of drugs more effective than any single drug:
-eg. scopolamine + promethazine with dextroamphetamine
VESTIBULAR REHABILITATION
-BPPV: effectively managed with vestibular rehabilitation

-nystagmus:
-predominant vectors are torsional in lower ear (posterior SCC) and vertical in upper
(contralateral - anterior SCC) ear
-latency: 5-15 seconds
-duration: < 30 seconds
-fatiguable
-horizontal SCC BPV:
-provocation with patient supine with rotation to head lateral position
-nystagmus exclusively horizontal in orientation
-duration of vertigo 30 seconds to 1 minute
-latency: 3 seconds
-not fatiguable
-liberatory manoeuver:
-performed as single tx - not repeated later unless symptoms returned
-primary goal is repositioning of otoconial debris within posterior SCC into vestibule
-eg. Epley manoeuvres
F.Ling - Medical Treatment of Vertigo (2)
1152
SURGICAL MANAGEMENT OF VESTIBULAR DISORDERS
PREOPERATIVE ASSESSMENT
-Ménière’s is most common vestibular disorder necessitating surgery

-Definite Ménière disease:
-two or more episodes of spontaneous rotational vertigo that lasts 20 minutes or longer
-audiometrically documented hearing loss on at least one occasion
-tinnitus or aural fullness in affected ear
-other causes excluded
-Certain Ménière disease:
-histopathologic confirmation to definition criteria
-Probable Ménière disease:
-one definitive episode of vertigo despite fulfilment of all other criteria
-Possible Ménière disease:
-cochlear or vestibular variants of Ménière disease when other causes have been excluded
-when hearing is useful, labyrinth-destroying procedures are avoided

-1/3 of pts with Ménière dz eventually have involvement of contralateral ear
-thresholds > 70 dB and speech discrimination > 20% warrant consideration of hearing preservation
surgery
SURGERY FOR BENIGN PAROXYSMAL POSITIONAL VERTIGO
-non-surgical techniques:
-Epley: canalith repositioning procedure
-Semont: liberatory manoeuver
-improved symptoms in 90%
-failure of one or both maneuvers after multiple repeated trials with debilitating symptoms is a prerequisite
for surgery
-surgical techniques:
-singular neurectomy
-nerve exits lateral aspect of IAC in the singular canal and courses inferiorly and
posteriorly to ampulla of PSCC
-intermediate segment is inferior-posterior to round window niche (sever the nerve at this
location)
-most common location is lateral to round window membrane (50%); 14-27% medial to
membrane
-transcanal approach
-complications:
-vertigo
-SNHL (20%; severe in 5%)
-extraordinarily difficult procedure
-PSCC occlusion
-transmastoid approach
-PSCC identified and bluelined
-laser partitioning of membranous labyrinth or packing with fascia or bone pate or bone
wax
-postoperative: dysequilibrium, transient sensorineural hearing loss
F.Ling - Surgery and Vestibular Disorders (1)
1153
OPERATIONS ON THE ENDOLYMPHATIC SAC (EXTERNAL SHUNTING)
-unknown therapeutic mechanism of sac surgery fuels controversy about its role in the management of
vertigo
-no controlled studies have documented the efficacy of sac surgery
-it appears that the benefit of sac surgery is limited in duration and that less invasive procedures can
provide similar benefit, although studies are not conclusive
-complete elimination of vertigo can be achieved by as many as 50% of patients, improvement occurs
among an additional 25%
-complications:
-SNHL (total 1%; mild-moderate 20%)
-CSF leak
-bleeding from injury to sigmoid sinus or jugular bulb
VESTIBULAR NERVE SECTION
-risk of facial paralysis

-various approaches:
-posteriorly through retrolabyrinthine or retrosigmoid craniotomy
-vestibular portion of eighth cranial nerve is superior to cochlear portion
-80% successful
-greater likelihood of incomplete neurectomy
-middle fossa approach
-superior and inferior vestibular nerves are sectioned laterally in internal auditory canal
-90% successful
-complications:
-disequilibrium, headache, hearing loss, CSF leak
-wound infection, facial paralysis, tinnitus
-middle fossa approach:
-labyrinthine artery injury total hearing loss
-greater risk of facial nerve injury
-memory disturbance from temporal lobe retraction
-retrolabyrinthine approach:
-greater incidence of CSF leak
-retrosigmoid approach:
-headache more common
LABYRINTHECTOMY
-final surgical option for management of vertigo

-various approaches:
-transcanal: -stapes removed vestibule drained of perilymph
-saccule removed under direct vision
-hook used to probe ampullar ends of SCCs
-transmastoid: -complete excision of all five end organs
-postop: vigorous horizontal nystagmus present; accompanied by vertigo
-elimination of vertigo > 85%
-wound infection, haemorrhage and facial nerve injury rare
1154
SUPERIOR CANAL DEHISCENCE SYNDROME
-defect in bony labyrinth, caused by altered postnatal bone development

-most common symptom: Tullio Phenomenon vertigo in response to loud sound
-symptoms also induced by changes in middle ear or intracranial pressure
-fast phase of nystagmus directed at affected ear in response to sound or positive pressure
-tx: avoid offending stimuli
-if debilitating symptoms canal resurfacing or occlusion via middle cranial fossa craniotomy
PERILYMPH FISTULA
-definition: abnormal patency between inner and middle ear that allows flow of perilymph
-causes:
-temporal bone trauma:
-subluxations or fracture of stapes footplate and rupture of round window membrane
-minor changes in middle ear or intracranial pressure (less accepted theory)
-diagnosis by surgical exploration of middle ear with visualization of fluid leak in oval or round window
but it is still very subjective
-no good objective tests
-commonly reported symptoms:
-aural pressure
-disequilibrium exacerbated by exertion
-conductive or sensorineural hearing loss
-tx:
-initial bed rest - some defects seal spontaneously
-surgery only if symptoms are progressive and dizziness is debilitating
-transtympanic endoscopic approach used
-oval and round windows scrutinized for presence of fluid
-if fluid identified blood patch is placed
1155
TEMPORAL BONE NEOPLASMS AND LATERAL CRANIAL BASE SURGERY
(From Cummings - Ch 167)
SUBTOTAL TEMPORAL BONE AND TOTAL TEMPORAL BONE RESECTIONS
-subtotal temporal bone resection allows en bloc resection of

medial surfaces of mesotympanum, leaving air cells of
petrous apex and portions of bony labyrinth
-indicated for middle ear malignancies
-total temporal bone resection involves an en bloc resection
of temporal bone, including petrous apex and sigmoid sinus
General surgical approach
Incision
-large C-shaped postauricular incision or Y-shaped incision
can be designed with a central island removed
-preauricular incision may be used for EAC involvement
Proximal vascular control, neck dissection

-should preoperative imaging indicate lymphadenopathy, a
supraomohyoid modified neck dissection can be performed
-proximal vascular control of carotid artery and internal
jugular vein attained
Infratemporal fossa dissection

-masseter attachment to zygoma is disattached
-mandibular osteotomy is performed from mandibular notch to angle of mandible
-mandibular condyle is separated from glenoid fossa
-temporalis muscle elevated off skull in a subperiosteal
fashion and reflected inferiorly, still attached to coronoid
process
-superior infratemporal fossa dissection should allow
identification of foramen spinosum and foramen ovale.
Temporal craniotomy
-temporal craniotomy expose superior surface of petrous
bone
Subtotal temporal bone resection

-vertical petrous portion of ICA is identified
-resection is performed by drilling with diamond burs
through glenoid fossa and across eustachian tube orifice
-mobilization of ICA is just distal to first genu
Osteotomy
-a groove may be drilled along floor of middle fossa
connecting glenoid fossa area, lateral IAC, and
posterosuperior mastoid
-osteotome is inserted into carotid canal just distal to first
genu and pointed toward internal auditory canal
-temporal bone specimen is brought out Subtotal temporal bone resection
F.Ling - Infratemporal Fossa (1)
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Total temporal bone resection
(A) frontotemporal-
retroauricular-cervical skin flap is
rotated forward
-external ear canal has been
transected
-facial nerve has been transected
just beyond stylomastoid foramen
-TMJ opened, and
mandibular ramus resected
-cranial nerves IX through XII and
jugular and carotid vessels are
exposed to neck
(B) temporal and suboccipital

craniotomy has been extended over
transverse sinus and lateral
posterior fossa
-zygomatic osteotomy and partial
mastoidectomy have been
performed
-osseous middle fossa floor has
been partially resected to expose
second (V2) and third (V3)
divisions of cranial nerve Vand
greater superficial petrosal nerve
-middle meningeal artery has been
transected
(C) eustachian tube, and tensor

tympani muscle have been
transected
-ascending and transverse
segments of petrous internal
carotid artery (ICA) have been
unroofed, and ICA has become
mobilized anteriorly
(D) temporal and retrosigmoid

dura have been opened
-lateral sinus had been ligated at its junction with sigmoid
-tentorium has been opened along inferior edge of mandibular nerve, trigeminal ganglion, and roof, with
interruption of superior petrosal sinus
(E) with cerebellum retracted medially, cranial nerves V and VII through XI can be seen. labyrinthine (internal
auditory) artery has been transected at its origin from anterior inferior cerebellar artery
(F) cranial nerves VII through XI have been transected, and underlying dura has been incised as posterior border of
en bloc resection of petrous bone. petrous bone specimen then is disconnected from any remaining attachments and
removed. PICA—Posterior inferior cerebellar artery
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Reconstruction
-facial nerve and other appropriate CN can be cable grafted
-dural defects are closed as needed with fascia or pericranium
-temporalis muscle can be rotated and sutured to surrounding soft tissue
Infratemporal fossa approaches
Postauricular approaches to infratemporal fossa

-Fisch divided these techniques into three basic approaches:
-Type A: -dissection entails radical mastoidectomy, anterior transposition of facial nerve,
exploration of posterior infratemporal fossa, and cervical dissection permitting
access to jugular bulb, vertical petrous carotid, and posterior infratemporal fossa
-Type B: -dissection explores petrous apex, clivus, and superior infratemporal fossa
-Type C: -allows exposure of nasopharynx, peritubal space, rostral clivus, parasellar area,
pterygopalatine fossa, and anterosuperior infratemporal fossa.
Closure of external auditory canal

-EAC is closed in a watertight blind sac
Removal of external auditory canal wall skin and tympanic membrane

-skin of osseous EAC wall is elevated circumferentially down to annulus
-incudostapedial joint is separated, tensor tympani tendon is cut, and neck of malleus is nipped, allowing
total removal of canal wall skin, tympanic membrane, and attached manubrium
Cervical dissection
-done as needed to expose inferior margins of tumor
-to gain cervical control of vascular structures if needed
Extratemporal facial nerve dissection

-facial nerve is dissected out to tertiary branches by cutting overlying parotid gland and freeing it from
underlying tissues
-this exposure is required for anterior transposition in type
A approach
-in type B and C approaches, facial nerve transposition is
not required; only frontal branch is followed distally to
allow its preservation when zygoma is transected
Radical mastoidectomy
-radical mastoidectomy removes air cell tracts lateral and
adjacent to otic capsule
-stapes suprastructure is removed to prevent inner ear
trauma
-facial nerve is skeletonized in preparation for transposition
-eustachian tube is obliterated with bone wax impregnated
with bone dust and a muscle plug
-removal of EAC, tympanic membrane, ossicles, and air
cells of temporal bone lateral to otic capsule constitute
radical mastoidectomy.
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Type A approach
-facial nerve transposition
-facial nerve skeletonized and freed of its bony
canal 180° circumferentially from geniculate
ganglion distally to stylomastoid foramen
-air cells of mastoid tip are exenterated lateral to
digastric ridge
-occlusion of sigmoid sinus
-bone is removed over posterior fossa dura anterior
and posterior to sigmoid sinus to allow ligation
-exposure of jugular bulb and internal carotid artery
-exposure of posterior infratemporal fossa now
permits isolation of vertical intrapetrous ICA
-with removal of bone over carotid artery and
beneath otic capsule, jugular fossa is exposed for
tumor removal
-tumor removal
-after exposure and distal control of ICA is
accomplished, tumor may be carefully removed
-jugular vein is ligated to prevent tumor and air
embolism
-closure of wound
-fascia lata provides best material for reconstruction, although lyophilized dura can be used to seal
defect
Type B approach
-differs from type A approach as facial nerve transposition usually is not required
-reflection of temporalis muscle still attached to coronoid process and zygoma allows retractor to expose
superior infratemporal fossa
-limits of operative exposure in type B approach are defined by middle cranial fossa (MCF) floor,
mandibular condyle, and reflected temporalis muscle
-thinning bone under MCF dura improves exposure
-petrous apex lesions, such as cholesteatoma or low-grade chondrosarcomas, may be removed at this point
with careful anterolateral retraction of ICA
Type C approach
-type C approach is an anterior extension of type B
approach
-permits posterolateral access to rostral clivus,
cavernous sinus, sphenoid sinus, peritubal space,
pterygopalatine fossa, and nasopharynx and to areas
exposed by type B approach
-in essence, permits access anterior to foramen
lacerum up to posterior aspect of maxillary sinus and
nasopharynx
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AGING AND AUDITORY SYSTEMS - PRESBYCUSIS
(From Cummings)
AGING OF AUDITORY SYSTEM
-characteristically results in bilateral symmetric neurosensory hearing loss in the frequencies above 2000
Hz
-increasing difficulty discriminating consonants in words
-ability to ignore competing speech also becomes impaired
-maintaining communication requires increasingly greater effort and energy
-30% of population over age 65 have significant hearing impairment
TYPES OF PRESBYCUSIS
Sensory presbycusis
-characterized by hair cell loss
-high-frequency, bilaterally symmetric sensorineural loss most frequently diagnosed in the elderly in the
clinical setting
-eventually, speech frequencies are lost
-degeneration of the organ of Corti - initially in the most basilar region and progressing apically about 15
mm along cochlear duct
-flattening and distortion with eventual loss of hair cells
-accumulation of lipofuscin, the aging pigment
Neural presbycusis
-associated with loss of spiral ganglion cells and axons; relative sparing of the organ of Corti
-gradual hearing loss with moderate slope towards high frequencies
-disproportionately severe decrease in speech discrimination
-basilar turn hearing usually normal
-apical innervation affected encoding of speech frequency and auditory information severely hampered
-associated with other neural deficits
Strial (metabolic) presbycusis

-slowly progressive familial neurosensory loss
-beginning in 3rd-6th decades and progresses slowly
-flat across all tested frequencies - excellent ability to discriminate speech
-excellent results with amplification
-some degree of atrophy of the stria vascularis
-organ of Corti and spiral ganglion cells usually unaffected
Inner ear conductive presbycusis (Cochlear presbycusis)

-bilateral symmetrical SNHL with upward slope towards high frequency
-preserved speech discrimination
-no anatomical correlates known
-hypothesis that stiffening of the basilar membrane causes hearing loss
-evidenced by hyalinization and calcification of membrane
-other associated changes include cystic degeneration of strial elements and atrophy of the spiral
ligament
F.Ling - Presbycusis (1)
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PROPOSED ETIOLOGIES
Vascular
-proposed as the cause of hearing loss in aging persons but insufficient histopathologic evidence
-progressive involution of human cochlear vasculature from fetus through the aged
-devascularization of capillaries and arterioles found in spiral ligament associated with aging
Diabetic presbycusis
-diabetic angiopathy narrowing of vessel lumens
-clinical audiologic and pathologic studies of the correlation between diabetes and presbycusis are
conflicting and contradictory
-in well-controlled studies, no correlation between sensorineural hearing loss and diabetes was found
Noise
-noise-induced HL may arise from mechanical damage, metabolic exhaustion or vascular changes
GENETIC CONSIDERATIONS
-typical hearing loss is basin-shaped curve with good discrimination and no recruitment
-pathologically, the most prominent feature in this disorder is atrophy of the stria vascularis, which is
parallel to Schuknecht’s strial atrophy category
HEARING AND DEMENTIAS
-studies of the cochlea in temporal bones from patients with confirmed Alzheimer’s disease showed lack of
degeneration in the cochlea, which is typical of Alzheimer’s patients
TREATMENT
-amplification remains the mainstay of treatment for presbycusis
F.Ling - Presbycusis (2)
1161
CONGENITAL AURAL ATRESIA
(From Schuknecht - Laryngoscope 99; Sept 1989)
INTRODUCTION
-hypoplasia of EAC
-bilateral in ~30% of cases
-associated ipsicranial cephalic anomalies when they occur in syndrome are generally negative
prognosticators for successful corrective surgery for conductive hearing loss
-surgery delayed until the process of pneumatization of temporal bone is advanced: about 5 yoa
-aids:
-amplification and assistive auditory devices
-lip-reading instruction
-special education
-parental guidance
-immediate surgery for:
-partial meatal atresia that is developing obvious canal cholesteatoma
-total atresia with otologic or radiologic evidence of cholesteatoma, otitis media, or mastoiditis
-pre-surgical work-up:
-audiometry to determine status of better hearing ear
-ECoG to determine bilaterality of hearing
-CT scan to assess:
-extent of pneumatization
-appearance of ossicles
-location of facial canal
-configuration of bony labyrinth
-presence of possible cholesteatoma formation
CLASSIFICATION
-Type A: meatal atresia

-limited to fibrocartilaginous part of EAC
-meatoplasty required
-Type B: partial atresia

-narrowing and tortuosity of fibrocartilaginous and bony parts of EAC
-partial visualization of TM
-short or curved manubrium
-may have deformed malleus and incus
-Type C: total atresia

-totally atretic canal but well developed pneumatization of tympanic cavity
-partial or complete bony atresia plate
-tympanic membrane usually missing
-head of malleus and body of incus usually fused
-facial nerve occasionally takes more anterior course: may partially overlap oval window
-Type D hypopneumatic total atresia

-all the features of type C as well as reduced pneumatization of temporal bone
-commonly seen in Treacher Collins syndrome
-abnormal course of the facial nerve and bony labyrinth; precludes successful surgery for
improvement of hearing
F.Ling - Congential Aural Atresia (1)
1162
TECHNIQUE OF ATRESIAPLASTY
-Type I Atresiaplasty (Meatoplasty)

-for type A atresia
-endaural incisions made
-conchal cartilage and soft tissue removed to create adequate canal
-unepithelialized surfaces covered with STSG
-Type II Atresiaplasty (Canaloplasty)

-constructing EAC in association with a mechanism for sound transmission through middle ear
without entering mastoid
-drilling occurs until head of malleus and body of incus are exposed
-temporalis fascia graft positioned to bridge tympanic space
-Type III Atresiaplasty (Canaloplasty with Strut)

-includes removal of malleus and incus and introduction of a strut to bridge gap from head of
stapes to fascial graft
-Type IV Atresiaplasty (Mastoidectomy with Stapediopexy)

-tympanic graft is placed on head of stapes
-wide-field tympanomastoidectomy is performed using post-auricular approach
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COMPLICATIONS OF SURGERY

-meatal stenosis
-graft failure
-acoustic trauma
-high-tone hearing loss form manipulation of ossicles
DISCUSSION
-criterion for successful operation

-obviates need for a hearing aid in bilateral atresia
-eliminate handicap of unilateral hearing loss in unilateral atresia
-threshold of hearing (average pure-tone threshold for 0.5, 1, 2, and 4 kHz) can be brought to 20
dB or better
-canaloplasty is superior to mastoidectomy with stapediopexy in improving the hearing
-many surgeons recommend delaying surgery in unilateral cases until adulthood, when patients can make
their own decision based on the risks and benefits
-the risk of surgical complications will be minimized and the chances for a successful hearing result are
increased if the middle ear and mastoid size are at least two thirds of the normal size and if all three
ossicles, although deformed, can be identified
-if average canal diameter < 4mm then risk of cholesteatoma formation is ~ 50%
-preponderance of cholesteatomas developed in canals < 2mm
Grading system for candidacy for surgery of congenital aural atresia

-stapes present 2
-oval window open 1
-middle ear space large and favourable 1
-facial nerve position favourable 1
-malleus-incus complex well formed 1
-mastoid well pneumatized 1
-incus and stapes connected 1
-round window visible and open 1
-appearance of external ear is normal 1
= 10 points
-total score < 6 points - not surgical candidate

-total score > 6 points - candidate for aural atresia repair
Hearing results
-standard to obtain minimal CHL with < 25 dB hearing threshold in at least 75% of pts
-Chandrasekhar: ABG of 30 dB in 60%
-Schuchtnecht: 50% of pts with 30 dB or better hearing
Alternatives
-bone anchored hearing aids
-bone conduction hearing aids
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Review of Anatomy: The Auricle and Temporal Bone Page 1 of 6
Ear and Temporal Bone
TEMPORAL BONE
 Five segments:
 squamous
 mastoid
 tympanic
 zygomatic
 petrous
 contains portions of carotid artery and jugular venous drainage system
 intimately related to dura of middle and posterior fossa
 articulates anteriorly with condyle of mandible
 mastoid air cell system communicates with middle ear
 facial nerve passes through en route to muscles of facial expression.
 Temporal Bone Dissection

 Middle Fossa Approach
 Lateral Transmastoid Approach
EAR
 divided into three parts
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file:///C:/Users/user/Desktop/Dr%20flings%20Notes/Contents/tbone.html 3/22/2013
 A. External Ear
 protects tympanic membrane
 collects and directs sound waves and plays a role in sound
localization
 skin of external ear normally migrates laterally from umbo of malleus
in tympanic membrane to external auditory meatus (at a rate of 2- 3
mm per day)
 Auricle - elastic cartilage covered with closely adherent skin configuration

is intricate, and extremely difficult to duplicate
 External Auditory Canal

 Lateral Portion
 cartilaginous with thick, loosely applied skin containing
ceruminous and sebaceous glands
 Medial Portion
 very thin skin directly over bone, no skin appendages
 comprises two- thirds of total canal in adults, less in infants and
children.
1166
 B. Middle Ear
 communicates with nasopharynx via eustachian tube
 transmits and amplifies sound waves from tympanic membrane to
stapes footplate converting energy from air medium to a fluid medium
of membranous labyrinth
 three ossicles
LEFT EAR VIEWED POSTERIORLY
 tympanic membrane
 ovoid, three- layered structure consisting of squamous epithelium
laterally, respiratory mucosa medially, and an intervening fibrous
layer
 apex maintained medially by support of malleus
 fibrous layer thickens laterally to form annulus, an incomplete ring
which is attached to surrounding bone
 superior to lateral process of malleus, ring is deficient, andÇarea is
known as pars flaccida
 majority of drum is composed of pars tensa.
1167
LEFT EAR VIEWED EXTERNALLY
 Ossicles
 from lateral to medial: malleus, incus, and stapes
 handle and lateral process of malleus attached to tympanic
membrane
 Spaces - middle ear cleft divided into spaces in reference to annulus.

 Epitympanum
 superior to tympanic membrane
 contains body of incus and head of malleus
 communicates with mastoid via aditus
 Mesotympanum
 on a level with ear drum
 oval and round windows, located posterosuperiorly on medial
wall, communicate with inner ear
 long process of incus projects into posterior quadrant to
articulate with stapes which sits in oval window
 facial nerve, usually covered by a bony canal, crosses
posterior superior quadrant superior to stapes, then courses
inferiorly between middle ear and mastoid air cells.
1168
 Protympanum
 in this anterior recess of middle ear, eustachian tube exits to
communicate with nasopharynx
 ETT runs in close proximity to carotid artery.
 Hypotympanum
 jugular bulb curves through hypotympanum
 usually covered by bone, but may be dehiscent and extend into
middle ear space.
 C. Inner Ear
 consists of a fluid- filled labyrinth which functions to convert
mechanical energy into neural impulses
 bony labyrinth is subdivided into smaller compartments by
membranous labyrinth
 fluid surrounding membranous labyrinth is called perilymph; fluid
within is called endolymph
 There are three main divisions of bony labyrinth.
 Vestibule
 just medial to oval window, and contains utricle and saccule
 vestibule is an antechamber, leading to both cochlear and
1169
semicircular canal.
 Cochlea
 anterior to vestibule
 bulges into middle ear and its bony covering is promontory
 communicates with middle ear via round window
 Semicircular Canals
 project posteriorly from vestibule
 detect angular acceleration
 superior, posterior and lateral, or horizontal canals.
1170
ELECTRONYSTAGMOGRAPHY
OVERVIEW
-calibration:
-upward swing of pen right
-downward swing of pen left
-limitations:
-deals primarily with only one major vestibular tracts (VOR)
-ignores vestibular-spinal tracts
-limited to horizontal SCC and superior branch of vestibular nerves
-anterior posterior, otolith organs and inferior branch of vestibular nerves not stimulated
-results can be affected by attention and medications
-therefore ENG provides limited information about total vestibular system function
-purpose of ENG:
-detect organic pathology within at least a portion of vestibular system
-monitor change in vestibular function
-identify central vs peripheral vestibular pathways
-vestibular lesions involving the vestibular end organs and vestibular nerve are classified as
peripheral
CENTRAL SUBTESTS
1. Gaze (fixation) test:

-to identify presence of spontaneous eye motion during visual fixation
-types of eye movement:
-nystagmus, ocular flutter, disconjugate eye position and drift, square waves
-normal gaze:
-able to maintain steady ocular fixation when looking at fixed targets in a visual field
-affected by acute, unilateral peripheral vestibular lesion or by a central lesion
-Alexander’s Law:
-nystagmus beats most intensely when eyes are deviated toward side of the fast phase of
the nystagmus
-central lesion if:

-direction-changing gaze nystagmus
-unilateral peripheral lesion if:
-direction-fixed gaze nystagmus
-one peripheral vestibular system is weaker in its neural output than the opposite
side
-nystagmus will beat away from weaker ear
-follows Alexander’s law
-increases in intensity and amplitude when visual fixation is eliminated
-true rotatory gaze nystagmus will not register on strip chart recorder
-antiseizure medications, barbiturates, alcohol may cause direction-changing gaze nystagmus and
poor ocular fixation
-deviation of eyes beyond 30o causes physiologic "end point" nystagmus
F.Ling - ENG (1)
1171
-Rotatory gaze nystagmus:
-brainstem lesion, often vestibular nuclei (eg. MS, 4th ventricle cysts, masses in 4th ventricle)
-cerebellar disease
-Vertical gaze nystagmus:

-CNS disease, usually brainstem
-upbeating gaze nystagmus common
-down-beating gaze nystagmus with lateral gaze
-lesions of cervico-medullary junction
-Arnold Chiari malformation: cerebellar tonsils pushed down into foramen magnum
-basilar artery impression at junction of skull base and spinal column
-down-beating gaze nystagmus in primary gaze position
-lesions of vestibular nuclei: flocculus
-Periodic alternating nystagmus (PAN):

-changes direction every 2-6 min and included a null period each half cycle in primary gaze
position
-often secondary to cerebellar lesion
-can be caused by space occupying or vascular lesions of brainstem and midbrain
-Ocular square waves:

-central lesion or anxious patient
2. Saccade (refixation) test

-patient looks at two targets on either side (horizontal) or above and below (vertical) center gaze
-normal recording is a clean square wave pattern
-ocular dysmetria:
-usually cerebellar dysfunction
-undershoot: hypometric saccades
-overshoot: hypermetric saccades
-disconjugate eye movements:
-internuclear ophthalmoplegia (INO)
-adducting eye moves slower and later than abducting eye
3. Ocular pursuit test

-normal is sinusoidal wave pattern
-when pursuit system is impaired, small corrective saccadic movements replace smooth pursuit
movement ("catch-up saccades")
-affected by variety of conditions including age and alertness, examiner instructions and various
medications
-overriding gaze nystagmus can interfere with the tracing
-smooth pursuit affected by brainstem, cerebellar or cortex lesions
-affected also by peripheral vestibular lesions with intense spontaneous nystagmus
-may be the most sensitive subtest for detection of brainstem/cerebellar disorders
4. Optokinetic test (OKN)

-optokinetic system maintains visual fixation when head is in motion
-patient fixates visually on horizontal and vertical-moving stripes or objects
-abnormalities:
-asymmetrical nystagmic response, low-amplitude response, poor nystagmic waveform
morphology
-isolated optokinetic abnormalities are cortical: visual pathways of brainstem and cortex
F.Ling - ENG (2)
1172
-in conjunction with direction-changing nystagmus: lesion in brainstem or cerebellum
-spontaneous nystagmus generated from acute unilateral, peripheral vestibular lesion can cause an
optokinetic asymmetry that is dominant in the direction of the peripheral spontaneous nystagmus
-degree of asymmetry increases with the OKN target speed
PERIPHERAL SUBTESTS
1. Positional Tests
-to determine if changes in head position cause or modify nystagmus
-eyes close to eliminate effects of visual suppression
-positional nystagmus is considered to be nonlocalizing: can be peripheral or central lesion
-direction-fixed, positional nystagmus seen more commonly in peripheral vestibular lesions
-direction-changing, ageotropic positional nystagmus
-nystagmus that changes direction when head position changes and beats away from the
down ear in the supine-head-left (or right) positions
-more commonly in central lesions and in bilateral, peripheral vestibular lesions
-geotropic: fast phase beats toward undermost ear
-nystagmus needs to be at least 6-8 degrees/s to be considered significant
-if both peripheral vestibular systems are in fact neurologically equal, a nystagmus should not be
present, regardless of velocity
2. Dynamic positioning test (Dix-Hallpike)

-maneuver that places patient’s head into position that creates the response
-"classic Dix-Hallpike response":
-latency period from 1-10s once patient’s head in position
-subjective vertigo
-transient nystagmic burst
-fatiguability
-classic response: BPV most likely
-non-classic response: lesion can be either peripheral or central
-speed of maneuver is only mildly important
3. Caloric tests
-non-physiologic procedure to induce endolymph flow in SCC (primarily horizontal)
-creates temperature gradient from lateral to medial part of canal
-neck ventroflexed 30o horizontal SCC are placed in vertical plane
-water temperatures of 30oC and 44oC
-cold water:
-cooling endolymph causing fluid to become dense
-falls in vertically positioned canal
-bends cupula away from utricle (ampullofugal) neural inhibition relative to opposite
ear
-slow phase toward and fast phase away ("cold opposite") side of irrigation
-warm water:
-heating endolymph fluid less dense
-bends cupula toward urtricle (ampullopetal) neural stimulation relative to opposite
ear
-slow phase away and fast phase toward ("warm same") side of irrigation
-note slow-phase velocities are measured
F.Ling - ENG (3)
1173
-Unilateral weakness: [(RW+RC)-(LC+LW)]/[RC+RW+LC+LW] x 100; abnormal if > 25%
-Directional preponderance: [(RW+LC)-(RC+LW)]/ [RC+RW+LC+LW] x 100; abnormal if >
30%
-caloric abnormalities usually reflect peripheral lesions
Failure of fixation suppression (central)

-during caloric testing, normal patients should be able to suppress nystagmus by opening their
eyes and fixating visually on a target
-failure of fixation suppression suggests CNS pathology
-a reduction in nystagmus velocity of at least 40% is considered normal
-fixation index:
-slow wave velocity with eyes open/eyes closed
-if < 60% then normal
-if > 60% then significant - suggests central lesion
F.Ling - ENG (4)
1174
MENIERE’S DISEASE
-Endolymphatic hydrops: condition of increased hydraulic pressure within inner ear endolymphatic system
-excess pressure accumulation causes a tetrad of symptoms as follows:
-Fluctuating hearing loss
-Occasional episodic vertigo (usually a spinning sensation, sometimes violent)
-Tinnitus or ringing in the ears (usually low-tone roaring)
-Aural fullness (eg, pressure, discomfort, fullness sensation in the ears)
Pathophysiology:
-two fluids chambers inner ear: endolymph and perilymph
-attacks of hydrops caused by increase in endolymphatic pressure break in membrane separating
perilymph (a potassium-poor extracellular fluid) and the endolymph (a potassium-rich intracellular fluid)
-chemical mixture bathes the vestibular nerve receptors depolarization blockade and transient
function loss creates an acute vestibular imbalance vertigo.
-mechanical disturbance of the otolithic organs responsible for linear and translational motion detection
may produce nonrotational vestibular symptoms
-mechanical disturbance of the organ of Corti hearing loss and tinnitus
-apex of the cochlea is wound much tighter than the base
-more sensitive to pressure changes than base affects low frequencies (located at the
apex) more than high frequencies (located at the relatively wider base of the cochlea)
-symptoms improve after membrane is repaired and normal sodium and potassium concentrations are
restored.
Causes:
-Increased pressure of endolymph may be caused by a wide range of disorders (eg, metabolic imbalance,
hormonal problems, infections). Autoimmune diseases (eg, lupus, rheumatoid arthritis) may cause an
inflammatory response within the labyrinth. Allergy also has been implicated in many difficult-to-treat
Ménière cases.
Differential Diagnoses:
-Benign Paroxysmal Positional Vertigo
-CNS Causes of Vertigo
-Inner Ear, Autoimmune Disease
-Inner Ear, Evaluation of Dizziness
-Inner Ear, Labyrinthitis
-Inner Ear, Ménière Disease, Surgical Treatment Inner Ear, Perilymphatic Fistula
-Inner Ear, Tinnitus
-Thyroid, Thyrotoxic Storm Following Thyroidectomy
Other Problems to be Considered:
-Acoustic neuroma and other brain tumors

-Autoimmune processes (especially lupus, rheumatoid arthritis, sarcoidosis, periarteritis, giant cell,
arteritis, Susac and Cogan syndromes)
-Congenital anomalies
-Diabetes
-High cholesterol or triglyceride
-Inner ear inflammation
-Labyrinthitis
F.Ling - Meniere's Disease(1)
1175
-Lyme disease
-Microvascular compression syndromes
-Multiple sclerosis
-Neurosyphilis
-Otosclerosis
-Perilymphatic fistula
-Salt or water imbalance
-Thyroid disease
-Thyroid hormone disease
-Transient ischemic attacks and stroke
-Trauma
-Vestibular migraine
-Viral infections
Investigations:
-audiometry
-transtympanic electrocochleography (ECoG)
-to detect distortion of nerve-containing membranes of the inner ear (presumably due to pressure
fluctuations of the perilymph pressure) and may show evidence of cochlear involvement
-ECoG measures ratio of summating potential (probably arising from movement of the basilar
membrane) and action potential on the nerve in response to auditory stimuli
-Hydrops is suggested when the ratio is greater than 35%
-ECoG is most accurate when Ménière disease is active
-ENG
F.Ling - Meniere's Disease(2)
1176
ELECTRONYSTAGMOGRAPHY
ENG SUBTESTS - OCULOMOTOR EVALUATION
The visual system provides information about whether the environment is stationary or mobile. This is
accomplished by means of foveation. The visual system is subserved by the motor system, the premotor
system, and the command (control) eye movement system, which controls saccadic eye movements,
pursuit, and vergence.
The oculomotor portion of ENG assesses eye movement function for the various command eye movement
systems in the absence of vestibular stimulation. For oculomotor evaluation, the patient is presented with
various visual stimuli and asked to follow them while his or her eye movements are recorded.
SACCADES (calibration)
-also called the calibration test, evaluates the saccadic eye movement system
-this system is responsible for rapid eye movements and refixation of the target on the fovea.
Administration
-For saccadic testing, one may place dots on the wall or ceiling at specified distances from each other
(usually center and 10°, 20°, and 30° off center) and then instruct the patient to look back and forth
between the dots, keeping the head fixed
Interpretation
-test results are influenced by patient cooperation and visual acuity
-various drugs can also affect performance. Accuracy, latency, and velocity should all be taken into
consideration when interpreting saccades
Normal Saccades
F.Ling - ENG Abnormalities (1)
1177
Accuracy
Hypermetric
-aka calibration overshoot,
hypermetric saccades occur
when a patient has difficulty
measuring the distance
required for the muscular act
necessary for following the
target
-patients who consistently
exhibit hypermetric saccades
may have ocular dysmetria,
which is suggestive of a CNS
lesion at the level of the
cerebellum (fastigial nuclei)
Ocular flutter
-spiky overshoot; the patient
overshoots the target several
times with a short duration
between overshoots
-caused by brainstem and
CNS lesions:
-brainstem
encephalitis,
paraneoplastic
syndromes,
meningitis, and
intracranial tumours
Hypometric
-patient undershoots the
target
-patient fails to reach target
with first saccades and
makes successive saccades,
each one brining the eyes
closer and finally onto the
target
-suggestive of basal ganglia
pathology and lesions of the
dorsal vermis of the
cerebellum
Multistep saccades
-occur when a patient undershoots the target and then attempts to correct with multiple small
saccades; also suggestive of CNS pathology
Postsaccadic drift
-called glissade, it is seen as a drifting of eye movement after the saccade; consistent with
cerebellar pathology
1178
Pulsion
-seen in vertical saccades
in patients with posterior
inferior (Wallengberg’s
syndrome) or superior
cerebellar artery syndrome.
The pattern includes a
pulling to the left or right
of the eyes when
completing vertical
saccades.
Latency
Delayed Saccades
-disorders in latency are due
to prolongation of saccades
-examiner should rule out
inattention or uncooperative
behaviour, drowsiness, drug
intoxications
-prolongations of more than
400 ms in attentive and
cooperative patients may be
suggestive of CNS
pathology: lesions of frontal
or frontoparietal cortex or
basal ganglia
Asymmetrical latencies
-can occur in patients with
lesions in the occipital or
parietal cortex
-saccades in one direction
may be fine with a
prolongation of saccades in
the opposite direction
1179
Velocity
Saccadic slowing
-first rule out drowsiness
or drug effects
-saccadic slowing is
consistent with various
CNS or ocular disorders,
including oculomotor
weakness, degenerative
conditions (Huntington’s
disease, progressive
supranuclear palsy), basal
ganglia pathology
(Parkinson’s disease), and
cerebellar disorders.
Abnormally fast saccades

-usually an artifact and
may be due to technical
difficulties
-in some cases, abnormally
fast saccades may suggest
CNS or ocular pathology
(ie, ocular flutter).
Asymmetrical velocity
-can be observed as an asymmetry between the eyes or between directions
-may suspect ocular nerve or muscle pathology (ie, lesions or palsies)
-CNS pathology may also be indicated
-lesion in the medial longitudinal fasciculus causing internuclear ophthalmoplegia may
evidence as asymmetrical saccadic velocity
-two primary etiologies:
-multiple sclerosis: usually causes bilateral (but sometimes highly asymmetric) INO
-brainstem infarction: usually causes unilateral INO
1180
GAZE
-conducted to evaluate for the presence
of nystagmus in the absence of
vestibular stimulation
-essentially 3 types of information are
obtained:
-presence or absence of
spontaneous nystagmus (no
task or center gaze)
-presence, absence, or
exacerbation of nystagmus
with addition of off-center
gaze tasks to stress the system
-fixation suppression of
spontaneous nystagmus
Administration
-patient is instructed to look straight
ahead and then to fixate on a target 30°
to the right, left, up, and down -fixation
is maintained approximately 30
seconds in center gaze and 10 seconds
in eccentric gaze
-fixation suppression can be eliminated by having the patient'
s eyes open in a dark room with Frenzel
lenses or with dark goggles used for infrared assessment
Interpretation
Square-wave jerks
-caution must be exercised
in interpretation of
square-wave jerks
-many healthy
patients exhibit this
pattern with their
eyes closed, with
increasing
frequency with
increasing age
-in young patients,
considered abnormal if they
occur more frequently than 1 per second or with eyes open suggestive of a cerebellar disorder,
progressive supranuclear palsy, and cerebral hemispheric disease
Spontaneous nystagmus
-may indicate either central or peripheral pathology
-presence of nystagmus with eyes open is always diagnostically significant
-peripheral indicators
Horizontal or horizontal rotary
Suppressed by visual fixation
Nondirection changing
Exacerbated by gazing in the direction of the fast phase
1181
-central indicators
Vertical
Not suppressed by fixation
Direction changing
Alexander's law
-nystagmus evident with eyes open always beats in the same direction and increases when the
patient gazes in the direction of the fast phase
-nystagmus decreases or disappears when the patient gazes in the direction opposite to the fast
phase; often seen in peripheral vestibular disorders and occasionally in central disorders
Unilateral gaze-paretic (evoked)

nystagmus
-only occurs with eccentric
gaze in one direction
-elicited nystagmus beats in
the direction of the gaze
-consistent with CNS
pathology.
Bilateral gaze-paretic (evoked)

nystagmus
-when the patient gazes
right, nystagmus is elicited
that beats to the right; when
the patient gazes left,
left-beating nystagmus
occurs
-pattern suggests CNS
pathology
Brun’s nystagmus
-combination of unilateral
gaze-paretic nystagmus and
vestibular nystagmus, which
is evidenced as nystagmus
in both directions of a gaze
that is asymmetrical
-associated with extra-axial
mass lesions on the side of
the gaze-paretic nystagmus
-ie. tumours of
CPA such as
acoustic neuroma
-damage floccules
of cerebellum,
causing ipsilateral
gaze-paretic
nystagmus, and
also damage
vestibular nerve,
causing contralateral vestibular nystagmus
1182
Congenital nystagmus
-present at birth or develops
during infancy
-nearly always conjugate,
horizontal and quite intense
-often has a spiky
appearance and increases
with lateral gaze
-may decrease in velocity or
completely disappear with
eyes closed
-often has a null point
Rebound nystagmus
-burst of nystagmus lasting
approximately 5 seconds
that begins when the eyes
are returned to center gaze
-when present, may suspect
brainstem or cerebellar
lesions
Fixation suppression
-for peripheral lesions,
nystagmus that is evident
with eyes closed or in the dark should be suppressed by visual fixation
-if visual fixation does not suppress nystagmus, CNS pathology is possible
Periodic Alternating Nystagmus

-horizontal nystagmus that
reverses direction
approximately every two
minutes
-caused by lesion of nodulus
and uvula of cerebellum
-Arnold-Chiari
malformation
-multiple sclerosis
-cerebellar tumours,
cysts, abscesses, or
degenerations
Downbeat Nystagmus
-form of central vestibular
nystagmus
-caused by lesions of
vestibulocerebellum and
underlying medulla
-cerebellar degeneration,
craniocervical anomalies,
and brainstem infarction
1183
Upbeat Nystagmus
-caused by lesions of the medulla or anterior vermis of the cerebellum
-infarctions, tumours, degenerations and atrophies of the cerebellum, medulla and midbrain, and
multiple sclerosis
SMOOTH PURSUIT TRACKING
-smooth pursuit system is

responsible for following
targets within the visual
field
-tracking can be evaluated
horizontally and vertically
-as a rule, vertical tracking
is not as smooth as
horizontal, even in healthy
subjects.
-tracking is also affected
by attention and patient
cooperation.
Administration
-patient is instructed to
follow a sinusoidal
moving target with his or
her eyes only.
Interpretation
-tracking test results should
resemble a smooth sinusoid
-breakup of movement may
indicate CNS pathology in various
locations
-nystagmus may be seen in
tracking test results when also
observed in spontaneous (center
gaze) recordings
OPTOKINETIC
Administration
-patient tracks multiple stimuli
-may be in the form of stripes on a
rotating drum or a stream of
lighted dots across a light bar or
the field of an oculomotor
stimulator
-stimuli are moved at a rate of
300, 400, or 600 per second in
each direction
1184
Interpretation
-eye movements that are generated by moving fields resemble nystagmus
-if responses are not symmetrical, CNS pathology may be suspected
POSITIONING AND POSITIONAL TESTING
Positioning
Dix-Hallpike maneuver
-to assess the presence or absence of nystagmus associated with BPPV
-when test results are classically positive, canalith repositioning and vestibular rehabilitation therapy may
be indicated
Administration
-performed by turning a patient's head to the right or left and then briskly assisting him or her to a supine
position with the head hanging to the right or left
-if nystagmus is observed, the test is repeated to evaluate fatigability of the response
-maneuver should be completed prior to any other positional testing
-patients with BPPV present with a geotropic rotary nystagmus
Interpretation
-if rotary nystagmus is observed, the results must have the following 4 characteristics to be considered
classically positive:
-delayed onset - need to observe patient for at least 20 seconds
-transient burst of nystagmus - lasts about 10-15 seconds
-subjective report of vertigo
-fatigability
-when BPPV occurs, a peripheral lesion on the side that is down when the nystagmus occurs may be
indicated.
Positional tests
Administration
-examiner places the patient in each position and evaluates him or her for a minimum of 20-30 seconds
-mental tasking is used to keep the patient from suppressing nystagmus
-some standard positions used are as follows:
-head hanging
-supine
-supine, head right
-supine, head left
-lateral right
-lateral left
Interpretation
-if results are normal, no nystagmus is present
-for results to be considered abnormal:
-nystagmus observed in positional testing should exceed 60 per second
-change direction in any 1 position
-persist in at least 3 different positions
-be intermittent in all positions
1185
-peripheral indicators include the following:
-direction-fixed
-if direction changing in different positions, may be peripheral if geotropic; however, a horizontal
canal variant of BPPV should also be considered
-latency of onset
-fatigable
-central indicators include the following:

-if direction changing in different positions, may be central if ageotropic
-direction changing in a single position, which is a strong indicator for CNS pathology
-immediate onset
-not fatigable
CALORIC STIMULATION
Caloric stimulation
-vestibular stimulators include
water, air, and closed-loop cuff;
water and air are commonly used
Administration
-cool irrigations - the fast phase of
nystagmus beats in the direction
opposite to the stimulated ear (ie,
cool irrigation in the right ear
causes left-beating nystagmus)
-warm irrigations - nystagmus beats
in the direction of the stimulated ear
(ie, warm stimulation of the right
ear produces right-beating
nystagmus)
-when adequate data have been
recorded, fixation suppression
testing is conducted
Monothermal
-some clinics use monothermal calorics as a screening test for patients who have normal oculomotor,
positional, and positioning test
-only warm calorics are conducted
-if the responses from each ear are equivalent, testing is terminated
-if a difference in responses exists between the 2 ears, bithermal caloric testing is conducted.
Ice water calorics

-ice water calorics are used to determine whether residual vestibular function exists in patients who have
no caloric response with standard stimuli.
Interpretation
-in the normal vestibular system, adequate, equivalent responses should be obtained from each ear
-slow phase velocity is determined for each recording for use in the following calculations:
1186
-Unilateral weakness (UW) is used
to evaluate symmetry
-in many clinics, a UW
greater than 25% is
significant
-%UW = [(RC + RW - LC
+ LW)/(RC + RW + LC +
LW)] X 100
-a negative number
indicates a right unilateral
weakness, and a positive
number indicates a left
unilateral weakness
-unilateral weakness is
indicative of a peripheral
vestibular lesion involving
the nerve or end-organ on
the side of the weakness
-Bilateral weakness
-average caloric responses
of 60 per second or less are
consistent with a bilateral
weakness
-borderline bilateral
weakness is noted when the
average responses are
between 70-90 per second
-abnormally weak bilateral
responses may be due to
bilateral peripheral
vestibular pathology or
central interruption of VOR
-Directional preponderance (DP)

-if the patient has
spontaneous nystagmus,
directional preponderance is
evident
-reflects an imbalance of the
horizontal VOR
-indicates peripheral or
central vestibular
dysfunction
-in general, a directional
preponderance greater than
20-30% is considered
significant
-%DP = [(LC + RW - RC +
LW)/(RC + RW + LC +
LW)] X 100.
1187
Fixation suppression
-after each caloric stimulus, the patient is instructed to fixate on a light or other object
-fixation should normally eliminate or greatly reduce the induced nystagmus
-if visual fixation does not inhibit nystagmus, central pathology at the level of the brain stem is indicated
Interpretation
-compute the fixation index (FI):
-an FI of 0.60 or greater is considered significant (FI = EO/EC, where EO = nystagmus with eyes
open and EC = nystagmus with eyes closed)
SPECIAL APPLICATIONS
Pressure fistula test
Administration
The patient is placed in an upright position. While the patient is involved in mental tasks, recordings are
conducted with his or her eyes open in the dark (infrared goggles) or eyes closed with electrodes. The
presence or absence of spontaneous nystagmus is noted. Next, a probe from an immittance bridge is placed
in the ear canal, and a seal is obtained. Pressure is then varied from 0-200 mm H2O and held for
approximately 15 seconds. Pressure is then decreased to - 400 mm H2O and held for 15 seconds. The
patient is questioned for subjective symptoms.
Interpretation
The presence of a fistula is confirmed if pressure causes nystagmus.
Tullio phenomenon
This is not as routinely used as pressure fistula testing, but the Tullio phenomenon is an option for patients
on whom a hermetic seal cannot be obtained.
Administration
Follow the procedure for a pressure fistula test, but instead of varying the air pressure, present a 500-Hz
tone at 95 dB for no longer than 3 seconds. Monitor eye movements and ask the patient about his or her
subjective experience.
Interpretation
The Tullio phenomenon is positive if nystagmus is observed.
1188
CRANIAL NERVE VII
FACIAL NERVE ANATOMY
STRUCTURAL ANATOMY
Intracranial Segment
-23-24 mm
-segment from brainstem to internal auditory canal
-Nervus Intermedius: parasympathetic and sensory
root of facial nerve
-motor root joins with nervus intermedius in
CPA/IAC to form common facial nerve
Intratemporal Segments
-meatal
-labyrinthine
-tympanic (horizontal segment)
-mastoid (vertical segment)
1. Meatal
-8-10 mm
-from porus acousticus (fundus) to meatal foramen
-traverses in anterior superior quadrant of IAC
separated by falciform crest inferiorly and Bill’s
bar posteriorly
2. Labyrinthine
-3-5 mm
-from meatal foramen to geniculate ganglion
-narrowest segment of fallopian canal (0.68 mm
diameter)
-geniculate ganglion:
-located at first genu Middle fossa approach - GSPN (5); geniculate ganglion (7); facial nerve
meatal segment (10), labyrinthine segment (9), tympanic segment (12)
-cells bodies of sensory cells and taste
cells from anterior 2/3 of tongue and
palate
-greater superficial petrosal nerve:
-first branch of facial nerve
-carries preganglionic parasympathetic
fibers to lacrimal gland
3. Tympanic
-8-11 mm
-from geniculate ganglion to pyramidal eminence
(at second genu)
-courses above cochleariform process, oval
window and stapes; below lateral semicircular
canal
-most common site of dehiscence (40-50%) Lateral approach - facial nerve mastoid segment (1), tympanic segment (2),
labyrinthine segment (3), meatal segment (4); GSPN (5); cochleariform
process (6)
1189
4. Mastoid
-10-14 mm
-from pyramidal process to stylomastoid foramen
-nerve to stapedius
-chorda tympani:
-preganglionic fibers to submandibular and sublingual glands
-special sensory taste fibers
Extratemporal Segments
-postauricular nerve
-branch to external auricular and occipitofrontalis muscles
-nerve to stylohyoid
-nerve to posterior digastric muscle
-nerves to muscles of facial expression
-pes anserinus
-branching point of extratemporal segments in parotid gland
-two divisions:
-superior - temporozygomatic
-inferior - cervicofacial
-temporal branch:
-frontalis
-corrugator supercillii
-procerus
-upper orbicularis oculi
-zygomatic branch:
-lower orbicularis oculi
-abundant anastomotic supply with
buccal branch
-buccal branch:
-zygomaticus major and minor
-levator anguli oris
-buccinator
-upper orbicularis oris
-marginal mandibular branch:
-lower orbicularis oris
-depressor anguli oris
-depressor labia inferioris
-mentalis
-cervical branch:
-platysma
Blood Supply of Facial Nerve

-anterior inferior cerebellar artery labyrinthine artery
-supplies nerve within IAC
-middle meningeal artery petrosal artery
-supplies perigeniculate area
-supplies tympanic and mastoid segments
1190
FUNCTIONAL ANATOMY
Branchial Motor (Special Visceral Efferent)

-motor nucleus
-motor function to:
-stapedius
-stylohyoid muscle
-muscles of facial expression
Parasympathetic (General Visceral Efferent)

-preganglionic fibers in superior salivatory
nucleus (3 subsets):
a) superior salivatory nucleus nervus

intermedius greater superficial
petrosal nerve vidian nerve [in
pterygoid canal] [pterygopalatine
fossa] (sphenopalatine ganglion)
postganglionic fibers to lacrimal
and palatine glands
b) superior salivatory nucleus nervus

intermedius chorda tympani and
lingual nerve (submandibular
ganglion) postganglionic fibers to
submandibular and sublingual glands
c) superior salivatory nucleus nervus

intermedius tympanic plexus
lesser petrosal nerve (otic
ganglion) post ganglionic fibers
to parotid gland*
*parasympathetic innervation from

CN IX, but some describe
contribution from CN VII
Sensory (General Sensory Afferent)

-supplies sensation to auricular concha,
postauricular skin, wall of EAC and part of
tympanic membrane
-cell bodies housed in geniculate ganglion
Taste (Special Sensory Afferent)

-anterior 2/3 of tongue lingual nerve
chorda tympani geniculate ganglion (houses
cell bodies) nervus intermedius tractus
and nucleus solitarius
1191
The Halmagyi (Head Impulse)Test
What is it?
A clinical test of severe unilateral loss of horizontal SCC function: one large or several
small oppositely directed, compensatory, re-fixation saccades elicited by rapid horizontal
head rotation toward the damaged side.
How is it done?
• Patients sit upright and fix their gaze on a target about 3 m away. The examiner
stands in front, but to the side of the patient. The patient is instructed to look at
the target while your head is turned from one side to the other (ie. passively). The
patient’s head is then rapidly turned.
• The examiner looks for saccades. A patient will not make any saccades if the
horizontal canal on the side to which the head was turned is intact. If not intact, a
patient will make saccades in the direction opposite to which the head was turned.
These saccades can be recorded with standard ENG equipment.
• Initially tested on 12 patients with a surgically created complete unilateral canal
paresis. All 12 demonstrated predictable, clinically evident saccades with this
manoeuvre. None of the control patients demonstrated saccadic movement. The
response was equally strong in patients who had had a paresis for 1 week or 1
year.1
What is the test used for?

To detect a severe unilateral horizontal SCC paresis clinically.
Sensitivity and Specificity

• The specificity of the head impulse test was 91-100% and the sensitivity was 34-
45%.2,3 The test is very sensitive to the presence of a severe paresis (87.5%).3
• The positive predictive value was 0.92, the negative predictive value was 0.41.2
• A canal paresis value of 42.5 percent was considered to be the limit of the normal
response, as seen when the head impulse test was used to predict a normal or
abnormal result in a given patient.2
• It does not detect mild or moderate vestibular weaknesses.3
Conclusions
The head impulse test is a useful clinical test for the detection of severe unilateral
horizontal SCC paresis. Head impulse testing will not replace caloric testing but is a very
useful adjunct to it. This test is poor at detecting mild to moderate canal paresis.
References
1. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol 1988;45:737-9.
2. Perez N, Rama-Lopez J. Head-impulse and caloric tests in patients with dizziness. Otol Neurotol
2003;24:913-7.
3. Beynon GJ, Jani P, Baguley DM. A clinical evaluation of head impulse testing. Clin Otolaryngol
1998;23:117-22.
Kilty 2004-Summary of the Halmagyi (Head Impulse) Test

1192
Head-Shaking Nystagmus (HSN)
What is it?
A clinical test that looks for nystagmus that appears after vigorous horizontal (horizontal SCC) head-
shaking for about 15 seconds at a frequency of 2 Hz. The test is a high-frequency vestibular stimulus.
How is it done?
• Originally described by Kamei et al1, it required the patient to shake their head 30 times in a)the
horizontal plane, bent forward 30o b)in the horizontal plane, positioned normally, c)in the coronal
plane, and d)in the sagittal plane.
• An alternative method has been described that requires the patient to shake their head rapidly in a
sinusoidal manner at a frequency of 2 cycles/s for at least 20 cycles.2
• After the head shaking, the patient’s eye movements are observed for 30-60 s.
• It has been described using Frenzel glasses, but it is thought to be more accurately performed
when done with standard ENG monitoring equipment.
• Three types of nystagmus have been described:
1) Deficiency-type: nystagmus with a predominate horizontal component and a fast phase
directed toward the intact end organ. Occurs in nearly 75% of cases.
2) Recovery-type: nystagmus directed toward the the affected side, occurs following a 20
second latent period. Occurs in nearly 23% of cases.
3) Biphasic-type: a combination of the latter two types. Occurs in 1-2% of cases.
What is the test used for?

Evaluation for a peripheral vestibular system disorder. Numerous studies have looked at the sensitivity and
specificity of this test. In general the sensitivity is poor, making it an unreliable screening test.
Sensitivity and Specificity

• In a study with 1364 participants who presented with the complaint of dizziness, nearly 32% of
patients had HSN.3 Only 19% demonstrated a caloric weakness (> 20%). The sensitivity of the
test was 50%, and the specificity 73%. The sensitivity increased with an increase in the R/L
excitability difference such that with a >80% weakness, the sensitivity was 77% whereas the
specificity was 70%.
• In a group of ‘normal’ volunteers (not having experienced dizziness), HSN occurred in 25-30% of
participants.4,5 In 196 patients with a diagnosis of a peripheral vestibular lesion, 76 had a positive
HSN test (sensitivity= 38%). The sensitivity was greater with a diagnosis of Meniere’s disease
(58%), acoustic neuroma (48%), or vestibular neuronitis (50%). With a diagnosis of BPV, the
sensitivity was only 29%, the same as ‘normal’ volunteers.3
Conclusions
HSN is neither sensitive nor specific and is not to be used as a screening test. It is complementary to the
standard ENG examination, but generally does not provide any new information to the examination.
References
1. Kamei T, Kimura K, Kaneko H, Noro H. Reevaluation of the head shaking test as a method of nystagmus
provocation. J Otolaryngol (Japan) 1964;67:1530-4.
2. Hain TC, Fetter M, Zee DS. Head-shaking nystagmus in patients with unilateral peripheral vestibular lesions.
Am J Otolaryngol 1987;8:36-47.
3. Fujimoto M, Rutka J, Mai M. A study into the phenomenon of head-shaking nystagmus : Its presence in a
dizzy population. J Otolaryngol 1993;22:376-9.
4. Asawavichianginda S, Fujimoto M, Mai M, Rutka J. Prevalence of head-shaking nystagmus in patients
according to their diagnostic classification in a dizziness unit. J Otolaryngol 1997;26:20-25.
5. Asawavichianginda S, Fujimoto M, Mai M, Desroches H, Rutka J. Significance of head-shaking nystagmus
in the evaluation of the dizzy patient. Acta Otolaryngol (Stockh) 1999;Suppl 540:27-33.
Kilty 2004-Summary of Head-Shaking Nystagmus (HSN)

1193
Malignant Otitis Externa
Imaging Studies:
Technetium Tc 99 methylene diphosphonate bone scan

-based on binding to osteoblasts.
-test is not specific since tumors or bony dysplasias, in addition to osteomyelitis, can cause osteoblastosis.
-useful in the initial evaluation because a positive finding in the correct clinical context can lead to
confirmation of diagnosis
-test is not useful for assessing response to therapy since results remain persistently positive long after
clinical improvement due to continuous bone remodeling and reformation.
-may have limited usefulness for patients with a prior history of mastoiditis or otologic surgery
Gallium citrate Ga 67 scan

-very sensitive but is not specific because gallium binds to actively dividing cells, including inflammatory
cells, tumor cells, and osteoblasts.
-improvement of a positive test result correlates with therapeutic response
-baseline test usually is obtained at initial diagnosis for comparison with follow-up studies during treatment
-quantitative comparison of lesion to nonlesion side may improve interpretation of these studies for
distinguishing acute external otitis from MEO and for determining efficacy of therapy.
Indium In 111––labeled leukocyte scan

-attempts to provide same sensitivity as a gallium citrate Ga 67 scan but is more specific to an
inflammatory process.
-does not appear to provide an improvement in scintographic technique for helping to establish diagnosis.
-may be better than gallium citrate Ga 67 scans for assisting in establishing correct timing of disease
resolution.
-can be unreliable for imaging chronic osteomyelitis in other areas of body. Thus, accuracy of this
application needs further study.
CT scan and MRI both are useful for evaluating anatomic extent of soft tissue inflammation, abscess formation, and
intracranial complications.
-CT scan fails to diagnose early osteomyelitis because 30-50% of bone destruction is required to detect
osteomyelitis by CT scan.
-MRI provides poor bone resolution
-soft tissue manifestations regress on CT scan and MRI with response to therapy.
-one changes remain persistently abnormal on CT scan for at least one year and are not well demonstrated
by MRI. Thus, neither of tests can be used to determine osteomyelitis resolution.
-Most authors advocate obtaining a CT scan with initial evaluation for all patients, whereas Benecke
advocates obtaining this test selectively for patients with cranial neuropathy, extensive bone changes on
technetium scan, or poor clinical response to treatment.
-MRI and CT scan are equally sensitive in detecting soft tissue extent of disease, but MRI is more sensitive
for detecting intracranial complications
1194
NEOPLASMS OF THE EAR AND LATERAL SKULL BASE
PATHOLOGY
Paraganglioma: clusters (zellballen) of chief cells containing Extramedullary

norepinephrine and dopamine plasmacytoma: sheets of
monotonous round cells typical
of plasma cells
Eosinophilic granuloma: localized collection of

histiocytes and polygonal and sheet formation
Basal Cell Carcinoma: rim of palisading basaloid cells at

tumour margin
1195
Embryonal rhabdomyosarcoma: small round and Alveolar rhabdomyosarcoma: sheets of round, oval, or
spindle-shaped primitive mesenchymal cells in loose straplike cells arranged in trabecular pattern surrounding
myxoid or compact pattern empty alveolar compartments
Pleomorphic rhabdomyosarcoma: anaplastic

multinucleated spindle cells that form whorls and fascicles
with longitudinal striations
Chordoma: stellate, intermediate and vacuolated

physaliphorus or soap-bubble cells in mucoid matrix
growing in nests, cords or trabeculae
Cholesterol granuloma: cholesterol crystals

surrounded by multinucleated giant cells, round cell
infiltration, hemosiderin laden macrophages
1196
OTOPLASTY
PATIENT EVALUATION
-most common cause of aural prominence: overprojection of conchal bowl:

-excess cartilage
-enlarged auriculomastoid angle
-both
-lack of antihelical fold
-ideal age: 5-8 years - correction before child’s entry into school
-measurements from scalp to helix at:
-top of helical rim: 10-12 mm
-level of EAC: 16-18 mm
-level of antitragus: 22 mm
SURGICAL TECHNIQUE
-postauricular incision created - ellipse of skin removed for conchal set back
-resulting auriculomastoid angle should be no less than 30o
-creation of antihelix
-incorporation of adequate amounts of both perichondral layers when placing the Mustarde and conchal sutures
-achievement of symmetry
COMPLICATIONS
-haematoma risk of cartilage necrosis cauliflower ear

-excessive pain within the first 48 hours
-back to OR open wound, express clot, control of bleeding sites
-infection
-POD 3-4
-gram-positive cocci: Staphylococci or streptococci
-suppurative chondritis (rare) - requires conservative debridement
-leads to auricular deformity
-long term complications
-suture extrusion, suture release, keloid formation
-use of monofilament nylon sutures:
-less infection, granuloma formation and extrusion but risk of cutting through cartilage compared
to braided sutures
-poor cosmetic results
-telephone deformity
-undercorrection of superior and inferior aspects of the auricle
-absolute number of complications and poor results is higher in patients undergoing cartilage-
cutting techniques:
-sharp contours and stigmata of poor surgical technique may occur when cartilage is
incised
F.Ling - Otoplasty (1)
1197
PERIPHERAL VESTIBULAR DISORDERS
Definition: Vertigo is the hallucination of movement, either of self (subjective) or the environment (objective).
History
A minimum vertigo history should address the following:
1. duration of individual attack (hours vs days)
2. frequency (daily vs monthly)
3. effect of head movements (worse, better, or no effect)
4. inducing position or posture (eg. rolling onto right side in bed)
5. associated aural symptoms such as hearing loss and tinnitus
6. concomitant or prior ear disease and/or ear surgery
Vertigo duration
1. Vertigo lasting minutes to hours

a. Idiopathic endolymphatic hydrops (Ménière's disease)
b. Secondary endolymphatic hydrops
(1) Otic syphilis
(2) Delayed endolymphatic hydrops
(3) Cogan's disease
(4) Recurrent vestibulopathy
2. Vertigo lasting seconds

benign paroxysmal positional vertigo
3. Vertigo lasting days

vestibular neuronitis
4. Vertigo of variable duration

a. Inner ear fistula
b. Inner ear trauma
(1) Nonpenetrating trauma
(2) Penetrating trauma
(3) Barotrauma
VERTIGO LASTING MINUTES TO HOURS
MÉNIÈRE'S DISEASE
-endolymphatic hydrops and Ménière's disease in particular are final manifestation of a variety of
pathological insults which may be congenital, inflammatory, traumatic or idiopathic
-cause of Ménière's still remains unknown
-syphilis cause in ~7% of patients with Ménière-like syndromes and otosclerosis is associated with ~4% of
Ménière's
-viral infections postulated as one possible cause of endolymphatic hydrops but no specific viruses have
been associated with disease, and pathologic studies have not found histologic changes suggestive of viral
infection
1198
-Definite Ménière disease:
-two or more episodes of spontaneous rotational vertigo that lasts 20 minutes or longer
-audiometrically documented hearing loss on at least one occasion
-tinnitus or aural fullness in affected ear
-other causes excluded
-Certain Ménière disease:
-histopathologic confirmation to definition criteria
-Probable Ménière disease:
-one definitive episode of vertigo despite fulfilment of all other criteria
-Possible Ménière disease:
-cochlear or vestibular variants of Ménière disease when other causes have been excluded
Pathophysiology
-overaccumulation of endolymphatic fluid
-endolymph is produced at stria vascularis and is absorbed primarily by endolymphatic sac
-mechanisms that may lead to a disturbance of this system:
1. Damage to endolymphatic sac and subsequent impairment of it's ability to absorb

endolymph
2. Blockage of endolymphatic duct leading to sac
3. Overproduction of endolymph.
-derangement in endolymph / perilymph balance leads to following pathophysiologic alterations
1. Swelling of endolymphatic space bulging of basilar membrane and Reissner's

membrane into perilymphatic space and become tensed
2. Rupture of Reissner's membrane with leakage of potassium rich fluid (endolymph) into
perilymph causing interference with generation of action potentials
3. Slow leakage hypothesis due to increased pressure has been also postulated
4. Bulging of membranous labyrinth so that it interferes with function or anatomy of other
labyrinthine structures: receptors of posterior SSC, utricle and occasionally impinging
under stapes footplate
-an imbalance with the normal side is created, this being perceived as vertigo and hearing loss
Diagnosis
Clinical presentation
-recurring attacks of vertigo (96.2%) with tinnitus (91.1%) and ipsilateral hearing loss (87.7%)
-attacks often preceded by aura consisting of a sense of fullness in ear, increasing tinnitus, and a decrease
in hearing
-acute period of vertiginous symptoms lasts 2 to 6 hours
Disease course
-highly variable
-cluster of attacks separated by long remissions, there may be single, sporadic attacks or periods of
unrelenting, recurring attacks
-vertigo will cease spontaneously in 57% of patients in 2 years and in 71% after 8.3 years
-pts may be minimally inconvenienced or completely incapacitated
1199
-long term studies indicate that patients experience:
1. Average pure-tone hearing loss of 50 dB
2. Mean speech discrimination score of 53%
3. Average caloric response reduction of 50%.
4. Mean frequency of attacks: 6-11/year for first 20 years
5. Mean frequency of attacks diminishing to 3-4 /year after 20 years.
6. Bilateral disease occurred in 47% of patients observed for 20 years or more
History and physical findings
Vertigo
-severe vertigo in horizontal plane which is maximal at onset of attack characterizes
-head movement exacerbates this symptom
-Otolithic crisis of Tumarkin:
-sudden unexplained falls without loss of consciousness or associated vertigo are occasionally
described
-a consequence of an abrupt change in otolithic input, an erroneous vertical gravity reference
occurs generates an inappropriate postural adjustment via vestibulospinal pathway sudden fall
-occur in less than 2% of Ménière's patients
-Lermoyez variant:
-resolution of hearing loss and tinnitus with onset of vertigo
-Cochlear hydrops:
-fluctuating hearing loss, aural fullness, tinnitus without vertigo
Nystagmus
-direction varies over time course of attack
-phases of nystagmus:
-"irritative nystagmus": early in attack, nystagmus is often noted beating toward affected ear
-"paralytic nystagmus": later, nystagmus beats toward healthy ear
-"recovery nystagmus": as attack subsides and vestibular function improves, nystagmus often
reverses toward affected ear
-nystagmus is not reliable in establishing validity of this diagnosis
Hearing loss and tinnitus

-sensorineural hearing loss typically fluctuating and progressive
-often occurs coincident with sensation of fullness or pressure in ear
-audiometric pattern:
-low-frequency, fluctuating loss is encountered most commonly
-over time hearing loss flattens and becomes less variable with audiometric curve becoming flat in
75% of patients at 15 years
-hearing loss outcome:
-profound hearing loss in only 1 to 2%
-diplacusis
-perception of difference in pitch between two ears when presented with same pitched sound is
present in almost half these individuals
-tinnitus:
-most often described as roaring; increasing prior to an attack and during one, while decreasing
following an attack
1200
Investigations
-audiogram low frequency hearing loss
-ENG unilateral weakness
-ECoG increased SP/AP ratio
-glycerol dehydration test (historical):
-oral glycerol ingestion causes osmotic diuresis will improve symptoms temporarily within 30-
60 seconds
-help diagnosis only if patient seen during acute phase
Medical therapy
Prophylaxis
-medical treatment aimed at prevention of vertigo employ strategy of reduction in endolymph accumulation
-such protocols include
1. dietary modification
2. intermittent dehydration
3. diuretics
4. enhanced microcirculation of ear such as:
-adenosine triphosphate, isosorbide, histamine, and betahistine
5. reduction in immune reactivity with corticosteroid, immunoglobulin, and allergy therapy
6. stress reduction
Dietary modification and diuretics

-goal of salt restriction, diuretics, and hyperosmolar dehydration is to reduce endolymph volume by fluid
removal or reduced production
-vertigo is controlled in 60% and hearing loss is temporarily stabilized in 70% of patients receiving dietary
modification and diuretics
Vasodilators
-in belief that Ménière's disease is result of strial ischemia, vasodilating agents such as betahistine have
been used without any effect
-other agents utilized with same rationale include: papaverine analog eupavarine, nicotinic acid, adenosine
triphosphate, and dipyridamole
Symptomatic relief
Antivertiginous medications:
1. Antihistamines
2. Mild sedatives
3. Benzodiazepines
4. Antidepressants
5. Antinausea medications
-these are aimed at dampening severity of attack and primarily diminishing autonomic symptoms associated
with vertigo such as nausea and vomiting.
Surgical treatment
-reserved for those patients who have failed medical management and is estimated to be necessary in 10%
of individuals
-some patients will continue to experience motion intolerance and mild positional instability despite
effective surgical management, this is attributed to incomplete adaptation
1201
Hearing sparing procedures without damage to vestibular labyrinth
1. Endolymphatic sac decompression and its modifications

-reduction of endolymph volume via increased drainage or increased absorption
-complete control of vertigo is seen in 65% of patients and this diminishes to 50% or less with a
10 year follow-up
-hearing stabilization occurs in 55% of patients procedures
-efficacy of various endolymph drainage procedures has been seriously questioned
2. Labyrinthine fistula procedures:
a. Cody
b. round window shunt / cochleosacculotomy.
-aimed at providing a release of pressure from endolymphatic space to perilymphatic space in a
controlled fashion
-results disappointing and not consistent
-procedures are of historical interest
Procedures sparing Cochlea & destroying labyrinth
1. Vestibular neurectomy
a. Middle fossa approach
b. Suboccipital approach
-Both procedures require sectioning of vestibular nerve and sparing of facial and cochlear nerves
-do not interfere with progression of hearing loss which continues unabated
-both have similar results in controlling vertigo:
-approximately 95% will have complete symptomatic relief
2. Chemical vestibular ablation
-streptomycin and gentamicin, by virtue of their more selective vestibular toxicity, have been
instilled locally into middle ear as a treatment for unilateral Ménière's disease
-current protocols utilize injection of concentrated gentamicin into middle ear through a pressure
equalizing tube several times a day for two to four days
-effective in controlling vertigo in 90% of patients and produces inadvertent hearing loss in10 to
30%
-contraindications:
-infection
-only hearing ear
-contralateral dysfunction
Procedures destroying both labyrinth and cochlea
-Labyrinthectomy
-an effective treatment for vertigo in Ménière's patient when serviceable hearing is absent (pure-
tone average > 60 dB and discrimination < 50%)
-excellent results are reported using all aforementioned techniques, with resolution of symptoms
in greater than 90% of cases
Parenteral Streptomycin
-utilized only for bilateral Ménière's
-resultant ablation of peripheral vestibular function while leaving hearing largely unchanged
-low dose parenteral streptomycin is used to preserve some degree of vestibular function to
prevent oscillopsia and ataxia
1202
SECONDARY ENDOLYMPHATIC HYDROPS
Otologic syphilis
-early syphilis
-vestibular symptoms are less frequent
-vary from mild imbalance to symptoms of protracted vertigo with vegetative features lasting days
-late syphilis
-can present up to 50 years or more after exposure
-cochleovestibular symptoms indistinguishable from Ménière's disease
-early syphilis, disorder is due to treponemal meningoencephalitis affecting arachnoid space
-late syphilis disorder is due to gummatous involvement of otic capsule
Delayed endolymphatic hydrops

-characterized by attacks of vertigo identical to those of Ménière's disease in a patient who has had a
previous, profound loss of hearing in one or both ears
-diagnosis is based on a Ménière's-like pattern of presentation of vertigo and history of prior severe hearing
loss
-causes of initial hearing loss vary:
-head trauma (acoustic and physical), viral labyrinthitis (mumps, influenza), mastoiditis,
meningitis, diphtheria, measles, and early childhood deafness of unknown etiology are all reported
-dehydrating agents, such as Lasix, improve vestibular response of affected ear and form basis of lasix test
Cogan's syndrome
-characterized by interstitial keratitis and bilateral, rapidly progressive audiovestibular dysfunction
-autoimmune etiology
-progression to complete absence of vestibular function, manifested by ataxia and oscillopsia, is common
-hearing loss is bilateral and progressive, without spontaneous improvement and frequently becoming
profound
-treatment with high dose steroids
-if no improvement or progression, further immunosuppression with cyclophosphamide is
indicated
-Vogt-Koyanagi-Harada Syndrome
-similar to Cogan syndrome
-associated with granulomatous uveitis, depigmentation of hair and skin, aseptic meningitis, and
loss of eyelashes
Recurrent vestibulopathy
-individuals describe attacks of vertigo similar to those of Ménière's disease without audiologic symptoms
such as tinnitus, hearing loss, or a sensation of fullness in ear
-only 15% of recurrent vestibulopathy diagnoses will change over time to Ménière's disease because there
is addition of cochlear symptoms
-patients with this condition have better vestibular function on caloric testing than Ménière's and majority
(>80%) go on to resolution over several years
-cause is unknown and it occurs in younger people than Ménière's on average
-given good outcome of this disease recommendation for treatment is symptomatic control.
1203
VERTIGO LASTING SECONDS
BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)
-utricular degeneration liberate otoconia, which then float downward into inferior-most region of vestibule,
ampulla of posterior semicircular canal, once they deposit there, they alter specific gravity of cupola,
changing its response characteristics from a purely angular acceleration detector to one that is stimulated by
linear movements and gravity
-Hallpike position:
-nystagmus is torsional; top of eye beats toward undermost ear (geotropic) nystagmus
-nystagmus is counterclockwise, as viewed by observer, when head is hanging to right, and
clockwise in head-hanging-left position
-result of isolated stimulation of Posterior Semicircular Canal which results in activation of
ipsilateral superior oblique and inferior rectus muscles
-one of most common forms of vertigo, estimated at least as twice incidence of Ménière's
Diagnosis
History
-severe vertigo associated with change in head position
-symptoms on rising from a bending position, looking up to take an object off a shelf, tilting their heads
back to shave, or turning rapidly
-symptoms occur suddenly and last in order of seconds, but never in excess of a minute
-most common identifiable cause of BPPV is felt to be closed head injury
-other cited predisposing events include vestibular neuronitis, infections, and following stapedectomy
Physical findings
-clear-cut diagnosis of this disease entity is made by
(1) observing classic eye movements in association with Hallpike maneuver and
(2) a suggestive history
-nystagmus pattern that is pathognomonic of BPPV consists of following:
1. nystagmus is rotational and geotropic
2. there is a latency of onset (seconds)
3. duration of nystagmus is short (< 1 minute)
4. vertiginous symptoms are invariably associated
5. nystagmus disappears with repeated testing (fatigable)
6. nystagmus reverses its direction on return of head to upright position
Treatment
-majority of patients experience spontaneous resolution of BPPV within several months of onset
Medical treatment
1. Vestibular suppressants are ineffective.
2. Liberatory maneuvers
-Semont manoeuver
-Epley manoeuver
Surgical treatment
1. singular neurectomy
2. vestibular neurectomy
3. posterior semicircular canal occlusion
1204
VERTIGO LASTING DAYS TO WEEKS
Vestibular neuronitis
-typically presents with dramatic, sudden onset of vertigo and attendant vegetative symptoms, dizziness
lasts days, with gradual, definite improvement throughout course
-complete absence of auditory dysfunction or symptoms
-invariably follows a viral upper respiratory tract infection
-postural instability and motion instability with certain head movements is present for months subsequently
and in addition BPPV occurs subsequently in up to 15% of patients
-slow phase of nystagmus is toward affected side and hypofunction is observed on caloric responses
-treatment is supportive and symptomatic for vertigo and related vegetative symptoms
VERTIGO OF VARIABLE DURATION
INNER EAR FISTULA
-abnormal communication between perilymphatic space and middle ear or an intramembranous

communication between endolymphatic and perilymphatic spaces
-may vary from mild and inconsequential to severe and incapacitating
History
-considered as a possibility following trauma to inner ear
-mechanism of trauma can vary:
-barotrauma
-penetrating trauma
-surgical trauma such as stapedectomy, cholesteatoma surgery or trauma
-following physical exertion
-vestibular symptoms are variable and include episodic incapacitating vertigo, equivalent to a Ménière's
attack, positional vertigo, motion intolerance, or occasional disequilibrium
-disequilibrium following increases in CSF pressure such as nose blowing or lifting (so-called
Hennebert's phenomenon) has been noted, as has vertigo following exposure to loud noises (Tulio's
phenomenon)
Examination
-fistula test:
-positive pressure is introduced into suspect ear, either by rapid pressure on tragus, compressing
external canal, or via a pneumatic otoscope, while observing eyes
-positive fistula sign: conjugate contralateral slow deviation of eyes followed by three or four
ipsilaterally directed beats of nystagmus
-high false negative rate
-fiberoptic examination to middle ear through a myringotomy is currently investigational but holds promise
to select appropriate patients for surgical exploration
Treatment
-consist of following:
1. bed rest
2. head elevation
3. laxatives to reduce risk of increased intracranial pressure
4. monitoring of both hearing and vestibular function.
-if hearing loss worsens or vestibular symptoms persist, surgical exploration is warranted
-intraoperative identification of a fistula, reported in about 50% of individuals explored
1205
TRAUMA
Vertigo and ataxia are common sequelae of head trauma and may be caused by:
1. cervical trauma
2. central nervous system trauma
3. peripheral vestibular damage
Labyrinthine concussion
-often associated with hearing loss of variable degree, is result usually of blunt head trauma or barotrauma
-usually transient, with spontaneous resolution occurring over a matter of days to weeks
-hemorrhage in labyrinth may initiate a series of inflammatory steps that lead to fibrosis and ossification
with attendant audiovestibular dysfunction
Blast trauma
-includes such occurrences as open-handed slap to ear as well as actual explosions.
-tympanic membrane and ossicles can be injured but inner ear damage is most severe when conductive
mechanism is not damaged
-auditory loss most common in high frequencies and frequently recovers and vestibular damage is less
frequent
Penetrating trauma
-violation of labyrinth or 8th nerve by either fracture or stapes subluxation or direct injury results in
permanent and total audiovestibular dysfunction
-nystagmus beats in direction of healthy ear, and patient will fall and demonstrate past pointing in direction
of slow phase of nystagmus
-vertigo will gradually subside over ensuing days to weeks
Barotrauma
-during flying and especially during diving in deep water, visual and proprioceptive cues are less effective
-acute vestibular dysfunction leading to disequilibrium, disorientation, nausea, and vomiting can be
devastating in such a setting
Alternobaric trauma
-transient vestibular or auditory dysfunction believed to occur as a result of elevated and probably
asymmetric middle ear pressure
-a function of eustachian tube opening pressures
Atmospheric inner ear barotrauma

-barotraumatic injury is frequently permanent and occurs as a result of damage to inner ear
-hearing loss and tinnitus are universal complaints, whereas vertigo tends to be less common
-most commonly experienced by divers: both in free diving and scuba diving.
-two prevailing theories:
1. Implosive theory: force transmitted into footplate or round window
2. Explosive theory: force from CSF transmitted into inner ear and out of footplate or round window.
Treatment:
1. Conservative:
-Bed rest, head elevation, and close monitoring of hearing- and balance-related symptoms are
suggested.
2. Surgical:
-Tympanotomy and middle ear exploration are reserved for those cases with progressive hearing
1206
loss or failure of resolution of vestibular symptoms in 3 to 5 days
3. Individuals suspected of having sustained IEBT and have complete recovery should be advised to
refrain from diving for at least 3 months
4. In all instances, patient should be counseled to perform gentle Valsalva maneuvers at frequent intervals
during descent and to abort dive if middle ear pressure equilibration cannot be achieved easily.
1207
Dr. F. Ling's
Temporal Bone Dissection

LATERAL APPROACH
 1. Koerner's septum
 1. Temporal line
 2. M astoid air cells
 2. M astoid cortex
 3. External auditory canal skin
 4. Emissary veins
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 1. M astoid antrum  1. Sigmoid sinus

 2. Horizontal semicircular canal  2. Digastric ridge and posterior belly of digastric muscle
 3. Facial nerve (skeletonized mastoid segment)
 4. Chorda tympani
 5. Facial recess
 triangle bound by: chorda tympani, facial nerve and incus
buttress
 6. Round window
 opens into cochear scala tympani
 7. Pyramidal eminence containing stapedius muscle
 8. I ncus buttress
 9. I ncus body
 10. Horizontal semicircular canal
 11. Posterior semicircular canal
 12. Superior semicircular canal
1209
 1. Sigmoid sinus
 1. Jugular bulb
 2. Tegmen tympani
 2. Facial nerve (mastoid segment)
 3. Endolymphatic sac
 3. Subarcuate artery
 in dura of posterior fossa between posterior SCC and sigmoid
 4. Posterior semicircular canal (ampullated end)
sinus
 5. Superior semicircular canal (ampullated end)
 enters temporal bone at operculum which lies posterioinferiorly
 6. Horizontal semicircular canal (ampullated end)
from IAC
 7. Facial nerve (tympanic segment)
 lies at or below a line projected from axis of horizontal SCC
 8. Incus
(Donaldson's line)
 9. Malleus
 4. Epitympanum
Cog area (not shown)
 small bony bar anterior and superior to cochleariform process which

separates anterior epitympanum from rest of the attic
 geniculate ganglion lies deep and medial to this
1210

 3. Chorda tympani
 3. Geniculate ganglion
 4. Eustachian tube
 4. Facial nerve (labyrinthine segment)
 5. Jacobson's nerve (CN IX)
 5. Greater superficial petrosal nerve
 6. Promontory of cochlea
 6. Cochleariform process
 7. Vestibule
 7. Tendon of tensor tympani
 elliptical recess of utricle
 8. Superior vestibular nerve
 spherical recess of saccule
 9. I nferior vestibular nerve
 8. Sinodural angle
1211
 1. I nternal carotid artery  1. Cochlea

 2. Round window  scala vestibuli ("superior" to basilar membrane in
 3. Oval window cochleostomy)
 4. Jacobson's nerve and cochlear promontory  scala tympani ("inferior" to basilar membrane in
cochleostomy)
Sinus tympani is an area that cholesteatoma can hide to which access is  2. Tensor tympani muscle (cut)
difficult. It is bounded by:  3. Cochlear nerve to modiolus
 4. Facial nerve (meatal segment)
 pyramidal eminence (medial surface)  5. Facial nerve (labyrinthine segment)
 ponticulum (bony ridge between oval window niche and sinus  6. GSPN
tympani)  7. Facial nerve (tympanic segment)
 subiculum (bony ridge between round window niche and sinus  8. Facial nerve (mastoid segment)
tympani)  9. Vestibular nerve
1212
Dr. F. Ling's
Temporal Bone Dissection

M I DDLE FOSSA APPROACH
 1. Middle fossa floor  1. TM J in glenoid fossa

 2. M iddle meningeal artery  2. M alleus(head)
 leads to foramen spinosum which is the most anterior landmark for
 note tendon of tensor tympani from cochleariform process which
orientation in middle fossa approach attaches to neck of malleus
 3. Greater superficial petrosal nerve in facial hiatus  3. I ncus (body)
 lies 1 cm medial to foramen spinosum
 4. I nternal carotid artery
 axis of nerve runs medial to petrous pyramid
 5. GSPN
 4. Arcuate eminence  6. Cochlea (bluelined)
 landmark for superior semicircular canal (not for IAC)
 petrous apex air cells lie just anterior
 absent in 15%
 7. Geniculate ganglion
 5. Superior petrosal sinus  may be dehiscent in 25% of specimens
 8. Tensor tympani muscle
Finding I AC  Eustachian tube lies just lateral to muscle
 9. Facial nerve (labyrinthine segment)
 longitudinal axis of superior SCC forms a 60 degree angle with longitudinal  note falciform (transverse) crest below
axis of IAC anteriorly  10. Facial nerve (meatal segment)
 if no landmarks, then open attic 1.5 cm behind foramen spinosum and just  note cochlear nerve below
medial to junction of squamous and petrosal bone. Expose ossicles,
 11. Superior vestibular nerve
cochelariform process, and facial canal wich is followed to IAC.
 innervates superior and horizontal SCC and utricle
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 inferior vestibular nerve (not shown)

 lies below SVN
 singular nerve innervates posterior SCC
 ampullary nerve innervates saccule
 13. Bill's bar (vertical crest)
 14. Superior (anterior) semicircular canal
 15. Posterior semicircular canal
 16. Horizontal (lateral) semicircular canal
 17. Vestibule
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Temporal Bone Anatomy
1215
a. Anterior crus of
superior
semicircular
canal
b. Posterior crus of
superior
semicircular
canal
c. Mastoid air cells
d. Koerner’s
septum
e. Posterior margin
of temporal bone
or cerebellar
plate
1216
a. Anterior crus of
anterior
semicircular
canal
b. Crus communis
c. Posterior
semicircular
canal
d. Mastoid air cells
and cerebellar
plate
1217
a. Sigmoid sinus
b. Vestibular
aqueduct
c. Posterior
semicircular
canal
d. Anterior
semicircular
canal
e. Lateral
semicircular
canal
f. Internal auditory
meatus
1218
a. Internal auditory
meatus
b. Vesibule
c. Endolymphatic
sac
d. Vestibular
aqueduct
e. Posterior
semicircular
canal
f. Sigmoid sinus
g. Petrous apex
h. Lateral
semicircular
canal
i. Malleus head;
body an short
process of incus
1219
canal
b. Facial nerve
(labyrinthine
segment)
c. Geniculate
ganglion
d. Facial nerve
(tympanic
segment)
e. Malleus
f. Incus
1220
a. Basal turn of the
cochlea
b. Geniculate
ganglion
c. Facial nerve
(tympanic
segment)
d. Malleus
e. Internal auditory
meatus
f. Vestibule
1221
a. Pyramidal
eminence
b. External auditory
canal
c. Round window
niche
d. Tensor tympani
e. Tympanic
membrane
1222
a. Jugular bulb
b. Internal carotid
artery
c. Eustachian tube
d. Tensor tympani
1223
a. Glenoid fossa,
temporo-
mandibular joint
b. Internal carotid
artery
c. Jugular bulb
d. Sphenoid sinus
1224
a. Supra-
labyrinthine cells
b. Cochlea
c. Malleus head
d. Tegmen tympani
e. Mastoid air cells
f. Carotid artery
1225
a. Internal carotid
artery
b. Cochlea
c. Facial nerve
(labyrinthine
segment)
d. Facial nerve
(tympanic
segment)
e. Middle ear
(hypotympanum)
1226
canal
b. Tensor tympani
c. Facial nerve
(tympanic
segment)
1227
a. Facial nerve
(tympanic
segment)
b. Lateral
semicircular
canal
c. Scutum
d. Ossicles
e. Superior
semicircular
canal
1228
a. Posterior
semicircular
canal
b. Tegmen tympani
c. Vestibular
aqueduct
1229
Vestibulo-Ocular Reflex (VOR)
-head turns to left

-left horizontal SCC:
-fluid flows toward ampulla (ampulopetal flow)
-relative stimulation
-right horizontal SCC:
-fluid flows away from ampulla (ampullofugal
flow)
-relative inhibition
-eyes move toward side of inhibition (right)
Caloric Testing
-cool water endolymphatic fluid drops

-causes ampullofugal flow in SCC
-relative inhibition on involved side
-causes slow drift of eyes towards involved side
-compensatory saccades in the opposite direction
(“cold-opposite”)
-warm water endolymphatic fluid rises

-causes ampullopetal flow in SCC
-relative excitation on involved side
-causes slow drift of eyes towards opposite side
-compensatory saccades in the same direction as
stimulus (“warm-same”)
1230
LOCAL SKIN FLAPS:
ANATOMY, PHYSIOLOGY AND GENERAL TYPES
LOCAL FLAPS
-advantages:
-use of local tissue with better donor site match
-one stage in most instances
-low donor site morbidity
-disadvantages:
-random pattern blood supply with limited length
-distortion of surrounding structures
-not enough bulk for deep defects
VASCULAR ANATOMY
-three main types of flaps:

-local or random-pattern flaps
-axial-pattern flaps
-musculocutaneous flaps
-hierarchy:
-subdermal plexus
-basis for random-
pattern flaps
-direct cutaneous arteries
-run on top of muscles
and send branches to
skin
-basis for axial-pattern
flaps
-segmental blood vessels
-large named branches
of aorta that run
below muscle masses
-form basis for
musculocutaneous
flaps
-perforating branches
-pass through
overlying muscles
-supplies muscles and overlying subcutaneous tissue and skin
-most common vessel supplying local facial skin flaps
-angiosome: overlying portion of skin supplied by a single perforating vessel
-adjacent angiosomes interconnected by small choke vessels in subdermis
F.Ling - Local Skin Flaps (1)
1231
Random-Pattern Flaps
-rely on flow through dermal and subermal plexus
-limits length and width
-causes of skin flap failure:
-extrinsic: -wound infection
-systemic hypotension
-excessive tension
-haematoma
-intrinsic: -excessive flap length and random pattern blood supply
-pharmacologic vasoconstriction
-smoking
-peripheral vascular disease
Axial-Pattern Flaps
AXIAL-PATTERN FLAPS
-rely on blood from named direct cutaneous
arteries and veins that course along Nasolabial Flap -angular artery
longitudinal axis of flap Forehead flap -supratrochlear artery
Lateral forehead flap -superficial temporal artery
-blood supply considered secure for at least
Deltapectoral flap -perforating vessels of internal mammary
length of these vessels artery
Musculocutaneous Flaps
-designed around segmental artery and vein
-raised as a unit (skin, subcutaneous tissue, muscle and segmental vessels)
-eg. pectoralis major, trapezius, latisimus dorsi flaps
PHYSIOLOGIC CHARACTERISTICS OF LOCAL FLAPS
-random-pattern blood supply refers to interconnecting anastomoses within dermis and subdermal plexus
-arterial resistance is the primary determinant of the rate of
cutaneous blood flow
-changes in venous capacitance determine total amount of blood in
skin at any one moment
-arteriovenous shunts are ubiquitous precapillary communications
between arterial and venous circulations
-allow blood to bypass capillary bed and thus function as
regulators of blood flow
-shunts innervated by sympathetic nervous system
-increased sympathetic tone shunts narrow provide less
blood to the skin
-speculated that with complete opening (from sympathetic
denervation), blood shunted away from capillary bed and
compromises viability of distal end of flap
Length to Width Ratio

-rough guideline; cannot be relied on as an absolute determinant of
flap success
-surviving length of flap determined by perfusion pressure of feeding vessels and intravascular resistance
-increasing width of base simply adds vessels, all with same perfusion pressure facing similar resistance
surviving length of flap does not increase
1232
Delay Phenomenon
-skin flaps that are partially incised and undermined but not transposed survive to a greater length when
raised at a later date
-most likely d/t closure of arteriovenous shunts, increase in vessel caliber, increased vessel numbers with
reorientation along flap axis and conditioning of distal flap to tolerate ischemia
-delays of 10-21 days most common
-beneficial effect is lost after 3 weeks to 3 months
-random-pattern flaps:
-parallel incision along sides of flap, leaving ends connected
-flap undermined to disrupt perforating vessels
-end of flap incised at time of transfer
-axial-pattern flap:
-incising proposed margins of flap sufficient; undermining not needed
SKIN BIOMECHANICS
-elasticity of skin determined by collagen and elastin content

-tension on flap can impair viability
-skin creep:
-phenomenon whereby a flap placed under sudden constant tension for 5-15 mins has additional
increase in length beyond original stretch
-stress relaxation:
-skin adapting to increased stretch by increasing volume
-principle that allows tissue expansion or serial excision of lesions
-relaxed skin tension lines (RSTL):
-indicates most favourable orientation of defects or incisions to obtain maximum skin mobilization
with least tension for closure
-ensure least tension on wound to prevent scar widening
SKIN FLAP FAILURE
-most common cause is vascular insufficiency d/t excessive flap length with a random blood supply or
excessive tension
-vasoconstriction: nicotine, epinephrine, dopamine
-haematoma under flap:
-increases wound tension and pressure on feeding vessels
-haematoma breakdown products contributes to flap necrosis
-diabetes, hypertension, infection and compression of flap pedicle also affect viability
TYPES OF LOCAL SKIN FLAPS
True Rotation Flaps

-semicircular and rotates in an arc; dog-ear at base excised
-advantages:
-allows closure of large lesion by recruiting lax skin over a greater distance
-disadvantages:
-requires a wider base than the advancement flap
-requires extensive undermining and long peripheral incision (4-5x diameter of the defect)
-common uses: cheek, triangular defects
1233
Transposition Flaps
-eg. rhomboid, bilobed, nasolabial flaps, Z-plasty, Dufourmental
Rhomboid Flaps
-for each rhomboid defect, four possible flap orientations can be used for closure
-advantage is that main area of tension is across closure of donor site and spares any compromise of the
flap tip
Dufourmental Flaps
-variant of rhomboid flap
-used for defects that do not correspond to classic 60- to 120-degree dimensions
-imaginary lines extended from diameter of defect and one of the sides of the defect
-angle made by these lines is bisected by a line the same length as a side of the defect
-back cut made that runs parallel to long axis of defect and same length as one side of defect
1234
Bilobed Flaps
-uses skin laxity to distribute tension
over two flaps
-first flap designed to be as long as
defect, somewhat narrower and angled
at ~45o
-second flap is smaller than first and
again angled at ~90o
-work best on nose where tissue can be
borrowed from perinasal area
-advantages:
-distributes tension evenly
-disadvantages:
-risk of pin cushioning
-lengthy incision that rarely
exploits ideal RSTLs
-common uses:
-nasal tip/dorsum, lateral cheek
Interpolated flap
-donor site is separated from recipient site and pedicle must pass over or under intervening tissue to reach
recipient site
Advancement Flaps
-monopedicled:
-usually rectangular and are moved forward into a defect from one side
-bipedicled:
-advanced from both sides of defect
-useful in lips and forehead
-V-Y advancement flaps
-preserve underlying subcutaneous circulation and preventing pincushioning edema by means of
providing adequate venous and lymphatic drainage
-common uses:
-forehead, lateral lip, eyelid
REGIONAL PEDICLED FLAPS
Regional Cutaneous Flaps

-deltopectoral
-advantage:
-strong blood supply
-large amount of donor tissue available
-tunnel forms a favorable fistula
-disadvantage:
-requires second stage procedure for detachment (6-8 weeks)
-requires skin graft at donor site
-arterial supply:
-first 4 perforating vessels of internal mammary artery (second vessel is the largest)
-common uses: similar to pectoralis major flaps
1235
-midline forehead
-temporal
Regional Myocutaneous Flaps

-pectoralis major:
-advantage
-reliable (“the workhorse”)
-excellent reach (up to lateral canthus
-one stage procedure
-potential for simultaneous harvesting
-easy to harvest
-disadvantage:
-may be bulky
-potential for breast deformity in women
-potential hair transfer
-loss of pectoralis function
-arterial supply:
-pectoral branch of thoracoacromial artery
-common uses:
-internal and external defects of oral cavity, oropharynx, hypopharynx
-relatively contraindicated with ipsilateral radical mastectomies
-double paddle may be created by using lateral thoracic artery
-latissimus dorsi:
-advantage:
-large amount of available skin and soft tissue
-long vascular pedicle with extended arc of rotation (to vertex of scalp)
-less hair transfer
-potential for bilobed skin islands
-out of irradiated field
-disadvantage:
-requires repositioning
-propensity for seroma formation at donor site
-may be bulky in large patients
-requires extended tunnelling between pectoralis major/minor
-arterial supply: thoracodorsal artery
-common uses:
-similar to pectoralis major flaps
-trapezius:
-advantage:
-3 forms allows for versatility
-relatively flat and thin flap
-one-stage procedure
-disadvantage:
-relatively limited arc of rotation
-significant donor site morbidity (weakness of upper extremities, may require skin graft
for closure)
-weaker blood supply
-awkward positioning
-common uses:
-oropharyngeal and hypopharyngeal defects, lateral neck, posterior face
1236
-Flap Designs:
-superiorly based (upper) flap:
-vascular supply from occipital artery and paraspinal perforators
-reliable flap
-limited arc or rotation
-donor site may require a skin graft
-lateral island trapezius flap:
-vascular supply from superficial branches of transverse cervical artery
-may cover defects of the oropharynx, posterior oral cavity, and hypopharynx
-inferior (lower) flap:
-vascular supply from descending branches of transverse cervical artery and
dorsal scapular artery
-provides a long pedicle
-most commonly used trapezius flap
-sternocleidomastoid:
-advantage: donor site located close to defect
-disadvantage:
-tenuous blood supply to skin (not a true axial flap)
-rotation limited by accessory nerve
-arterial supply: occipital artery, superior thyroid artery, transverse cervical artery
-common uses:
-small defects in anterior lateral oral cavity and lateral oropharynx
1237
MICROVASCULAR FREE FLAPS
IN HEAD AND NECK RECONSTRUCTION
INTRODUCTION
Advantage:
-single-stage procedure, excellent perfusion, ability to preselect tissue characteristics of donor
tissue for given recipient site defect
-potential two-team approach
-possible functional restoration (sensation/motor)
-improved ability for spatial positioning of donor tissue
Disadvantage:
-requires microsurgical expertise and specialized instrumentation
-may require longer operating time
-possible colour and texture mismatch
-5-15% failure, most occur in first 24-72 hours; salvage rate on re-exploration ~50%
-neovascularization complete after 8 days
-vascularized muscle reduces to ~20% of tis mass, vascularized fat reduces to 40-60% of its mass
-may monitor flap clinically by examining colour, turgor, capillary refill, temperature, and quality of
dermal-mucosal bleeding
-revisions should be completed as possible to avoid no-reflow phenomenon, survival time may be extended
with free radical scavengers
-critical time of warm ischemia:
-jejunal flaps ~ 2 hours
-skeletal flaps ~ 6 hours
-cutaneous flaps ~ 8 hours
MICROVASCULAR FREE FLAP SELECTION

Flap Quality Advantages Disadvantages
Radial Forearm thin, pliable versatility, ease limited bulk, skin graft donor site
Lateral arm moderately thin primary closure of donor site small-caliber pedicle
Lateral thigh moderately thick large surface area of tissue, long pedicle challenging harvest
Temporoparietal fascia ultrathin can be transferred as pedicle flap challenging harvest, limited pedicle length
Rectus bulky versatility, ease of harvest risk of ventral hernia
Latissimus dorsi moderate bulk large surface area, ease of harvest lateral decubitus positioning
Gracilis thin muscle can be separated into functional units limited tissue available
FASCIAL AND FASCIOCUTANEOUS FLAPS
Radial Forearm Flap
Description
-skin of entire forearm, from antecubital fossa to flexor crease can be harvested
-most often used in reconstruction of oral cavity and base of tongue, partial and circumferential
reconstruction of pharynx, reconstruction of soft palate
-can be transferred as osteocutaneous flap with a segment of radius 10-12 cm long
F.Ling - Microvascular Free Flaps (1)
1238
-disadvantage is limited amount of bone
available and risk of pathologic fracture of
radius
Neurovascular Pedicle
-based on radial artery and its venae comitantes or
cephalic vein
-lateral antebrachial cutaneous nerve is primary
sensory nerve
Anatomic Variations
-greatest concern is integrity of ulnar arterial supply
to hand through palmar arches
-incomplete palmar arch puts vascular supply of
thumb and index finger in jeopardy
-detect with Allen test
Potential Morbidity
-vascular compromise to hand
-radius fracture for osteocutaneous flaps
-cosmesis of site
Lateral Arm Flap
Description
-moderately thin fasciocutaneous flap that
can be reinnervated for cutaneous
sensation with posterior cutaneous nerve
of arm
-donor side usually can be closed
primarily when width of harvested skin
limited to 6-8 cm
-based on terminal branch of profunda
brachii artery and posterior radial
collateral artery and its venae comitantes
-maximum pedicle length of 8-10 cm
-posterior cutaneous nerve of the
forearm used as vascularized nerve graft
Potential Morbidity
-radial nerve which lies in spiral groove of
humerus identified and protected
-injury leads to wrist drop
Technical Considerations
-lateral intermuscular septum 1 cm posterior to line drawn from insertion of deltoid and lateral epicondyle
-central axis of flap is based on intermuscular septum
1239
Lateral Thigh Flap
Description
-provides large surface area with expendable tissue
-flaps as large as 25x14 cm harvested
-most useful for intraoral and pharyngeal
reconstruction
Neurvascular bundle
-based on third perforator of profunda femoris
system
-pedicle length 8-12 cm
-lateral femoral cutaneous nerve of thigh for
reinnervation
Anatomic Variations
-terminal cutaneous branch of second or fourth
perforator of profunda femoris may provide
dominant arterial pedicle to skin
Potential Morbidity
-atherosclerosis of arteries
-proximity and vulnerability of sciatic nerve after adductor muscles are detached from linea aspera
Temporoparietal Fascial Flap
Description
-most commonly transferred as pedicled flap, but
can be used as free flap when arc of rotation is
inadequate
-ultrathin, highly vascular, pliable, and durable
-can be harvested with dimensions of 17x14 cm
-used for reconstruction of oral cavity, middle and
upper regions face, hemilaryngectomy defects
-temporoparietal fascia deep to skin and
subcutaneous tissue and superficial to temporalis
muscle fascia
-superficial temporal artery and vein located 3
cm superior to root of helix where vessels branch
into frontal and parietal division
Potential Morbidity
-injury to frontal branch of facial nerve
-secondary alopecia from dissection too superficial
Preoperative Considerations
-preoperative XRT, neck surgery, previous bicoronal incision, external carotid embolization
1240
MUSCLE AND MUSCULOCUTANEOUS FLAPS
Rectus Abdominis Flap
Description
-easy to harvest, long vascular pedicle and extremely
reliable
-used to reconstruct high-volume defects such as total
glossectomy defects, skull base defects and large
cutaneous defects
-disadvantages: poor colour match to facial skin and
tendency to become ptotic
-based on deep inferior epigastric system
-larger caliber vessels cf superior system
-musculocutaneous perforators are direct
branches and can supply much larger territory
of skin
-neurosensory supply: lower six intercostal nerves
Potential Morbidity
-can weaken anterior abdominal wall and predispose pt
to ventral herniation
-below arcuate line, anterior sheath must be
reapproximated to prevent herniation
-ileus can occur
Latissimus Dorsi Flap
Description
-used either as free or pedicled flap
-when transferred as muscle alone, muscle atrophies to
thickness of ~4 mm
-ideal for scalp reconstruction but poor for large
neck defects
-large volume defects require transfer as
musculocutaneous flap
-thoracodorsal artery and vein from subscapular vessels
-average length of pedicle is 9.3 cm (range 6 to 16.5 cm)
-thoracodorsal nerve provides motor innervation
Potential Morbidity
-if flap is pedicled, then risk of kinking and occlusion of
vessels flap necrosis
Technical Considerations
-pt positioned on bean bag in semi-decubitus position
-previous axillary lymph node dissection a relative
contraindication to use of flap
1241
Gracilis Flap
Description
-thin muscle flap from medial thigh
-primary use in head and neck has been facial
reanimation
-advantages of flap for facial reanimation are its
neuromuscular structure, long vascular pedicle and ease
of dissection
-terminal branch of adductor artery arising from
profunda femoris artery
-point of entrance of vascular pedicle into muscle is
consistently between 8 and 10 cm inferior to pubic
tubercle
-motor supply is anterior branch of obturator nerve
COMPOSITE FREE FLAPS
Fibular Osteocutaneous Flap
Description
-used for long-bone replacement after trauma or
cancer
-provides longest possible segment of
revascularized bone (25 cm)
-used for reconstruction of almost any mandibular
defect
-peroneal artery and vein provide primary blood
supply
-preoperative angiography or MRA are
recommended to ensure adequate arterial supply to
foot when peroneal artery is sacrificed
-peroneal communicated branch can be
harvested as vascularized nerve graft
Potential Morbidity
-in 5-10% of cases, blood supply to skin paddle is
inadequate
-functional deficits include weakness in
dorsiflexion of great toe
1242
Iliac Crest (Osteocutaneous and Osteomusculocutaneous) Flaps
Description
-used for reconstruction of segmental
mandibular defects
-up to 16 cm of bone can be harvested
-deep circumflex iliac artery and
vein which aries from lateral aspect of
external iliac artery
Potential Morbidity
-herniation of abdominal wall
Scapular and Parascapular (Fasciocutaneous

and Osteofasciocutaneous) Flaps
Description
-long length and caliber of vascular pedicle;
abundant surface area of relatively thin skin;
separation of soft tissue and bone flaps; ability
to combine scapular flap with latissimus dorsi
and serratus anterior muscles
-10 cm of bone can be reliably transferred;
adequate for placement of osseointegrated
implants
-based on circumflex scapular artery
-horizontally oriented scapular flap
based on transverse cutaneous
branch
-vertically oriented parascapular flap
based on descending cutaneous
branch
-pedicle length:
-7-10 cm when circumflex scapular
artery harvested at its takeoff from
subscapular vessels
-11-14 cm if subscapular vessels
transected at their junction with axillary artery and vein
Potential Morbidity
-injury to joint space (glenoid)
-harvest of scapular osteocutaneous flap requires detachment of teres major and minor muscles shoulder
weakness and limited ROM
-previous axillary node dissection is a contraindication to use of these flaps
1243
VISCERAL FLAPS
Jejunum
Description
-used in reconstructing circumferential pharyngoesophageal defects
-mesenteric vessels
Potential Morbidity
-most susceptible to primary ischemia
-stricture of upper or lower anastomosis in ~10% (lower than tubed cutaneous flaps)
Other Considerations
-extension of disease into proximal thoracic esophagus is an absolute indication for esophagectomy and
gastric pull-up
-external monitoring segment of jejunum is removed at beside on POD#7 by means of suture ligation of its
mesentery
Omentum and Gastroomentum
Flap Description
-used to cover large scalp defects, repair extensive midfacial defects, management of osteoradionecrosis
and osteomyelitis, facial contouring
-gastroomental free flap used for oral or pharyngeal defects; omentum used to provide carotid coverage
-right gastroepiploic artery
Potential Morbidity
-intraabdominal complications:
-gastric leak with peritonitis and intraabdominal abscess formation
-gastric outlet obstruction
-history of gastric outlet obstruction or peptic ulcer disease is a contraindication to this procedure
MICROVASCULAR RECONSTRUCTIVE APPROACHES TO DEFECTS IN THE HEAD AND NECK
Pharyngoesophageal Defects
-classified according to circumferential involvement (partial, near total and total)
-mechanism of postop voice production and use of postop radiation therapy also considered
-partial defects (50% of pharynx) and near-total (1 cm strip remains):
-primary closure cannot be performed without high risk of pharyngeal stenosis
-reconstructed with pedicled regional flaps or free tissue transfer
-if carotid protection believed beneficial, a pedicled regional flap can be used to protect vessel
-total defects:
-complete defect
-free tissue transfer has greatest effect
-three types of reconstructions commonly used:
-gastric transposition
-for tumour extension below cricopharyngeus into cervical esophagus
1244
transposition for technical and oncologic reasons (possibility of skip lesions in
proximal esophagus)
-not optimal for long oropharyngeal extensions because it can put tension on
mucosal closure
-free jejunal transfer
-large free fasciocutaneous transfers (RFFF, lateral thigh)
-provide better voice, less dysphagia and less donor-site morbidity than does
jejunum
Oral Cavity and Oropharyngeal Defects

-radial forearm flap has become the workhorse of soft-tissue oral cavity reconstruction
-when functional results are likely to be compromised by use of soft-tissue component of an osseous flap,
two flaps can be used
-in total glossectomy defects, muscle of a rectus or latisimus flap is used to reconstruct floor of mouth
-complex full-thickness defects can be closed with osteomusculocutaneous iliac crest flap, multipaddled
osteocutaneous scapula or a partially deepithelialized osteocutaneous fibular flap
Midfacial Defects
-free flaps used to in reconstructing maxilla to maintain midfacial projection in premaxillary, zygomatic
and infraorbital regions
-restore contour and projection of midface
-facilitate rehabilitation of an occlusal surface in upper jaw for mastication
-provide oronasal separation
-close orbit or provide platform for prosthetic rehabilitation of the eye
-to maintain functioning lacrimal system if globe is intact
-infrastructure defects (oral palate)
-combined infrastructure and suprastructure defects:
-maxillectomy with intact orbital rim
-effectively reconstructed with an obturator
-maxillectomy including infraorbital rim
-best reconstructed with free tissue transfer, either alone or in concert with prosthesis
-eg. osseocutaneous forearm flap for infraorbital rim reconstruction
-eg. iliac crest, fibular or scapular flap with osseointegrated implants
-maxillectomy including infraorbital rim and orbital contents
-additional tissue volume required for the orbit
-osseocutaneous scapular flap alone or osseocutaneous radial forearm flap in
combination with maxillary prosthesis used
-composite defects
-any of the other defects combined with facial skin
-osseocutaneous scapular flap has been most useful
-adequate bone stock to recontour most maxillary defects
Defects of Base of Skull

-bone defects associated with skull-base defects frequently reconstructed with split calvarial bone or
hydroxyapatite compounds
-principles of skull base reconstruction:
-support dural closure
-provide carotid coverage
-obliterate dead space
-support nonvascularized bone reconstruction
-restore calvarial and facial contour
-anterior defects that include orbit and maxilla are best reconstructed with a large-volume flap such as
1245
osseocutaneous scapular flap or a rectus flap
-lateral defects best reconstructed with scapular flap or lateral arm flap
SUMMARY
Flap Quality Sens. Via NV Supply Pedicle OI Disadvantage

b. /Bone imp.
Length
Radial -thin, pliable -yes 3+ -radial artery 10-12 -no -only 40% of radial bone may be
Forearm -lateral antecubital cm transferred
cutaneous nerve bone -donor site requires skin graft
Lateral Arm -moderately -yes 3+ -profunda brachii 8-10 -no -difficult to close primarily if > 6 cm
thin -posterior cutaneous cm -unattractive scar at donor site
nerve of arm -difficult to position for two-team
approach
Scapula -moderate bulk -no 2+ -circumflex scapular 10 cm -yes -requires detachment of shoulder girdle
-thin skin artery bone muscles
(transverse cutaneous -7-10 -requires lateral decubitus positioning
branch; descending cm or -smaller volume bone stock for
cutaneous branch) 11-14 endosseous implants
cm
pedicle
Fibula -moderate bulk -yes 1+ -peroneal artery 25 cm -yes -variable and tenuous blood supply to
-lateral cutaneous bone skin paddle
branch of peroneal -skin graft may be requires at donor
nerve site for osseocutaneous harvest
Iliac Crest -bulky -no 2+ -deep circumflex iliac 16 cm -yes -risk of inguinal hernia
artery bone -poor colour match to face
-temporary hip weakness with
paraesthesia
Rectus -bulky -yes 3+ -inferior epigastric -no -risk of ventral hernia

Abdominus artery
-last 6 intercostal
nerves
Latissimus -moderate bulk -no 3+ -thoracodorsal artery 6-16.5 -no -poor colour match
Dorsi -thoracodorsal nerve cm -potential shoulder disability
(maintains bulk) -awkward position for two-team
approach
Lateral -moderately -yes 3+ -third perforator of 8-12 -no -more difficult to harvest
Thigh thick profunda femoris cm -atherosclerosis of arteries
-large flaps -lateral femoral
(25x14 cm) cutaneous nerve
1246
MANDIBULAR RECONSTRUCTION
Anatomy of the Defect
Bony Defect
-a lateral (mandibular body) defect often causes minimal cosmetic and functional deformities
-some pts compensate well for malocclusion, making reconstruction unnecessary
-when mandibular symphysis is missing, severe functional and cosmetic deficits necessitate mandibular
reconstruction
-ramus defects - three scenarios:
a) proximal segment of condyle, coronoid process, and ramus superior to lingula
-allows superomedial proximal segment displacement by means of unopposed temporalis
and pterygoid muscle pull
-coronoidectomy aids proximal segment relocation and helps to obtain a better
neomandibular range of motion
b) complete disarticulation
-alloplastic joint replacement system can be used
-use of autogenous bone or costochondral graft for condylar reconstruction
c) oblique subcondylar osteotomy
-preserves condyle and posterior border of ascending ramus
-“Andy Gump” deformity: resection of anterior mandibular arch; difficult to reconstruct
Soft-tissue Defects
-pts who need additional soft tissue benefit from pedicled or free skin and muscle transplantation
-conventional mandibular reconstruction of irradiated tissue beds has low success rate (20-60%) and a high
complication rate (20-65%)
-Hyperbaric Oxygen therapy can improve quality of recipient bed
-improves radiation-related hypocellularity, hypovascularity, and hypoxia
-after 20 HBO tx (100% oxygen at 2.5 atm for 90 min), there is a greater cellular matrix of viable
fibroblasts and neoangiogenesis
-transcutaneous oxygen tension measurements after HBO therapy increased 150%
-vascular density plateaued at 80-85% for normal non-irradiated tissues after 18-22 HBO
treatments
-response of irradiated tissue to HBO has three phases:
-phase I:
-lag phase
-during first 8 treatments
-little change in tissue oxygen tension (30-50%)
-increased collagen synthesis and capillary budding
-phase II:
-rapid response phase
-18th to 22nd treatments
-oxygen tension increases logarithmically to plateau at ~82%
-neoangiogenesis with multiple capillaries in previously hypovascular tissue
-heightened fibroplasias evident
-phase III:
-plateau phase
-oxygen tension plateaus at 85% of the value for nonirradiated tissue
-correction of tissue hypoxia reduces stimulus to angiogenesis and further
treatments do not affect tissue oxygenation
F.Ling - Mandibular Reconstruction (1)
1247
-HBO enhances perfusion and allows healing and supports transplantation of nonvascularized bone
-success rate of HBO therapy for secondary mandibular reconstruction among pts who have
undergone radiation therapy is ~92%
-additional HBO is not needed even if there is a long delay between completion of HBO therapy
and surgery
MATERIALS
Alloplast
-implants include pins, trays and plates
-used as spacers or for internal fixation of bone grafts
-obviate prolonged maxillomandibular fixation
-metal mesh trays and retention screws can be used as spacers with autogenous corticocancellous bone
chips
-main disadvantage is difficulty of augmenting the neoalveolar ridge for dental implantation
without removing the tray
-bone plates and screws are alloplastic materials most widely used in mandibular reconstruction
Bone Grafts
-osteogenesis (Axhausen):
-initial bone formation in a transplant arises form cells that survive transplantation and proliferate
to form new osteoid
-phase I:
-starts after grafting and continues for 4 weeks
-determines the final size of bone graft, because phase II replaces phase I bone rather
than producing new bone
-phase II:
-pluripotential host cells are transformed into osteoblastic cells
-these cells remodel phase I bone and organize the graft
-host fibroblast are induced to grow into graft mediated by bone morphogenic protein
(BMP)
-influences genetic transformation of host pluripotential cells along osteoblastic
lines involved in synthesis of type I collagen and hydroxyapatite salts needed for
formation of bone matrix
-begins 2 weeks after start of osteogenesis, peaks at 6 weeks and wanes until 6 months
-four types of autogenous free bone graft material
-corticocancellous blocks
-cancellous bone
-cortical bone
-particular bone combined with cancellous marrow (PBCM)
-corticocancellous blocks:
-late resorption of central graft causes fractures
-d/t diminished phase I bone formation and poor early revascularization because thick cortical
bone makes a physical barrier that separates cancellous graft bone from host tissue
-cancellous bone:
-provide sufficient phase I bone formation
-gives excellent clinical results in management of selected small defects if mandibular structural
integrity has not been compromised
-in larger defect, pure cancellous bone provides insufficient rigidity
1248
-PBCM:
-offers best osteogenic potential
-provides sufficient viable endosteal osteoblasts and mesenchymal cells to support both phases of
osteogenesis
-allows rapid revascularization
-disadvantage is lack of structural integrity, which necessitates use of a crib as carrier
-allogeneic cribs of mandible, rib or iliac bone are used in mandibular reconstruction
-allogeneic mandible is most useful in reconstruction of ramus and TMJ or symphysis
-allogeneic mandible is hollowed out to form a crib
-crib is packed with PBCM
-allogeneic rib is split longitudinally and the two cortical strips are contoured to the surgical defect
-allogeneic iliac: ipsilateral ilium best mimics that of hemimandible
SURGICAL TECHNIQUE
-for nonvascularized bone grafting, an external approach eliminates contamination and infection of oral
cavity
-coronoidectomy releases fibrosed temporalis muscle
-if a plate is being used for graft fixation, it is contoured and fastened to proximal and distal segments with
three or four bicortical screws in each segment
Pedicled Flaps
Pectoralis Major Flap

-reliable
-used to resurface all mucosal defects of oral cavity and to manage external defects
Trapezius Musculocutaneous Flaps

-lower island flap
-based on transverse cervical and dorsal scapular vessels
-most reliable in oral cavity
-lateral island flap
-transfers skin and muscle over lateral clavicle and scapula
-transverse cervical vessels limit reach of this flap and make it unreliable for reconstruction of oral
cavity
-superior flap
Latissimus Dorsi Musculocutaneous Flap

-based on thoracodorsal artery and vein
-supplies largest area of tissue and has greatest reach of any regional pedicled flap
Deltopectoral Flap
-based on perforating branches of internal mammary artery
-limited reach of flap, need for staging
-limited use in contemporary reconstruction of oral cavity
Sternocleidomastoid Musculocutaneous Flap

-has been used to resurface defects of floor of mouth
-skin component is unreliable
1249
Temporalis Muscle Flap
-based on deep temporal artery and vein
-used to resurface limited defects of palatal and buccal mucosa
Vascularized Bone
-vascularized bone resists infection and extrusion
-particularly useful in previously irradiated oral cavity, where nonvascularized methods are prone to failure
-bony healing of vascularized bone is similar to fracture-type healing, rather than creeping substitution of
nonvascularized bone grafts
Distraction Osteogenesis
-process by which bone is stretched to elongate it or fill a bony defect
Timing of Reconstruction
-mastication muscle fibrosis and soft-tissue contracture make delayed reconstruction difficult
-avoiding primary reconstruction hinders functional and cosmetic results
-microvascular free vascularized bone transfer has greatly enhanced success of primary reconstruction of
segmental mandibular defects
-goals of primary oromandibular reconstruction:
-restore mandibular continuity
-restore lower facial contour
-maintain mobility of residual tongue
-reconstruct anatomic configuration of sulcus
-provide rehabilitation with functional lower denture
-improve mastication, deglutition, and speech
-restore sensation to denervated lower lip
-restore sensation to resurfaced portions of oral cavity
Vascularized Composite Bone Flaps

-ideal qualities of osseous component of composite free flap:
-well vascularized
-sufficient length, width, height
-natural contour that simulates shape of mandible
-minimal morbidity
-accessible for two-team approach
-ideal qualities of soft-tissue component of composite free flap
-well vascularized
-thin and pliable
-mobile relative to bone
-sensate
-lubricated
-minimal morbidity
-accessible for two-team approach
-eight vascularized, bone-containing composite free flaps available
Iliac Crest Osseocutaneous Free Flap

-blood supply from deep circumflex iliac artery and vein
-overlying skin supplied by direct perforators that traverse three muscle layers
-skin paddle often too bulky for intraoral use
-skin easily compromised by edema or torsion
-internal oblique muscle provides a thin, pliable soft-tissue flap for intraoral reconstruction
1250
-STSG usually placed over muscle
-donor site morbidity includes early gait disturbance and ventral hernia
Scapular Flap
-provides a large amount of soft tissue and 10-12 cm of bone
-based on circumflex scapular branches of subscapular vessels
-bone quality often is inadequate for dental implants
-harvesting requires intraoperative repositioning
Fibular Osseocutaneous Free Flap

-supplied by peroneal vessels
-provides sufficient length and thickness of bone
-bone requires several osteotomies to contour the neomandible
-skin flap is less reliable than are others for intraoral reconstruction
Radial Forearm Free Flap

-based on radial artery and cephalic vein
-provides thin, sensate, pliable skin
-segment of radius up to 10 cm long and ~40% of its circumference can be transferred with skin
-bone is small for dental implants and pathologic fracture occurs among as many as 25% of pts
Ulnar Osseocutaneous Free Flap

-has bone and skin similar to radial forearm flap
-limited experience using this flap
Lateral Arm Free Flap

-thin cutaneous flap based on profunda brachii vessels
-sensory supply via posterior cutaneous nerve
-bone 1/6 of humerus in circumference and 10 cm long can be transferred as a composite flap
Dorsalis Pedis Flap

-thin, sensate cutaneous flap from dorsal foot
-based on dorsalis pedis artery and superficial peroneal nerve
-skin is thinnest and most pliable
-second metatarsus can be used - bone size is limited
-little use in oromandibular reconstruction
Rib Osseocutaneous Flap

-based on intercostal vascular pedicle, blood supply to skin is marginal
-reduced popularity of this flap in head and neck reconstruction
Restoring Sensory Feedback

-may cause disturbance in deglutition and aspiration
-sensate flaps, but poor bone:
-radial forearm, ulnar forearm, lateral arm, dorsalis pedis, and rib
-combine these flaps with fibular or iliac crest to improve functional outcome
Graft Fixation
-advantages:
-prevents shearing of neocapillaries revascularizing graft
-provide stability
1251
-disadvantages:
-stress shielding will interfere with bone remodelling
-screws can loosen and from cutaneous sinus tracks
Dental Rehabilitation
-use of dental implantation after bony mandibular reconstruction allows stable and retentive prosthetic
restoration
-types:
-conventional tissue-borne denture - least stable
-implant-born denture
-fixed retrievable prosthesis, most stable
-load is completely supported by the implants
-implant-assisted denture:
-load is shared by mucosa and the implants
-less expensive than implant-borne prosthesis
FUNCTIONAL ASSESSMENT
-functions of oral cavity:
-deglutition
-mastication
-oral competence
-taste
-articulation
-oral hygiene
-respiration
-airway protection
1252
SURGICAL RECONSTRUCTION AFTER MOHS SURGERY
ONCOLOGIC CONSIDERATIONS
-most common skin cancer is BCC followed

TREATMENT STEPS IN MOHS SURGERY
by SCC
-recurrence rate of BCC can range from 7- -tumour excision
50% -specimen orientation section cutting
-mapping of section
-Mohs micrographic surgery (MMS) used to -histologic examination
decrease recurrence rate to 4% -if tumour is present, directed re-excision of that section based on
-all tumour resection margins are subjected to tumour map
histologic examination -repetition of steps until tumour is completely resected
-MMS particularly useful for skin tumours
that are:
-recurrent, incompletely excised, clinically aggressive, morpheaform or sclerotic
-larger than 2 cm in greatest dimension, have ill-defined borders
-occur in high risk area
-in areas of critical cosmetic importance: tip of nose, ala, upper lip, eyelids, helix of ear
-MMS preserves the greatest amount of normal tissue
-in tumours with high recurrence rate, reconstruction is delayed 12-18 months to allow early detection of
recurrence:
-skin grafts used when recurrence likely unless grafting impairs function
-allows preservation of local tissue for reconstruction after final cure
-adjuvant radiation for:
-massive, highly aggressive, or invasive tumours
-when tumour resection margins are uncertain
-when gross tumour is left behind
-when there are multiple recurrences
RECONSTRUCTION OPTIONS
Healing by Secondary Intention SUGGESTED FACIAL DEFECT

-simplest method RECONSTRUCTION
-scar can distort nose, mouth or eyelids
-excellent results for small defects in selected locations (tip Small defects
-primary closure
of nose, medial canthus, parts of auricle) -primary closure with M-plasty
-healing by secondary intention
Primary Closure Moderate-sized defects
-usually for defects < 2cm -local skin flaps
-skin grafts for some defects
-for cheeks, forehead, neck and around lips Large defects
-M-plasty at ends can decrease scar length -regional flaps
-skin grafts
Skin Grafts Large, complex defects
-microvascular free flaps
-excellent results for shallow defects -distant pedicled flaps if free flap is not
-useful interim covering when tumour recurrence is likely possible
-allow reconstruction of large defects
-colour and texture match not as good
-FTSG donor sites:
-preauricular and postauricular areas
-melolabial fold
-upper inner arm
F.Ling - Mohs Surgery Reconstruction (1)
1253
-supraclavicular area
-upper eyelid
Local Flaps
-provide excellent colour and texture match and minimal contraction
-most commonly used: advancement, rotation, transposition, and V-Y flaps
Regional Flaps
-forehead flaps and neck flaps often are considered regional flaps for facial reconstruction
Distant Flaps
-pectoralis major musculocutaneous flap
-deltopectoral flap
-trapezius flap
-latisimus dorsi
Free Flaps
-required for massive defects
-requires microvascular anastomosis
Tissue Expanders
-used when there is inadequate adjacent tissue for reconstruction
-expansion performed over 6-12 weeks
-useful for scalp and forehead defects
-rapid expansion used for immediate acquisition of additional tissue
-expansion over 15-30 minutes
-0.5 to 2.5 cm of additional skin can be gained
RECONSTRUCTION OF ANATOMIC SITES
-aesthetic masses (anatomic unit) of the face:

-forehead
-periorbital region
-nose
-lip
-cheeks
-chin
-if possible, tissue used from same anatomic unit as defect
Nose
-for smaller skin defects, primary closure or local skin flaps usually are appropriate on dorsum, sidewall, or
tip
-larger defects may require paramedian forehead flap
Cheek
-small defects closed primarily
-small to moderate defects best closed with local flaps
-rhomboid flap
-rhomboid flap with M-plasty modification
-triangular advancement flap from melolabial region
1254
-moderate to large defects:
-rotation flap of cheek skin
-elevated superficial to parotid gland and facial musculature
-rotation flap of neck skin
-preauricular incision extended into neck and flap elevated superficially to platysma
-lower cheek defects can be closed with cervical transposition flaps
-can be elevated deep to platysma to enhance flap blood supply
Forehead
-skin less mobile
-small lesions excised along horizontal axis and closed primarily
-moderate defects closed with advancement, rotation, and transposition flaps
-skin graft or healing by secondary intention may be reasonable
Temple Region
-small defects closed primarily with M-plasty
-moderate defects: V-Y closure
-large defects: secondary intention, skin grafting or tissue expanders
Medial Canthal Region

-small, thin defects of medial canthal region heal well by secondary intention
-large lesions reconstructed with FTSG or local transposition flap
Eyelid
-skin defects usually amenable to primary closure, FTSG, or use of rotation flaps
Auricle
-small helical skin defects closed primarily
-small skin defects in other auricular areas repaired with skin grafts or allowed to heal by secondary
intention
Lips
-defects less than one-half lip width:
-closed primarily
-shield incision or W-plasty
-defects one-half to two-thirds lip width

-midline Abbe flap or Karapandzic flap
-lateral/commissure defects Estlander flap
-defects greater than two-thirds width

-usually necessitate cheek use of advancement or transposition flaps
-massive or total lip defects can necessitate use of regional, distant, or free flaps
1255
SCAR CAMOUFLAGE
SCAR ANALYSIS
-upon maturation, an ideal scar is level with the surrounding skin, is of good colour match, is narrow, is
parallel to or lies within favourable skin tension lies, and lacks obvious straight lines
-early revision with realignment of scar can accelerate its maturation
-healing wounds incorporate high fibroblastic activity, thus dermabrasion can be beneficial as early as 6
weeks after wounding
SCAR CAMOUFLAGE TECHNIQUES
Excisional Techniques
TECHNIQUES OF SCAR REVISION
AND CAMOUFLAGE
Fusiform Excision
-useful only when scar lies in favourable position Excisional Techniques
-incision placement
-scar excised elliptically with opposing angles of 30o or less
-fusiform excision
-shave excision
Shave Excision -scar repositioning
-for scars that are acceptable narrow but have contours elevated a -serial partial excision
few millimetres above surrounding skin can be improved by means
Irregularization Techniques
of shave excision -Z-plasty
-healing occurs by re-epithelialization -W-plasty
-Geometric broken-line resurfacing
Scar Repositioning
Adjunctive techniques
-small scars that lie close to relaxed skin tension line can be -steroids
repositioned by means of excision -dressings, medications
-often involves sacrifice of tissue between scar and desirable site -cosmetics
Serial Partial Excision

-used when size and elasticity of a scar prohibit one-stage excision and closure
-normal skin is undermined and stretched in stages to fill area of resected scar until all of the scar is excised
Scar Irregularization
Z-Plasty
-lengthens scar and changes its direction
-helpful for scars that cross relaxed skin
tension lines, distort anatomic landmarks,
or make bands or webs across concavities
-two angles and three limbs of equal length
-60o increases length of scar
75%
50%
25%
-correctly designed Z-plasty uses lateral
limbs that parallel relaxed skin tension line
of interest
F.Ling - Scar Camouflage (1)
1256
W-Plasty
-useful around areas of convex curvature,
such as along mandibular border, antihelical
fold or dorsum of the nose
-advantages: segments with shorter limbs are
used and technique does not cause overall
lengthening of the scar
-usefulness is limited on broad, flat surfaces
such as the cheek, because result is a
predictable, regularly irregular scar that is
somewhat conspicuous
Geometric Broken-Line Closure

-involves disruption of the linearity of a scar
-consists of irregular geometric patterns with
mirror-image pattern on opposite side
-shapes are no longer than 6 mm in any
dimension
-best technique for most long, unbroken
facial scars
Dermabrasion and Laser Resurfacing

-to level skin and promote re-epithelialization with new collagen production
-only papillary dermis should be injured and preserve adnexal structures
-abrading into reticular dermis risks subsequent scarring
-patient selection important:
-risk of pigment inconsistency higher among dark-skinned patients
-history of vitiligo, collagen vascular disease, and hypertrophic or keloid scar formation as well as
active herpes simplex an increase risk of unfavourable results
-concurrent use of OCP can precipitate melasma, a type of hyperpigmentation
-milia (small epidermal cysts) are not uncommon after dermabrasion
-can be minimized and postoperative healing facilitated if wound is covered with ointment or a
semiocclusive dressing until epithelial resurfacing has occurred, usually within first week
ADJUNCTIVE TECHNIQUES
Steroids
-to manage or prevent hypertrophic scars and/or keloids
-intralesional injection of triamcinolone acetonide
-injection into fat can cause atrophy
-concentration used varies from 10-40 mg/mL
-other complications:
-dermal and subcutaneous atrophy
-hypopigmentation
-telangiectasias
Silicone Sheets and Gels

-can be used alone or combined with laser therapy to aid resolution of hypertrophic scars
Mechanical Forces
-pressure and massage aid in resolution of hypertrophic scars
1257
Dressings, Medications, and Cosmetics
-topical antibiotic or pure petrolatum ointment used on sutured wounds minimizes crusting and retards
bacterial contamination
1258
NASAL RESTORATION WITH FLAPS AND GRAFTS
Large Nasal Defects
-nasal subunits:
-dorsum
-nasal side wall (2)
-alar/nostril sill (2)
-soft triangle (2)
-columella
-tip
-type of skin:
-thin, smooth mobile:
-dorsum and sidewalls, columella
-thick, pitted, with sebaceous glands:
-alae and upper part of nasal tip
BLOOD SUPPLY
-paramedian forehead flap:

-axial flap
-branches of dorsal nasal arteries, supratrochlear arteries, and supraorbital arteries
-vessels quickly pass through frontalis muscle and come to lie just below dermis of skin
forehead flap can be thinned nearly to the dermis while preserving axial vessels
-nasolabial flap:
-perforating vessels through levator labia superioris
-septal mucosal flaps:
-dorsal blood supply: anterior ethmoidal artery
EVALUATION FOR NASAL RECONSTRUCTION TREATMENT
-What does the pt want? -Small superficial defects (<1.5 cm):

Healing by wound contraction, simple wound closure, -thick-skinned zones: Bilobed flap of Zitelli
staged aesthetic reconstruction? -thin-skinned zones: Full-thickness preauricular skin graft or
-Diagnosis. simple transposition flap
What surface forms are missing?
What tissue layers are missing? -Large superficial defects:
What internal anatomic structures are missing? -thick-skinned zones: Paramedian forehead flap
-Enumerate donor materials for each surface form and tissue -defects isolated to alar lobule: nasolabial subunit flap
layer. Replace tissues in like kind. -thin-skinned zones: preauricular full-thickness skin graft
-Patient’s general health.
Cigarette smoker? -Loss of cartilage or bone:
Low serum albumin? -reconstruction of a nasal subsurface framework with primary
-Condition of skin. bone and cartilage grafts
Cigarette smoker? -cartilage graft always required for alar reconstruction
Radiation damage?
Numerous comedones -Full-thickness unilateral defects:
-lining reconstruction with septal or bipartite intranasal lining
flaps
-Midline full-thickness defects and total nasal reconstruction:

-full-thickness septal pivot flaps for lining and support
F.Ling - Nasal Restoration (1)
1259
Large Superficial Defects:
Paramedian Forehead Flap:

-for non-smokers, distal end of flap can be safely thinned to thickness of normal skin in nasal tip
-if defect is large or very long, an intermediate operation to thin the middle portions of the pedicle is
needed 21 days after the first procedure
-pedicle can be divided 12 days after surgery - but most people wait at least 21 days
1260
Reconstruction of a Framework for
Nasal Tip:
-autologous material required:

-cranial, ilial, and
costal bone
-septal, auricular and
costal cartilage
-cartilage can be harvested and
shaped to form nasal cartilages
nasal tip framework
reconstructed
-skin covered with paramedian
forehead flap
Lining of the Lower Nasal Vestibule:

-requires flaps that are thin, soft and highly
vascular
-from nasal vestibules and nasal septum
-eg. full-thickness alar defect:
-remove remaining alar sub-unit
-forehead flap for nasal cover, graft
of septal cartilage for internal
framework, septal mucosa for lining
-septal mucoperichondrium can be
elevated if left attached by a 1.2 cm
pedicle in the region of upper lip and
nasal spine
-highly vascular septal lining flap
allows placement of septal cartilage
grafts into defect at primary operation
-cartilage framework: lateral crus of
alar cartilage, upper lateral cartilage,
central armature for right ala
-septal flap inside vestibule is cut 3 weeks later
1261
Lining, Support, and Coverage for Large Full-
thickness Defects
-lining for defects that involve lower two
thirds of nasal vestibule can be harvested
from remaining vestibule and from
ipsilateral septum as a bipartite flap
consisting of a bipedicled portion and a
septal portion that have a common base
-two-part flap mobilized by means of
transverse incision of vestibular skin and
cartilage 8 mm above defect
-vestibular lining skin and cartilage are
mobilized and delivered to alar margin and
fixed with sutures
-septal flap incised and delivered to
maintain a 1.2 cm base over upper lip and
nasal spine
-two flaps sutured together to form a soft
and vascular vestibular lining
-subsurface framework of cartilage
reconstructed
-complications:
-vascular compromise of flap
-infection
-epistaxis
-emergencies:
-local vascular compromise: managed by
means of releasing tight sutures within 24
hours
-infection: antibiotics and aspiration of
hematoma
1262
NASAL RESTORATION WITH FLAPS AND SMALL GRAFTS
Small Nasal Defects
DEFECT ANALYSIS AND PERTINENT ANATOMY
-upper third:
-nasal bones
-thin skin
-little functional concern with defects in this zone
-middle third:
-skin thin medially but thick laterally
-lateral nasal artery immediately cephalic to supra-alar crease
-lower third:
-tip, alar lobule, columella, and soft-tissue triangle
-thick sebaceous skin
-poorly healing scars
-dynamic collapse of external nasal valve may occur - requires nonanatomic cartilage grafting to
prevent collapse
FUNCTIONAL CONSIDERATIONS COMMON OPTIONS IN THE MANAGEMENT OF SMALL

CUTANEOUS DEFECTS
-depth of defect can cause nasal obstruction
-eg. -loss of underlying bone or cartilage Upper third: Full-thickness skin graft
Glabellar transposition flap
-loss of fibroareolar integrity of alar Healing by secondary intention
lobule and lateral middle third of
nose Middle third: Bilobe transposition flap
-will require structural reinforcement One-inch closure (midline)
Full-thickness skin graft
Single-stage forehead flap
FLAP SELECTION Lower third: Bilobe transposition flap

Composite graft (alar rim)
One-inch closure (midline)
-aesthetic subunits are not as important in Melolabial flap (columella, ala)
management of small defects - however Full-thickness skin graft, delayed
attempt is made to maximize camouflage by
positioning flaps and scars along subunit
borders
TECHNIQUES
Skin and Composite Grafts

-consider delay - enhances vascularity, fills depression and improves surface contour
-square wound borders
-bevel edges toward defect to smooth transition with native skin
-skin grafts:
-supraclavicular, preauricular, melolabial and postauricular areas
-composite graft:
-root of helix for small but deep defects around alar rim
-multilayered closure required
1263
Primary Closure
-for midline defects of middle or lower third of nose
Rhomboid Flap
-versatile flap with predictable scars and vectors of tension
-laxity usually from lateral nasal wall and medial cheek
-inferiorly based flap tends to cause fewer problems with postoperative congestion and edema
Bilobed Flap
-allows distribution of tension farther from primary defect to control degree of tension along alar margin
-wide undermining in the supraperichondrial plane essential for all transposition flaps
Single-stage Forehead Flap

-deepithelialized pedicle
-tunnelled under intact glabellar skin
-does not require pedicle division
Reiger Flap
-glabellar skin with unilateral base on medial brow and supratrochlear region
-for large defects of upper third of nose
1264
SURGERY FOR EXOPHTHALMOS
-exophthalmos:
-condition of altered thyroid metabolism that causes protein depositions within EOMs, increasing
bulk as much as 10-fold
-an abnormal autoimmune response caused by T lymphocyte
-consequences:
-thickening of muscles
-fat herniation
-proptosis
-upper and lower eyelid retraction
-divergence of gaze
PATIENT EVALUATION
-any pt with unilateral or bilateral exophthalmos should be presumed to have thyroid disease
-Graves disease:
-increased total and free T3, total and free T4, reverse T3 uptake, clearance and release of iodine
131 and serum assays of TRH
-US of orbit can confirm suspicion of orbital thyroid disease thickening of EOMs
-CT/MRI: pathognomonic enlargement of recti muscles readily identified
-a particularly revealing physical sign is a hyperaemia over lateral rectus muscles
-pseudotumour cerebri
-most common differential diagnosis to consider
-CT/MRI can show generalized edema of soft tissues
-use of high-dose steroids usually improves proptosis within 24-48 hours
-lymphoma of the orbit
-usually elderly pt
-more localized mass seen on scan usually near apex, proptosis may be acentric
-space-occupying masses:
-metastatic tumour, vascular anomaly, neurofibroma retinoblastoma unilateral proptosis
-congenital shallowness of orbits (eg. Apert syndrome and Crouzon disease)
MANAGEMENT
-disease self-limited in most pts

-progressive untreated disease blindness d/t corneal exposure or optic neuropathy
-endocrinology evaluation and management of hyperthyroidism required
-suppression of thyroid activity through subtotal thyroidectomy, iodine 131 ablation, or exogenous
thyroid hormone
-acute deterioration in 1-2% decreased visual acuity or field defects
-treatment of choice is 80-120 mg of prednisone daily for 14 days
-if vision does not improve, decompression indicated
-exophthalmos persists in 5% even after pts become euthyroid
F.Ling - Surgery for Exophthalmos (1)
1265
SURGICAL TREATMENT
-indications for surgical decompression:

-early stage: if steroids fail to regain visual acuity or if steroids are required for long-term
maintenance
-late stage:
-when palpebral retraction, exophthalmos, or oculomotor involvement is seen, cosmetic
decompression
-eye findings stable for 6 months
-functional indications:
-decreasing visual acuity, visual field defects, abnormal visual-evoked potentials, disk edema
-significant lid retraction, corneal exposure with keratitis not responsive to conservative medical
management
Orbital Decompression
Superior Orbital Decompression

-involves unroofing entire superior orbital wall by frontal craniotomy
-advantage of removing large amount of orbital bone for decompression
-use limited
-usually indicated in cases of traumatic injury to orbit, biopsy of apical masses, volume expansion of
congenitally contracted orbit
-bony roof of orbit carefully removed from just anterior to optic foramen to anterosuperior orbital rim
-titanium mesh fabricated to form covering for orbital roof
-considered only for severe cases of contracted orbit associated with proptosis and decompressions
performed for orbital trauma
Medial Orbital Decompression
-approached through standard external ethmoidectomy incision or through coronal

forehead approach
-ethmoidectomy approach:
-medial canthal tendon displaced laterally
-lacrimal sac elevated out of lacrimal fossa
-anterior and posterior ethmoid arteries identified and ligated
-complete ethmoidectomy performed
-medial orbital periosteum incised longitudinally with axis of orbit, allowing orbital fat to herniate
through periosteal defect into ethmoidectomy cavity
Inferior Orbital Decompression

-creates a large orbital floor blow-out fracture, but spares injury to infraorbital nerve
-approach through subciliary eyelid incision and Caldwell-Luc maxillary antrostomy
-course of infraorbital nerve identified and bone is removed medial and lateral to this
-medially bone removed to lacrimal fossa and laterally removed to thick bone of zygoma
-periorbita incised longitudinally to allow orbital fat to herniate into maxillary sinus
-forced duction testing performed to ensure that muscles of inferior orbit are not hindered by
entrapment
Lateral Orbital Decompression

-approach via coronal direct rim incision, extended lateral canthotomy, or direct lateral incisions
-direct lateral incision made as an extension of subciliary incision or as a lateral canthotomy
-periosteum over lateral orbital rim exposed, it is incised widely directly over rim and exposed
1266
-lateral rim can be removed by drill, osteotome or saw still attached to periosteum and then later
replacement into its proper position to maintain cosmesis
-lateral orbital bone removed as much as possible until thick bone of skull base encountered
-periorbita incised and orbital fat gently teased out to protrude into newly created space
-lateral extension of orbital fat limited by position of temporalis muscle
Endoscopic Intranasal Decompression

-used to decompress medial and medioinferior floors of orbit
-cannot decompress orbital floor lateral to infraorbital nerve and cannot extensively open periorbita
for exposure and extrusion
-maxillary ostium enlarged to provide optimal exposure of orbital floor
-ostium enlarged superiorly to level of orbital floor and inferiorly to roof of inferior turbinate
-lamina papyracea removed to level of ethmoid arteries
-using sickle knife, orbital periosteum incised to allow orbital fat to protrude into ethmoid cavity
-with endoscope alone, ~3 mm of exophthalmos can be corrected
Orbital Fat Removal

-an alternative procedure to orbital decompression
-approaches: upper lid crease and subciliary
-orbital septum in both lids opened longitudinally and fat compartments debulked
-6 mm of proptosis reduction can be gained
Other Interventional Treatment

-XRT an alternative for late sequelae of stable dysthyroid ophthalmopathy
-200 cGy of fractionated photon radiation administered over 2 weeks
-mainly stabilizes or improves condition, but exophthalmos does not resolve
COMPLICATIONS
-untreated disease:
-progressive optic neuropathy blindness
-corneal exposure keratitis
-endophthalmitis
-diplopia
-corneal abrasion after decompression
-scleral protector, Frost suture, lubrication for protection
-optic nerve compromise
-from lengthy retraction
-retrobulbar hematoma
-injury to infraorbital nerve
-ectropion
-retinal hemorrhage
-occurs almost exclusively in diabetic patients
-orbital cellulitis or abscess if significant sinusitis occurs
EMERGENCIES
-retrobulbar hematoma
-retinal vascular oclusion
-corneal ulcer
1267
FACIAL REANIMATION
INTRODUCTION
-goals of facial rehabilitation:

-protect eye from corneal
exposure
-provide balanced smile
-improve oral competence
-improve mastication
-four types of reanimation methods:
-neural methods
-musculofascial
transpositions
-facial plastic procedures
-prosthetics
ANATOMY
-extracranial course of facial nerve:

-stylomastoid foramen
innervates posterior belly of
digastric
-enters parotid gland pes
anserinus divides into two
branches:
temporofacial
cervicofacial
GENERAL CONSIDERATIONS
-immediate eye protection: moisture

chambers, artificial tears and
ointments
-waiting period of at least 12 months
before attempting a surgical
interruption that may result in
irreversible damage to facial nerve
-if paralysis has occurred <12-18 months (before significant muscle atrophy or loss of motor endplates)
may consider end-to-end anastomosis, interpositioning, crossover grafting, and upper eyelid gold weight
implants
-if paralysis has occurred >12-18 months with significant muscle atrophy or facial nerve cannot be grafted,
may consider musculofacial transpositions, static procedures, and upper eyelid gold weight or spring
implants
F.Ling - Facial Reanimation (1)
1268
TECHNIQUES
Facial Nerve Anastomosis

-for disruption d/t trauma, benign tumours or iatrogenic injury
-mobilization of the nerve within 30 days is acceptable:
-maximum axoplasmic flow within 3-4 week period nerve has best physiologic opportunity to
regenerate
-nerve endings freshened and 8-0 nylon or smaller sutures applied to reapproximate epineurium
-a plumb line dropped from lateral canthus: injuries distal to this line repair not required
Facial Nerve Repair with Grafts

-used to reduce tension at anastomosis site
-used if tumour resection involves facial nerve
-common nerves used:
-great auricular nerve:
-located superficial to SCM perpendicular to a line drawn between mastoid and angle of
mandible
-sural nerve:
-lateral aspect of leg
-1-2 cm lateral to saphenous vein, medial and posterior to lateral malleolus of ankle
Crossover Technique
-three basic techniques:
-hypoglossal facial
-spinal accessory facial
-facial facial
-require following conditions:
-irreversible facial nerve injury
-intact mimetic function
-intact motor endplate function
-intact proximal donor nerve
-intact distal facial nerve
-commonly used in pts post-excision of acoustic neuromas
-results unpredictable: many pts have synkinesis
-7-to-11 crossover:
-morbidity: loss of trapezius function
-try to use only branch to SCM
-7-to-7 crossover:
-inconsistent results
-more sophisticated free muscle flaps or second
donor nerve usually required
-7-to-12 crossover:
-identify and cut facial nerve at stylomastoid foramen via parotidectomy approach
-nerve then isolated to pes anserinus
-identification of hypoglossal nerve inferior to digastric muscle nerve transected as distal as
possible and sutured directly to main trunk
-pts may have subtle articulation problems
Muscle Transposition Techniques

-used when there is no intact facial neuromuscular system:
-Mobius Syndrome: congenital absence of facial nerve
-loss of motor endplates from long-standing facial nerve interruption for at least 3 years
1269
-other cranial nerves sacrificed and cannot use crossover techniques
-Temporalis Muscle Transposition:

-used mostly for reanimation of corner of mouth
-incision in preauricular crease and extending to superior temporal line dissection above SMAS
to avoid injuring peripheral nerve
-expose temporalis muscle incise muscle down to periosteum using middle 1/3 of muscle
-creation of large tunnel over zygomatic arch
-second incision in nasolabial fold to expose orbicularis oris
-temporalis muscle attached with permanent sutures to orbicularis oris
-Masseter Muscle Transposition:

-advantage:
-avoids large facial incision
-disadvantage:
-less muscle to be used
-vector force more horizontal, providing less superior angulation to corner of mouth
-modification of technique:
-using fascial sling from fascia lata graft of thigh
-sling passed around anterior half of masseter muscle and ends are sutured to orbicularis
oris muscle
1270
Ancillary Procedures
-include:
-facial plastic procedures (rhytidectomy, blepharoplasty, browlift)
-prosthetic implants (gold implants, spring implants)
-canthopexy and lid tightening techniques
-lateral tarsal strip procedure:
-used for ectropion or lower lid laxity
-tarsorrhaphy:
-partial suturing of eyelids, permanent procedure, does not reanimate, results in visual
field deficits and cosmetic deformity
Free Muscle Flaps

-technically difficult and require microvascular techniques
-gracilis, seratus anterior, or extensor digitorum brevis
-two stages:
-nerve graft harvested and attached to opposite normal side
-6-9 months later a free muscle flap with its neurovascular bundle intact is anastomosed
1271
1272
FACIAL ANALYSIS
DEFINITION OF TERMS
-trichion (Tr): -midline at hairline

-glabella (G): -prominence in midsagittal plane, above root of nose
-nasion (N): -corresponds to nasofrontal suture; superior to sellion
-sellion: -soft tissue, deepest point of nasofrontal angle
-radix (R): -root of nose
-rhinion (Rh): -junction of bony and cartilaginous nasal dorsum
-thinnest skin of nose
-supratip break: -just cephalic to tip defining point
-tip defining point (Tp):
-anteriormost projection of nasal tip corresponding to medial cephalic portion of lateral
crura of lower lateral cartilages
-infratip lobule: -portion of lobule inferior to tip defining point
-infratip break: -junction of columella and lobule
-subnasale (Sn)
-superior vermillion border (Vs)
-inferior vermillion border (Vi)
-stomion (St): -embrasure of lips
-menton (M): -inferiormost border of chin
-columellar point (Cm):
-anteriormost soft tissue point of nasal columella
-alar crease (A): most posterior portion of nose
-mentolabial sulcus (Ms): dip in chin
-pogonion (Pg): -most prominent anterior projection of chin
-gnathion (Gn): -junction of line tangent to menton and pogonion
-cervical point (C)
-tragion (Tr): -point at supratragal notch of ear
F.Ling - Facial Analysis (1)
1273
-nasofrontal angle (NFA)
-nasofacial angle (NfcA)
-nasolabial angle (NLA)
-male: ~90o-105o
-female: ~95o-120o
-mentocervical angle (MCA)
-Frankfort plane: line extending from superior

margin of EAC to inferior border of infraorbital rim
GENERAL FACIAL ASSESSMENT
-major aesthetic masses: forehead, eyes, nose, lips, chin

-ideal width to length ratio of face: 3:4
-vertical fifths: each fifth approximately one eye width
-horizontal thirds
-profile view assess for degree of convexity
1274
Forehead
-most important characteristic of forehead from surgical standpoint is the NFA
-advancing NFA superiorly will effectively lengthen nose
-deepening the angle at surgery will alter dorsal profile nasal projection effectively increased
Eyes
-inner intercanthal distance ~ width of one eye ~ 3.5cm
-interpupillary distance ~ 6.5 cm
-outer intercanthal distance ~ 9.5 cm
-female brow positioned above supraorbital rim with higher arch

-male brow position over or slightly inferior to supraorbital rim with little arch
-upper eyelid covers 2-3 mm of superior iris

-lower lid lies within 1-2 mm of inferior limbus
1275
Nose
-nasal length: nasion to tip defining point
-desirable nasal width ~ 70-75% of nasal length
-polly-beak deformity caused by fullness in the supratip region
-tip projection: extent of protusion of nasal tip from anterior facial plane
-tip rotation: degree of inclination of NLA

-more rotation acceptable in shorter individuals than taller ones
-increasing rotation effectively increases projection but decreases nasal length
-nasal base:
-columella to lobule ratio ~ 2:1
-lobular width = 75% of nasal base width
-ala:lobule = 1:1 (on lateral view)
-columellar show = 2-4 mm
1276
Lips
-lateral aspect of oral commissures should lie along vertical line tangent to medial limbus of iris
-interlabial gap: no more than 3 mm
-incisor exposure:
-no more than 2 mm with lips in repose
-no more than 2/3 of maxillary incisor on full smile
Ears
-top of helix should be on horizontal line with lateral eyebrow
-inferior attachment at level of alar-facial junction
-longitudinal axis on lateral view posteriorly inclined ~20o off vertical
-angle of protrusion from posterior scalp ~
20o
Dental Occlusion
-mesial: toward midline of dental arch
-distal: away from midline of dental arch
-buccal: toward cheek
-lingual: toward tongue
Angle’s Classification:
Class I: normal occlusion

-mesiobuccal cusp of maxillary
first molar in occlusion with buccal
groove of mandibular first molar
Class II: retrognathia

-buccal groove of mandibular first
molar lies distal to mesiobuccal
cusp of maxillary first molar
Class III: prognathia

-buccal groove of mandibular first
molar lies mesial to mesiobuccal
cusp of maxillary first molar
METHODS OF FACIAL ANALYSIS
-Cephalometrics: involves measurement of bony landmarks on x-ray (radiographic craniofacial relationships)

-Photometrics: direct consideration of soft-tissue proportions on facial photographs
1277
OF THE AESTHETIC SURGERY PATIENT
Effects of Aging on the Face

-skin:
-thinned epidermis
-decreased subcutaneous fat
-dermis loses elastic fragments (elastosis)
-decreased melanocytes and Langerhans’ cells
-decrease in Type I collagen (mature) and increase in Type III collagen (immature)
-reduced vascular supply (especially in smokers)
-skeletal:
-thinned skull and mandible (especially in edentulous patient) resulting in an excess skin envelope
-laryngeal skeleton and hyoid descends
-forehead midface:
-weakened supportive matrix between SMAS and overlying fat pad results in deepened melolabial
crease
-hypotonic facial muscles results in festooning and facial rhytids
-neck:
-jowling,
-chin ptosis
-ptotic submandibular glands
-platysma banding from loss of tone resulting in loss of cervicomental angle
SELECTION OF PATIENTS
Concept of Deformity
-surgeon needs to understand pt’s self-image, what the pt describes as the deformity and how the pt wants
the defect corrected
-surgeon mus also counsel pt about the surgeon’s perception of the problem
-pt and surgeon must agree on existence of deformity and the style and degree of desired change before
surgery is undertaken
Preoperative Interviews
-pt’s ability to accept the surgical result is highly correlated with the degree to which pt has been prepared
-interviews should address:
-what are the pt’s expectations
-are the expectations realistic and reasonable
-can the expectations be fulfilled
-can the pt be satisfied
-computer imaging:
-greatest danger in its use is “implied promises”
Poor Candidates for Cosmetic Facial Plastic Surgery

-unrealistic expectations
-multiple physician visits
-psychiatric instability
-smokers have >12x increased risk of skin sloughing and scarring
F.Ling - Preop Evaluation of Cosmetic Pt (1)
1278
Traditional and Contemporary Views
-paranoid schizophrenic is a potentially dangerous patient - thorough psychiatric evaluation recommended
-borderline personality disorders:
-poorer candidates for aesthetic surgery
-predominant in malpractice cases
-existence of preoperative depression is not an absolute contraindications to surgery, but there is a risk of
the depression intensifying
F.Ling - Preop Evaluation of Cosmetic Pt (2)
1279
SURGICAL ANATOMY OF THE NOSE
F.Ling - Surgical Anatomy of the Nose (1)
1280
TOPOGRAPHIC ANATOMY AND LANDMARKS
-topographic subunits:
-in reconstruction of external nasal defects, it is often
preferable to resect and replace an entire topographic
subunit with skin of like colour, character, and texture
rather than simply filling the existing primary defect with a
skin graft or pedicle flap
-consist of:
-nasal dorsum
-nasal sidewalls (2)
-nasal tip (including infratip lobule and columella)
-alar lobules (2)
-depressions of supraalar facets (2)
SKIN AND SUBCUTANEOUS TISSUES
-nasal skin thinner, more mobile, and more easily repositioned in cephalic 3/5 of nose
-relatively devoid of subcutaneous tissue and sebaceous glands
-skin more thicker, glandular quality caudally
-skin is thin at rhinion and thick at nasion and supratip area
-slight skeletal hump at rhinion exists even when external epithelial profile line is relatively
straight and devoid of an external humped appearance
DISSECTION PLANES
-ideal soft-tissue preservation for potential cushioning and camouflage achieved by dissection in immediate
supraperichondrial plane (sub-SMAS) over upper and lower lateral cartilages and subperiosteal elevation
over bony dorsum
-ideally, anaesthetic infiltration should be placed precisely in this supraperichondrial (sub-SMAS) plane in
the lower half of the nose to aid in vascular dissection
MIMETIC MUSCLES INFLUENCING THE NOSE
-elevator muscles
-procerus
-levator labia-superioris alaeque nasi
-anomalous nasi
-depressor muscles
-alar nasalis
-depressor septi nasi
-compressor muscles
-transverse nasalis
-compressor narium minor
-minor dilator muscles
-dilator naris anterior
-synergistic action of levator labia superioris and depressor septi nasi can profoundly depress nasal tip
caudally, “round up” supratip area, and temporarily lengthen nose considerably
1281
-mimetic muscles encased and interconnected within SMAS
-dissection deep to SMAS layer results in ease of dissection, minimal bleeding, minimal damage to
neurovascular structures supplying nasal tip skin, avoidance of damage to intact SMAS layer, and reduced
scarring during healing more predictable healing
BONY SKELETON
-consists of paired nasal bones and ascending (frontal) processes of maxilla

-nasal bones:
-inferoposteriorly, bones are fused to perpendicular plate of ethmoid
-commonly jointly deviated in twisted nose deformity
-in rhinoplasty, only sufficient periosteum should be elevated as an intact layer medially and
laterally to gain access to bony nasal hump, preserving all other periosteal attachments over bones
of maxilla to stabilize and support bony fragments after completion of lateral osteotomies
-overlap upper lateral cartilages
-lateral osteotomies:
-if positioned too high on nose may lead to aesthetic and functional sequelae, manifested by
airway compromise and palpable or visible step deformity over lateral nasal wall
-lacrimal sac at potentially at risk but damage is rare
CARTILAGINOUS SKELETON
Cartilaginous Pyramid
-composed of quadrangular septal cartilage and upper lateral cartilages
-cephalic end rigid and fixed while caudal end very flexible
-upper lateral cartilages extend a variable distance beneath caudal portion of nasal bones and are securely
fixed to bony undersurface
-reconstruction of certain twisted noses may require division of upper lateral cartilages from septum to
realign the nasal framework
-profile alignment often requires greater quantitative reduction of cartilaginous hump
-mucoperichondrium continuous from septal cartilage to undersurface of upper lateral cartilages should be
preserved in most pts
-division of this anatomic area of the valve as a “routine’ step in rhinoplasty serves no useful
purpose
-upper lateral cartilage to alar cartilage attachment represents one of the major supports to projection of the
tip and is interrupted by almost all incisional approaches for access to nose in rhinoplasty
-“scroll”
-inferior edge of upper lateral cartilage may recurve outwardly and met with a corresponding
incurving of cephalic margin of alar cartilage
-may result in abnormal width of nose in middle third or supratip area
-nasal valve:
-angle between caudal quadrangular cartilage and distal upper lateral cartilages
Nasal Septum
-mucoperichondrium enveloping quadrangular cartilage inserts into bony-cartilaginous articulation with
maxillary crest at base of septum, where mucoperiosteum covering bony nasal floor also is inserted
-maxillary-premaxillary approach:
-gaining access to bony septal floor by elevating and bringing into continuity two subperichondrial
and mucoperiosteal flaps by sharp or semisharp dissection (“superior and inferior tunnels”)
-portion of septum anterior to piriform aperture provides vital support for nasal dorsum and tip
1282
-angles of the caudal septum:
-anterior septal angle
-midseptal angle
-posterior septal angle
-membranous septum:
-composed of bilateral external layers
of the vestibular skin with intervening
subcutaneous areolar tissue
-in pts with overactivity of tip while
speaking, it is desirable to divide fibers
of depressor septi nasi that traverse
membranous septum to insert over
caudal septum
-complete transfixion incisions sacrifice the
attachment of medial crura footplates to caudal
septum, thereby at least temporarily diminishing
one of the major tip support structures
Alar (Lower Lateral) Cartilages

-anatomy of alar cartilages and their relationship to one another influence the choice of incision and
surgical approaches
-large bulky cartilages may require bipedicle flap or an open approach for adequate analysis and
surgical contouring
-widely separated alar cartilages, exhibiting varying degrees of bifidity and clefting may require
suture narrowing or vertical interruption for narrowing refinement
-tip-defining point:
-site of highest projection
-highest medial cephalic portion of lateral crus and is manifest externally by a light reflex
ANATOMIC TIP SUPPORT MECHANISMS
Major
-size, shape, and resilience of medial and lateral crura of lower lateral cartilages
-medial crural footplate attachment to caudal border of quadrangular cartilage
-attachment of upper lateral cartilages (caudal border) to alar cartilages (cephalic border)
Minor
-ligamentous sling spanning paired domes of alar cartilages
-cartilaginous septal dorsum
-sesamoid complex extending the support of the lateral crura to piriform aperture
-attachment of alar cartilages to overlying skin and musculature
-nasal spine
-membranous septum
1283
INTRODUCTION TO RHINOPLASTY
INITIAL CONSULTATION
-determine pt’s motivations and goals for surgery

-nasal evaluation:
-airway evaluation:
-obstruction:
-right-sided, left-sided, or both
-fixed or changing
-rhinorrhea, hay fever
-epistaxis
-sinusitis
-external nose:
-profile:
-radix
-dorsal height
-tip projection
-tip rotation
-alar columellar relation
-nasolabial angle
-caudal septum
-chin projection
-frontal view:
-straightness
-bony-cartilaginous transition
-tip bulbousness
-tip definition
-alar-columellar relation
-basal view:
-dorsal line
-tip definition
-nostril symmetry
-alar base width
-nasal tip support:
-position and strength of anterior septal angle
-shape and position of caudal septal border
-thickness and flexibility of LLC
-nasal skin:
-thickness, dryness, fine wrinkles, sun damage
-informed consent:
-risks: bleeding, infection, intranasal scarring, palpable or visible irregularities, unsatisfactory
cosmetic appearance, potential for CSF leak, meningitis and death
-patient education:
-postoperative course:
-nasal and eyelid swelling and possibly two black eyes
-intranasal packing/splints explained
-photographs taken at initial consult
-pt to avoid ASA or NSAIDs 2 weeks prior to surgery
F.Ling - Rhinoplasty (1)
1284
ANAESTHESIA
-local anaesthesia:
-advantages:
-less bleeding
-recovery faster
-lower cost
-cocaine:
-4% solution (maximum dose ~5 mL for most adults)
-maximum dose = 3 mg/kg
-effective for 2 hours
-mechanism of action: blocks re-uptake of NE and dobutamine at adrenergic endings
-lidocaine:
-maximum dose: 3-5 mg/kg
-with epinephrine, max dose: 7 mg/kg
-0.5% lasts 1 hour (2 hours with epi)
-1% lasts 1.5 hours (3.5 with epi)
-bupivicaine:
-maximum dose = 3 mg/kg
-lasts 3-10 hours
OVERVIEW OF SURGERY
-two major areas of surgical change: tip and dorsum

-osteotomies usually performed last because swelling can obscure fine anatomic detail
Incisions
-hemitransfixion:
-allows access to columella, medial crura, and premaxillary area
-open incision:
-best access for tip and dorsal nasal work
-intercartilaginous incision:
-for minimal tip work
-intracartilaginous incision:
-parallels LLC cephalic border, 2-6 mm closer to nostril opening
-incision through LLC
-trims cephalic border of LLC, removing a 3-5 mm strip of cartilage
-rim incision:
-made at caudal border of LLC
-often combined with intercartilaginous incision for delivery of LLC
Hump Reduction
-skin of upper nose separated from bone and cartilage
-periosteum is incised and subperiosteal plane undermined to nasofrontal angle
-dorsal line needs slight middorsal “hump” to compensate for thinner skin here
-reduction begun with scalpel removal of cartilage
-bony hump then reduced to join with cartilaginous dorsum
-small bony humps or irregularities can be adjusted by rasping
-larger humps usually removed with osteotomes
1285
Medial and Lateral Osteotomies
-“open roof” deformity after hump is
removed
-osteotomies disconnect bones both medially
and laterally mobilized nasal bones are
repositioned medially
-medial osteotomy performed first
-beginning at open roof superior
edge, cut starts with osteotomes
next to septum and curves gently
outward and upward to nasofrontal
suture line
-lateral osteotomy:
-begins above floor of piriform
aperture, lateral to anterior inferior
turbinate
-if begun lower, may narrow nasal
valve, causing obstruction
-osteotomes kept parallel to floor during
main length of osteotomy; if angled the underlying bone cannot support repositioned bones and a step-off
or asymmetric positioning can occur
-“high” osteotomies: result in obvious step-off in bone at middorsal level
-lateral osteotomy usually not carried superior to intercanthal line
-intermediate osteotomy:
-performed between medial and lateral ones
-permit satisfactory narrowing of flattened noses
1286
1287
EXTERNAL RHINOPLASTY APPROACH
-external rhinoplasty approach provides maximal exposure of upper and lower lateral cartilages
-advantages:
-helpful in diagnosis, cartilage manipulation, and precise application of cartilage grafts
-disadvantages:
-transcolumellar incision, increased surgical time, increased tip edema
-result in minimal loss of tip support by dividing only skin attachments to lower lateral cartilages (minor tip
support mechanism)
-prior surgical incision such as lateral rhinotomy, extended bilateral alotomies, or excessive thinning of
overlying skin can compromise blood supply to skin-soft tissue envelope
VASCULAR ANATOMY OF THE NOSE
-major arteries, veins and lymphatics of nasal tip run above SMAS of nose
-arteries:
-lateral nasal a. - from facial artery
-follow cephalic margin of lateral crura to meet paired columellar vessels
-dorsal nasal a.
-columellar a.
-important to dissect below musculoaponeurotic layer of the nose minimizes tip edema
SURGICAL TECHNIQUE
-1% lidocaine with 1:100000 epinephrine injected into nasal tip, columella and along caudal margin of
lateral crura
-incisions: transcolumellar incision made at level of midcolumella and bilateral marginal incisions
-cone incisions are made, converse scissors are used to dissect caudal to medial crura without damaging
caudal margin of lower lateral cartilage
-submuscular plane just above lateral crura is identified and tissue is bluntly dissected toward cephalic
margin of lateral crura
-fibrous connections released in midline
-blunt dissection continued toward osseocartilaginous junction
-options:
-columellar strut:
-sutured into precise pocket between medial crura to provide support or correct buckled medial or
intermediate crura
-caudal extension graft:
-appropriately shaped flat piece of septal cartilage harvested from posteroinferior region of
septum
-will enhance nasal length, tip projection and alar-columellar relationship
-dome-binding suture:
-increases tip projection and narrows domes
-dome division with excision of superiorly based triangle of cartilage:
-to narrow the domes
-cartilage usually excised at the domes if decreased projection is desired
-if tip rotation is needed, cartilage can be excised lateral to domes
-shield-shaped tip grafts can be used to increase tip support and projection, provide shape to infratip lobule
and camouflage tip asymmetries
F.Ling - External Rhinoplasty (1)
1288
-thin skin is a relative contraindication for tip grafts because graft may become visible when
edema resolves and skin thins over time
INDICATIONS FOR EXTERNAL RHINOPLASTY
-cases that require extended surgical exposure for diagnostic or technical reasons
-asymmetry of nasal tip cartilages or middle nasal vault
-inadequate tip projection
-structural deficiency
-specific nasal deformities:
-crooked nose deformity
-secondary and revision rhinoplasty
-cleft-lip nasal deformity
-saddle-nose deformity
-benign nasal tumours
-closure of septal perforations
COMPLICATIONS
-dissection out of submuscular plane excessive bleeding, postop edema, scarring and irregularity of skin-
soft tissue envelope
-irregularity of transcolumellar incision
-lateral notching of transcolumellar incision
-results from stretching of upper columellar flap effectively increases horizontal width of
columellar flap
F.Ling - External Rhinoplasty (2)
1289
REFINEMENT OF THE NASAL TIP
ANALYSIS AND DIAGNOSIS
-quality of skin:
-essential indicator of surgical outcome and plays significant role in preoperative planning
-extremely thick skin, rich in sebaceous glands and subcutaneous tissue least likely to achieve
desirable refinement and definition
-thin skin: offers no cushion to camouflage or contour imperfections
-undesirable progressive skin retraction over years
-tip recoil:
-tests the inherent strength and support of the nasal tip
-weak tips may require additional struts or grafts
-note asymmetry of alar cartilage
-assess septum, columella
-evaluation of nasal spine and caudal septal angle
-position and inclination of nasofrontal and nasolabial angles,
shape and size of alae, overall width of middle and upper thirds of
nose, and relationship of nose to rest of the facial features and
landmarks are evaluated
SURGICAL TECHNIQUES
-nasal tip commonly approached as distinctive and separate part of

rhinoplasty operation
-tip support mechanisms must be respected:
-Major supports:
-alar cartilage size and shape; medial rural
footplate attachment to caudal margin of septum;
upper lateral cartilage attachment to alar
cartilage
-Minor supports:
-interdomal soft tissue; cartilaginous dorsum;
alar cartilage attachment to embracing skin;
membranous septum
F.Ling - Refinement of Nasal Tip (1)
1290
-preservation, reduction or enhancement of tip projection are considered
-preferred nasal tip surgery terms:
-incisions: transcartilaginous, intercartilaginous, marginal
-approaches: delivery, nondelivery (cartilage splitting, retrograde), open (external)
-techniques:
-volume reduction with residual complete strip; weakened complete strip; suture
modification of complete strip; interrupted strip
Nondelivery Approaches
-cartilage splitting:
-for pts who need only conservative or minimal tip refinement and rotation
-few millimetres of medial-cephalic portion of lateral crus removed
-disturbs little of normal anatomy and consistently heals predictably and with symmetry with
minimal scarring
Delivery Approaches
-visual presentation of alar cartilages as bipedicle chondrocutaneous flaps
-must maintain a complete strip at least 5 mm wide
-can achieve greater volume reduction
-used when significant defatting or scar resection is required
-transdomal suturing:
-pts with extremely thin skin, delicate alar sidewalls and bulbous cartilage, predictable refinement
with horizontal mattress suture
-strengthen tip support and can be used to enhance tip projection
-interrupted strip techniques
-used when more significant cephalic tip rotation is indicated in more severe tip deformities
-residual complete strip is divided somewhere along its course, excessive portions of lateral and
occasionally medial crus removed, and cartilages are reconstructed
-dangers:
-asymmetric healing and scarring
-sacrifice of tip support
-over-rotation of tip
Open (External) Approaches

-potential indications:
-cleft-lip nose deformity
-severe tip asymmetry
-marked overprojection
-significant underprojection
-eccentric anatomy
-difficult tip revisions
-teaching
-advantages:
-precise direct-vision diagnosis
-bimanual surgery
-exposure
-disadvantages:
-more operative edema and scarring
1291
Tip Projection
-preservation:
-ensure major and minor tip supports are left largely intact or reconstructed
-complete strip techniques recommended
-avoid complete transfixion incision which destroys vital support provided by medial crural
footplate overlap of caudal septum
-techniques to increase projection:
1. autogenous cartilage struts positioned below or between medial crura
2. plumping grafts of cartilage into base of columella through low lateral columellar incision
3. for widely splayed medial crural footplates resecting excessive intercrural soft tissue and
suturing medial crura (transdomal or interdomal suture)
4. autogenous cartilage tip grafts (supradomal graft or shield graft)
5. cephalic rotation of tip
-techniques to decrease tip projection:
1. full transfixion incision
2. lower septal angle
3. shorten medial and/or lateral crura
Tip Rotation
-rotation ultimately results from planned surgical

modifications of alar cartilages
-maintenance of residual complete strip tends to
resist upward rotation during healing
-the more cephalic margin excised, the
more rotation occurs
-interrupted strips foster more significant
rotation of nasal tip and can be controlled
and calibrated by excision of a base-up
triangle from the lateral aspect of the lateral
crus
-techniques to increase tip rotation:

1. remove hump
2. shorten caudal septum
3. shorten lateral crura
4. shield graft
5. premaxillary augmentation
6. augment medial crura
7. augment columellar-labial angle
-adjunctive tip rotation techniques

-septal shortening with high septal
transfixion
-reduction of convex caudal medial crura
-resection of membranous columellar skin
-techniques to create an illusion of cephalic tip

rotation:
-placement of contoured cartilage grafts placed in infratip lobule, columella, and nasolabial angle
1292
-techniques to decrease tip rotation:
1. excise caudal septum near
spine
2. dorsum augmentation
Tip Volume
-techniques to decrease lobule volume:

-excising cephalic border of alar cartilage
-complete strip
-interrupted strip
-weakened strip
-minimum 4-8 mm of residual strip must be preserved
1293
SPECIAL CONSIDERATIONS IN RHINOPLASTY
CLEFT-LIP NOSE
TIMING OF REPAIR OF CLEFT LIP,

NOSE AND PALATE
3 mo -tip rhinoplasty
-cleft-lip repair
-closure nasal floor
-myringotomy and tube
placement
12-18 mo -palatoplasty
4-7 yr -columellar lengthening
8-16 yr -orthodontic treatment
9-11 yr -alveolar cancellous bone grafting
14-16 yr -definitive nasal reconstruction
14-17 yr -orthognathic surgery
-typical unilateral cleft-lip nose deformity

-deviation of nose to affected side
-lower dome
-flattened or crimped lateral crus
-caudal displacement of alar rim with horizontal nostril axis
-loss of nasal sill
-depressed or missing bony floor
-bilateral cleft-lip nose deformity:
-more symmetric
-columella is shortened to greater extent
-tip projection and support are less adequate
-both nostrils oriented horizontally
-most commonly, reconstruction of nasal floor and sill and reshaping of lower lateral cartilages are
performed primarily; major septal and bony pyramid reconstruction is often delayed
SURGERY OF THE NONWHITE NOSE
-nonwhite pt generally has thicker skin with more subcutaneous adipose tissue in nasal tip
-nasal bones usually small in both length and height
-low dorsum gives appearance of wider nose
-nasal spine usually much less significant structure
-augmentation may be needed to increase nasal height
-Gore-Tex usually used to build up significant depression but cannot provide support
-irradiated cartilage may be used
-other materials: Silastic, Mersilene mesh
-tip definition may be required cartilage graft used
SADDLE-NOSE DEFORMITY
-caused by significant loss of profile in bony and cartilaginous dorsum

-dorsal augmentation with autogenous bone or cartilage preferred materials
-creation of an L-shaped strut inserted via open approach
F.Ling - Special Considerations Rhinoplasty (1)
1294
-cartilage grafts:
-septal cartilage
-rib graft
-auricular graft
-bone grafts:
-mastoid cortex
-iliac crest
-calvarial bone
-alloplastic materials:
-risk of infections and extrusion
-Silastic, Gore-Tex, Mersiline, Proplast, Supramid,
-heterografts:
-bovine cartilage and bone (largely abandoned d/t resorption)
-homografts:
-demineralized bone
-high resorption rate
-irradiated cartilage
-high resorption rate
-unnatural feel
-acellular dermis (Alloderm)
ALAR BASE RESECTIONS
-proportion b/n height of infratip lobule and nostrils: 1:2

-proportion b/n ala and tip in lateral view is 1:1
-black nose tends to be broader and less projected and has more horizontally oriented nostrils than white
nose
-alar width is about same as distance between medial canthi
-alar base resection done to decrease width or flare of ala
-when projection is reduced significantly, resulting alar flare needs to be addressed with alar
resection
-an acute orientation of alar axis is a contraindication to alar resection because it would create an overly
narrowed base
-sill = nostril rim between
attachment of medial crura
and attachment of ala to
face
-lack of a clearly
defined sill a
relative
contraindication to
alar base resection
-nostrils and alar margin considered
as two concentric circles:
-inner circle or outer circle
can be narrowed or varying
degrees of both
1295
TWISTED NOSE
-evaluation:
-examine overall facial symmetry
-examine relationship of nose to face
-evaluate septum
-evaluate nasal spine: shape and position relative to
midline and medial crura
-evaluate bony pyramid: length height and any
convexity or concavity
-middle third of nose: depressions of one or both
upper lateral cartilages, deviation of dorsal septum,
profile abnormalities
-tip: position of domes, deficits of medial or lateral
crura, problems with support, contour
abnormalities
-alae, nostrils examined from frontal, basal and
lateral views
Surgical Technique
-an inadequately straightened septum is most
common reason for less-than-ideal postoperative
result
-high septal deviation in keystone area (region of
overlap of upper lateral cartilage by nasal bones)
associated with C-shaped external deviation at rhinion
-corrected via septoplasty
1296
-sequential osteotomies performed
-if above inadequate to straighten the angulation, light morselization, cross-hatching or
partial-thickness cuts can be performed on dorsal septum in keystone area
-sequential osteotomies:
-“opening a book”
-if pyramid deviated to left, lateral osteotomy cut made on opposite side medial
osteotomy made on right medial osteotomy made on left left lateral osteotomy made
-tip-work:
-free all soft-tissue attachments from lower lateral cartilages to allow them to return to
midline position
-existing cartilage is rearranged and grafting of deficits performed
-middle-third:
-contoured if needed
-simple depressions usually treated with onlay grafts
-C-shaped depressions can be camouflaged with onlay grafting
-collapse of one or both upper lateral cartilages can be addressed with spreader graft
placed between septum and upper lateral cartilage
AGING AND RHINOPLASTY SURGERY
-for children, cosmetic nasal surgery should be delayed until child has reached an age of essentially full
nasal growth (age arbitrary: 15-17)
-aging and the nose:
-changes in position of nasal tip
-major and minor tip support weakens with age descent of the nasal tip over the years
-changes in quality of nasal cartilage and bone
-changes in thickness and elasticity of skin
-nose divided into three parts:
-fixed upper part: nasal bones
-semimobile midportion: upper lateral cartilages and septum
-lower mobile part: lower lateral cartilages
-with age, the middle and lower parts become longer and more prominent; nasolabial angle becomes less
than the ideal 90o
-loss of bone and fat in premaxillary area may make nose appear more prominent
-goal is to reconstitute tip support mechanisms whenever possible
-dorsal-hump removal is performed conservatively in the older patient
1297
REVISION RHINOPLASTY
-as a general rule, revision rhinoplasty is not undertaken for at least 1 year after primary rhinoplasty
-most frequent complications requiring surgical intervention include knuckling (bosseleation), pinching,
columellar retraction, polly beak, alar retraction, midnasal asymmetry, saddling
BOSSELATION
-bosses: knoblike protuberances in

dome areas
-most common nasal tip deformity in
revision surgery
-etiology:
-major alterations of lobular
cartilage in original surgery
-sharp edges from previous
surgery
-complete rim strip that is too
narrow
-treatment:
-correction performed through
small slot incision careful
dissection and retraction
allows exposure of the boss
-raise low side (alar
septal graft)
-lower high side
(shave excision)
-combination of
above
PINCHING
-cause: excessive excision of lateral crural elements

-results in collapse of external nasal valve
-treatment:
-replacement with septal cartilage
-precise pocket created via rim incision
-graft fitted and incision closed
ALAR RETRACTION
-etiology:
-excessive cartilage and vestibular skin excision that results in scarring and retraction of the ala
-prevented by leaving at least 2-3 mm rim strip and not sacrificing any vestibular skin in
the primary rhinoplasty
-poor alar-columellar relationship
-congenital causes
-lateral crural cartilage and membrane excised
F.Ling - Revision Rhinoplasty (1)
1298
-treatment:
-shorten columella
-shorten contralateral ala
-cartilage graft (minimal retraction)
-auricular minicomposite (severe retraction)
-cymba concha graft
-ideally best to replace left ala with right cymba concha and vice versa
-skin is rolled out and graft placed in the vestibule
COLUMELLAR RETRACTION
-etiology:
-congenital
-alar-columellar disproportion
-traumatic
-iatrogenic resection of caudal septum
-treatment:
-raise ala
-cartilage graft
-composite graft
-used if membrane and cartilage are deficient
POLLY-BEAK FORMATION
-definition:
-postsurgical convexity of supratip relative to rest of nose, such that the lower two-thirds of nose
takes on the convex profile of a parrot’s beak
-etiology:
-inadequate dorsal cartilaginous septal resection
-excessive dorsal septal resection
-results in dead space in supratip area
-excessive tip cartilage resection
-leads to loss of tip support
-exuberant supratip scar tissue
-excessive bony pyramid reduction
-shortened columella
-excessive excision of domes of alar cartilage
-treatment:
-supratip massage
-high cartilaginous septum or exuberant scar tissue excise tissue excess through unilateral
intercartilaginous and complete septocolumellar incision
-augmentation of tip support and projections
-augmentation of dorsal profile
-steroid injections
1299
MIDNASAL ASYMMETRY
-etiology:
-nasal bone disparity
-subluxated upper lateral cartilage

-usually secondary to trauma
-overexcised upper lateral cartilage
-septal deviations
-treatment:
-appropriate nasal bone restructuring
-onlay grafts
-bolster subluxed upper lateral cartilage and camouflages the deformity by filling
concavity with appropriately shaped septal or conchal cartilage
-spreader grafts
-improve function of internal valve and appearance of midnasal area
-septal corrections
SADDLE-NOSE DEFORMITY
-etiology:
-congenital
-traumatic
-iatrogenic
-excessive resection of bone or cartilage from nasal dorsum
-treatment:
-retrodisplacement of tip
-for overprojecting tip causing relative concavities of pyramid
-lateral osteotomies
-raises dorsal profile line slightly and aids in closing open roof deformity
-autogenous graft
-septal cartilage best choice
-can be layered
1300
-other materials:
-conchal cartilage, temporalis fascia
-autogenous outer table cranial bone, iliac bone, rib cartilage implants
-disadvantages:
-irregularities, resorption, morbidity associated with harvesting body sites
-alloplastic graft
-supramid, gore-tex, mersiline, proplast
-silastic implants
-disadvantages:
-inflammation
-dislocation
-rejection
1301
BLEPHAROPLASTY
SURGICAL ANATOMY
-pretarsal orbicularis: muscular ring superficial to

tarsus
-preseptal orbicularis: muscular ring superficial to
orbital septum
-orbicularis: outer muscular ring that extends under
eyebrow and over inferior orbital rim
-orbital septum contiguous with tarsal plates

-orbital fat compartments occupy:
-two spaces in upper lid:
-central and medial compartments
divided by superior oblique muscle
-three spaces in lower lid
-central and medial compartments
divided by inferior oblique muscle
-central and lateral compartments
separated by a fascial sling
-Whitnall’s ligament:
-dense fibrous connective tissue that functions as a fulcrum for levator muscle
-Lockwood’s ligament:
-dense fibrous connective tissue that functions as a fulcrum for lower lid
-superior tarsal plate height: 8-9 mm
-inferior tarsal plate height: 4-5 mm
Layers above eyelid crease

-skin
-orbicularis muscle
-orbital septum
-orbital fat
-levator aponeurosis
-Muller’s muscle
-tarsal portion
EVALUATION
-ideal upper eyelid and brow in women:

-positioned medially at orbital rim, centrally just at or slightly above orbital rim, laterally above
orbital rim
-lid crease < 10 mm above lid margin
Indications
-blepharochalasis:
-rare condition of unknown cause
-may be familial, characterized by recurrent attacks of lid edema resulting in thin, redundant eyelid
skin and sunken appearance from fat herniation
-hereditary hypertrophy of skin and orbicularis muscle
F.Ling - Blepharoplasty (1)
1302
-dermatochalasis:
-laxity of eyelid d/t aging
-acquired draping of excess kin over lids, usually from actinic damage, thins eyelid skin, allows
for prolapse of orbital fat, progressive ptosis occurs with aging
-pseudoherniation:
-orbital fat protrudes through a lax orbital septum behind orbicularis muscle, baggy lids
Motivational History
-family history of baggy lids
-long-term desire for reversal of progressively deteriorating lid appearance
-no pt should expect external-world changes as a result of surgery
Medical History
-control fluid retention
-no ophthalmic conditions
-pt with full-blown dry-eye syndrome should not undergo blepharoplasty
-previous blepharoplasty
-secondary procedure must be conservative to avoid lagophthalmos or significant scleral show
Ophthalmic Evaluation
-check visual acuity, visual field tests, motility, ocular tension, measure scleral show, proptosis,
fundoscopic exam
-normal Bell’s phenomenon:
-assess adequate protection of the globe, evaluating by forcing the lids open and observing the
upward rotation of the globe to protect the cornea
Evaluation of Upper Lid-Brow Complex

-if a substantial amount of upper lid skin redundancy is actually infrabrow skin, removing this apparent
skin redundancy may depress the brow further do brow lift instead
-an upper lid blepharoplasty in the presence of an uncorrected unilateral ptosis will make the brow problem
more obvious
-evaluated lateral hooding; determine orbicularis oculi muscle hypertrophy or redundancy
-evaluate skin type:
-thin skin: requires conservative resection of fat from central compartment and conservative
resection of orbicularis to avoid a hollow look in central upper lid sulcus
-thick skin requires more aggressive surgical approach
-evaluate any lagopthalmos (incomplete eye closure): presence dictates conservative blepharoplasty
Evaluation of Lower Lid

-to determine type of surgical approach:
-transconjunctival:
-used only when there is fat pseudoherniation and either absent or very minimal
redundant skin or lax orbicularis muscle
-used mostly in younger patients
-external subciliary incision:
-for skin redundancy and muscle swag
-skin-muscle flap approach
-used mostly in older patients
-evaluate strength or laxity of lower lid (snap test):
-a slow return indicates caution with skin excision and the possible need for a horizontal lid-
shortening procedure
-1-2 mm of skin laxity can be addressed with CO2 laser; beyond 3 mm, it is probably best to used the skin-
1303
muscle flap
-palpate orbital rim to determine extent of bony margin contributing to lower lid appearance
THE OPERATION
Anesthesia
-local anaesthesia
-eyelids maintain anaesthesia for the shortest period
Upper Lid
-complete before beginning surgery on lower
lids
-mark upper lid crease: upper anatomic
boundary of tarsal plate
-should be at least 8 mm above upper
lid margin
-carry line medially into sulcus into
nasal junction
-carry line laterally to sulcus between
lateral orbital rim and lid
-grasp redundant skin with forceps:
-lower blade is at marked lid crease, upper blade is in region of maximum estimated excision
-with forceps blade closure, the upper lid margin should not elevate
-skin marked at several points and then connected into a line
-medial skin redundancy should always be underestimated slightly if pt has large medial fat compartment
-prevents tenting of skin and hypertrophic scarring
-depth of excision is to orbital septum
-orbital septum is opened sharply and fat is teased into wound and removed
-skin closed with subcuticular Prolene sutures
Lower Lid
Skin-Flap Approach:
-start at lateral canthal mark 2.5 mm below lid margin in subciliary crease
-small skin flap developed for 3 mm to expose and preserve pretarsal fibers orbicularis
oculi (preserves tension)
-separate pretarsal and preseptal muscle to puncta exposes lateral, central and medial
fat compartments
-fat removal done in lateral to medial direction
-before clamping medial fat pocket, observe and preserve inferior oblique muscle
-hemostasis must be absolute to avoid bleeding medial fat stump that could retract back
into the orbit
-skin-muscle flap draped superiorly and excision done with small scissors while patient is looking
upward with mouth open thus placing maximum tension on lower lid
-there should be no wound gap after excision
-lid suspension suture:

-used if some redundancy remains and allows further excision of skin
-placed b/n lateral orbicularis in skin-muscle flap and lateral orbital periosteum in a
vertical direction
1304
Transconjunctival Approach:
-local anaesthetic injected into subconjunctival space from puncta medially to the lateral canthus
-incision made with fine electrodissection needle (Colorado needle) through conjunctiva along
inferior tarsal border
-dissection carried immediately over orbital septum and under orbicularis
-separate orbital septum from orbicularis down to orbital rim
-exposes the three fat compartments removed after clamping
-sutures not required to close transconjunctival incision
POSTOPERATIVE CARE
-avoid looking downward for next 24 hours: downward gaze could allow skin-muscle flap to slide
inferiorly over underlying orbicularis septum
-sedentary activities for the first 3 days
-mild activities may resume on POD 10
-contact lenses may be safely used at POD 9-10
COMPLICATIONS
COMPLICATIONS
-severe cutaneous ecchymosis
Hematoma -haematoma
-more common after lower lid blepharoplasty -subconjunctival ecchymosis
-chemosis
-has palpable firmness
-lagophthalmos
-wound reopened and bleeding vessel cauterized -scleral show
-ectropion
Subconjunctival Ecchymosis -pigmented, wide, too low scars
-loss of vision
-resolves completely in 3 weeks
-dry-eye syndrome
-reassurance
EMERGENCIES
Chemosis -progressive haematoma
-severe dry-eye syndrome
-related to lower lid blepharoplasty -vision loss
-can resolve quickly (days) or remain for up to 6 weeks
-reassurance
Lagophthalmos
-usually mild after upper eyelid surgery
-minor tearing treated with ointments
Ectropion
-postoperative squint exercises and upward massage can reverse minor scleral show
-if caused by horizontal lid laxity that was unrecognized, horizontal lid-shortening procedure required
-may be due to downward displacement of skin-muscle flap simple releasing incision which elevates the
flap and redrapes it may resolve the problem
Poor Scars
-requires secondary scar excision
-scars result when wound is repaired over a large dead space
-can be treated by injecting very small amounts of Kenalog
Loss of Vision
-usually follow haematoma formation
-rapid decompression of a progressing retrobulbar haematoma is essential to preserve vision
1305
THE AGING FACE (RHYTIDECTOMY)
ANATOMY
Layers of Facial Planes

-skin
-subcutaneous fat
-SMAS
-mimetic muscles
-deep facial fascia
-deep elements (eg. facial nerve, parotid
duct, buccal fat)
Facial Nerve Relationships
-Temporal Branch:
-courses along line from earlobe to
zygomatic arch at point midway
between tragus and lateral canthus
-over zygomatic arch then
penetrates deep temporal fascia into
undersurface of superficial temporal
fascia
-Zygomatic Branch:
-courses 1 cm below zygomatic arch in a superior and medial direction from tragus to lateral
canthus
-Marginal Branch:
-exits the parotid 1 cm below mandibular angle, deep to platysma within the submandibular gland
fascia (superficial to the facial vein)
Superficial Muscular-Aponeurotic System (SMAS)

-fan-like structure that envelops face and forms bassi for resuspending sagging facial tissues
-translates facial muscle action to dynamic action in the facial skin
-continuous with platysma, superficial temporal fascia, perioral, nasolabial and periorbital muscles
-adherent to parotidomasseteric fascia (continuation of deep cervical fascia in the neck and deep temporal
fascia above zygomatic arch), dermis of cheek, and zygomatic arch
-located above parotid fascia, facial nerve, and facial artery
Osseocutaneous Retaining Ligaments:

-skin attachments to bone
-zygomatic ligament:
-attaches from zygomaticomaxillary suture (McGregor’s patch) to overlying malar skin
-mandibular ligament:
-attaches from anterior mandible to overlying parasymphyseal skin
Fascia-Fascia Retaining Ligaments:

-skin attachments to fascia
-parotid ligament: attaches to overlying skin
-masseter ligament: supports soft tissue of the medial cheek superiorly over the mandibular body
(attenuation results in jowls)
F.Ling - Rhytidectomy (1)
1306
PATHOPHYSIOLOGY
-intrinsic factors:
-histological changes in aging skin:
-thinning of epidermis
-retraction of rete pegs
-decreasing numbers of protective melanocytes
-dermal elastic filaments become thin and fragmented
-dermal collagen thickens but is reduced in amount
-reduced vascular supply to skin
-subcutaneous fat atrophy with gravitational redistribution of soft tissues
-extrinsic factors:
-sun-damage:
-actinic damage from UVA
-reduction in structural elements wrinkles
-growth of thickened, poorly organized fibers: elastosis
-increased amount of immature type III collagen
-decreasing vascular supply
-increasing cellular dysplasias actinic keratoses
-cigarette smoking decreases vascular supply
-increases skin slough 12x
Diseases of Premature Aging

-Cutis Laxa:
-associated with hernias, emphysema, aneurysm
-rhytidoplasty helpful
-Progeria:
-associated with growth retardation, early atherosclerosis
-rhytidoplasty not helpful
-Werner Syndrome:
-high pitched voice, diabetes, osteoporosis
-rhytidoplasty not helpful
ASSESSING CANDIDACY
-benefits of rhytidectomy limited to tightening and resupporting lower 2/3 of face

-intrinsic defects of tissues are not well addressed by suspension rhytidectomy
-ie. wrinkles will need to be addressed by resurfacing techniques
-contraindications:
-absolute:
-significant bleeding diatheses
-ASA class IV or V (dangerously compromising medical condition)
-relative:
-adverse healing: diabetes, chronic steroid therapy, connective tissue abnormalities
-psychiatric illness that involves a distorted perception of reality (eg. schizophrenia,
paranoid delusional disorder)
-psychological assessment: motivation for surgery
1307
General Considerations
-must assess the full face
-consideration for facial resurfacing, brow-lift, blepharoplasty, or rhinoplasty done
-adjunctive chin an cheek augmentation may be necessary
-assess position of hyoid bone:
-high and posterior hyoid bone is ideal, allowing maximum elevation of submental contour and
greatest definition between submentum and neck in profile
-evaluate for jowling
-evaluate for deepened melolabial crease, chin ptosis, increased distance from ciliary margin to malar
crescent
-generally, older pt with voluminous sagging skin or pt with fat face and neck would not be as good a
candidate as thinner 40- to 50-yo pt because postoperative skin draping with such excess is less satisfactory
-ideal candidate:
-40-50' s, good bony framework, strong cheekbones and chin, normally placed hyoid bone, thin
face, good elasticity, and stable weight
Avoiding Problems
-full evaluation of facial nerve function
-note any facial asymmetry
-note any scars or lesions
-deep nasolabial folds and downturned oral commissure will not be adequately addressed with
rhytidectomy
-smokers have 12x more risk of skin slough 2o vasoconstriction and higher incidence of haematoma
formation
-prior face-lift may complicate proposed procedure
PREOPERATIVE PREPARATION
-stop smoking 1 month prior to surgery

-aspirin, steroids, NSAIDs discontinued 2 weeks prior to surgery
SURGICAL PLANNING
-general anaesthesia generally considered

-patient marked in upright position
-incisions:
-women:
-should preserve temporal hair tuft and posterior hairline in women
-bring temporal incision forward into inferior aspect of temporal tuft at root of the helix
in female patients
-incision line gently curved in an anterosuperior direction indicated by patients hairline
-incisions can be post-tragal
-men:
-may need to shave behind ear, because beard skin may become relocated to postauricular
area
-temporal hair tuft generally will be thinner in width and density
-pre-auricular incision to preserve a non-hair-bearing area directly anterior to tragus
1308
OPERATIVE STAGE
-two-layer cervicofacial rhytidectomy with suspension of SMAS

-provides longer lasting results than suspension of skin alone
-surgical adjuncts:
-liposuction
-used for cervicofacial, submental, periparotid, and jowl regions
-allows for shorter flaps and less risk of hematomas
-platysmaplasty
-in absence of midline platysmal plication, SMAS suspension pulls anterior margins of
platysma laterally, actually weakening support for submental fat
-chemical peels should not be completed concurrently
-laser resurfacing techniques may be considered 6-12 months postoperatively
Flap Elevation
-+/- submental liposuction through submental incision: can help provide wider undermining
-+/- playsmaplasty: inspect submental fat, plication of platysma
-incisions made through pre-auricular incision
-earlobe dissected completely free
-superficial flap elevation in region of temporalis fascia prevents injury to frontal branch of facial nerve,
which crosses zygomatic arch
-flap may be liposuctioned under direct vision
SMAS Suspension
-imbrication techniques:
-involve direct incision, resection or undermining of SMAS fascia with reapproximation or
overlap of cut SMAS fascia edges
-increased sharp dissection increases risks of bleeding, nerve injury and skin slough
-plication techniques:
-avoids direct cutting and undermining of SMAS layer
-folding of SMAS fascia on itself and secures tissues with buried sutures
-suspension vectors:
-first vector:
-from angle to mandible to fascia near superior mastoid cortex
-affects cervicomental angle and angular bony contour of mandible
-second vector:
-originates in SMAS of cheek and mandibular ramus near anterior border of parotid and
extends posterosuperiorly toward preauricular sulcus and tragus
-third vector:
-extends from posterior border of cervical platysma in a predominantly superior direction
to SCM fascia in region of mastoid tip
-pull that is too posterior creates a distinctly unattractive and artificial appearance: widen and flatten the
oral commissure
Flap Closure
-skin is redraped over ear
-excess skin is removed
-“pixie or satyr” earlobe:
-complication in which an elongated earlobe is directly attached to facial cheek skin
-prevented by leaving generous amount of perilobular flap skin around ear lobe
-leave a generous portion of extra skin for post-tragal incisions in order to sufficiently cover tragal cartilage
without tension
1309
COMPLICATIONS
Nerve Injury
-incidence 0.4-2.6%
-most commonly injured nerve is sensory greater auricular nerve
-motor branch most vulnerable to direct, technical injury is frontal branch of zygomatic-temporal division
-superficial location
-traverses mid-portion of zygomatic arch
-avoid deep-plane dissection
-other nerve branches:
-marginal mandibular nerve
-platysma transsection and excessive SMAS traction in region near angle of mandible
and inferior mandibular border can result in nerve paralysis
-buccal nerve:
-aggressive dissection medial to anterior border of parotid
Hematoma
-most common and feared complication (15%)
-require immediate evacuation and control of bleeding source
-pain, swelling or firmness of buccal region
-reduction of haematoma incidence:
-intraop hemostasis
-closed suction drainage
-shorter flaps and two-layer face-lift
-liposuction preservation of vascular septae
-sequelae:
-skin necrosis
-infection
-prolonged ecchymosis
-alopecia
-subcutaneous nodules and skin puckering
-scar contracture
Skin Slough and Necrosis

-higher risk for smokers, longer and thinner flaps, and hematomas
-prevented by maintaining dermal-subdermal plexus (avoid overaggressive liposuction) and a tension-free
closure
Incisional Problems
-active hypertrophic scars
-satyr earlobe
-elongated earlobe from excessive inferior tension at lobule
-tx: V-Y advancement flap
-blunted and anteriorly dislocated tragus
-elevated temporal hairline
-ingrown hairs
-persistent hemosiderin deposits
Alopecia
-from poorly planned incisions and excessive tension
-avoid poorly placed incisions or tension
1310
THE AGING NECK
ANATOMY
-ideal neck has an acute cervicomental angle of 90o or less with hyoid bone at the apex of this angle
-aging of the neck
-collagen fragments and elastin fibers degenerate overlying integument atrophies and stretches
-perforating septa from underlying platysma support skin against gravity and create horizontal
rhytids
-insulating layer of fat thickens
-platysma is intimately connected to lower facial musculature (SMAS)
-function of the platysma is to stabilize chest muscles against the jaw during heavy lifting
-mandibular projection is important in determining strength or weakness of cervical profile
-a congenitally weak chin or one acquired by bone absorption and ptosis of mental muscles and
soft tissues allows enhancement of postoperative profile by simple augmentation
MANAGEMENT
-facelift operation is the cornerstone of surgery for the aging neck

-class I and II used to redrape skin
-class II fat must be removed liposuction
-limits of liposuction:
-inferior jawline superiorly
-SCM posteriorly
-cricoid inferiorly
-technique of liposuction:
-infiltration of tumescence solution
-fat removed first from midline
-fat further aspirated with diagonal tunnels coming from incisions placed under lobule of
the ear
-submental tuck:
-exposure of mandible periosteum in midline
-ellipse of fascia and muscle is excised in midline from mandible to notch of thyroid cartilage
-submental fat removed
-submental musculature is reconstituted in the midline
-cervicoplasty:
-3-4 cm submental incision made
-subcutaneous layer of fat peeled from platysma
-in midline, fascia-muscle complex incised form mandible to thyroid notch
-deep submental fat removed to expose mylohyoid and digastric muscles
-reconstruction submental triangle done by suturing anterior bellies of digastric muscle with
permanent braided suture
-platysma layer closed
-tangential shaving of up to three fourths of anterior belly of digastric raises hyoid bone
F.Ling - The Aging Neck (1)
1311
THE AGING FOREHEAD
FOREHEAD ANATOMY
-blood supply:
-lateral: external carotid superficial temporal artery zygomaticotemporal artery
-medial: ophthalmic artery supraorbital artery and supratrochlear artery
-nerve supply:
-central forehead: supraorbital and supratrochlear nerves (branches of V1)
-lateral sensation: lacrimal (V1), zygomaticofacial (V2), zygomaticotemporal (V2),
auriculotemporal (V3)
-motor function: temporal branch of facial nerve
-layers of scalp:
-S: skin
-C: subcutaneous tissue
-A: aponeurosis and frontalis
-L: loose areolar tissue
-P: pericranium
-muscles:
-frontalis muscle:
-interdigitates with orbicularis oculi
muscle, skin of eyebrows and root of
nose
-raises eyebrows forms horizontal
forehead rhytids
-corrugator supercilii muscles:
-draws eyebrows medially
-associated with vertical glabellar
rhytids
-procerus muscle:
-draws medial edge of eyebrow downward
-causes horizontal glabellar rhytids
F.Ling - The Aging Forehead (1)
1312
PHYSIOLOGY OF AGING
-with aging, upper third of face undergoes several

changes:
-loss of skin elasticity
-decreased bulk of subcutaneous tissue
-increased skull bone resorption
-ptosis of forehead, glabella, temple and
eyebrows
skin redundancy in infrabrow and
upper eyelid and hooding of skin
-with descent of eyebrows, pt tends to increase frontalis
muscle activity to dynamically elevate brows rhytids
become deeper and permanent as fascia contracts and
causes a permanent skin crease even when muscle is at
rest
Forehead Aesthetics
-eyebrow position:
-medial end in line with vertical drawn at ala of nose
-apex in between vertical drawn from lateral limbus and lateral canthus
-lateral end at an oblique line drawn through ala of nose and lateral canthus
-in men brow is more commonly at level of supraorbital rim; women brow arches higher
ASSESSMENT AND PLANNING
Ptosis
-must differentiate between lateral eyelid hooding that is a result of upper eyelid skin redundancy and that
due to ptosis of the eyebrow
-relaxation of frontalis muscle to assess
-aggressive upper eyelid blepharoplasty may result in further brow ptosis
-correction of temple ptosis improves lateral canthal crow’s feet
Rhytids
-note forehead, glabellar, and temple rhytids
Hairline Patterns
-women with medium to low hairlines are candidates for standard coronal or endoscopic forehead lift
-women with high hairline might benefit from trichophytic lift, which maintains their hairline position and
reduces vertical height of their high forehead
-male patients beware of male pattern baldness
-may require direct and mid-forehead lifts, which seek to camouflage incision in natural subunit
boundaries
Skin Type
-fair- and thin-skinned pts usually heal with more ideal scars that those with dark and thicker or sebaceous
skin
Asymmetries
-passive and dynamic asymmetries of eyebrows noted
-dynamic eyebrow asymmetries should not be altered surgically
1313
-passive asymmetries are not usually corrected unless it is the pt’s expressed wish may alter unique facial
characteristics
Bony Contour
-women with prominent supraorbital rim and excessive forehead bossing may appear masculinized may
benefit from bone reduction
MANAGEMENT
-non-surgical techniques to improve forehead appearance:

-sun avoidance
-cosmetics
-tretinoin cream
-collagen fillers
-chemical peels
-Botox
SURGICAL PROCEDURE AND TECHNIQUE HIGHLIGHTS
-indication for forehead and brow lifts:

-elevate ptotic and asymmetric brows
-address upper eyelid hooding
-reduce glabellar and forehead creases
-three surgical groups:
-coronal forehead lift and its trichophytic and pretrichial modifications
-direct brow lift and its modifications
-endoscopic forehead lift
1314
Coronal Forehead Lift
-standard procedure of choice for rejuvenation of upper face
-ideally for pt with generalized ptosis and rhytids of upper face and normal or low hairline
-high hair lines in women and male pattern baldness
-not useful to correct brow asymmetries
-advantages:
-well-concealed incision behind hairline
-good exposure of forehead muscles allowing accurate and extensive myoplasty
-disadvantages:
-elevation of frontal hairline
-hypesthesia posterior to incision line
Technique:
-incision made 4-6 cm posterior to frontal hairline; cant incision parallel to hair follicles to
minimize hair loss
-dissection in subgaleal (supraperiosteal) plane and superficial to superficial layer of deep
temporal fascia
-beware of frontal branch over zygomatic arch
-perform myotomy of corrugators, procerus, and central frontalis muscle
-make skin excision anterior to incision (usually 12-18 mm of scalp)
-expect up to 5 mm of stretch-back
-place suction drain for 24 hours if needed
Bilateral Temple Lift

-same incision as coronal forehead lift, except incision is carried from just above anterior helical root up to
mid-pupillary line but does not extend completely across midline scalp
-for men or women with primarily lateral eyebrow ptosis and upper eyelid hooding
-does not allow myoplasty procedures in forehead
-does not appear to offer longer lasting results seen with coronal forehead lift
Pretrichial Lift
-primary indication is for a high hairline and long vertical height to forehead in women
-does not raise anterior hairline to unaesthetically high level
-resection of redundant forehead skin reduces vertical height of forehead
-advantage:
-allows same wide access to forehead musculature as coronal lift
-disadvantages:
-broader area of anesthesia
Trichophytic Forehead Lift

-indicated where there is a desire to maintain hairline at its preoperative position or to reduce height of
forehead
Mid-forehead Lift
-for pts with significant forehead rhytids in which the scar can be camouflaged
-more closer and more direct approach to glabella and does not distort hairline
-major disadvantage is potentially unsatisfactory scar
1315
Direct Brow Lift
-indicated primarily for men with bushy eyebrows
-advantages:
-long-lasting lift as a result of excellent orbicularis
muscle suspension
-best technique to correct brow asymmetries or
unilateral brow ptosis
-more effective to correct marked ptosis of lateral
eyebrow
-disadvantage:
-eyebrow scar
-loss of hair follicles
-no effect on forehead, glabellar or temple ptosis and
cannot be used to improve forehead or glabellar
rhytids
Technique:
-skin incised directly above brows, inferior edge of incision just within brow hairs
-skin excised down to but not including frontalis
-supratrochlear and supraorbital nerves preserved
-includes suspension of orbicularis oculi to pericranium
Indirect Brow Lift

-essentially same procedure as direct brow lift, but skin excision is performed bilaterally at some distance
above eyebrow in forehead
-men who have male pattern baldness or women who have thin and light hair with a high hairline are
potential candidates
-advantages:
-ability to conceal forehead incision within a skin crease and at same time achieve a relatively
proximal suspension for the eyebrow
-disadvantages:
-relatively selective use
Browpexy
-performed through infrabrow incision
-may be indicated in pt primarily concerned about fullness or puffiness in lateral portion of upper eyelids
-lateral prominence in infrabrow region d/t prominent supraorbital margin or brow fat pad may be
improved with this technique
-use restricted to pts who have only mild to moderate eyebrow ptosis
Technique:
-performed through upper blepharoplasty incision
-dissection plane suborbicularis oculi
-fusiform fat excision
-may or may not also elevate brow
-if used to elevate brow, permanent suture suspension needed
Endoscopic Forehead Lift

-allow correction of brow ptosis and reduction of forehead and glabellar rhytids
-direct endoscopic visualization affords ability to identify and preserve supraorbital and supratrochlear
neurovascular bundles
-sensory neuropathy and scarring are decreased d/t incision size reduction, change in incision placement,
1316
and lack of skin excision
-high hairlines in women
-male pattern baldness
-tight, thick skin
-extensive bony attachements in Asians and American Indians
Technique:
-three to six small vertical incision just behind frontal hairline
-subperiosteal dissection plane
-dissection anteriorly and posteriorly
-endoscopic visualization and instrumentation
-supraorbital and supratrochlear nerves preserved
-myoplasty may be performed
-no scalp excision, therefore most surgeons fixate scalp in elevated position (screws, sutures,
tissue glue etc.)
COMPLICATIONS
-bleeding
-may be encountered from superficial temporal artery in coronal, pretrichial or trichopytic lifts or
from supratrochlear or supraorbital arteries
-sensory nerve injury

-permanent hypesthesia or anaesthesia centrally just posterior to coronal lift incision, up to 2 cm in
diameter not uncommon
-browplasty procedure results in temporary hypesthesia over lateral eyebrow margin for several
months
-motor nerve injury

-frontal branch of facial nerve at risk in zygomatic region
-lagophthalmos
-usually a problem in cases of previous or concurrent upper blepharoplasty with excessive skin
removal
-scar widening
-most often occurs in temporal region
-infection
-rare
-increased following haematoma development in diabetic pts
EMERGENCIES
-haematoma can compromise vascularity of flap and contribute to hair loss

-requires immediate evacuation and control of bleeding site
-corneal ulceration
-d/t lagophthalmos
-requires ophthalmic drops and ointment and an eye shield or tarsorrhaphy is necessary
1317
CONGENITAL AURICULAR MALFORMATION
ANATOMY AND EMBRYOLOGY
-important landmarks:
-helix
-superior crus
-inferior crus
-scapha
-antihelix
-cymba conchae and cavum conchae
-external ear located in lower neck
as mandible develops, ear ascends to side of head
-hillocks:
1 tragus
2 helix
3 cymbum
4 scapha
5 antihelix
6 antitragus
-muscles:
-intrinsic: major and minor helices, tragus, antitragus, transverse and oblique
-external: anterior auricularis, superior auricularis, posterior auricularis
-blood supply:
-superficial temporal a.
-posterior auricular a.
-occipital a.
-venous drainage:
-posterior auricular v.
-external jugular v.
-superficial temporal v.
-retromandibular v.
-lymphatics:
-parotid nodes
-cervical lymph nodes
-motor innervation:
-CN VII:
-temporal branch anterior and superior auricularis
-posterior auricular branch posterior auricularis
-lesser occipital nerve
-mastoid branch of lesser occipital nerve
-greater auricular nerve (C2, C3)
-auriculotemporal nerve (CN V3)
-Arnold’s nerve (CN X) supplies concha
F.Ling - Congenital Auricular Malformation (1)
1318
COMMON AURICULAR DEFECTS
-protruding ear:
-auriculocephalic angle > 30o
-cryptotia:
-pocket ear deformity
-cup ear deformity:
-constriction of helix and scapha
-colobomata:
-clefts of the ear
-lobule deformities
-microtia and anotia
PROTRUDING EARS
-vertical axis inclined 20o posteriorly

-vertical height ~ 6 cm
-width ~ 55% length
-helical rim protrudes 1-2 cm from skull
-measurements from scalp to helix at:
-top of helical rim: 10-12 mm
-level of EAC: 16-18 mm
-level of antitragus: 22 mm
-angle of protrusion ~20-30o
-superior aspect usually level with brow
-auricular landmarks of deformity:
-very poor antihelical fold
-overdeveloped concha
-abnormally formed scapha
-obvious lack of superior and inferior crus surrounding fossa triangularis
-otoplasty best begun before child starts school, b/n ages 5 and 6
-ear is at 85% of adult size and before the age of social stigmatization
Surgical Techniques
Mustarde Technique
-to correct underdeveloped antihelical fold
-involves placing several horizontal mattress sutures along scapha in a curved line to create an antihelical
sulcus
-problems: -sutures may become noticeable or could erode trough postauricular skin
-may fail to maintain proper curve of antihelical fold
Converse Technique
-an island of cartilage is created that sits anteriorly to the rest of the conchal cartilage
-cartilage produces a normal appearing fold
-allows more permanent retraction of auricle and is potentially more permanent correction of antihelix
1319
Farrior Technique
-combination suture and cartilage sculpting technique
-incisions made through cartilage on conchal rim only; then longitudinal wedges are removed at level of
superior crus and future antihelical fold
-an incision then is made through cartilage at level of antihelical fold, creating an island
Pitanguy Technique
-uses smaller island flap and conchal set back suture
-for pts with small amount of antihelical cartilage
Furnas Technique
-for overdeveloped concha
-if conchal bowl too large, an island of cartilage can be removed to narrow it and allow proximal portion to
lie firmly against mastoid
-placement of conchal mastoid sutures as far posteriorly to avoid narrowing of EAC
Complications and Emergencies

-chondritis
-inadequate correction (most common)
-haematoma
-“telephone ear” deformity:
-caused by too much flexion of antihelix at a level equal to mid-portion of ear and inadequate
flexion at superior and inferior poles
CONGENITAL MALFORMATIONS
Classification
-Marx:
-Grade 1: abnormal auricle with all identifiable landmarks
-Grade 2: abnormal auricle without some identifiable landmarks
-Grade 3: microtia is recognized by a very small auricular tag (“peanut ear”)
-Grade 4: anotia
-Weerda:
-Grade I: mild deformity with a slightly dysmorphic helix and antihelix
-major structures are present, and no additional cartilage is necessary during surgical
repair
-Grade II: all major structures present to some degree, but repair requires cartilage or skin
-Grade III: few, if any, landmarks; peanut and anotic ears
Syndromes Associated with Malformations

-Treacher-Collins Syndrome
-hemifacial microsomia
-Goldenhar syndrome
-Down syndrome
Surgical Reconstruction of Auricular Deformities

-correction of microtia usually begins at age of 6 years
-best material is autogenous rib cartilage
-option of osseointegrated prosthesis
1320
Surgical Planning and Treatment
TREATMENT OF CONGENITAL MALFORMATION OF
-photodocumentation AURICLE
-high-resolution CT scan of temporal bones
obtained Stage I: -auricular reconstruction (creation of cartilaginous
-at least 2-3 months allowed between stages framework with autogenous rib cartilage)
Stage II: -Lobule transposition
of reconstruction Stage III: -atresia repair (by otologist)
Stage IV: -tragal reconstruction
-Auricular Reconstruction (I): Stage V: -auricular elevation
-no stripping of perichondrium
during rib harvesting
-most common complication: atelectasis
-others: PTX, pneumomediastium, pneumonia
-sculpt cartilage to form framework
-framework implanted on side of head
-Lobule transposition (II):

-inferiorly based pedicle flap created
-flap then transposed into framework
-Atresia repair (III):

-drill out of temporal bone to create canal
-framework is then maneuverer into proper position
-Tragal Construction (IV)

-harvest composite graft
-J-type incision with anterior chin elevation
-placing composite graft and suturing anterior limb
-Auricular Elevation (V)

-incision made in postauricular area; covering with STSG
Complications
-skin necrosis overlying cartilage framework
-chondritis
-reabsorption of cartilage
-malposition of auricle implant
-tissue breakdown of skin graft or posterior aspect of ear
-keloid formation
1321
CHIN AND MALAR AUGMENTATION
CHIN AUGMENTATION
Methods of Evaluation of Chin Projection

-Legan angle:
-angle contained by lines from
glabella to subnasale and
subnasale to soft tissue pogonion
-should be 12+/-4 degrees
-Merrifield Z-angle:
-created by Frankfort horizontal
line and line connecting soft-
tissue pogonion and most
anterior part of lip
-Z angle should be 80+/-5
degrees
-Gonzales-Ulloa:
-determines chin projection
based on a line perpendicular to
Frankfort horizontal line that intersects nasion
-chin should approximate this line
Chin Implants EVALUATION OF CHIN AND MALAR AREAS

-alloplastic implants:
-deficiency of chin or malar projection with secondary disharmony
-Silastic (most common) according to predetermined facial proportions
-e-PTFE -effects of proposed changes or enhancement of pt’s overall facial
-porous polyethylene aesthetics
-acrylic -determination of the adjunctive procedure to accomplish desired
results such as facelift, rhinoplasty, liposuction
-after implant placement there is a 70% gain in -overall facial features, including dental occlusion, skin texture,
soft-tissue projection: anatomic proportions, prior facial trauma, and emotional stability
-ie: at 10 mm implant will provide 7 mm
soft-tissue increase
MANAGEMENT OF CHIN DEFICIENCIES
-intraoral insertion:
-risk of intraoral contamination, suture -alloplasts vs. sliding genioplasty
line irritation, larger incision line, -alloplasts: simpler, removable, fewer complications
-sliding genioplasty: useful in asymmetric jaws and extreme
inability to stabilize implant internally
microgenia
-extraoral insertion: -intraoral vs. extraoral alloplast placement
-avoids irritation and potential -intraoral:
contamination -bothersome suture lines
-anterior geniobuccal sulcus scar contracture
-allows implant to be suture stabilized to
-extraoral:
periosteum -external scar
-subperiosteal placement of implant is desirable
Operative Procedure (extraoral insertion) -various alloplastic materials and shapes are available commercially
-final soft-tissue augmentation represents70% of implant width
-local or general anaesthesia applied
-10-15 mm incision made in submental crease
carried down to and through periosteum
-periosteal elevation then made with a Joseph elevator
-superior and lateral subperiosteal envelope created
-avoid injuring mental nerves
-implant then placed within subperiorsteal envelope
-intraoral insertion via gingiva-buccal incision
F.Ling - Chin and Malar Augmentation (1)
1322
Complications
-displaced implant:
-implant may slide too far superiorly and obliterate anterior gingival-lip sulcus abnormal smile
-lateral displacement implant should be appropriately sutured to periosteum
-infection of tissue reaction:
-extremely rare
-antibiotics given if reaction does not resolve within 10 days, implant is removed and 8 weeks
should elapse before attempting to reinsert it
-bony resorption:
-occurs in almost all alloplastic implants
-may cause a problem to underlying teeth
-results in loss of projection
-improper size selection
-should wait at least 3 months before replacing implant to see what swelling and tissue reaction
will actually do to the appearance
-mental nerve injury from lateral dissection
-hypertrophic scar
Sliding Genioplasty
-indications:
-more severe cases of retrognathia
-insufficient vertical height
-hemifacial atrophy
-failed implant
-advantages:
-using pt’s own tissue
-can be used to decrease vertical
height of chin if necessary
-disadvantages:
-increased surgical time
-longer healing time
-risk of injury of anterior teeth and membranes around chin and lip area
-loss of lip competence (poor reapproximation of mentalis muscle)
Operative technique:
-incision made anterior to gingivobuccal sulcus and extends just laterally to cuspid teeth
-carried through orbicularis and mentalis muscles which will be reconstructed later
-periosteum is elevated inferiorly and laterally
-an osteotomy is made below cuspid apices and mental foramina at an appropriate angle
-inferior segment is advanced and held in place with four-screw cross-plate
-procedure can be combined with chin implantation to enhance contour
MALAR AUGMENTATION
-indications:
-lack of malar prominence
-adjunct to face-lift surgery if pt has deepened melolabial folds
-accentuation of malar prominence, creating a more pleasing aesthetic appearance
-asymmetry of malar prominence from congenital deformity, surgical resection or incomplete
reduction of malar fracture
1323
Evaluation
-decision mainly based on aesthetic appreciation than actual measurements
-when malar prominence falls more than 5 mm posterior to nasolabial groove on a true lateral projection,
there is usually a deficiency of the malar area
Implant Selection
-silastic:
-advantages:
-can be inserted into smaller pocket
-infection can be treated with implant in place
-disadvantages:
-tends not to stay in original position and must be anchored with suture at initial insertion
-forms surrounding capsule that may be palpated as surgical site matures
-reinforced e-PTFE:
-advantages:
-forms no capsule and has good tissue fixation
-disadvantages:
-large pocket required for insertion
-must be removed if infection occurs in immediate area
-porous polyethylene:
-advantages:
-has average pore size that ranges from 100-250 um
-allows for tissue ingrowth with minimal soft-tissue reaction
-disadvantages:
-not as flexible as silastic or reinforced e-PTFE
-must be removed if infection occurs
Operative Procedure
-intraoral incision placed just inferior and slighly anterior to parotid duct, 3 cm long
-incision carried down to periosteum
-elevation superior and lateral over malar and zygoma
-porous implants pressure loaded with clindamycin and saline
-implant placed over cheek
Complications
-malpositioned implant
-must be surgically removed and replaced
-infection
-implant removed
-new implant should not be reinserted for 6-8 weeks
-intraoral implant exposure
-implant removed, size adjusted, and reinserted
1324
CHEMICAL PEELING
Skin Anatomy
Epidermis
-stratum corneum: no nucleus, keratin in cytoplasm,
loosens then desquamates
-stratum granulosum: 3-5 layers thick, flattened,
keratohyalin granules
-stratum spinosum: basophilic cells
-stratum basale: single layer of cuboidal cells at basal
lamina
Epidermal-Dermal Junction:
-rete pegs: epidermal projections into dermal layer
-papillae: dermal, vascularized projections into
epidermal layer
Dermis:
-papillary dermis: collagen and elastin fibers
-reticular dermis: denser layer
Subcutaneous layer:
-contains fat and fibrous tissue
Principles of Chemical Peeling

-uses:
-remedy scarring
-treat actinic and other keratoses and pigmentary irregularities
-rejuvenate wrinkled photo-aged skin
-postacne scars
-scar revision
-address texture, decrease oiliness, size of pores
-peels classified by depth of penetration:

-very superficial: exfoliates stratum corneum down to stratum granulosum
-superficial: damages or causes necrosis of epidermis b/n stratum granulosum and basal cell
layer
-medium: causes necrosis of epidermis and wounding of papillary dermis
-deep: causes necrosis and wounding from epidermis down through papillary dermis
and into reticular dermis
-reparative processes:
-epidermis growth and thickening triggered by removal of stratum corneum as well as with deeper
damage of epidermis to basal layer
-deposition of some collagen and dermal glycosaminoglycans activated by epidermal wounds
-production of collagen and dermal ground substance generated with dermal wounds
-timeline:
-5 days: epidermis regenerates
-1 weeks: epidermis loosely attached to dermis
-2 weeks: new collagen deposits, youthful look
-1 month: pigment returns
-6 months: epidermis at normal thickness
-10 months: dermis normalizes
F.Ling - Chemical Peeling (1)
1325
-depth of penetration factors:
-agents used and their concentrations
-method of applications and layers of application
-use of pre-peel keratolytic agents
-use of degreasing agents
-use of occlusion or semi-occlusion of peeled skin
-skin thickness
-pilosebaceous gland activity and density
-anatomic location
-contraindications:
-active herpetic lesions
-pustular acne
-history of keloids
-collagen diseases
Trichloroacetic acid peels

-coagulation necrosis limits injury to epidermis and some papillary dermis
-superficial peel (10-30% TCA)
-medium-depth peel (30-40% TCA)
-for actinic keratoses, dyschromia and some wrinkling
-pretreatment with Jessner solution, glycolic acid or CO2 to increase penetration
-deep peel (45-50%)
-for wrinkles and rhytides
-can be performed on darker-skinned pts with less likelihood of permanent hypopigmentation than
with phenol
Jessner peel
-mixture of resorcinol, salicylic acid, and lactic acid in ethanol
-used to freshen skin, to treat acne and to lighten epidermal pigmentation
Glycolic acid peels

-superficial peeling agents to soften and smooth skin, improve skin texture and tone, enhance clarity and
correct minor photo-aged changes
-adjunct in decreasing epidermal pigmentation
-MOA: causes dis-cohesion of corneocytes in stratum corneum; deposition of collagen
Phenol peels
-indications:
-aging skin with fine and deep wrinkles
-photodamaged skin
-multiple, diffuse actinic keratoses
-pigmentary abnormalities
-superficial acne scars
-stucco keratoses
-deep dermal peel
-liquefaction necrosis resulting in deep dermal injury
-complications and caveats:
-pigmentary changes for darker skinned pts: hyperpigmentation or hypopigmentation
-relative contraindication: skin treated with x-rays destroyed adnexal structures needed for
1326
cutaneous regeneration
-previous used of systemic Accutane is a risk factor for scarring
-flap necrosis and scarring if used in conjunction with facelift
-toxicity:
-phenol is absorbed into circulation
-significant cardiac arrhythmias
-related to surface area of phenol applied: face is peeled in segment of no more than 25%
of facial area with 10-15 minute pause between segments
-renal and hepatic toxicity
-contraindications:
-areas treated with external beam radiation
-renal, cardiac, hepatic disease
-formulations:
-Baker’s solution:
-contains liquid phenol (88% phenol concentrate), distilled or tap water, liquid soap,
croton oil (enhances keratolytic and penetrating action)
COMPLICATIONS
-hyperpigmentation
-hypopigmentation
-scarring
risk factors:
-deep peels in keloid-forming patients
-peels that extend into reticular dermis
-post-radiation skin (lack of adnexal structures)
-Accutane therapy (wait 12 months to allow sebaceous glands to recover)
-excessive abrasion prior to application
-cardiac arrhythmia (with phenol)
-renal toxicity (with phenol)
-herpes simplex activation
-prophylactic valcyclovir started 48 hours before the peel and continued for 10-12 days
-cutaneous infection
-streptococcus or staphylococcus infection (uncommon)
-pseudomonas infections (uncommon)
1327
CERVICOFACIAL LIPOSURGERY
-adipose tissue
-mesodermal origin
-subdermal perivascular connective tissue containing adipoblasts preadipocytes adipocytes
-blood supply:
-< 1cm: from descending branches of subdermal plexus
-suctioning fat in direction upward toward subdermal plexus will cause greater
fat atrophy
-> 1cm: from ascending fascial arteries
-suctioning fat over fascia will cause greater fat atrophy
-volume and distribution of cervicofacial fat are strongly influenced by genetic factors
-surgical changes in fat volume should be considered permanent in cervicofacial region
-fat transplantation:
-reinjection of liposuctioned fat small cystic cavities lined with fibrous tissue in center or fat
which provide a useful matrix for providing volume
-6-9 months required for graft stabilization
-small, uniform quantities that maximize surface area-to-volume ratio
INDICATIONS AND CONTRAINDICATIONS
-indications:
-improve contour for correcting congenital or traumatic deformity
-correct lipoma and lipodystrophies
-defat flaps
-removal of localized fat deposits (wattles and jowls)
-correction of asymmetries
-adjunct to face/neck lift
-enhancement of malar eminences
-limited to subdermal volume changes
-difficult to obtain good results with pts with thin and lax skin
-fine rhytids cannot be corrected
-excessive or loose skin will remain redundant
-generalized obesity
-collagen vascular diseases
-endocrine disorders
-bleeding disorders
-inelastic skin, cellulitis or pitting defects, stretch marks, minimal to minor wrinkling, age of 55
and older, history of hypertension or diabetes
-injection of synthetic polymers produce significant complications:

-deformity and inflammatory tissue destruction
F.Ling - Liposuction (1)
1328
PREOPERATIVE ASSESSMENT AND WORKUP
-submental and submandibular areas (wattle and jowls) examined

-mandibular contour and cervicomental angle
-buccal and parotid areas
PROCEDURES AND TECHNIQUES
Liposuction
-standard: blunt suction technique of Illouz
-less damage to vascular and lymphatic arcades
-septae are left to nourish skin with perforating vessels less possibility of skin loss
-small suction cannula creates more subcutaneous tunnels and decreases likelihood of surface
irregularities
-start with blunt tipped 4- or 6- mm cannula with suction apertures 8 to 10 mm from end
-cobra-tipped cannula for dense fibrotic tissue but more likely to cause neural, vascular and skin damage
-“wet technique”
-tumescence solution (hypotonic salt solution with lidocaine and epinephrine)
-advantages:
-decreases blood loss and aids in dislodgement and separation of tissue planes
-disadvantage:
-fluid distorts surgical area, more difficult to determine actual volume of fat removed
-higher incidence of post-surgical edema and ecchymosis
-“dry technique” more applicable in head and neck
-does not use tumescence solution
-ultrasound-assisted liposuction:
-20-40 kHz ultrasonic frequency at cannula tip forms microcavities or bubbles eventually
bubbles implode
Applications for Liposuction and Lipocontouring

-six appropriate areas:
-submental
-submandibular
-preparotid
-lower nasolabial
-upper nasolabial
-malar fatpad areas
-improve chin/neck contour:
-direct approach: via submental incision
-indirect approach: via bilateral postauricular incisions
-deep nasolabial folds and redundant medial cheek fat:
-incision at nasal aperture
Lipoinjection
-harvest with 18-gauge or larger cannula
-inject small quantities (usually in 0.1 ml increments) beginning distally
-overcorrect by about 30%
Applications for Lipoinjection

-six areas that respond well to lipoinjection:
-glabellar frown line
1329
-inframalar groove
-cheek hollows
-nasolabial fold
-oral commissure
-mentum
COMPLICATIONS
-Minor:
-ecchymosis
-dyesthesia
-irregularities, bulges, depressions
-pigmentation changes
-Major (rare)
-neural and vascular injury
-haematoma/seroma
-infection
-skin loss
1330
MANAGEMENT OF BENIGN FACIAL LESIONS
EPIDERMAL LESIONS
Actinic Keratosis:
-small multiple erythematous lesions on sun-exposed areas
-10-20% develop into SCCa
-actinic cheilitis: occurs on vermilion border of lips
-tx: -usually cryotherapy
-multiple lesions: dermabrasion, chemical peeling or topical 5-FU
Actinic keratosis
Cutaneous Horn:
-hyperkeratotic conical lesions whose height is at lease half their largest diameter
-various types of lesion may be present at their bases (actinic keratosis, verruca,
SCC, seborrheic keratosis)
Cutaneous horn
Seborrheic Keratoses:
-brownish black verrucous stuck-on appearance
-tx: -dermal curettage
Keratoacanthoma:
Seborrheic keratosis
-clinically and histologically can resemble SCC
-occur in elderly people on sun-exposed areas
-rapid growing reaching full size in 6-8 weeks then involuting spontaneously (less
than 6 months)
-can also occur with Muir-Torre Syndrome
-genetic syndrome characterized by a combination of sebaceous tumors of
the skin and one or more internal malignancies, most often colon cancer
-types of sebaceous skin neoplasia include sebaceous adenoma, sebaceous
Keratoacanthoma
epithelioma, sebaceous carcinoma, and keratoacanthoma
-tx: -observation or complete excision
-avoid shave biopsy because histologic changes at lesion base are
important in differentiating from SCCa
Cysts:
-often compressible and may have visible puncta
Epidermoid cyst
Millia:
-small, yellowish white, 1-2 mm papules
Comedones:
-open (blackheads) - occur with acne vulgaris
-closed (whiteheads)
-histologically: dilated cystic hair follicles filled with keratinous and lipoid material
F.Ling - Benign Facial Lesions (1)
1331
SKIN-APPENDAGE TUMOURS
Trichofolliculomas:
-solitary
-central pore with white wool-like tuft of hair
-tx: -shaving, punch excision or CO2 laser
Tricoepitheliomas: Tricofolliculoma
-small, flesh-coloured papules
-solitary or multiple (AD) cluster around central face
-can occur with cylindromas
-tx: -shaving, punch excision or CO2 laser
Trichilemmomas:
-small pink to brown facial papules
-multiple hamartoma syndrome (Cowden disease) Multiple tricoepitheliomas
-AD
-associated with high incidence of breast cancer, other visceral
malignancies
-fibrous hamartomas of breasts, thyroid and GI tract
Sebaceous Hyperplasia:
-2-3 mm yellow to orange lobulated papules with slight umbilications
-can occur with cyclosporine use Syringoma
-feature of acne rosacea
Syringomas:
-intraepidermal eccrine duct adenomas
-predominantly in women at puberty - multiple lower eyelid lesions
-tx: -excision
Hydrocystomas:
Hydrocystoma
-uncommon cystic periorbital lesions
-translucent bluish quality
-tx: -excision
Pilomatrixomas:
-tumours differentiating toward hair cells
-solitary, hard, deep-seated nodules
-common in children and young adults
-tx: -excision Pilomatrixoma
Nevus Sebaceus:
-tumour differentiating toward sebaceous glands
-congenital lesion presenting as a solitary, often linear, slightly raised, orange-
yellow hairless plaque on scalp or face
-basal cell carcinoma develops in 5-7%
-tx: -excision
Nevus sebaceus
1332
NON-SKIN-APPENDAGE TUMOURS
Vascular Tumours:
Hemangiomas:
-congenital:
-nevus flammeus
-vascular malformation (port wine stain)
-medial nevus flammeus:
-lightens with age and not associated with
underlying abnormalities
-lateral nevus flammeus:
-darkens with age
-associated with leptomeningeal angiomatosis
(Sturge-Weber syndrome) or osteohypertrophy
and arteriovenous fistulae (Klippel-Trenaunay Nevus flammeus
syndrome)
-tx: tunable dye lasers
-capillary haemangiomas
-appear b/n 3rd and 5th weeks of life
-grow for months and then regress
-70% regress by age 7
-tx: -usually resolve spontaneously
-treat those that ulcerate, encroach on vital structure
(nose, eyes, mouth) or are frequently traumatized
Capillary hemangioma
intralesional corticosteroids used
-cavernous haemangiomas
-appear at any age
-association with Maffucci syndrome (dyschondroplasia
and osteochondromas) or blue rubber-bleb nevus syndrome
-Kasabach-Merritt syndrome: Cavernous hemangioma

-consumptive coagulopathy rarely developing with
widespread haemangiomas secondary to coagulation within
the haemangioma
-acquired:
-pyogenic granuloma
Ectasias:
-telangiectasias
-occur in many conditions:
-scleroderma, dermatomyositis, radiation dermatitis, chronic Pyogenic granuloma
alcoholism, liver disease, pregnancy, childhood, Osler-
Rendu-Weber disease
-venous lakes
-deep blue cutaneous nodules typically on lips, ears, or face
-arteriovenous malformations
1333
Fibrous Tumours
-skin tags
-fibrous papules
-adenoma sebaceum
-uncommon but characteristic feature of tuberous sclerosis
-actually angiofibromas
-tx: dermabrasion, CO2 laser, or argon laser
-hypertrophic scars Adenoma sebaceum
-keloids
Fatty/Muscular Tumours
-lipoma
-leiomyomas: arise from erector pili hair follicle smooth muscle
Neural Tumours
-neurofibromas
-benign nerve sheath tumours
Melanocytic Tumours
-tumours of nevus cells (melanocytic nevi), epidermal melanocytes, or dermal
melanocytes
-melanocytic nevi:
congenital or acquired
-histological classification:
-Junctional: flat pigmented Junctional nevi
-Dermal: flesh coloured and dome shaped or pedunculate
-Compound: in between
-Spitz nevus:
-epithelioid and spindle cell nevus
-benign but can resemble malignant melanoma histologically
-epidermal melanocytes:
Dermal nevi
-freckles (ephelides)
-lentigines
-lentigo senilis (actinically induced)
-lentigo simplex
-may become malignant lentigo maligna or lentigo maligna
melanoma
-dermal melanocytes:
-nevi of Ota
-unilateral blue-brown-black discolourations of the periorbital Compound nevi
region, temple, forehead, malar area and nose
-rarely undergo malignant degeneration
-blue nevi
-no malignant potential
Spitz nevus
1334
Inflammatory Lesions
-warts (verruca vulgaris)
-HPV infection
-molluscum contagiosum
-poxvirus
-shiny, flesh-coloured to pink, dome-shaped, firm papules with central umbilications
THERAPEUTIC CONSIDERATIONS:
Dermal Curette
-semi-sharp round to oval blade of variable size
-blade will not normally cut through normal collagen
Electrosurgery
-electrodesiccation
-healing by secondary intent may take 2-3 weeks
Cryotherapy
-tissue destruction determined by volume of cryogen applied, duration of exposure and technique used
-NO, fluorocarbon sprays and liquid nitrogen
Intralesional Corticosteroid Therapy

-side effects: atrophy, hypopigmentation
-significant systemic absorption when more than 20 mg injected in single session
-used to soften keloids or hypertrophic scars (10-40 mg/ml) repeated every 2-3 weeks to minimize systemic
toxicity
Chemical Peeling
-actinically damaged skin
Dermabrasion
-can be more predictable than chemical peeling because extent of wounding can be more precisely
controlled
Laser Surgery
-precise margination, good control of destruction depth, good hemostasis, decreased postoperative pain,
and target specificity
Hemostatic Agents
-Monsel solution (ferric subsulfate) - protein coagulant; permanent discolouration
-aluminium chloride
-silver nitrate
1335
MANAGEMENT OF ALOPECIA
Medical Treatment of Androgenetic Alopecia

ETIOLOGY OF ALOPECIA
-directed against dihydrotestoterone (DHT)
-finasteride: -androgenic alopecia (male pattern
-competitive and specific inhibitor of type II 5-alpha-reductases baldness)
(enzyme that converts testosterone into DHT) -autoimmune disease
-burns
-may reduce libido and sexual potency -chemotherapy
-minoxidil: -dermatologic disorders (eg. psoriasis)
-MOA unclear -radiation exposure
-does not have any known effect on production, excretion, or -neoplasms
-traction
interactions of human androgens
Hairline Design TREATMENT OF ANDROGENETIC

-frontotemporal triangle is formed by recession of frontal hairline ALOPECIA
superiorly and the temporal hairline posteriorly
-apex of the triangle is designed to fall on a vertical line that intersects the Finasteride (Propecia)
Minoxidil (Rogaine)
lateral canthus Hair-bearing autografts:
-follicular unit grafts
-micrografts
-minigrafts
PATIENT EVALUATION
-standard circular grafts
-scalp reduction
-prevent moving follicles at risk for future alopecia into cosmetically -extensive scalp reduction
important areas on the scalp any future hair loss will result in exposed -flaps
-tissue expansion
scars over scalp
-low density donor hair may be a contraindication to hair transplantation
results in very thin hair density from transplantation procedures
-older pts generally have well-established patterns of alopecia
METHODS OF TREATMENT
Autograft Hair Transplantation
Donor Site
-found on sides and back of head and is limited anteriorly be a vertical line through the EAC
-superior border of safe donor area in mid-occipital region generally located beneath horizontal line that
intersects superior attachment of auricles to the scalp
-strip of follicles no larger than 1 cm is removed
-ensure no transection of follicles
-individual grafts are then made
Recipient Site
-grafting requires 2-4 sessions
-grafts inserted, evenly spaced apart and maintaining adequate circumferential bridge around each graft
-this maintains adequate circulation around each graft
-maintain consistent graft angling of follicles
-two methods to achieve density and refinement within transplanted hairline regions:
a) Exclusive use of follicular unit grafts

-microscopic cluster of closely united follicles
-usually contains one-four hairs
F.Ling - Alopecia (1)
1336
b) Combination of minigrafts and micrografts
-minigrafts contain 3-8 hairs
-create higher-density hair more posteriorly
-micrografts have only 1-2 hairs
-refine outer perimeter of transplanted recipient site
-soften transition zone between bald forehead skin and transplanted frontal
hairline
-wait 4 months between each session
-newly transplanted grafts enter telogen effluvium phase and lose preexistent hair over 2-6 weeks
-new hair begins growth in about 10-16 weeks
Sequelae and Complications

-severe forehead edema
-arteriovenous fistula
-haematoma
-infection, necrosis
-poor hairline design
-scarring, telogen
Scalp Reduction
-excision of bald skin from crown and central scalp regions
-hair bearing scalp is undermined and advanced superiorly to cover excision site
-scalp reduction patterns:
-midline sagittal ellipse, Y pattern, lateral crescent
Extensive Scalp Reductions

-to eliminate alopecia in crown and vertex regions
-do not provide hair in frontal region
-bilateral occipitoparietal (BOP) flap and bitemporal (BT) flap
-require staged ligation of occipital vessels 2-6 weeks before actual reduction procedure
-require identification of superficial temporal arteries (STA)
-extensive undermining of scalp, hair-bearing BOP advanced superomedially and anteriorly to
replace a horseshoe-shaped bald area adjacent to donor fringe
-BT flap procedure performed 2-3 months after BOP flap
-complications:
-reduced blood supply inherent to these large flaps can result in temporary telogen
-risk of necrosis of flaps
-widening of mid-scalp scar
-visible scar formation in anterior temporal incision line
-thinning hair density within donor scalp regions
Tissue Expansion
-useful in pts with MPB who would benefit from hair-bearing flap or a scalp reduction but are limited by
poor scalp flexibility
-scalp expanders: temporoparietal and occipital donor regions
-does not provide coverage to frontal regions
-frequent expansion (2-3x/wk) until pain tolerance reached
-scalp reduction is then performed
-complications: infection, haematoma, exposure of implant, implant failure
Juri Flap
-pedicled transposition flap based on STA
-for frontal hairline restoration
F.Ling - Alopecia (2)
1337
LASER SKIN RESURFACING
-laser produces thermally induced exfoliation with superior precision, depth control, and uniformity with
additional beneficial therapeutic effects on collagen
SKIN ANATOMY
-total skin thickness: 1.5-4.0 mm
-epidermis: 0.04-1.5 mm
-keratinocytes
-melanocytes in basal layer
-dermis:
-superficial papillary dermis
-deeper, thicker reticular dermis layer
-contains fibroblasts: collagen and elastin production
-appendiceal structures
-hair, sebaceous glands, sweat glands
-neck skin has relative lack of pilosebaceous glands increased risk of scarring and delayed
healing
-age related changes in skin:
-thinning of epidermis and dermis
-flattening of dermal-epidermal junction
-collagen and elastin fibers become fragmented and degenerate
-decrease in number of appendiceal structures
LASERS IN SKIN RESURFACING
-CO2 laser most commonly used

-water is the target chromophore
-selective photothermolysis:
-selective heating of target tissue determined by laser wavelength and is of sufficient energy to
exceed vaporization threshold (5 J/cm2 for skin)
-exposure time is less than thermal relaxation time defined as time required for volume of target
tissue to dissipate 50% of its heat (1 msec for skin)
-advantage of laser resurfacing:
-realignment of collagen and elastin fibers correlate with thicker and smoother textured skin
-continued clinical improvement observed for up to 18 months
F.Ling - Laser Skin Resurfacing (1)
1338
INDICATIONS AND PATIENT SELECTION
-indications:
-rhytids
-dyschromias
-scarring conditions:
-superficial/shallow acne
-elevated scars more favourable than depressed scars
-immature more favourable than mature scars - ideally 6-8 weeks following scar
formation for optimal results
-skin lesions:
-lentigines and seborrheic keratoses
-actinic keratoses
-early superficial basal cell carcinoma
-adjunct to other facial rejuvenation procedures (eg. blepharoplasty, rhytidectomy)
-avoid using laser on area where there is subdermal undermining
-contraindications:
-active or recent use of isotretinoin (Accutane) impaired ability of pilosebaceous apparatus to
reepithelialize wound
-skin resurfacing delayed 6 months to 2 years after discontinuation of medication
-active infection
-other areas of caution

-history of HSV resurfacing may cause reactivation
-prior resurfacing procedures (eg. chemical peeling, or dermabrasion) alters anatomy of skin
-lower lid laxity who have undergone prior blepharoplasty increased risk of developing
ectropion
-radiation therapy, collagen vascular disease (eg. scleroderma), hypertrophic scars or keloids
-dynamic (present in animation) vs static (present in animation and repose) rhytids
-dynamic rhytids:
-attached to facial musculature - not very responsive to laser resurfacing
-horizontal forehead lines, glabellar frown lines, periorbital crow’s feet, nasolabial folds
-static rhytids:
-correctable with laser
resurfacing
FITZPATRICK CLASSIFICATION OF SUN-REACTIVE SKIN
-classification systems of skin: TYPES
-Glogau classification
-Fitzpatrick: Skin Type Skin Color Sunburn Tan
-light skin (Type I) to dark I White Yes No
skin (Type VI)
-types I-III will tolerate II White Yes Minimal
resurfacing without
III White Yes Yes
significant risk of
pigmentation changes IV White No Yes
-types IV-VI at increased
V Brown No Yes
risk
VI Black No Yes
1339
PREOPERATIVE PREPARATION
-skin preparation initiated approximately 6 weeks prior to resurfacing procedure

-agents commonly used:
-retinoic acids
-epidermal thickening
-enhanced collagen regeneration
-new vessel formation
-reduced cellular atypia
-uniform disbursement of melanin granules
-alpha-hydroxy acids
-diminishes corneocyte adhesion better penetration of laser
-hydroquinone
-bleaching agent that down-regulates melanin production
-used in patients who are prone to develop hyperpigmentation after resurfacing
-prophylatic oral antiviral and antibacterial medications
TECHNIQUE
-protection of patient, personnel and surgeon

-local, regional or general anaesthetics based on pt’s and surgeon’s preference
-depth of tissue vaporization by varying laser parameters and number of passes with laser
-chin has thickest skin
-eyelids have thinnest skin
-using recommended CO2 laser settings, depth after one pass ~60-80 um.
-usually 1-5 passes are required depending on area
-must wipe away dessicate white debris; if left on, will act as thermal conductor
-pink colour superficial papillary dermis
-tan-grey colour deeper papillary dermis
-yellowish hue upper reticular dermis; do not go beyond or adnexal structures will be injured leading to
scarring
-neck usually left untreated to avoid risk of poor healing and scar formation
POSTOPERATIVE CARE
-application of semi-occlusive dressing to promote wound healing:

-open: vaseline
-closed: composite foam, hydrogel, plastic mesh, polymer film
-laser wound re-epithelialized in 7-10 days
-sun protection for at least 3-6 months
SEQUALAE AND COMPLICATIONS
-common sequelae: usually resolves

-erythema: lasts 3-5 months
-edema and pruritus
1340
-complications:
-milia:
-epithelial inclusion cysts from follicular plugging with occlusive dressings during
reepithelialization
-resolve spontaneously
-contact dermatitis:
-d/t decreased barrier function of de-epithelialized skin
-antibiotic-containing ointments, soaps, moisturizers and cosmetics
-tx: low-potency topical steroid ointments
-HSV infections:
-most common infections seen as consequence of laser resurfacing
-vesicles usually absent dx based on high clinical suspicion
-failure to treat with antivirals lead to scarring or disseminated infection
-bacterial and fungal infections:
-less common
-usually d/t Staph aureus and Pseudomonas aeruginosa
-hyperpigmentation:
-common following skin resurfacing in patients with Fitzpatrick skin type III or higher
-pts with darker skin types are treated prophylactically with hydroquinone in preoperative
period
-postop hyperpigmentation also tx with hydroquinone
-hypopigmentation:
-delayed; may be observed up to 1 year
-permanent and few treatments available
-can occur with any skin type
-scarring:
-increased if: isotretinoin use, keloid tendency or previous resurfacing procedures
-also from excessive tissue ablation into deep reticular dermis
-regional variations: perioral, mandibular and neck areas
-tx: topical and intralesional steroids, silicone dressings and pulsed dye laser
-ectropion:
-previous lower blepharoplasty at increased risk
-lower lid laxity
-requires surgical repair
COMMON LASER TYPES
-CO2 Laser:
-invisible beam
-primarily absorbed by water
-excellent for cutting, coagulation, or ablating (depending on area of focus)
-Nd:YAG Laser:
-near-infrared beam, invisible
-primarily absorbed by pigmented tissues
-deeper penetration
-more scatter than CO2 lasers
-indicated for cutaneous lesions (port-wine stains, telangiectasia, hemangiomas, etc.)
1341
-KTP Laser:
-visible laser, primarily absorbed by oxyhaemoglobin
-may use a fiberoptic carrier
-indicated for cutaneous lesions and as a cutting tool
-Argon Laser:
-visible, broad-band blue light
-primarily absorbed by oxyhaemoglobin
-depth of penetration between CO2 and Nd:YAG lasers
-Flashlamp-excited Dye Laser:

-visible, yellow light
-vascular sensitive
-less scarring and hypopigmentation than Nd:YAG and argon lasers
-indicated for cutaneous vascular lesions
ERBIUM LASER
-produces more superficial ablation than CO2 laser

-advantage:
-faster healing time with less erythema
-useful in treating more superficial rhytids
-disadvantage:
-less skin tightening
-increased bleeding
-unable to manage deeper wrinkles and more severe photodamage
1342
TISSUE EXPANDERS
-advantages:
-avoids distant flaps, allows for hair-bearing skin
-disadvantages:
-requires multiple procedures, deformity from expansion device
-common uses:
-face and neck, scalp (alopecia), preauricular region (otoplasty), concurrent procedure with serial
excisions
Biomechanical Properties:
-collagen: stores strain energy applied during deformation of skin
-elastin: most linearly elastic biosolid known determines elastic property
-glycosaminoglycans: binds collagen and elastin fibers
-hyaluronate: type of GAG that binds fluid to form a gel
-Biological Creep:
-property of conventional tissue expanders
-permanent changes in microanatomy
-increases epithelial mitotic activity and subdermal vasculature
-results in net increase in surface area
-Mechanical Creep:
-no change in microanatomy
-displaces fluid and extracellular substances
-realigns collagen fibers by breaking bonds with GAGs and elastin fibers
-no net increase in surface area
-Stress Relaxation:
-decrease in stress when skin is held under constant pressure
Techniques:
-base should be 2.5 times area of defect
-rectangle expander has best expander volume-to-skin area
-most expanders used in head, face, and neck are from 1-250 ml
-Conventional tissue expansion technique:
-expand over 4-6 weeks of use
-relies on biological creep
-Rapid intraoperative tissue expansion:
-expansion and deflation of prosthesis in operating room over 3 minute intervals (typically 3
cycles)
-no true net gain of skin surface area
-relies on mechanical creep
-important to match expander to geometric configuration of the expansion site
-serial injections of saline performed weekly
-W-shaped or V-shaped incision recommended as universal incision for insertion of a tissue expander
Specific Site Considerations
Scalp
-used to correct male-pattern baldness
-used to close defects after tumour excision or to repair scar tissue
-implant placed in loose subgaleal connective tissue, superficial to periosteum
F.Ling - Tissue Expanders (1)
1343
Auricle
-postauricular skin, which lies over a bony prominence and is thinner than scalp, can become necrotic at
pressure points can expose the implant
-this skin is expanded more slowly than is the more flexible skin of the face and neck
Face
-expander inserted extraperiosteally beneath frontalis muscle
-expanded forehead flap can be used repeatedly for nasal reconstruction
-cheek can provide enough tissue by means of expansion to resurface almost one third of ipsilateral face
-for traumatic and burn scars, after Mohs tumour excision, or for congenital skin lesion
-expander placed through preauricular face-lift incision
Neck
-skin of neck amenable to expansion, although not used as much as skin of scalp and face
Complications:
-current rate is 5-7%
-infection
-extrusion and leakage
-neuropraxia or vascular compromise
-bone resorption
-skin necrosis
-hematoma
F.Ling - Tissue Expanders (2)
1344
OTOLARYNGOLOGY FACTS AND POINTS
Anatomy of the Ear
1. The temporalis muscle attaches to the squamosa portion of the temporal bone.
2. The anterior boundary of the tympanic cavity is the carotid wall, eustachian tube, tensor tympani.
3. Meckel’s cave is a concavity in the superior part of the temporal bone.
4. Gradenigo syndrome is associated with inflammation of the following cranial nerve in the Dorello canal:
VI
5. Trautmann triangle is determined by the sigmoid sinus, bony labyrinth and superior petrosal sinus or dura.
6. The upper limit of normal for the diameter of the internal auditory canal in an adult male is 8 mm.
7. The posterior semicircular canal and saccule are innervated by the inferior vestibular nerve
8. The inferior tympanic artery to the middle ear is a branch of the ascending pharyngeal artery.
9. The superior portions of the utricle and saccule and the superior and horizontal semicircular canals are
supplied by the anterior vestibular artery.
10. The lobule of the ear has sensory innervation from C2,3 via lesser occipital nerve.
11. The average size of the footplate is 1.41 x 2.99 mm.
12. The scala vestibular and scala media are separated by the Reissner membrane.
13. In the adult, the eustachian tube is approximately 35 mm.
14. The auricle of the ear has reached adult shape by the following week of gestation: 20th.
15. Congenital microtia occurs in 1:20,000.
Audiology
16. The human ear is capable of hearing the frequency range form 20-20,000 Hz.
17. In audiology, speech noise is white noise with the following frequencies filtered out: below 300 Hz and
above 3000 Hz
18. The decibel scale is logarithmic and incorporates a ratio. All of the following are used for reference levels:
intensity, sound pressure, hearing, sensation level.
19. The effective vibrating part of the tympanic membrane is approximately 55 mm2.
20. The transformer ratio of the middle ear is about 22:1. This translates into approximately 25 dB.
21. In 1960, Bekesy outlined his theory of hearing. He stated that when the stapes footplate moves in and out
of the oval window, there is a resulting upward and downward movement of the basilar membrane, which
causes distortion of the endolymph. This theory is called the Travelling Wave Theory of Hearing.
22. A saucer shaped (SNHL) audiogram is most indicative of congenital hearing loss.
23. A double peaked impedance audiometry pattern can be seen in the use of a high frequency probe tone in a
“B” tympanogram.
24. A type As tympanogram is consistent with otosclerosis.
25. The above tympanogram is a type Ad.
26. During a Carhart Tone Decay Test, one presents a tone at the threshold for the following number of
seconds: 60.
-a tone is presented for 60 seconds. If the tone disappears, raise the stimulus level and continue
until the patient can hear for 60 seconds. If this last level is 20 dB or more above threshold, the
test is positive for retrocochlear pathology.
27. The following test is similar to the Carhart test but it incorporates rest periods during the testing. It is the
Owen Test.
-test to help rule out retrocochlear pathology.
28. In Bekesy Audiometry when there is a continuous tracing above the pulsed tracing, this is indicative of a
functional hearing loss. This is called a Bekesy type V.
29. In acoustic reflex testing, the reflex will likely be an absent if there is conductive pathology or a
sensorineural hearing loss greater than 60 dB.
30. In high resk neonates, the following percentage of the screen group will have hearing loss using BERA: 3-
F.Ling - ENT Facts and Points (1)
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4%.
31. The audiometric test that is based on the principle that one increases the volume of one’s voice in the
presence of background noise due to the fact that the noise is heard and interferes with self-monitoring is
called the Lombard test.
32. A positive Bing test is indicative of normal hearing.
-it is a tuning fork test in which the tone is louder with the ear canal occluded.
33. The tuning fork test in which the tuning fork is placed against the mastoid and then, when it is no longer
heard, is placed against the tragus while the examiner gently occludes the meatus is called the Lewis test.
-no a good test, and interpretation of the test is neither simple nor consistent.
34. According to OSHA, Permissible Noise Exposure over an 8-hour day should not exceed 90 dB.
35. Earmuffs, custom-fitted earplugs, or disposable earplugs each provide the following amount of sound
attenuation: 20-40 dB.
Electrical Response Audiometry
36. The origin of the summating potential is the hair cells and is a direct current shift of the baseline of the
recording.
37. The generator site for wave V of the ABR is thought to be the inferior colliculus.
38. The ABR generated by a broad-band click stimulus has its major contribution from the following
frequency range: 3000 to 4000 Hz.
39. A patient has a 60 dB hearing level at 4000 Hz in the suspect ear. To correct the latency of the ABR for
this patient, the following time interval should be deducted: 0.1 ms.
-for responses to a standard 80 dB nHL broadband click, deduction of 0.1 ms for each 10 dB that
the 4 kHz hearing loss exceeds 50 dB.
40. The least interaural latency difference considered suspicious for an acoustic tumour is 0.2 ms.
-the interaural difference in wave V latency (IT5) will normally be 0.2 ms. Greater than 0.2 ms
seen in more than 96% of acoustic tumours
41. The cochlear microphonic originates from the hair cells.
42. The most accurate non-invasive test for acoustic tumour diagnosis is MRI.
43. The normal latency of the fifth wave of the ABR is in the range of 5-6 ms.
44. The origin of wave I of the ABR is the auditory nerve.
45. The normal value of the wave III-V interval is approximately 2 ms.
Vestibular System and Its Disorders
46. The kinocilia are located at the end of each hair cell nearest the tallest stereocilia.
47. The utricle is primarily sensitive to linear movement.
48. A 40 year old patient is having a caloric test done. Stimulating the right ear with water warmer than body
temperature results in the following directional movement of endolymph: ampullofugal.
49. The endolymphatic potential across the membrane separating the endolymph from the peilymph is 80 mV
50. In electronystagmography testing (ENG), investigators use the following percentage difference between
right-beating and left-beating nystagmus to be significant in the Jongkee formula for directional
preponderance: 25-30%.
51. A 50 year old male presents with vertigo. During his ENG testing, he has a right-beating nystagmus with
left ear down and a left-beating nystagmus with right ear down. This is suspicious of positional alcohol
nystagmus.
-cupula is rendered a floating object by alcohol diffusion. It becomes gravity dependent and
produces a peripheral vestibular abnormality secondary to the prior 24- to 48-hour ingestion of
alcohol.
52. Simultaneous binaural bithermal stimulus testing produces diagnostic information and is what percentage
more sensitive than the alternate binaural bithermal method done? 55%
53. A 60 year old male is suspected of having a central lesion. One of the most reliable sings would be failure
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of ocular fixation.
54. Alternate bithermal caloric responses may reveal an abnormality about 50% of the time while simultaneous
bithermal caloric responses increase the yield to 80% in the following condition: Meniere disease
55. On ENG testing of a 23 year old female with symptoms of unsteadiness, it was noted that there was
evidence of anterior internuclear ophthalmoplegia on testing eye movements. This is indicative of multiple
sclerosis.
56. Nystagmus present when gazing in the direction of the fast component and in straight gaze is termed
second-degree nystagmus.
-suggests a central origin. Also, vertical or diagonal nystagmus suggests a central origin.
57. Positional nystagmus, when the direction of the nystagmus remains fixed regardless of the position of the
head during the positional testing although it may be stronger in a particular direction, is termed Nylen type
II nystagmus.
-this implies either a peripheral lesions or a central lesion.
58. Aschan type I nystagmus is when the nystagmus is nonfatigable and persistent: its direction changes with
head position.
59. The Kobrak test is a simple caloric test that is done with the patient in the upright position and the head
tilted back at 60o angle.
60. The directional preponderance test is a standardized test to measure canal paresis and directional
preponderance and in this test the patient is placed in supine and the head is elevated at a 30o angle.
61. The principle of ENG is based on the difference in electrical potential between the retina and the cornea.
62. In a positive fistula test, stimulation of the ear with positive pressure results in nystagmus to the same side.
63. The Charcot triad (nystagmus, scanning speech, intention tremor) may be associated with multiple
sclerosis.
64. The rare variant of Meniere disease in which there is a dramatic restoration of hearing after an acute attack
of vertigo is called Lermoyez syndrome.
65. Internuclear ophthalmoplegia is a disturbance of the lateral movements of the eyes characterized by a
paralysis of the internal rectus on one side and weakness of the external rectus on the other, and if it is
bilateral it is pathognomonic of multiple sclerosis.
Speech, Language, and Voice
66. A speech impairment that occurs with CVA or another neurologic problem in which substitutions and
additions of sounds in words is termed apraxia.
-dysarthria is a central or peripheral nervous system deficit resulting in muscle slowness,
weakness, or incoordination.
67. When a child tends to repeat what is said to him or her it is termed echolalic.
68. The frequency of voice that is considered optimal for adult men is at 125 Hz. For women: 225 Hz.
69. A 40 year old male presents to his MD with a voice disorder. He is diagnosed as having flaccid dysarthria.
His most likely diagnosis contributing to this is myasthenia gravis.
-flaccid dysarthria is a voice disorder that occursn in lower motor neuron or primary muscle
disorders such as MG and tumours and strokes involving the brainstem nuclei.
70. Amyotrophic lateral sclerosis is a condition in which a voice disorder may present as mixed dysarthria.
71. One of the most important tests in detecting vibratory asymmetries and submucosa scars is
strobovideolaryngoscopy.
72. The region of the intermediate and deep layers of the lamina propria is called the vocal ligament.
73. The volume of air remaining in the lungs at the end of expiration during normal breathing, which may be
divided into expiratory reserve volume and residual volume, is called functional residual capacity.
74. This medication has been used in treatment of performance anxiety but can produce thrombocytopenic
purpura, mental depression, and bronchospasms among other adverse reactions: Beta blockers.
75. The theory of speech that suggests that the contribution of a particular speech manoeuver to the spectrum
depends on its relation to the nodes or antinodes of the standing waves is called the perturbation theory.
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Congenital Deafness
76. Hereditary deafness occurs in the following incidence of live births: 1:4000
77. The Mondini-Alexander classification of inner ear developmental anomalies is incomplete development of
the bony and membranous labyrinth. The cochlea may be represented by a single curved tube and the
vestibular labyrinth is not developed.
78. If a mother is infected with rubella druing the first trimester, the percentage of children with deafness at
birth is 5-10%.
79. In a congenital syphilis patient, when there is vertigo and nystagmus on stimulation with high intensity
sound such as the Barany noise box, it is called Tullio phenomenon.
80. Leopard syndrome is a form of hereditary congenital deafness associated with variable SNHL, pulmonary
stenosis, hypogonadism, and ocular hypertelorism.
81. Tietze syndrome is a hereditary congenital deafness associated with profound deafness, absent eyebrows,
blue irides, and albinism.
82. the autosomal dominant hereditary congenital deafness syndrome associated with widely spaced medial
canthi, flat nasal root in 75% of cases, confluent eyebrows, white forelock, and coloured irides is
Waardenburg disease.
83. Achondroplasia is associated with saddle nose, frontal and mandibular prominence, mixed hearing loss and
dwarfism.
84. The hereditary congenital deafness syndrome associated with syndactylia, craniofacial dysostosis,
hypoplastic maxilla, exophthalmos, and a flat conductive hearing loss is Apert syndrome.
85. The hereditary congenital deafness syndrome associated with cranial synostosis, parrot-beaked nose, short
upper lip, mandibular prognathism, and premature closure of the cranial suture lines is Crouzon syndrome.
86. Klippel-Feil syndrome is a hereditary congenital deafness associated with SNHL, short neck due to fused
cervical vertebrae, external auditory canal atresia, and spina bifida.
87. The syndrome of congenital deafness, pigeon breast, scoliosis, thin elongated individuals with long spidery
fingers and hammer toes is Marfan.
88. A 6 month old male presents with hearing loss, optic atrophy, sclerotic brittle bone, choanal atresia, and
fluctuating facial nerve paralysis. The most likely diagnosis is Albers-Schonberg disease.
89. Treacher Collins syndrome is associated with malformation of ossicles, antimongoloid palebral fissure,
mandibular hypoplasia and a normal IQ.
90. A 1 year old male presents with micrognathia, cleft palate, mixed hearing loss, hypoplastic mandible,
mental retardation, and breathing difficulties when sleeping. The most likely diagnosis is Pierre Robin
syndrome.
91. Vander Hoeve syndrome or osteogenesis imperfecta is an AD congenital hearing loss syndrome associated
with fragile bones, loose ligaments, hearing loss, and 60% have blue sclera.
92. Alport syndrome is suspected in a 4 month old baby. One of the most helpful tests in making the diagnosis
would be a urinalysis.
93. Fanconi anemia syndrome, Alstrom syndrome, Van Buchem syndrome, and Mohr syndrome all share the
same trait of autosomal recessive inheritance.
94. Hallgren syndrome, Alstrom syndrome, and Cockayne syndrome all share the same trait of associated
visual loss.
95. Hurler syndrome (gargoylism) is a hereditary congenital deafness syndrome associated with mental
retardation, dwarfism, mixed hearing loss, forehead prominence, and abnormal mucopolysaccharides are
deposited in tissues.
96. Laurence-Moon-Bardet-Biedl syndrome is associated with congenital deafness, obesity, dwarfism, mental
retardation, and retinitis pigmentosa.
97. Pendred syndrome is a hereditary congenital deafness syndrome associated with a “U”-shaped audiogram,
diffuse goiter development at puberty, and a normal IQ. This syndrome constitutes the following
percentage of hereditary deafness syndromes: 10%.
98. The syndrome associated with retinitis pigmentosa, polyneuropathy, ataxia, and SNHL is Refsum
syndrome.
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99. With regard to congenital abnormalities of the middle and external ear, when one has microtia, atretic
canals, and abnormal ossicles it is termed a class III abnormality.
100. The hereditary congenital deafness syndrome that is autosomal recessive and is associated with retinitis
pigmentosa, ataxia, and vestibular dysfunction is Usher syndrome.
Cochlear Implants
101. The F0 (fundamental frequency) is mainly responsible for pitch in cochlear implant technology. This is a
frequency range from 100-200 Hz.
102. The most prominent cell in the matrix of the spiral ligament are type I fibroblast cells.
103. The nucleus multichannel cochlear implant is 25 mm long and contains approximately 22 electrodes.
104. There are 13 to 16 million people in the US with hearing loss. Of these, there are approximately how many
thousand with severe to profound hearing loss: 150,000-200,000
105. One notable exception to having cochlear implant is Michel deformity.
106. The current minimum age limit for implantation of a cochlear implant is age 1 year.
107. A 4 year old child has had a cochlear implant inserted in her right ear at age 3. She presents with
longstanding (4 months) bilateral noninfected middle ear effusions. The next step is to suggest no
treatment at present and observe for infection
108. A 5 year old female had a cochlear implant inserted successfully. The parents are told that if she has any
further surgery she should avoid monopolar cautery.
109. Several factors are involved in predicting a more rapid or greater improvement in speech reception and
production in children after cochlear implant surgery. This indicates: postlingual onset of deafness,
implantation during the preschool years, a shorter period of auditory deprivation, participation in an oral
communication therapy program.
110. The children who have been the most obvious candidates for a cochlear implant are those who have
demonstrated no response to warble tones in the sound field with appropriate hearing aids or responses
suggestive of vibrotactile rather than auditory sensation. This aided response is with no response above
1000 Hz but in the lower frequency having responses at levels greater than 40-50 dB HL.
Neurotology and Skull Base Surgery
111. The anterior margin of the foramen magnum os formed by the basioccipital synostosis.
112. All of the following are characteristisc os neurofibromas associated with Von Reckinghausen disease:
multiple, nonencapsulated, incorporate axons, malignant degneration.
113. In performing a translabyrinthine removal of an acoustic neuroma, spinal fluid may be decompressed by
opening the cochlear aqueduct.
114. In performing a middle fossa procedure to remove an acoustic neurma, generally the anterior limit of the
dissection is the middle meningeal artery.
115. Transposition of the following nerve routinely occurs during a transcochlear approach: CN VII
116. The greater and lesser wings of the sphenoid bone are separated by the superior orbital fissure.
117. the trigeminal ganglion lies in the Meckel cave.
118. Anterior to the jugular foramen lies the carotid canal.
119. For large lesions of the cerebellopontine angle, the following approach will allow the surgeon to obtain the
widest field of view: suboccipital.
120. Characteristics of glomus tumours include all the following: multicentric origin, metastatic change is rare,
familial tendency, associated with neuropeptide secretion
Facial Nerve Paralysis
121. A 40 year old male presents at your office with an acute facial nerve paralysis. The differential diagnosis
should include all the following: Lyme disease, herpes zoster, sarcoidosis.
122. The facial nerve is not fully developed until a child is 4 years old.
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123. The incidence of Bell’s palsy per 100,000 population is 20-30.
124. A family history of Bell’s palsy is present in 8%.
125. The labyrinthine segment of the facial nerve extends from the fundus of the IAC to the facial hiatus, where
the fallopian is narrowest. This segment is approximately 3 to 5 mm.
126. The facial nerve has thousands of fibers. Seventy percent are myelinated and 30% sensory and
secretomotor. The total number of fibers is approximately 10, 000.
127. A 60 year old male presents to your office with 24 hour history of right otalgia, dysgeusia, and hyperacusis.
You should expect in 48 hours he may develop Bell palsy.
128. On testing the facial nerve in a 40 year old male with facial nerve paralysis, there is a difference between
the two sides in minimal nerve excitability testing. A difference of how many mA suggest nerve
deprivation: 3.5 mA.
129. The incidence of severe degeneration in facial nerve paralysis with herpes zoster is approximately 40%.
130. Which of the following tests is used to predict facial nerve function ro return 6-12 weeks before clinical
evidence of return of function: electromyography.
131. A 24 year old male presents with blistering of his right conchal bowl, facial nerve paralysis, and pain.
Viral testing would show rising titers to the following virus: varicella-zoster.
132. The incidence of facial paralysis in newborns is the following: 0.25% of live births.
133. A newborn child has on examination facial diplegia, bilateral loss of abductors of the eye, extremity
anomalies, and aplasia of the brachial and thoracic muscles. The most likely diagnosis is Mobius
syndrome.
134. A large children’s hospital in the midwest did a retrospective analysis of facial nerve paralysis in newborns
over a 20 year period. Their study showed the following percentage of facial nerve paralysis was due to
birth trauma: 80%.
135. a 14 year old female was involved in an incident during which she sustained a knife wound to the central
left cheek. she had a facial nerve paralysis and repair was carried out within 24 hours. She most likely had
the following repair: epineural repair
136. A 60 year old male presents with a peripheral facial nerve paralysis. He has a firm 2x3 cm parotid mass.
Needle aspiration indicates a malignant tumour. The most common diagnosis is adenoid cystic carcinoma.
137. The following is disruption of the nerve trunk: neuropraxia.
138. A survey, at a large New York hospital, of temporal bone fractures revealed the following percentage of
fractures involved the facial nerve: 20%.
139. A 30 year old female presents to your office with recurrent orofacial edema, recurrent facial palsy, and
lingua plicata (fissured tongue). The most likely diagnosis is Melkersson-Rosenthal syndrome.
140. An 18 year old male form Connecticut presents to your office with a facial nerve paralysis, generalized
malaise, an erythematous skin lesion, regional lymphadenopathy, and a history of having camped outdoors
the previous week. The most likely diagnosis is Lyme disease.
Syndromes and Eponyms
141. Auriculotemporal syndrome (Frey syndrome) is associated with aberrant innervation of the sweat glands by
parasympathetic fibers of the IXth cranial nerve.
142. A 35 year old male presents to your office with indolent ulcers of the mucous membranes and skin with
stomatitis as well as anogenital ulceration, iritis, and conjunctivitis. He has Behcet syndrome.
143. A 45 year old female presents to your office with a history of crocodile tears characterized by residual
facial paralysis with profuse lacrimation during eating. She has Bogorad syndrome.
144. The symptom complex that occurs in individuals working in high pressure when they are returned too
suddenly to normal pressure is called Caisson disease
145. Cavernous sinus syndrome is caused by thrombosis of the cavernous intracranial sinus and is associated
with involvement of the following nerves: II, III, IV and V1
146. The syndrome of nonsyphilitis interstitial keratitis associated with vertigo, tinnitus, ataxia and progressive
SNHL is called Cogan syndrome.
147. Costen syndrome is a symptom complex involving an abnormality of the TMJ - impaired bite and is
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characterized by tinnitus, vertigo and pain in the frontal, parietal, and occipital areas.
148. DiGeorge syndrome involves cardiovascular and craniofacial anomalies and abnormalities of the thymus
gland.
149. The syndrome associated with leukopenia, arthritis, and enlarged lymph nodes and spleen is termed Felty
syndrome.
150. A 50 year old male presents to your office with a symptom complex of acute suppurative otitis, pain in the
eye and temporal area, abducens paralysis and diplopia. He has Gradenigo syndrome.
151. A 40 year old man presents to the office with Horner syndrome. He has paralysis of the cervical
sympathetic nerves and therefore has ptosis, mosis, anhidrosis and enophalmosis.
152. Vernet syndrome (jugular foramen syndrome) is associated with involvement of cranial nerves IX, X and
XI.
153. Multiple endocrine adenomatosis type IIA (Sipple syndrome) is associated with hyperparathyroidism,
pheochromocytoma and medullary carcinoma of the thyroid.
154. Rollet syndrome is associated with involvement of cranial nerves III, IV, and VI.
155. One of the most reliable clinical tests for hypocalcemia is the facial twitch obtained by tapping the
distribution of the facial nerve. This is called Chvostek sign.
Embryology of Clefts and Pouches
156. In the embryology of the fetus, the derivatives of the five arches (pharyngeal or branchial) are of a
combination of mesodermal origin.
157. During the course of embryonic development, the third arch artery is the precursor of the carotid artery.
158. The thymus gland is derived from the ventral aspect of the third pouch.
159. The second branchial arch gives rise to the geniculate ganglion VII.
160. The cartilage bar of the fourth branchial arch forms thyroid cartilage and cuneiform cartilage.
161. The ventral (thyroid) diverticulum that descends between the first and second arches can forma a
thyroglossal duct cyst but usually it atrophies by the sixth week of gestation.
162. In the fetus, the tongue is fully developed by the 20th week.
163. The hard palate is formed in the fetus by the ninth week.
164. The incidence of esophageal atresia in cases of tracheoesophageal fistulas is slightly greater than 90%.
165. The hyoid bone is usually calcified by age 2. The thyroid cartilage starts to calcify at age 20.
Cleft Lip and Palate
166. The muscle that is the primary elevator of the soft palate is the levator veli palatini.
167. An incomplete cleft lip involves a portion of the lip and may form a muscular diastasis with intact
underlying skin to a large cleft with only a small band of residual tissue connecting the two sides of the lip.
This band is call the Simonart bar.
168. The embryologic development of the lip and palate occurs between 4 and 7 weeks.
169. a newborn child is noted to have an incomplete cleft of the palate. This probably occurred at the following
point in embryologic development: 7 to 12 weeks.
170. In your office, you have a mother who had a cleft palate repaired as a child. She has one child without
congenital deformities but she is 12 weeks pregnant. You can advise her that the chance of this child
having a cleft palate alone is 6%.
171. The incidence of a cleft deformity per live births is 1:680.
172. A child is seen in the neonatal nursery with a cleft palate deformity. The parents are very anxious to have
this repaired. You suggest they should wait until 10 to 12 months.
173. You are asked to see a child in the newborn nursery with a cleft lip deformity only. The parents want an
idea of when this can be surgically repaired. You tell the parents this can usually be done at 10 weeks.
174. Lip adhesion is a preliminary procedure used in the therapy of cleft lip repair. In the procedure, there are
usually laterally based flaps obtained from the lip itself. The procedure is usually done at 1 to 4 weeks.
175. One of the palatoplasties done for a soft palate deformity using posteriorly and anteriorly based unipedicle
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microperiosteal flaps is called an Oxford palatoplasty.
176. The procedure used to close the soft palate cleft with closure of the hard palate at a later date is called
Schweckendick procedure.
177. The most common complication of palatoplasty procedures is hypernasal speech (30%). Fistula formation
is from 10-21%.
178. The Dibbell technique is a procedure to correct the nasal ala, the lateral alar margin and the lip.
179. The technique used to lengthen the columella in cleft lip repair is the Bardach.
180. The primary complication of a pharyngeal flap initially is hemorrhage.
Immunology and Allergy
181. Type I is an IgE mediated reaction via mast cells, type II is a cytotoxic reaction, type III is an immune
complex-mediated reaction, and type IV is a cell-mediated reaction.
182. The third most abundant serum immunoglobulin that inhibits the adherence of microorganisms and alien
macromolecules is IgA. IgG is the major antibody of secondary responses, IgM is the predominant
antibody in early immune response, IgD is found in large quantities in circulatory B cells, and IgE is found
in basophil and mast cells. IgA is the predominant Ig in seromucous secretions.
183. Tests of B-cell function include measurement of serum levels of immunoglobulins, antibody response
following immunization, and the presence of plasma cells
184. The principle organs that serve as sites for proliferation and development of cells involved in immune
responses include all the following: bone marrow, Peyer patches, lymph nodes, spleen.
185. Cellular hypersensitivity occurs 24-72 hours after antigen introduction.
186. Tests of T-cell function: lymphocyte count and morphology, E-rosette assay, allogenic skin graft rejection,
delayed hypersensitivity skin tests.
187. Corticosteroids affect the sodium pump, reduce capillary permeability, and stabilize lysosomal membranes.
188. In chemotaxis, there is a very organized movement of cells.
189. 13-20% of US population suffers from allergic disease.
190. An allergen is an antigen that causes allergic reaction.
The Chest
191. The volume of gas that is either inspired or expired during each normal respiratory cycle is called the tidal
volume.
192. One of the most useful tests for asthmatics to monitor the severity of an asthmatic attack is the forced
expiratory volume.
193. A flow volume loop demonstrating decreased expiration and inspiratory curves is indicative of pulmonary
COPD.
194. A flow volume loop demonstrating decreased inspiratory curve is indicative of extrathoracic obstruction.
195. A measure of the distensibility of the lung parenchyma is called the compliance.
196. Decreased compliance is indicative of pulmonary fibrosis.
197. Normal lung function is considered to have an alveolar-arterial gradient of less than 20 mmHg.
198. FEV1 should be the following percentage or greater of the predicted volume from a normative chart: 80%
199. Total lung capacity for males is 6L; 4.2L for females.
200. A class I congenital genesis of the lung has been classified by Schneider as total genesis of the lung
201. A methemoglobin level of this degree produces cyanosis: 75 mg/dL
202. The leading primary pulmonary carcinoma in women is squamous cell carcinoma.
203. The triad of apical lung tumour, vocal cord paralysis and Horner syndrome is called Pancoast syndrome.
204. The thyroidea ima artery is present in the following percentage of the population: 10%.
205. The following percentage of mediastinal tumours are malignant: 30%.
206. A 6-month old child is taken to the operating room to have a peanut removed from her right main stem
bronchus. The size of the bronchoscope you would most likely choose would be 3.5 mm.
207. In the adult male, the average distance from the incisor teeth to the hiatus is 38 cm.
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208. The most common cause of hemoptysis related to the lung is bronchiectasis.
209. The most common cause of dysphagia lusoria is an abnormal subclavian artery
210. The ligamentum arteriosus is an abnormality of the following branchial arch: 4th.
Related Ophthalmology
211. The floor of the orbit is formed by the orbital plate of the maxilla, orbital surface of the zygoma, and the
orbital process of the palatine bone.
212. A 20 year old male sustained eye trauma and ti was determined he had a displaced trochlea. The physical
exam would have revealed diplopia on downward gaze.
213. A 35-year old male presents to your office with proptosis, excessive lacrimation, periorbital edema and
photophobia. one test that would be helpful in making a diagnosis would be a TSH assay
214. The superior orbital fissure transmits the superior orbital vein, ophthalmic vein, orbital branch of the
middle meningeal artery, recurrent branch of the lacrimal artery, and cranial nerves III, IV, VI, V1
215. The usual causative organism in cavernous sinus thrombosis is coagulase-positive S. aureus.
216. The orbital decompression procedure in which the floor and the medial wall of the orbit are removed to
allow expansion into the ethmoid and maxillary sinuses was first described by Ogura.
217. The lateral rectus muscle is innervated by the following cranial nerve: VI nerve.
218. The muscles involved with movement of the eyes down and to the right are right inferior rectus and left
superior oblique.
219. The procedure for decompression for malignant exophthalmos in which an ethmoidectomy is done and the
floor of the frontal sinus is removed is described by Sewell.
Related Neurology
220. Internuclear ophthalmoplegia is pathognomic of multiple sclerosis.

221. The Charcot triad in multiple sclerosis includes nystagmus, scanning speech, and intention tremor.
222. A 40 year old female presents to your office with papilledema, headache, vomiting and a giant imbalance.
She has also paroxysmal positional nystagmus in all directions. An MRI scan is most likely to reveal a
cerebellar glioma.
223. A 65 year old male is seen on consultation in the hospital with spontaneous nystagmus, ipsilateral Horner
syndrome, ipsilateral loss of pain and temperature sensation, and ipsilateral rectus muscle and facial
weakness. He has Wallenberg syndrome.
224. A 75 year old male with a history of ASHD presents to your office with a history of recurrent vertigo that
lasts for several minutes and is associated with nausea and vomiting. He also gets visual illusions and
hallucinations, drop attacks, visual field defects, and diplopia. The most likely diagnosis is vertebrobasilar
insufficiency.
225. A mother brings to you her 8 month old child who periodically gets episodes of head tilt, pallor, vomiting
and agitation. The episodes of head tilt can last from a few hours to 3 days. You make the diagnosis of
paroxysmal torticollis. The treatment is none, the condition will resolve by age five.
226. A 12 year old boy is brought into your office by his parents. He has a history of periodic episodes of
difficulty swallowing and diplopia. He also notices that he gets weak after exercise and at the end of the
day. After examination, the next step is to order a tensilon test - r/o myasthenia gravis.
227. A 65 year old farmer presents with history of fever, parotid swelling, uveitis, and transient bilateral facial
nerve paralysis. The most likely diagnosis is uveoparotid fever of Heerfordt.
228. A 45 year old female presents to your office with a history of headache and visual symptoms. On
examination you discover the patient has bitemporal hemianopsia. The most likely diagnosis is pituitary
adenoma.
229. A sense of foul smell when none is present is called cacosmia.
230. The following medication has been used in the treatment of anosmia: vitamin A.
231. Friedreich ataxia is an autosomal recessive disorder in which patients lose their ability to ambulate
independently 10-20 years after onset. The most life-threatening aspects of the disease are related to
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cardiac manifestations.
232. Refsum syndrome is a familial disorder that is believed to be inherited in an autosomal recessive fashion.
Patients have retinitis pigmentosa, cerebral ataxia, and SNHL. Serum analysis would reveal elevated
phytanic acid.
233. The second most common cerebral pontine angle mass lesion is a meningioma.
Nasal Endoscopy and Its Surgical application
234. The incidence of accessary ostia from the maxillary sinus is approximately: 20-30%
235. The Onodi cell is the most posterior of the posterior ethmoid cells.
236. A clinical bony dehiscence of the c cavernous portion of the carotid canal is present in 22% of patients.
237. As a landmark, one uses the anterior ethmoid artery. It is important to know that this can be absent
unilaterally in the following percentage of patients: 14%; bilaterally absent in 2% of patients.
238. The range of bacteria involved in acute sinusitis include S. pneumoniae, S. aureus, H. influenzae and
Streptococcus pyogenes.
239. The most common fungal sinus infection in an otherwise healthy patient is Aspergillus niger.
240. Woodworkers have an increased incidence of this type of tumour in the maxillary sinus: adenocarcinoma
241. An anatomic variation of the ethmoidal infundibulum can be related to the following cells: Haller cell
242. The most common sinus involved in inflammatory sinus disease is the ethmoid sinus.
243. A 30 year old immunosuppressed female had a CT scan that showed metallic densities within the maxillary
sinus. Another test that may be helpful would be a T2-weighted MRI will demonstrate reduced signal
intensity in a patient with fungal sinusitis.
244. Squamous cell carcinoma is the most common true neoplasm of the paranasal sinus. The incidence is
approximately 1:200000.
245. The incidence of CSF rhinorrhea in patients who suffer serious head trauma is 2-3%. Accidental trauma is
the cause of 80% of the patients with CSF rhinorrhea.
246. The most common postoperative complication of endoscopic sinus surgery is synechia.
247. Only 20% of patients with CSF rhinorrhea develop meningitis as their initial symptom.
Antimicrobial Therapy in Head and Neck Surgery
248. In the general population, the incidence of anaphylaxis as a result of the use of penicillin-based antibiotics
is 1:10,000
249. Staph aureus has a high resistance to ampicillin
250. One of the major side effects of long-term isoniazid treatment is peripheral neuropathy.
251. Cephalexin has very poor coverage against: hemophilus, pseudomonas, and bacteroides
252. Cefuroxime has poor coverage against bacteroides and pseudomonas.
253. Erythromycin can significantly elevate theophylline levels in the bloodstream.
254. Tetracycline antibiotic suspension has been helpful against aphthous stomatitis.
255. Ciprofloxacin has poor activity against anaerobes.
256. Erythromycine is very effective against Legionella pneumophilia.
257. Ciprofloxacin exerts its antibacterial activity via the inhibition of bacterial topoisomerase II.
258. With long-term amphotericin administration, one should monitor renal function
259. Vancomycin can be ototoxic in high doses.
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REVIEW QUESTIONS IN FACIAL PLASTICS
AND RECONSTRUCTIVE SURGERY
Local Skin Flaps: Anatomy, Physiology and General Types
1. What are the advantages (3) and disadvantages (3) of local flaps?
2. What types of vessels are the basis of musculocutaneous flaps? Axial-pattern flaps?
Random-pattern flaps?
3. What is an angiosome?
4. What are four axial-pattern flaps and their supplying arteries?
5. What is the delay phenomenon?
6. What is “skin creep”? What is “stress relaxation”?
7. What is the significance of relaxed skin tension lines?
8. What are some of the causes of skin flap failure (8)?
9. How do you construct a Rhomboid flap? A Dufourmental flap? A bilobed flap?
10. What are the three types of advancement flaps?
11. What are the steps involved in survival of a STSG (5)?
12. What examples of regional cutaneous flaps (3)?
13. What are examples of regional myocutaneous flaps (4) and their blood supply?
Microvascular Free Flaps in Head and Neck Reconstruction
14. What is the blood supply of:

-radial forearm free flap
-lateral arm flap
-lateral thigh flap
-temporoparietal fascial flap
-rectus abdominal flap
-latisimus dorsi flap
-gracilis flap
-fibular osteocutaneous flap
-iliac crest
-scapular flaps
-jejunum
15. Which flaps are sensate(3)? Which nerves are involved?
16. Which free flaps provide the most bulk (2)?
17. Which free flaps can be osseocutaneous (4)? How much bone can be harvested from
each?
18. Which free flaps provide a large surface area of tissue (3)?
19. Which osseocutaneous flap has poor supply to its skin paddle?
20. Which free flap provides the longest neurovascular pedicle?
21. Which free flap is predominantly used in facial reanimation?
Surgical Reconstruction after Mohs Surgery
22. What are the indications for Mohs surgery?

23. What are the basic treatment steps in Mohs surgery?
24. What are the reconstructive options for Mohs surgery (6)?
25. What are possible donor sites for FTSG (5)?
26. What are the aesthetic masses of the face (5)?
F.Ling - Facial Plastics Review (1)
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27. What are methods are used to close small to moderate defects of the cheek? Moderate
to large defects of the cheek (2)?
28. What method is used to close small thin defects of medial canthal region?
Mandibular Reconstruction
29. Which portion of the mandible, when missing, causes severe functional and cosmetic
deficits?
30. After how many treatments of hyperbaric oxygen does the vascular density plateau? At
what percentage does this plateau occur compared to normal non-irradiated tissue?
31. How is hyperbaric oxygen beneficial for the reconstruction of irradiated bone?
32. Which regional flap provides the largest area of tissue and has the greatest reach of any
regional pedicled flap?
33. What are the goals of primary oromandibular reconstruction?
34. What are the ideal qualities of the osseous component of a composite free flap (5)?
35. What are the ideal qualities of the soft-tissue component of a composite free flap (7)?
36. Which free flaps are able to accept osteointegrated implants (2)?
37. What is the blood supply of the following free flaps?
-iliac crest
-scapular
-fibular
-radial forearm
-lateral arm
38. Which flaps are capable of sensation (5)?
39. What is the maximum amount of bone that can be harvested from the radius without
severely compromising the residual radius?
Tissue Expansion in Reconstruction
40. Which component of skin stores strain energy?

41. Which component of skin determines the elastic property?
42. What is biological and mechanical creep? What is stress relaxation?
43. How many times should the base of the expander be compared to the defect?
44. What shape of expander has the best volume-to-skin area?
45. Contrast conventional tissue expansion with rapid intraoperative tissue expansion.
46. What are the complications of volume expanders (5)?
Scar Camouflage
47. What are some excisional techniques for scar camouflage (4)?
48. A Z-plasty with angles of 60-, 45- and 30-degrees will increase the length of the scar by
what percentage?
49. What are other scar irregularization techniques (2)?
50. Which patients should not have dermabrasion or laser resurfacing (5)?
51. What are the complications of intralesional steroids for scar revision (3)?
Facial Reanimation
52. What are the four broad categories of facial reanimation methods?
53. In a patient with newly diagnosed facial nerve paralysis, what is the surgeon’s most
immediate concern?
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54. How long do you wait before attempting a surgical interruption that may result in
irreversible damage to the facial nerve?
55. List the different techniques used for facial reanimation (5).
56. What are common nerve grafts used for repair (2)?
57. What conditions are required before performing nerve crossover techniques (5)?
58. Which crossover technique is the most reliable?
59. What is Mobius syndrome?
60. When would muscle transposition techniques be employed (3)?
61. What are the two methods of muscle transposition? What is an advantage and
disadvantage of each technique?
Facial Analysis
62. What is the Frankfort plane?

63. What is the nasofrontal angle? The nasolabial angle? The nasofacial angle? The
mentocervical angle? What are their approximate values?
64. What are the major aesthetic masses of the face?
65. What is the meaning of “vertical fifths” and “horizontal thirds”?
66. What is the relationship between the interpupillary distance and intercanthal distance?
67. What is the relationship between the intercanthal distance and the alar-alar distance?
68. How is female brow position different from male brow position?
69. What is the desirable length to width ratio of the nose?
70. Define tip projection and tip rotation.
71. What is the approximate columella to lobule ratio?
72. What is the approximate lobule to nasal base ratio?
73. What is the approximate ala to lobule ratio?
74. What is an acceptable amount of columellar show?
75. The lateral aspect of the oral commissure will lie along a line tangential to which
structure?
76. On lateral view, what is the posterior inclination of the longitudinal axis of the ear off the
vertical?
77. What is the angle of protrusion of the ear from the posterior scalp?
78. Define the three classes of dental occlusion according to Angle.
Surgical Anatomy of the Nose
79. What are “aesthetic subunits” of the nose? What do they consist of (5)?
80. In terms of dissection planes, what is the ideal plane of dissection over the upper and
lower lateral cartilages? Bony dorsum?
81. What are the elevator muscles of the nose (3)? The depressor muscles (2)? The
compressor muscles (2)? The dilatory muscles (1)?
82. What is the tip defining point?
83. What are the major tip support mechanisms of the nose (3)?
84. What are the minor tip support mechanisms of the nose (6)?
85. What are the legs of the nasal “tripod” (3)?
Introduction to Rhinoplasty
86. What is generally involved in at the initial consultation for rhinoplasty (5)?
87. What are the main points to evaluation for the nose (4)?
88. What is the maximum dose for cocaine in most adults? How long does it last?
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89. What is the maximum dose for lidocaine in adults, with or without epinephrine? How
long does it last?
90. What are the different types of incision in rhinoplasty (5)?
91. What is an “open roof” deformity?
92. Where do you begin a lateral osteotomy? What happens if this is done too low? What
happens if this is done too high?
93. What is an intermediate osteotomy?
External Rhinoplasty Approach
94. What are the advantages (3) and disadvantages (3) of an external approach?
95. Which minor tip support mechanism is lost with external approach?
96. What are relative contraindications to external approach because of compromised blood
supply to the skin-soft tissue envelope (3)?
97. Where do the major arteries of the nose run in relation to the SMAS?
98. What are the arteries that supply the skin of the nose (3)?
99. Which two incision are used for the external approach?
100. What are the indications for the external approach?
101. What is the most common complication of an external approach?
Refinement of the Nasal Tip
102. What is the most important anatomical factor that is important in dictating the potential
surgical outcome of nasal tip refinement?
103. What is tip recoil and how is it important in the evaluation of the nasal tip?
104. What are the major (3) and minor (6) tip support mechanisms of the nose?
105. What are the different approaches to the nasal tip (3)?
106. When is a cartilage splitting technique used?
107. What incisions are used for a cartilage delivery approach (2)?
108. What technique is used when more significant cephalic tip rotation is required in more
severe tip deformities?
109. What technique is used to achieve narrowing refinement of the broad tip?
110. What are potential indications of the open rhinoplasty approach (7)?
111. What methods can be employed to enhance tip projection (5)?
112. What methods can be employed to enhance tip rotation (7)?
113. What methods are used to reduce the volume of the nasal tip (3)?
Special Considerations in Rhinoplasty
114. What are some of the features of a unilateral cleft-lip nose deformity (6)?
115. What are some of the features of a non-white nose (4)?
116. What materials can be used to augment a saddle-nose deformity (5)?
117. What are the disadvantages of alloplastic materials (2)?
118. What is the main disadvantage of demineralized bone and irradiated cartilage?
119. With regards to the orientation of the alar axis, when is it contraindicated to perform alar
resection and why?
120. For a twisted nose, what is the suggested order to perform the osteotomies? What can
be done if after performing the osteotomies, there is still a depression on the lateral side
of the nose?
121. When should cosmetic surgery be delayed in children?
122. What are some of the changes in the nose related to aging (3)?
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Revision Rhinoplasty
123. As a general rule, when should revision rhinoplasty be undertaken?

124. What is the most common nasal tip deformity in revision surgery?
125. What is the etiology of bosselation? How can this be corrected?
126. What is the main cause of nasal tip pinching?
127. What is the main cause of alar retraction? What are methods used to correct this (3)?
128. What is a polly-beak deformity? What causes this (4)? How can this be corrected
based on its cause?
129. What techniques are used to correct midnasal asymmetry (4)?
Blepharoplasty
130. Which eyelid abnormalities can be corrected with blepharoplasty?

131. How many orbital fat compartments occupy the upper lid? Lower lid?
132. Which muscle divides the central and medial compartments of the upper lid? Lower lid?
133. The superior lid crease is present at what distance from lid margin?
134. What are the surgical approaches to lower lid blepharoplasty? When are they used?
135. Which extraocular muscle is most at risk of injury in blepharoplasty?
136. What are the complications of blepharoplasty (6)?
The Aging Face (Rhytidectomy)
137. What are the histological changes in the aging skin (5)?
138. What are two major extrinsic factors to aged skin?
139. What part of the face does rhytidectomy address?
140. What is the SMAS?
141. What are the four basic types of rhytidectomy?
142. What are two surgical adjuncts to rhytidectomy to address the lower 2/3 of the face?
143. What is the most common complication of rhytidectomy?
144. What is the most common nerve injured during rhytidectomy?
145. What is the most common branch of the facial nerve injured and why?
146. What are the complications of rhytidectomy (6)?
147. What is the ideal position of the hyoid for good results post-facelift?
148. What patient factor will increase the risk of skin slough approximately 12 times?
149. What are methods to address deep nasolabial folds (4)?
The Aging Forehead
150. What is the blood supply to the forehead (3)?

151. What is the innervation of the forehead (4)?
152. What are the layers of the scalp (5)?
153. Which muscle forms vertical rhytids?
154. Which muscles forms horizontal forehead rhytids?
155. Which muscle forms horizontal glabella rhytids?
156. How do you determine ideal eyebrow position?
157. What features should be assessed in the analysis of the forehead (6)?
158. What are three methods of forehead/eyebrow lift? What are the advantages and
disadvantages or each?
159. What are the complications of forehead/eyebrow lift (5)?
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Chin and Malar Augmentation
160. What are the three methods of evaluating chin projection?

161. What types of alloplastic implants are available (4)?
162. How much reduction in gain occurs several months after implant placement?
163. What are the two surgical options for chin implantation and what are the advantages
and disadvantages of each?
164. What are the complications of chin augmentation?
165. What other surgical method can be used to augment the chin? What are the indications
(4) and what are the possible complications (3)?
Congenital Auricular Malformation
166. What is the approximate normal angle between the ear and the head?
167. Name the various landmarks of the external ear.
168. What is the blood supply to the pinna (3)?
169. What is the venous drainage of the pinna (4)?
170. What is the motor (2) and sensory (4) innervation of the pinna?
171. What are the two major deformities that cause outstanding ears and what are the
surgical techniques used to correct them?
172. What are the complications of otoplasty (4)?
173. What are the five stages involved in auricular reconstruction?
174. What are the alternatives to microtia reconstruction?
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REVIEW QUESTIONS IN GENERAL OTOLARYNGOLOGY
Degenerative and Idiopathic Diseases
1. What are the three clinical forms of fibrous dysplasia? Which is the most common form?
2. What are the features of McCune-Albright syndrome (3)?
3. What is the typical radiographic appearance of fibrous dysplasia (1)?
4. What are the biochemical abnormalities seen in Paget’s disease (3)?
5. What is the medical treatment of Paget’s disease (3)?
6. What is the difference between Mikulicz disease and Mikulicz syndrome?
7. What are the sialographic features of autoimmune parotid disease (2)?
8. What are the features of Sjogren syndrome (3)?
9. Which autoantibodies are implicated in Sjogren syndrome (2)? Which other autoantibodies may
be elevated?
10. How is Sjogren syndrome diagnosed?
11. What are the treatments available for recurrent acute sialadenitis (3)?
12. What is the differential diagnosis of recurrent bilateral nontender parotid swelling (5)?
13. What are the three histologic features of Wegener’s?
14. What are the treatments available for Wegener’s (4)?
15. What is the typical histologic picture of T-cell lymphoma? What are the treatments available
(3)?
16. What are the features of Churg-Straus syndrome (3)?
17. What are four causes of non-neoplastic, non-traumatic subglottic stenosis?
18. What is amyloid composed of? What stain will identify it?
19. What is the histologic feature in sarcoidosis (1)?
20. In the head and neck, where do sarcoid deposits most frequently occur?
21. What two biochemical tests can be used to diagnose sarcoidosis?
22. What is the main medical treatment of sarcoidosis?
23. What are the clinical features of relapsing polychondritis?
24. What is the cause of Hashimoto thyroiditis? What is the test used to diagnosis this condition?
25. What is Riedel struma?
Connective Tissue Diseases
26. What are the autoantibodies associated with the following disorders?:
-SLE (2)
-RA (2)
-Sjogren (2)
-systemic sclerosis (2)
-polymyositis/dermatomyositis (1)
-mixed connective tissue disease (1)
-Wegener’s (1)
27. Which autoimmune disease is associated with skin and mucosa lesions, malar rash, nasal
septal perforation, pericarditis, arthritis, and renal failure?
28. Which autoimmune disease is associated with dysphagia, tight perioral skin and calcinosis?
29. What is the underlying pathophysiology of polyarteritis nodosa?
30. What are the laryngeal (1) and otologic (3) manifestations of Wegener’s granulomatosis?
31. What is the diagnosis of a patient presenting with temporal headaches, jaw claudication and an
elevated ESR?
32. What are the features of Behcet’s disease (2)?
33. What are the features of Cogan syndrome (3)?
F.Ling - General Otolaryngology Review (1)
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34. What are five clinical features of Kawasaki disease? What important investigation is required to
follow these patients?
35. What is the treatment of Kawasaki disease (2)?
Granulomatous Diseases of the Head and Neck
36. What are the three clinical forms of Histiocytosis X?

37. What is the histology of a pyogenic granuloma? Where is it most commonly found?
38. What is the pathology of necrotizing sialometaplasia?
39. Which organism is seen in cat-scratch disease? What stain is used to identify this organism?
40. Which disease is characterized by visible cutaneous sinus tracts, lymphadenopathy and sulfur
granules seen on histology?
Anatomy and Physiology of the Salivary Glands
41. Which pharyngeal pouch are the major salivary glands derived from?
42. What type of cells is predominantly seen in the parotid, submandibular and sublingual glands?
43. Which nerve carries postganglionic parasympathetic fibers from the otic ganglion to the parotid
gland? Aberrant innervation to skin can cause which syndrome?
44. What are the functions of saliva (7)?
45. Draw the secretory unit.
46. What is the parasympathetic innervation of the parotid gland: in terms of preganglionic nerve,
ganglion, postganglionic nerve?
47. What is the parasympathetic innervation of the submandibular and sublingual gland: in terms of
brainstem nuclei, preganglionic nerve, ganglion?
48. What is the primary neurotransmitter of the parasympathetic?
49. What is the composition of saliva (6)?
50. In the unstimulated state, which gland has the highest salivary flow? Which gland has the
highest salivary flow in the stimulated state?
51. For problems of hypersecretion, what surgical procedures can be done (4)?
Non-neoplastic Diseases of the Salivary Glands
52. What is the most common viral disorder involving the salivary gland? What other viruses can
affect the salivary glands (3)?
53. What organisms are usually seen in acute suppurative sialadenitis (3)?
54. What are three granulomatous diseases that can affect the salivary glands?
55. What is Heerfordt syndrome?
56. How is Sjogren syndrome diagnosed? What is seen on biopsy?
57. What percentage of calculi occur in the submandibular vs. parotid vs. sublingual glands?
58. What are the treatment options of a submandibular calculi?
59. What are some causes of non-inflammatory nonneoplastic enlargement of the salivary glands
(sialadenosis) (6)?
Controversies in Salivary Gland Disease
60. What is the accuracy of FNAB in determining malignant versus benign tumours?
61. What percentage of salivary gland tumours are diagnosed as malignant on frozen section but
are found to be benign on permanent sections?
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62. What percentage of salivary gland tumours are diagnosed as benign on frozen section but are
found to be malignant on permanent sections?
63. What test has the highest predictive value for recurrence in patients with adenoid cystic
carcinoma?
64. What is the incidence of cervical metastasis due to oral or major salivary gland adenoid cystic
carcinoma?
65. What is the 10 year survival rate for patients with adenoid cystic carcinoma who have cervical
metastasis?
Upper Digestive Tract Anatomy and Physiology
66. List the six anatomic valves that are involved in deglutition.
67. List the four phases of swallowing and describe what occurs in each of the phase.
68. What are the two pressure generators during swallowing?
69. What effect does bolus volume have on both airway closure and cricopharyngeal opening
duration?
70. During the pharyngeal phase, which components can be exerted by voluntary control (2)?
71. What are two postural maneuvers that can be performed to decrease the risk of aspiration?
72. What is laryngeal penetration?
Upper Airway Anatomy and Function
73. What are the functions of the upper airways (4)?

74. Speech consists of three component processes, what are they?
75. What are five conditions that are required for pronation?
76. What is the vocal cycle?
77. How is the volume of speech controlled?
78. How is the frequency of speech controlled?
Tracheotomy and Intubation
79. What are the indications for tracheotomy (4)?

80. What is a Bjork flap? Why should it not be used in children?
81. For an emergency tracheotomy, what is the best incision that should be performed?
82. What are the contraindications of a cricothyrotomy (2)?
83. What is the most common intraoperative complication of tracheotomy?
84. What is the most common early postoperative complication of tracheotomy?
85. What is the most common late postoperative complication of tracheotomy?
86. What cuff pressure causes occlusion of submucosal capillaries?
87. What are the complications of percutaneous dilatational tracheotomy? What is the most
common?
Taste
88. What is hypogeusia? Ageusia? Dysgeusia?

89. Name the four different types of taste papillae and their location.
90. What is the role of the glossopharyngeal nerve in taste? Which brainstem nuclei does it
terminate on?
91. What is the role of the facial nerve in taste? Which brainstem nuclei is involved?
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92. What other nerves are involved in taste sensation (2)?
93. How can you clinically differentiate dysgeusia caused by a genuine stimulus versus a taste
phantom?
94. What are some of the causes of taste disorders?
Stomatitis
95. What are some infectious causes of stomatitis (4)? What are some noninfectious causes (6)?
96. What is the treatment of herpes gingivostomatitis in the immunocompetent and
immunocompromised patient?
97. What is Vincent’s gingivitis and what two organisms are usually implicated?
98. Which conditions are usually associated with desquamative gingivitis (5)? How is a diagnosis
made?
99. What is the pathophysiology of cicatricial pemphigoid and bullous pemphigoid? What is seen on
histopathology? How do these two diseases differ clinically and histopathologically? How are
these diseases treated?
100. What is a positive Nikolsky sign?
101. What condition is caused by autoantibodies directed against desmosome-monofilament
complexes, affects Ashkenazi Jews, with pathology that demonstrates intraepithelial clefting,
Tzank cells and acantholysis?
102. What condition is associated with target lesions, an rapid explosive onset of macules, papules,
vesicles, bullae or places? What are the severe forms of this condition that may require ICU
admission (2)?
103. What condition has a histology of hyperkeratosis, Civatte bodies, liquefactive degeneration of
basal cell layer and a sandlike lymphocytic infiltration in lamina propria?
104. What are the different clinical variants of lichen planus (5)?
105. What are the various clinical presentations of candidiasis (6)?
106. What are the three clinical presentations of aphthous ulcers?
107. What is the differential diagnosis of white lesions in the oral cavity (15)?
Pharyngitis
108. Tissues of the pharynx are prone to reactive changes because of which predominant tissue?
109. What is the differential diagnosis of pharyngitis (15)?
110. What are the complications of GABHS pharyngitis (3)?
111. A 9-year-old boy develops a paroxysmal cough and difficulty breathing. A throat culture reveals
a non-motile pleomorphic gram-negative coccobacillus. What is the most likely organism?
112. Which viruses can cause a mononucleosis like picture (3)?
Odontogenic Infections
113. Sublingual space infection occurs from which infected teeth?

114. Submandibular space infection commonly occurs from infection of which teeth?
115. What is Ludwig’s Angina? What spaces does it involve?
116. What are the organisms involved in odontogenic infections?
117. Which antibiotics are usually used?
118. Which organism is most commonly involved in osteomyelitis?
119. What imaging studies can be used to diagnose osteomyelitis and what are their findings?
120. What infection is characterized by anaerobic branching gram-positive filamentous organisms,
suppurative fistulous tracts through skin with sulfur granules seen in the exudate?
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121. What are the complications of odontogenic infections (10)?
Snoring and Obstructive Sleep Apnea
122. What are the two stages of sleep?

123. Which part of sleep do obstructive events most commonly occur and why?
124. What are the three distinct syndromes of sleep related airway obstruction and what are their
features?
125. What are the three different types of sleep apnea?
126. What is the respiratory disturbance index (RDI)? What is the apnea index (AI)?
127. How is OSA diagnosed based on RDI and AI?
128. What is the classification of OSA and hypoxemia severity?
129. What are the pharyngeal dilator muscles (5)?
130. What are anatomic causes of sleep apnea (10)?
131. What are signs and symptoms of OSA (6)?
132. What are the complications of OSA (7)?
133. What is the Mueller manoeuvre and what is its significance?
134. What are the components of polysomnography (9)?
135. What is the MSLT?
136. What blood test should be done on newly diagnosed patients with OSA?
137. What are the conservative (2), nonsurgical (3) and surgical (6) options for treatment of OSA?
138. How effective is UPPP for snoring? For OSA?
139. What are the indications for tracheotomy for OSA (6)?
140. Which two treatments significantly decreases morbidity and mortality from OSA?
Deep Neck Infections
141. What are the neck spaces that involve the entire length of the neck (4)?
142. What are the suprahyoid neck spaces (4)?
143. What are the anterior, posterior, superior and inferior boundaries of the retropharyngeal space,
danger space and prevertebral spaces?
144. What are the boundaries of the parapharyngeal space (7)?
145. What are the contents of the prestyloid and poststyloid compartments of the parapharyngeal
space?
146. Which fascial layer(s) make up the carotid sheath?
147. What are the organisms seen in the majority of DNIs?
148. Which type of streptococci are commonly seen in pharyngeal infections?
149. Which type of streptococci are commonly seen in odontogenic infections?
150. What diagnostic test is required in DNIs to assess for a serious life-threatening complication? If
this complication is present, what needs to be done in addition to draining the deep neck
abscess and giving IV antibiotics.
151. What is the most common cause of a submandibular space infection?
152. Where do submandibular space infections gain access to the lateral pharyngeal space?
153. What is the treatment of submandibular space infections?
154. What are the other spaces that are in direct contact to the parapharyngeal space?
155. How does the presentation of infections involving the pre- and post-styloid space differ?
156. Which syndrome is associated with suppurative IJV thrombosis?
157. What are some signs of impending bleeding from carotid artery erosion?
158. What is the surgical approach for drainage of a parapharyngeal space abscess?
159. At what age do retropharyngeal lymph nodes usually involute?
160. What is the surgical approach for drainage of a retropharyngeal space abscess?
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161. What is a Pott’s abscess?
162. What is the most common organism involved in prevertebral space infections?
163. What are the complications of deep neck infections (10)?
164. What is the organism involved in Lemierre syndrome? What is the treatment?
Esophageal Disorders
165. What are the three regions of natural constriction in the esophagus and approximately what
level are they during rigid esophagoscopy in the adult male?
166. What are the layers of the esophagus (4)?
167. Define primary, secondary and tertiary peristalsis.
168. What decreases LES pressure (5)?
169. What are the advantages of rigid (5) and flexible (5) esophagoscopy?
170. What are common ENT manifestations of GERD?
171. What are the treatment options of GERD?
172. What are the complications of reflux (5)?
173. What are the four manometric findings of achalasia? What are the treatment options (3)?
174. What are the findings on barium swallow for diffuse esophageal spasm (1)? What are the
treatment options (3)?
175. What is the difference seen on barium swallow between achalasia and scleroderma?
176. What are the treatment options for cricopharyngeal dysfunction causing dysphagia (2)?
177. What are the features of Plummer-Vinson syndrome (6)?
178. Where does Zenker’s diverticulum occur? What are the treatment options (2)?
179. What is the most common organism infecting the esophagus in the immunocompromised host?
180. What is the most common benign tumour of the esophagus?
181. What are the two most common malignant tumours of the esophagus?
182. What is Boerhaave syndrome?
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REVIEW QUESTIONS IN HEAD AND NECK ONCOLOGY
Principles of Chemotherapy in the Management of Head and Neck Cancer
1. What are the main mechanisms of action of chemotherapeutic drugs (5)?

2. What is the role of chemotherapy in head and neck cancer (2)?
3. What is the mechanism of action of methotrexate? What are the main side effects (4)?
4. What is the mechanism of action of cisplatin? What are the main side effects (4)?
5. What is the mechanism of action of 5-FU? What are the main side effects (3)?
6. What are the advantages and disadvantages of induction chemotherapy?
7. What are the complications of chemotherapy (8)?
Principles of Radiation Oncology
8. What is brachytherapy?
9. How does radiation induce cell death?
10. What are the four R’s of radiation oncology?
11. Which phase in the cell cycle are tumour cells more radiosensitive? radioresistant?
12. What are the advantages and disadvantages of preoperative radiation therapy?
13. What are the advantages and disadvantages of postoperative radiation therapy?
14. What are the complications of radiation therapy?
15. What is hyperfractionation?
16. What is accelerated fractionation?
17. What is hypofractionation?
18. What dose of radiation is usually needed for subclinical disease? Microscopic disease?
Clinically palpable disease?
19. What are the indications for adjuvant radiation treatment?
20. What are the contraindications of radiation therapy?
Cutaneous Malignancy
21. In descending order of incidence, what are the three most common cutaneous malignancies?
22. What are some risk factors for developing cutaneous malignancies (8)?
23. Name a syndrome in which patients have a propensity to develop BCCs. What is the mode of
inheritance? What are other features of this syndrome (3)?
24. What are the five subtypes of BCC? Which is the most aggressive/dangerous and why?
25. What is the rate of metastasis for BCC?
26. What are the treatment options for BCC (5)?
27. What is the metastatic potential of cutaneous SCCa?
28. What are the factors associated with a high-risk SCCa?
29. What are some histological features of SCCa (5)?
30. What are the five histologic variations of cutaneous SCCa?
31. What is the most common premalignant lesion of the head and neck? What is the treatment of
this lesion (3)?
32. Briefly, what is Bowen’s disease?
33. What is the name of an epithelial tumour with a rapid growth within 2 months with involution that
occurs in males and older patients most commonly on the nose?
34. What margins should be taken for small BCC? What margins should be taken for aggressive
BCC and SCCa?
35. What are the indications for Moh’s surgery (4)?
F.Ling - Head and Neck Oncology Review (1)
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36. What is the treatment of the N0 and N+ neck in cutaneous SCCa?
37. Describe the TNM classification for skin carcinoma.
Malignant Melanoma
38. What are the risk factors for developing melanoma (6)?
39. What are the clinical characteristics of a lesion that is suspicious for melanoma (5)?
40. What are the four clinicopathologic types of melanoma?
41. Describe the Clarke and Breslow classification of melanomas.
42. When can elective neck dissection be offered in the management of melanoma?
43. What is sentinel node biopsy and when can it be used?
44. What is the primary modality of treatment?
45. What are the typical resection margins for lesions that are in situ, 1-2 mm, 2-4 mm and greater
than 4 mm thick?
46. When is a radical neck dissection advocated?
47. What other adjuvant treatments are available (3)? When are they used?
48. In general, what are the treatment options for superficial, intermediate and deep melanomas.
Include discussion for N0 and N+ disease.
49. What are the adverse effects of interferon?
Neoplasms of the Nose and Paranasal Sinuses
50. What are the risk factors associated with nasal and paranasal sinus malignancies (7)?
51. What is the differential diagnosis of benign epithelial tumours (5), malignant epithelial tumours
(6), benign non-epithelial tumours (4), malignant non-epithelial tumours (8)?
52. What are the advantages and disadvantages of MRI and CT scan for evaluation of sinonasal
malignancies?
53. What are the three types of papilloma?
54. Which HPV types are more associated with benign disease? Which types are more associated
with malignant disease?
55. What is the rate of malignancy with inverted papilloma?
56. What are the top two common malignant tumours of the sinonasal tract? Which risk factors are
associated with each?
57. Describe the histology of an esthesioneuroblastoma (2).
58. What is the treatment modality for lymphoma and extramedullary plasmacytoma?
59. Describe the T staging for maxillary sinus tumours.
60. What is Ohngren’s line and what is its significance?
61. List the various surgical approaches to sinonasal tumours (6).
62. List in descending order the three most common sites of origin of sinonasal tumours.
63. What are the pathways to orbital invasion (3)?
64. What is the rate of cervical and distant metastasis? What is the recommended treatment for the
N0 neck?
65. What are absolute contraindications for craniofacial resection of sinonasal tumours (6)?
66. What are the complications of treatment for sinonasal cancers (10)?
67. What are the reconstructive options post-extirpation of sinonasal malignancies (3)?
Orbital Tumours
68. What is the most common primary intraconal orbital neoplasm in the adult?
69. What is the most common vascular tumour of the orbit and periocular tissue in infancy and
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childhood?
70. What is the most common malignant primary tumour of the orbit in children?
71. What is the most common epithelial neoplasm of the orbit?
72. What is the most common malignant epithelial neoplasm of the lacrimal gland?
73. What is the differential diagnosis of an orbital tumour (vascular, hematopoeitic, neural,
mesenchymal)?
74. What are the signs and symptoms of an orbital tumour (5)?
75. What is the most common metastatic orbital tumour?
76. What orbital condition is characterized by poorly localized orbital pain, eyelid swelling showing
multiple tissues in the orbit affected on CT?
77. What is the most common primary cyst of the orbit?
78. What is the most common eyelid malignancy?
Salivary Gland Neoplasms
79. Of the major salivary glands, neoplasms are found in which gland the majority of the time?
What is the percentage?
80. What is the proportion of benign vs malignant neoplasms in the parotid, submandibular and
sublingual glands?
81. What is the most common salivary gland neoplasm in children? What is the second most
common?
82. What is the most common malignant salivary gland neoplasm in children? What is the second
most common?
83. What is the most common benign neoplasm in adults? What is the second most common?
84. What is the most common malignant parotid neoplasm in adults?
85. What is the most common malignant submandibular gland neoplasm in adults? What is the
second most common?
86. Briefly, in terms of pathogenesis of salivary gland neoplasms, what is the multicellular theory?
What is the bicellular theory?
87. According to the multicellular theory, which cells of the salivary gland unit are the following
tumours derived from:
-mucoepidermoid carcinoma
-adenocarcinoma (2)
-oncocytic tumors
-acinic cell carcinoma (2)
88. For each of the pathologic descriptions, name the tumour:
-multiple cystic spaces with a double layer of oxyphilic granular cells and lymphoid
stroma projecting into the cystic spaces.
-chondromyxoid stroma, incomplete encapsulation with pseudopod extensions.
-serous acinar cells with clear cytoplasm arranged in a cystic, papillary, vacuolated or
follicular pattern.
-aggregates of mucoid cells separated by strands of epidermal cells; positive keratin and
mucous staining.
-glandular formation of cylindric cells of variable height forming papillae, acini or solid
masses.
-intracellular keratinization, intercellular bridges, keratin pearl formation.
-basaloid epithelium arranged in cylindric formations in an eosinophilic hyaline stroma
and perineural invasion.
-solid nests of epidermoid cells with few mucoid elements; positive stain for keratin and
mucin.
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89. What percentage of Warthin tumours are bilateral?
90. Histologically, how can one differentiate a high-grade MEC from SCCa?
91. Histologically, how can one differentiate a MEC from an adenocarcinoma?
92. Which salivary tumours have a propensity for perineural invasion (4)?
93. Which malignant salivary gland neoplasm shows the greatest propensity for distant metastasis?
94. What is the most important etiologic factor for the development of tumours of the major salivary
glands (esp. MEC)?
95. What normal structures can be mistaken for salivary gland neoplasms (3)?
96. In general, what is the treatment for malignant salivary tumours (include discussion of
histological grade, and the N0 and N+ neck) (4)?
97. Which malignant tumours are low-grade (2) and which are high-grade (5)? What is the
approximate 5 year survival for low- vs high-grade malignancies?
98. What are the five methods of locating the facial nerve?
99. What are the complications of parotidectomy (5)? Which is the most common complication?
100. Which branch of the facial nerve is most at risk for injury?
101. What is Frey syndrome? What is the cause? What are the treatment options (5)?
102. What are the poor prognostic indicators for salivary gland neoplasms (6)?
Lip Cancer
103. What are the functions of the lips (3)?

104. What is the sensory innervation of the upper and lower lip?
105. What is the blood supply of the lips? Where do these arteries run?
106. Describe the lymphatic drainage of the upper and lower lip.
107. Compare the relative frequency of cancers affecting the upper lip to the lower lip.
108. What percentage of malignancies of the lip are due to squamous cell cancer?
109. What are the main risk factors for development of lip cancer (4)?
110. What are other lesions that are seen on the lips (5)?
111. What are poor prognostic indicators for lip cancer (6)?
112. What is the TNM staging for lip cancer?
113. What are the treatment options for early lesions T1-T2?
114. What are the treatment options for late lesions T3-T4?
115. At which T stage would you consider treatment to the N0 neck?
116. What are the indications for postoperative radiation (6)?
117. What reconstruction options are for lip defects that are less than ½ of the lip? ½ to 2/3 lip? More
than 2/3 lip?
118. What flap is appropriate to reconstruct a 75% defect in the lower lip including commissure?
119. What is the most significant functional disadvantage of the Karapandzic flap reconstruction?
120. In an Abbe flap reconstruction, what is the width of the flap compared to the area of the defect?
Neoplasms of the Oral Cavity
121. What are the subsites of the oral cavity (7)?

122. Which foramina permits tumour spread from the palate into the anterior nose?
123. What is contained within these foramina?
124. Which foramen is a potential rout for spread for hard palate neoplasm though pterygopalatine
fossa to skull base?
125. What is the lymphatic drainage of the tongue with respect to its anterior, lateral and central
portions?
126. What is the lymphatic drainage of the floor of mouth with respect to its superficial mucosa and
deep collecting system?
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127. Excluding lip cancer, what are the top three most common subsites of the oral cavity that
develop squamous cell carcinoma?
128. What are the risk factors for developing oral SCCa (6)?
129. What is the TNM staging for squamous cell carcinoma of the oral cavity?
130. What is the differential diagnosis of other oral cavity tumours (8)?
131. What are the three gross pathology forms of SCCa?
132. What are poor prognostic factors associated with SCCa of the oral cavity (6)?
133. What are the treatment options for early T1-T2 lesions? Late T3-T4 lesions?
134. For most oral cavity lesions, when is elective treatment of the N0 neck considered based on T
stage?
135. Which subsite of the oral cavity has a higher predilection for verrucous carcinoma? How does
this diagnosis affect treatment (2)?
136. Which subsite of the oral cavity has equal incidence of SCCa and salivary gland malignancies?
137. What is the preferable mode of therapy for early primary retromolar trigone SCCa?
138. Alveolar carcinoma is most commonly located where in the oral cavity?
139. Of oral cavity cancers treated primarily with radiotherapy for cure, what is the subsite with
highest complication rate?
140. What are some options for reconstruction of oral cavity defects (4)?
Odontogenic Cysts, Tumours and Related Jaw Lesions
141. What is the differential diagnosis for a mass in the jaw (mandible or maxilla) (10)?
142. What are the two most common cystic lesions in the jaw? What is the pathogenesis and what is
their typical radiographic appearance?
143. Why is the differentiation of an odontogenic keratocyst from other cysts important?
144. Which syndrome is associated with multiple kertaocyts, BCC, bifid ribs, frontal bossing and
hypertelorism?
145. What is the most common epithelial odontogenic tumour? Where is it most commonly located?
What is its typical radiographic and histologic characteristic? How is it treated?
146. Name two other epithelial odontogenic tumours.
147. Which odontogenic tumour is common in young women and has benign self-limited growth?
148. How are odontogenic lesions diagnosed (ie. investigations etc..)
149. What are the basic treatment modalities and give an example of the type of lesion that the
treatment would be used for (3)?
150. What are the complications of odontogenic cysts, tumours and related jaw lesions (3)?
Neck Dissection
151. List the different types of neck dissections.

152. What are the poor prognostic factors that can be seen from a neck dissection.
153. Which structures are spared in a modified radical neck dissection type I? Type II? Type III?
154. What are the different types of selective neck dissections and which nodal levels do they
involve? What are their indications?
155. What are the different nodal levels?
156. What structures can be involved in an “extended” neck dissection?
157. List the complications from a neck dissection.
158. When is elective neck dissection considered?
159. When is postoperative radiation considered?
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Controversies in Management of N0 Neck in Squamous Cell Carcinoma of the Upper
Aerodigestive Tract
160. What are the three options in the management of the N0 neck in SCCa?
161. What are histologic features that may be predictors of cervical metastasis?
162. What are the disadvantages of elective neck irradiation?
Lymphomas of the Head and Neck
163. What are the risk factors for the development of lymphomas (6)?
164. What are the sites and presenting symptoms of NHL in the head and neck (10)?
165. What is the major the limitation of FNA in the evaluation of lymphoma?
166. What immunohistochemical studies are used to differentiate lymphoma from other high grade
malignancies?
167. Describe the Working Formulation classification of NHL and list examples under each category.
168. Which type of NHL is the most common in the head and neck?
169. Which site of involvement of NHL has a higher propensity for CNS involvement?
170. What drugs are involved in the CVP and CHOP regimens?
171. In general, how are lymphomas treated (2)? What are the complications of these treatments?
172. What is the treatment for lymphoma causing an impending airway obstruction?
173. What are the features of tumour lysis syndrome (4)?
Thyroid Disease and Surgery
174. In terms of development, where does the thyroid gland originate from?
175. What is the lymphatic drainage of the thyroid gland (3)?
176. What biochemical marker is used to measure the completeness of thyroid ablation after surgery
or radioisotope therapy?
177. What is the most common benign thyroid neoplasm?
178. What is the limitation of FNAB when it comes to follicular neoplasms?
179. What are the four types of thyroid malignancies?
180. What are the histologic features of papillary thyroid carcinoma?
181. What are the histologic subtypes of papillary thyroid carcinoma (6)?
182. What is the main mode of spread for papillary thyroid cancers? What is the main mode of
spread for follicular carcinomas?
183. What tumours are involved in the MEN II syndromes?
184. From which cells do medullary thyroid carcinomas originate?
185. What is the typical histologic appearance of medullary thyroid carcinoma?
186. What is the most common site of metastasis of medullary thyroid carcinoma?
187. What is the significance of RET-proto-oncogene?
188. What is the treatment of medullary thyroid carcinoma (2)?
189. What is the risk of malignancy of a solitary thyroid nodule?
190. What are the prognostic factors in thyroid malignancies (4)?
191. How do high and low risk malignancies differ in terms of recurrence and mortality rates?
192. What is the rationale of radioactive iodine therapy? What are the risks of this type of therapy
(3)?
193. What are the complications of thyroidectomy (5)?
194. What are the manifestations of Graves disease (3)?
195. Which drugs are used in suppressive therapy for hyperthyroidism (4)? What treatments are
available if the patient fails suppressive therapy (2)?
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Parathyroid Disease and Surgery
196. What is primary, secondary and tertiary hyperparathyroidism?

197. What are the causes of hypercalcemia?
What is the most common cause in outpatient population? Inpatient population?
198. What are the clinical manifestations of hypercalcemia?
199. What are the embryologic precursors to the parathyroid glands?
200. What are some aberrant sites of the parathyroid glands?
201. What are the key features to the MEN-type syndromes?
202. List the different pre-operative localization tests to detect parathyroid adenomas.
203. Briefly list the medical options for hypercalcemia.
204. What are the functions of PTH?
205. What are the complications of parathyroid surgery?
Nasopharyngeal Cancer
206. What are the boundaries of the nasopharynx (5)?

207. What are the anatomic subsites of the nasopharynx (3)?
208. With regards to the nasopharyngeal mucosa, what types of tissue are present?
209. List the WHO histopathologic types of nasopharyngeal carcinoma.
Which type carries the worst prognosis?
Which types are more radiosensitive?
Which type is the most common? least common?
210. Which ethnic populations are more susceptible to nasopharyngeal carcinomas (4)?
211. What are some risk factors to developing NPC?
212. NPC susceptibility genes are linked to which chromosome?
213. What are the top five signs or symptoms for NPC? What is the most common sign or symptom?
214. What are the potential local routes of spread for NPC? What neurological deficits are observed?
215. What is the incidence of distant metastasis? What sites are affected?
216. Which serologic tests are useful in screening for occult disease? Which WHO types of NPC
does this screen for?
217. Which test can provide prognostic information for NPC? Which WHO types does this apply to?
218. What is the TNM staging for nasopharyngeal cancers?
219. List the prognostic indicators for nasopharyngeal carcinoma (5).
220. What is “Ho’s line”? What is its significance?
221. What is the main treatment modality for NPC?
What is the role for brachytherapy?
What is the role for surgery? What is the most frequently indicated surgical procedure other
than biopsy?
What is the role for chemotherapy?
222. For recurrent or residual disease, what are the surgical approaches available?
223. What are some treatment related complications?
Oropharyngeal Cancer
224. What are the anatomic boundaries of the oropharynx?

225. What are the anatomic subsites (6)?
226. What is the lymphatic drainage of the oropharynx?
227. What are the contents of the prestyloid compartment of the parapharyngeal space?
228. What are the contents of the poststyloid compartment of the parapharyngeal space?
229. What are the nerves responsible for referred otalgia in oropharyngeal cancers (2)?
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230. What are the different types of cancer that can occur in the oropharynx (5)?
231. What is the most common malignancy of the palatine tonsil?
232. What is the most common presenting symptom?
233. What are the histologic variants of SCCa in the oropharynx (6)?
234. Describe the TNM staging of oropharyngeal cancers.
235. What are the treatment options for early (T1-T2) oropharyngeal cancers?
236. What are the treatment options for advanced (T3-T4) oropharyngeal cancers?
237. What features of the primary tumour will make it surgically unresectable (3)?
238. What are the different surgical approaches to the oropharynx (7)?
239. What are the indications for postoperative radiation?
240. What type of reconstruction is required for large surgical defects?
241. What are the complications of treatment (radiation and surgical)?
Hypopharyngeal Cancer
242. What are the superior and inferior limits of the hypopharynx?
243. What are the anatomic subsites of the hypopharynx?
244. What is the lymphatic drainage of the hypopharynx?
245. What is the most common malignancy of the hypopharynx? What are some other malignancies
that can affect this area?
246. What are the risk factors?
247. List some features of Plummer-Vinson syndrome. How is this related to hypopharyngeal
malignancy?
248. List the subsites in order of decreasing incidence of malignant involvement.
249. What is the incidence of occult lymph node metastasis in the N0 neck?
250. What is the incidence of distant metastasis?
251. What is the incidence of palpable nodal metastasis at presentation?
252. What is the incidence of coexisting primary malignancies in patients with one head and neck
cancer?
253. What is the risk of patients with primary head and neck cancers to develop a second primary
within 5 years?
254. Describe the TNM staging for hypopharyngeal cancers.
255. What are treatment options for early (T1-T2) hypopharyngeal cancers?
256. What are treatment options for late (T3-T4) hypopharyngeal cancers?
257. What are indications for partial laryngopharyngectomy (4)?
258. If radiation therapy is to be used primarily, generally what type fractionation scheme is used?
259. What levels must be addressed in the management of the N0 neck?
260. What levels must be addressed in the management of the N+ neck?
261. What are the options for surgical reconstruction (6)?
262. What is the mortality rate associated with gastric pull-up?
Cervical Esophageal Cancer
263. What is the superior and inferior limits of the cervical esophagus (2)?
264. What are the layers of the esophagus (4)?
265. What is the blood supply of the cervical esophagus (1)?
266. What is the nerve supply to the cervical esophagus (1)?
267. What is the lymphatic drainage of the cervical esophagus (2)?
268. What is the most common tumour of the cervical esophagus?
269. What are the major risk factors for cervical esophageal cancer (2)?
270. What is the most common abnormal finding? What other symptoms/signs are seen (3)?
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271. What investigations can be carried out to diagnose cervical esophageal cancer (3)?
272. Describe the T-staging of cervical esophageal cancer.
273. What is the general management of an early esophageal cancer with extension to the
postcricoid area and involvement of the thoracic esophagus?
274. What is the general management option for advanced esophageal cancer?
275. Overall, what is the prognosis for esophageal cancer (poor, moderate, or excellent)?
276. For gastric pull-up, what are the reasons one must perform a total esophagectomy (3)?
277. What is the operative mortality of the gastric pull-up?
Vertical Partial Laryngectomy and Laryngoplasty
278. In terms of laryngeal carcinoma, what percentage involves the glottis, supraglottis, and
subglottis?
279. For glottic cancers, what is the risk of nodal involvement for T1 and T2 lesions (1)? T3 lesions?
280. What are the various histologic stages of glottic lesions (5)?
281. What proportion of dysplastic lesions eventually progress to carcinoma?
282. What is “microinvasive” carcinoma?
283. What is Ackerman’s tumour? What features make it different from regular carcinoma (4)?
284. What are the treatment options for early glottic carcinoma (6)?
285. What are relative contraindications for laser microscopic excision (4)?
286. What are the general contraindications for open partial laryngectomy (5)?
287. What are the contraindications for cordectomy (2)?
288. What are the indications for VPL (5)?
289. What structures are removed in a VPL (4)? What other structure is removed in an extended
VPL (1)?
290. What is used to line the laryngeal lumen after VPL (1)? What can be used to add bulk if voice
quality is poor post-VPL?
291. For lesions involving only the anterior commissure what open partial technique can be used?
292. What are some complications of VPL (7)?
Supraglottic Laryngectomy
293. What are the patient selection criteria for supraglottic laryngectomy (5)?
294. What is the most common reason for local or regional recurrence after treatment of a T1 or T2
supraglottic cancer?
295. What is the risk of nodal metastasis for a T1, T2, T3 and T4 supraglottic carcinoma?
296. What are the indications and contraindications for supraglottic carcinoma?
297. What structures are removed (7)?
Supracricoid Partial Laryngectomy
298. What are the main indications for supracricoid partial laryngectomy with cricohyoidopexy?
299. What are the contraindications of this procedure?
300. Cricohyoidepiglottopexy is used for what type of cancer?
301. What structures are removed (4)?
Advanced Cancer of the Larynx
302. Describe the three anatomic regions of the larynx and their approximate levels.
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303. What are the tissue barriers to the spread of cancer (6)?
304. What are the boundaries of the pre-epiglottic space?
305. What are the boundaries of the paraglottic space?
306. What are the most common sites of cartilage invasion by cancer (5)?
307. Which (named) nodes do glottic cancers first spread to?
308. What is the differential diagnosis of a laryngeal lesion (7)?
309. Describe the TNM staging of supraglottic, glottic and subglottic cancers.
310. What are the surgical options for advanced supraglottic carcinomas (4)?
311. What are the treatment options for advanced glottic carcinoma?
312. What are the treatment options for subglottic carcinoma?
313. Which chemotherapeutic agents are commonly used for organ preservation (2)?
314. What are the complications of surgery and radiation for advanced laryngeal cancer?
Management of Intractable Aspiration
315. What are some of the etiologies of aspiration (4)?

316. What are the four phases of swallowing? What occurs during each phase?
317. What is the effect of tracheostomy on swallowing (5)? In a patient with a tracheostomy, what can
be done to improve swallowing and prevent aspiration?
318. What are the non-surgical options to help prevent aspiration (4)?
319. What are three compensation techniques that can be used to help with swallowing?
320. What are the surgical options for intractable aspiration (6)?
Voice Rehabilitation After Laryngectomy
321. What are the options for alaryngeal speech (5)?

322. What is a contraindication to voice restoration?
323. What are some of the causes for speech failure with TEP (5)?
324. What is the most common cause for TE speech failure?
325. What are the treatment options for persistent pharyngoesophageal spasm after successful
primary TEP (3)?
326. What are some of the complications of TEP (5)?
Tracheal Tumours
327. What percentage of tracheal tumours are malignant versus benign?

328. What are the two most common primary malignant tumours of the trachea?
329. What are the most common benign tumours of the trachea (3)?
330. What are signs and symptoms of tracheal tumours (6)?
331. What is the blood supply to the trachea (2)?
332. What is the average length of the adult trachea?
333. What is the maximum amount of tracheal resection allowed?
334. What are the options to decrease tension on the anastomosis of the tracheal resection (6)?
335. What are the complications of a tracheal resection (4)?
336. How do SCCa and ACC differ in terms of presentation and prognosis?
Vascular Tumours of the Head and Neck
337. What is the most common head and neck tumour in children?
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338. A child has a subglottic hemangioma, what percentage will have other cutaneous hemangioma?
339. What syndrome is associated with capillary malformations of the face?
340. Where do juvenile nasopharyngeal angiofibromas originate from?
341. What are the surgical approaches for the exenteration of JNAs (4)?
342. What are 3 malignant vascular tumours of the head and neck area?
343. What type of cells are paragangliomas derived from?
344. What two cell types are seen histologically in paraganglioma?
345. What are the anatomic locations of paraganglioma (5)?
346. What is the “rule of 10's” for carotid body tumours?
347. If a patient has a paraganglioma and is symptomatic with high blood pressure and tachycardia,
what tests should be done (3)?
348. How do you differentiate a carotid body tumour from a glomus vagale?
349. What is the Shamblin classification of carotid body tumours (3)?
350. What is the significance of Brown’s sign?
Cranial-Base Surgery
351. What is lateral medullary syndrome?

352. What vein drains the temporal lobe and enters the transverse sinus at a position medial to the
superior petrosal sinus?
353. What methods are used to evaluate cerebrovascular perfusion (2)?
354. What structures are transmitted via the following foramina:
-cribriform plate (1)
-optic canal (2)
-superior orbital fissure (6)
-inferior orbital fissure
-foramen rotundum (1)
-foramen ovale (1)
-foramen spinosum (1)
-sulcus tubae auditive (1)
-foramen lacerum
-carotid canal
-stylomastoid foramen (2)
-jugular foramen (4)
-internal acoustic meatus (2)
-hypoglossal canal (1)
-foramen magnum (5)
355. What are extracranial landmarks that help identify the floor of the anterior cranial base?
356. What are the boundaries of the infratemporal fossa?
357. What artery supplies a temporoparietal facial flap? Which artery supplies the temporalis
muscle?
358. Which arteries supply the pericranial flap?
359. What are the layers of the scalp?
360. What are some approaches to the anterior cranial base (4)?
361. What are three approaches to the middle cranial base?
362. What are some approaches to the posterior cranial base (4)?
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REVIEW QUESTIONS IN LARYNGOLOGY
Laryngitis
1. What are some viruses associated with laryngitis?

2. Which organism is associated with acute laryngotracheitis?
3. Which laryngeal structure is most commonly involved in acute laryngotracheitis? How does this
manifest on x-ray?
4. What organisms are usually involved in secondary bacterial laryngitis (3)? Which antibiotics are
generally used?
5. Which organism is involved classically in epiglottitis?
6. What is the management of acute epiglottitis?
7. What condition presents with thick, gray-green plaquelike membranous exudates over pharynx
and larynx (1)?
8. What are some possible sequelae of laryngopharyngeal reflux (5)?
9. What is “pseudosulcus vocalis”?
10. What is the gold standard for diagnosing reflux?
11. What class of medications is implicated in angioedema?
12. Hereditary angioedema is thought to be due to deficiency of what?
13. What are some autoimmune conditions that can give laryngitis (2)?
14. A patient with long-standing laryngitis and is found to have a supraglottic lesion. This is biopsied
and it demonstrates an amorphous red-staining material with Congo red. What is the
diagnosis?
15. What are the areas of involvement with tuberculous laryngitis (3)? Which is the most common?
16. Name other chronic granulomatous diseases of the larynx (6)
17. You biopsy a laryngeal lesion and the pathology reports “pseudoepithelial hyperplasia”. What is
the differential diagnosis (5)?
18. In the immunocompromised host, what pathologic lesions can be found in the larynx (4)?
19. Radiation induced laryngitis is a diagnosis of exclusion. What other conditions should be ruled
out first (4)?
Hoarseness and Vocal Cord Paralysis
20. What type of epithelium constitutes the mucosal layer of the vocal cords?
21. What are the 5 layers of the true vocal cord and what do they consist of?
22. Which muscles are the adductors (3), abductor (1) and tensor (1) of the vocal cords?
23. Which brainstem nucleus is responsible for the motor function of the larynx?
24. What clinical findings are seen with paralysis of the SLN (3)? What laryngoscopic findings are
seen (3)?
25. What should be elicited in the patients’ history in the evaluation of hoarseness (10)?
26. What investigations should/can be performed in the evaluation of hoarseness and/or vocal cord
paralysis (10)?
27. Classically, which nerve(s) is/are injured if the vocal cords are in a cadaveric position?
Paramedian position?
28. What are the top three causes of stridor in children (in order)?
29. What is the most common cause of vocal cord paralysis in children? What are other causes
(5)?
30. For children with unilateral vocal cord paralysis, what is the main modality of treatment?
31. What percentage of newborns with bilateral vocal cord paralysis require tracheotomy?
32. What is the most common cause of vocal cord paralysis in adults? What are other causes of
vocal cord paralysis (15)?
F.Ling - Laryngology Review (1)
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33. What is the medical management of unilateral vocal cord paralysis?
34. How long should you wait before performing surgery for unilateral vocal cord paralysis?
35. What are the surgical options for unilateral vocal cord paralysis (4)?
36. For endoscopic medialization, what materials are available (4)? Which of these materials is
falling out of favour and why?
37. What are the surgical options for bilateral vocal cord paralysis (5)?
Benign Lesions of the Larynx
38. Which portion of the vocal folds are vocal cord nodules located? How do you manage them?
39. What is the most common benign lesion of the adult larynx?
40. What is the most common benign lesion of the child’s larynx?
41. What are the two types of vocal cord polyps?
42. Where are mucous retention cysts of the larynx most commonly found (2)? What is their
surgical management if involving the vocal cords?
43. What is the main causes of vocal cord granuloma (2)? How are they treated?
44. What is the risk of transmission of HPV in the birth canal?
45. Which subtype of HPV is responsible for more aggressive papillomatosis?
46. What are the two most common sites for laryngeal papillomatosis?
47. What are the non-surgical option for treatment of papillomatosis (4)?
48. Which type of cells do granular cell tumours originate from?
49. What is the most common site of a granular cell tumour?
50. If the larynx is involved, what are the most common site for a granular cell tumour?
51. What is the most common nerve of origin for neurogenic tumours?
52. Is laryngeal amyloid a localized or systemic problem?
53. What is the most common area affected in laryngeal amyloidosis?
54. What is seen on histology in laryngeal amyloidosis (2)?
55. What is the classic histology seen in sarcoidosis (1)?
56. What is the treatment of sarcoidosis?
57. What is capillary ectasia? In whom is it most commonly seen? What is the management?
58. What are the two histological types of intracordal cysts?
59. What is a glottic sulcus? What is seen on stroboscopic examination? What is the treatment?
60. What is a condition seen in middle-aged women who are chronic smokers causing a decreased
pitch in voice?
61. What is the pathophysiology of an intubation granuloma?
62. What are the two forms of laryngeal papillomatosis? Which is the more aggressive form?
63. Which type of patients are vocal cord nodules most often seen (2)?
Laser Surgery of the Larynx
64. What are the applications of laser in laryngology (5)?

65. What criteria must be met before contemplating laser excision of laryngeal cancer (5)?
66. What are the advantages of surgical treatment of early glottic cancers versus radiation therapy?
Laryngeal and Pharyngeal Function
67. What are the functions of the larynx (5)?

68. What is the most important pharyngeal dilator?
69. What are the three fundamental components in the process of speech?
70. What are the requirements for phonation (5)?
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71. What is the voice cycle?
72. What is the “body-cover” concept of phonation?
Voice Analysis
73. What is the GRABAS scale and how is it used?

74. What is the maximal phonation time (MPT) required for speech? What is it in the average male
and female?
75. What is the significance of a prolonged MPT? A shortened MPT?
76. What is the phonation quotient?
77. What is the fundamental frequency? What is its approximate value for men and women?
78. Define shimmer and jitter.
79. What are factors that will increase or decrease phonatory flow rate?
80. What determines the loudness of voice? What determines the pitch?
Neurologic Evaluation of the Larynx and Pharynx
81. What are some speech and swallowing symptoms suggestive of neuropathology (6)?
82. Which progressive disease can present with monotonous and raspy voice, velopharyngeal
incompetence, visible fasciculation in tongue, and difficulty with swallowing?
83. What disorder presents with easy fatigue with muscle use, ptosis, difficulty speaking, breathing
or swallowing with repetitive movements? Which test can confirm this condition?
84. Which condition consists of relapsing and remitting sensory and motor deficits, vertigo, tremor,
scanning speech and dysphagia?
85. What condition results from infarction of the central tegmental tract? How can this condition be
corrected?
86. Which condition is characterized by generalized bradykinesia with sluggish articulation and
monotone voice with decreased loudness?
87. What is adductor and abductor dysphonia? How can they be treated?
Phonosurgical Procedures
88. What are the laryngeal framework surgery classification according to Isshiki (4)?
89. What are the complications of vocal fold medialization by injection (5)?
90. What are the advantages and disadvantages of medialization thyroplasty over medialization by
injection (5)?
91. What are some surgical procedures to alter pitch (4)?
Controversies in Laryngology
92. What are the principle indications for stroboscopy (4)?

93. What is the main indication for laryngeal electromyography?
94. With regards to paralysis, what are good and poor prognostic findings on EMG?
95. What are the causes of vocal process granuloma (4)? What are the indications for surgery (4)?
96. What best prevents development of prolonged postoperative dysphonia after vocal cord
surgery?
97. What is the indication for absolute voice rest?
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REVIEW QUESTIONS IN OTOLOGY AND NEUROTOLOGY
Development of the Ear
1. Which branchial arches is the pinna derived from? Which hillocks do these arches contribute
to? What part of the pinna do these hillocks eventually form?
2. What are the embryologic derivatives of the tympanic membrane?
3. What are the embryologic derivatives of the ossicles?
4. Where is the usual location of a congenital cholesteatoma?
5. What is the incidence and most common site for facial nerve dehiscence?
6. What is the incidence of coexisting middle/outer ear and inner ear abnormalities?
7. At what gestational age does the membranous labyrinth obtain adult shape? Adult size?
8. Which inner ear structure continues to grow into the third trimester?
9. Which structures develop from the pars superior and pars inferior portions of the developing
otocysts?
10. What are the classifications of inner ear maldevelopment and what are their approximate
incidences?
11. What is the most common histopathologic finding in congenital deafness?
12. What is Bing-Siebemann dysplasia?
13. Malformations of the cochlea are believed to be due to disruptions during the first 4 to 7 weeks
of development. What malformations are seen if this disruption occurs before 4 weeks GA? At 5
weeks GA? At 6 weeks GA? At 7 weeks GA?
14. What is the most common radiologically detectable abnormality of the inner ear?
Anatomy and Physiology of Hearing
15. What features aid sound localization?

16. How does the middle ear achieve impedance matching of sound transmission? What pressure
gain does this result in?
17. What is the transforming ratio?
18. How much conductive loss occurs with a tympanic membrane perforation? A tympanic
membrane perforation with stiff ossicles?
19. What are the general functions of the middle ear muscles?
20. Name the different divisions of the cochlea. What type of fluid is contained within each division?
What are their electrolyte concentrations with regards to Na and K (high vs low)?
21. Where is perilymph produced? Where is endolymph produced (2)?
22. Where is endolymph absorbed?
23. In terms of the basilar membrane, which end is wider? Which end is stiffer? Which end is
narrower? Which end is more flexible?
24. Compare and contrast inner versus outer hair cells with regards to:
-percentage of neurons that innervate the cochlea
-type of neurons
-afferent or efferent innervation
-relative cell number
-arrangement of stereocilia
-attachment to the tectorial membrane
-hair cell to ganglion cell ratio
25. What is the “cochlear amplifier”?
26. List the four gross cochlear potentials. What do each of these potentials represent?
27. Briefly describe the tonotopic arrangement of the basilar membrane.
28. What are the four types of OAEs?
F.Ling - Otology Neurotology Review (1)
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29. Briefly describe the central auditory pathway from cochlea to auditory cortex.
30. What is recruitment?
31. What is the significance of the tuning curve?
Vestibular Function and Anatomy
32. What are the 5 organs that sense acceleration?

33. How many degrees from the horizontal plane is the lateral SCC angled?
34. What are the kinocilium? How does deflection of the stereocilia in relation to the kinocilium
affect nerve transmission?
35. In the horizontal canals, maximal excitation occurs with which type of endolymphatic flow?
36. In the anterior and posterior canals, maximal excitation occurs with which type of endolymphatic
flow?
37. What are the functional canal pairs (3)?
38. What type of acceleration do the saccule and utricle sense?
39. What is the orientation of the polarization vector in the saccular macula? In the utricular
macula?
40. Which organs does the superior vestibular nerve innervate? The inferior vestibular nerve?
41. For each SCC, which extraocular muscles are excitatory(2) and inhibitory(2)?
Balance Function Tests
42. When are formal balance function tests indicated (4)?

43. What are the vestibular subtests in ENG (4)?
44. What are the oculomotor subtests in ENG (3)?
45. What is the corneal retinal potential?
46. How is nystagmus characterized (2)?
47. What are the different types of nystagmus (4)?
48. What findings on ENG are suggestive of a central disorder (6)? A peripheral disorder (5)?
49. What three positions are used in positional testing?
50. What percentage of unilateral hyporeactivity is considered significant?
51. What percentage of directional preponderance is considered significant?
52. What type of lesion causes saccadic overshoot or undershoot dysmetria?
53. What other conditions can cause slow saccades or increase latency?
54. What condition causes saccadic pursuit?
55. What is rotatory chair testing used for (3)?
56. What is phase, gain and symmetry with regards to rotational chair testing?
57. What are the 6 conditions of dynamic posturography?
58. Which conditions do patients with bilateral ototoxicity fall (2)?
Electronystagmography
59. Which vestibular tract does ENG mainly deal with?

60. Which SCC and vestibular nerve branch is tested?
61. What is Alexander’s Law?
62. In a unilateral peripheral lesion, which direction is the nystagmus in relation to the weaker ear?
63. Can positional nystagmus differentiate peripheral vs central lesions?
64. How many degrees must nystagmus need to be before it is considered significant?
65. What temperatures are tested on caloric testing?
66. How is unilateral weakness and directional preponderance calculated?
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67. What is the fixation index and what value is considered significant?
Assessment of Peripheral and Central Auditory Function
68. What is a dB? What is the reference sound pressure (dynes/cm2)?

69. What is the reference level for dB HL? dB SL?
70. What is the sound intensity (dB HL) for whispered speech, conversational speech, and
shouting?
71. What are the octave frequencies? What are the interoctave frequencies (2)?
72. What are the speech frequencies (range)?
73. How do you calculate the pure-tone average?
74. What is the interaural attenuation for air conduction with over the ear headphones vs insert
headphones? What is the interaural attenuation for bone conduction?
75. What is the test-retest variability in pure-tone audiometry?
76. What is masking? What is crossover?
77. What is the speech reception threshold? What are spondees?
78. How is speech recognition measured?
79. What are the different types of tympanograms and what are their significance?
80. What is the normal threshold level to elicit an acoustic reflex?
81. What is the afferent and efferent portions of the acoustic reflex?
82. Where are the electrodes placed for ABR?
83. What type of stimulus is used to elicit an ABR? What level of hearing loss would preclude an
ABR?
84. What is the approximate latency of wave I, III, and V? What is the approximate interwave
latencies of I-III, III-V, and I-V?
85. What do each of the waves in the ABR represent?
86. What are the features of conductive or mixed hearing loss on ABR (3)? Sensory hearing loss
(3)? Retrocochlear hearing loss (3)?
87. What are the three components of the ECochG?
88. When is the SP/AP ratio abnormal for ear canal electrode, tympanic membrane electrode, and
transtympanic electrode?
89. What are the cortical auditory evoked responses (3)?
90. What are the two classes of OAEs?
91. What are the three types of evoked OAEs?
92. What are the clinical applications of OAEs (5)?
Neurophysiologic Intraoperative Monitoring
93. What are three methods that can be used to monitor the auditory system intraoperatively?
94. What is the most sensitive method? What is the least sensitive method?
95. Which method best senses changes in cochlear blood supply?
96. Which three surgeries place the facial nerve at risk?
97. Excluding operations for acoustic neuroma, which segment of the facial nerve is most commonly
injured?
98. What anaesthetic considerations should be made when monitoring the facial nerve?
Imaging Studies of the Temporal Bone
99. In terms of tissue signal characteristics, what are the signal intensities for fat, CSF, nasal
mucosa, and soft tissue in a T1, T2 and contrast enhanced T1 MRI?
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100. What infectious condition of the external auditory canal can be mistaken for a malignancy?
101. What is coalescent mastoiditis?
102. What is a Bezold abscess?
103. What is a cholesterol granuloma? What are the MRI signal characteristics?
104. What are the MRI characteristics of a petrous apex cholesteatoma?
105. What is the most common site for labyrinthine fistula secondary to bony erosion from a
cholesteatoma?
106. What is the most common primary tumour of the middle ear?
107. What is the most common positive imaging finding in individuals with congenital SNHL? What
syndrome is this commonly associated with?
108. What are the MRI characteristics of an endolymphatic sac tumour?
109. What condition is associated with a “double ring sign” around the cochlea?
110. Where is the facial nerve most commonly injured in a longitudinal and transverse temporal bone
fracture?
111. What is the most common cause for objective pulsatile tinnitus and a vascular hypotympanic
mass?
112. What is the most common CPA tumour? Second most common? Third most common?
113. What are the MRI characteristics of an acoustic neuroma? A meningioma?
Infections of the External Ear
114. What is the lymphatic drainage of the external auditory canal?

115. What are the nerves involved in the cutaneous sensory innervation of the external auditory canal
(5)?
116. What are the two most common bacteria seen in acute otitis externa? What other bacteria can
be seen?
117. According to Senturia, otitis externa has three stages. What are they?
118. What are the principles of treatment for acute external otitis (4)?
119. What is necrotizing external otitis (NEO)?
120. Which population is affected by NEO (2)?
121. What are the salient features of NEO (4)?
122. Which organism is implicated the majority of the time? What other organisms can be involved?
123. What is the most common cranial nerve affected in NEO?
124. What are the stages of NEO?
125. What diagnostic imaging options are available for NEO and when are they used (4)?
126. List the treatment for NEO (5).
127. What is the role of surgical therapy in NEO? What is the prognosis?
128. Which organism is implicated in furunculosis or carbunculosis of the external auditory canal?
129. Which organisms are implicated in bulbous myringitis (3)? What is the general treatment?
130. Which organisms are implicated in otomycosis (3)?
131. What are the available treatments for otomycosis (6)?
Neoplasms of the Ear and Lateral Skull Base
132. What is the most common true neoplasm of the middle ear?
133. Which tumours contain “zellballen” of chief cells containing norepinephrine and dopamine?
134. What is Brown’s sign?
135. What is Vernet syndrome? Villaret syndrome?
136. What investigations are required for glomus tumours (3)?
137. What surgical approaches are available for glomus tympanicum (2)? Glomus jugulare?
138. In which location of the temporal bone are hemangiomas most common?
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139. A chronic bloody draining ear is suggestive of what type of pathology?
140. Which type of lesion is characterized by a rim of palisading basaloid cells with central necrosis
and ulceration?
141. Name four glandular tumours of the EAC.
142. Which tumour is characterized by solitary cystic lesions originating from primitive hair matrix
cells?
143. Which disease is associated with endolymphatic sac tumours?
144. What are the three clinical types of Langerhans Cell Histiocytoses?
145. What are the three types of rhabdomyosarcoma?
146. What lesion is characterized by stellate, intermediate and vacuolated physaliphorus or soap-
bubble cells in mucoid matrix growing in nests, cords or trabeculae?
147. What is the pathogenesis of cholesterol granulosa (4)?
Congenital Aural Atresia
148. Briefly describe the embryological development of the EAC.

149. T/F. There is a correlation b/n degree of microtia and extent of facial nerve abnormality.
150. What is the most common anomaly of facial function?
151. What is the classification of atresia according to Schuknect (4)?
152. What two important investigations are required for evaluation of atresia?
153. What is the non-surgical management of unilateral and bilateral atresia?
154. What conditions require immediate surgical repair (2)?
155. What is the recommendation with regards to timing for unilateral atresia repair?
156. For bilateral atresia repair, what is the timing of surgery? Why is this age selected? Which ear
is selected first?
157. What are the minimum criteria for bilateral repair (2)?
158. For unilateral repair, what are the 9 criteria considered in the grading system for candidacy for
surgery? Who would be a candidate based on this grading system?
159. A preponderance of cholesteatomas will develop in stenotic canals less than ___ mm.
160. What are the two basic approaches to atresia repair?
161. What are the surgical landmarks for the anterior approach? In which part of the middle ear
cavity does the ossicular mass usually lie?
162. What are common facial nerve abnormalities that can be seen (3)?
163. According to Schuknecht what are the four types of atresiaplasty?
164. What is the most common complication of atresia repair? What are other complications (4)?
165. In terms of hearing result, what percentage of carefully selected patients will have hearing
improvements to 20-30 dB HL?
Intratemporal and Intracranial Complications of Otitis Media
166. What are four early signs of impending complications?

167. What are the four intratemporal and six intracranial complications of otitis media?
168. What are the common bacteria seen in acute suppurative otitis media?
169. What are the common bacteria seen in cholesteatoma?
170. What are the common bacteria seen in chronic otorrhea?
171. What are the common bacteria seen in acute mastoiditis?
172. What are the treatment options for mastoiditis? What conditions mandate surgery (4)?
173. What id Gradenigo syndrome? How is this treated?
174. What is the difference between serous and suppurative labyrinthitis? How is the sequelae of
hearing loss different between these two types of labyrinthitis?
175. What is the most common cause of facial paralysis in the context of infection? What is the
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management in the context of an acute otitis media and facial nerve paralysis?
176. What are some signs of sigmoid sinus thrombophlebitis? How is this diagnosed?
177. In cases of sigmoid sinus thrombophlebitis, when should a clot be removed? What else needs
to be done?
178. What are the four clinical stages of brain abscess?
179. What is the most common intracranial complication arising form middle ear infections?
180. What is otic hydrocephalus? What is the theory behind its development? How is this treated?
181. What are the potential routes of spread that can cause meningitis from otitis media (6)?
182. What are the three mechanisms for the development of a subdural abscess in the context of
otitis media?
Middle Ear and Temporal Bone Trauma
183. What are the possible chief symptoms of a temporal bone fracture (5)?
184. How can temporal bone trauma cause vertigo (6)?
185. How can temporal bone trauma cause sensorineural hearing loss (5)?
186. How can temporal bone trauma cause conductive hearing loss (3)?
187. How can temporal bone trauma cause facial weakness or paralysis (4)?
188. Compare and contrast longitudinal versus transverse temporal bone fractures with regards to
location, frequency, type of hearing loss, incidence of facial nerve paralysis, and degree of
trauma associated.
189. What investigation is required for penetrating trauma to the temporal bone?
190. What are the suggested indications for early surgical exploration in patients with facial nerve
paralysis (3)?
191. What is the most common area of facial nerve injury in patients with longitudinal fractures?
Transverse fractures? Penetrating trauma?
192. If surgical exploration is required, what approach is used for longitudinal fractures if hearing is a
concern? In a transverse fracture where hearing is a concern? In a transverse fracture where
hearing is not a concern?
193. What are the complications of temporal bone trauma?
194. What long term complication is related to tissue entrapment from temporal bone trauma?
195. Which emergencies require immediate surgical intervention in temporal bone trauma (2)?
Cholesteatoma
196. What is the proposed theory of pathogenesis of congenital cholesteatoma?

197. Where is congenital cholesteatoma most often found? What is the usual shape?
198. What are the different types of acquired cholesteatoma (2)? Based on these two types, what are
the proposed theories of acquired cholesteatoma (7)?
199. What are the factors involved in bone resorption secondary to cholesteatoma (3)?
200. What are the three common locations of origin of cholesteatomas? Of these three, which is the
most common?
201. What is Prussak’s space? What are it’s boundaries?
202. What is the most common site of ossicular damage?
203. What are the surgical goals in the management of cholesteatoma (5)?
204. What are the boundaries of the facial recess?
205. What is the difference between a radical and a modified radical mastoidectomy?
206. What is involved in the Bondy procedure?
207. What is the most common site of labyrinthine fistula formation?
208. What is the most common site of nerve involvement in a facial paralysis secondary to
cholesteatoma?
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209. What are the two areas at risk for recurrences of a cholesteatoma?
210. What are the complications of cholesteatoma (5)?
Surgery of the Mastoid and Petrosa
211. Why is the inferior portion of a postauricular incision placed more posteriorly in children under 2
years of age?
212. What is the significance of the temporal line?
213. What are the indications for a simple mastoidectomy (4)?
214. What is Koerner’s septum? Where does it originate from?
215. What are the boundaries of the facial recess?
216. What are the landmarks of the facial nerve within the mastoid (6)?
217. Where is the most common area of dehiscence of the facial nerve?
218. What is the most common site of injury of the facial nerve?
219. What are the advantages and disadvantages of canal-wall-up versus canal-wall-down
mastoidectomy?
220. What are techniques used to minimize postoperative chronic infections following canal-wall-
down mastoidectomy (5)?
221. What is the Bondy procedure?
222. What percentage of petrous apices are pneumatized?
223. What are the air cell tracts to petrous apex (6)?
224. What are the complications mastoid surgery (8)?
225. What should be done in a patient who has total facial nerve paralysis in the postoperative
period?
Reconstruction of the Tympanic Membrane and Ossicular Chain
226. What is the difference between myringoplasty and tympanoplasty?

227. What are the two surgical options for reconstruction of a central TM perforation? What are the
advantages and disadvantages of each technique?
228. What are the different types of tympanoplasty according to Wullenstein classification?
229. What is a PORP? What is a TORP?
230. What are the indications for tympanoplasty (4)?
231. What are the contraindications for tympanoplasty (3)?
232. What are the different approaches for a subtotal, small posteroinferior or anterior perforation?
233. What are the complications of tympanoplasty (5)?
Otosclerosis
234. What is the most common site for otosclerotic lesions? Where are other areas that they can
occur (5)?
235. What are three theories for the cause of sensorineural hearing loss in otosclerosis?
236. What is the mode of inheritance of otosclerosis?
237. Approximately what percentage of the population is affected by otosclerosis?
238. How does pregnancy affect hearing in otosclerosis?
239. What is Schwartze’s sign? In what percentage of patients with otosclerosis is it seen in?
240. What are the audiometric findings in otosclerosis?
241. What is Carhart’s notch?
242. What is the “on-off” effect?
243. What inherited, systemic disease is associated with otosclerosis?
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244. What is the maximal conductive loss in otosclerosis?
245. In general, what are the treatment options for otosclerosis?
246. What are the absolute contraindications to surgery?
247. What are the intraoperative, short term and long term risks and complications of stapedectomy?
248. What are the causes for failure of stapedectomy?
Acute Paralysis of the Facial Nerve
249. Describe the intratemporal segments of the facial nerve and their approximate lengths.
250. Where is the most common site of dehiscence of the facial nerve?
251. What does the extratemporal segment innervate (4)?
252. Which muscles are innervated by the frontal branch of the facial nerve (4)? The marginal
mandibular (4)?
253. What is the blood supply to the facial nerve (3)?
254. List the four different types of innervation of the facial nerve and their functions.
255. How is the facial nerve located in a middle cranial fossa approach?
256. What are three areas of dehiscence of the facial nerve?
257. What is the differential diagnosis of acute facial nerve paralysis (15)?
258. What is the differential diagnosis of bilateral facial nerve paralysis (6)?
259. What is Melkersson-Rosenthal syndrome?
260. Describe the 4 electrophysiologic tests for evaluation of facial nerve function. What do each
indicate and what are their limitations?
261. List the House-Brackmann classification for facial paralysis.
262. What is the most common cause of facial paralysis? What is the second most common?
263. What is the etiology, treatment and prognosis of Bell’s palsy?
264. What is Ramsay Hunt syndrome?
265. How do you decide when to explore a facial laceration?
266. What are the options for interpositional grafts for the facial nerve?
267. What is Mobius syndrome?
268. What are the conservative and surgical options for eye care in facial paralysis?
Otologic Manifestations of Systemic Disease
269. List the viral causes of SNHL.

270. What is Hennebert’s sign?
271. What diagnostic tests are used for syphilis (2)?
272. What is the causative organism of Lyme disease? What are some ENT symptoms of this
disorder?
273. What are the common otologic problems seen in AIDS?
274. How can relapsing polychondritis be differentiated from infectious chondritis clinically?
275. Which disease is associated with conductive and sensorineural hearing loss, brittle bones, and
blue sclera?
276. What disorder is associated with progressive cranial neuropathies caused by nerve compression
at the foramina from faulty remodelling of bone.
277. What is the treatment of Paget’s disease?
278. What are the otologic complications of fibrous dysplasia (3)?
Infections of the Labyrinth
279. What structure is implicated in the spread of middle ear infections to the labyrinth?
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280. What is the arterial supply of the stria vascularis (2)?
281. What three organisms account for 70% of cases of bacterial meningitis?
282. Which organism is associated with hearing loss post meningitis?
283. What area of the labyrinth is affected by fungal meningitis?
284. Which congenital viral infections is associated with hearing loss?
285. What are some histologic findings associated with viral infections of the labyrinth?
286. How is CMV infection diagnosed (3)?
287. What are some features of congenital rubella infection?
288. What is three conditions are required for the diagnosis of idiopathic sudden sensorineural
hearing loss?
289. What are the treatments for SSNHL?
290. What symptom complex is seen in mumps (4)?
Noise-Induced Hearing Loss
291. With regards to temporary threshold shifts, the magnitude of the shift is dependent on what three
factors?
292. Which are more hazardous, high-frequency or low-frequency sounds?
293. In terms of frequency, where do loud pure tones cause the greatest TTS.
294. How does NIHL differ with presbycusis in terms of progression?
295. What are some of the reasons for the 4-kHz notch in NIHL (4)?
296. If a person has a unilateral complete facial nerve paralysis and works in a dangerously loud
environment, how would his hearing compare in the ear on the paralysed side to the other?
297. What is the primary site of injury for NIHL?
298. What is the pathology of TTS vs PTS?
299. What is impulse noise? At what critical level is impulse noise most hazardous?
300. At what levels on the dBA scale does the risk grow rapidly for NIHL?
301. What is the most important non-occupational exposure for NIHL?
302. What are the key points in the diagnosis of occupational NIHL (8)?
303. How do you calculate the monaural impairment (MI) and the overall hearing handicap (HH)?
304. At what time weighted average exposure does the OSHA require hearing protection for
workers?
305. What is the 5 dB “trading rule”? What is an 8-h exposure to 90 dBA equivalent to at 4 hours, 2
hours, 1 hours?
Ototoxicity
306. What is the mechanism of action of aminoglycosides in ototoxicity?

307. Where does early damage occur in aminoglycoside ototoxicity? After what period is the damage
permanent?
308. Which are the vestibulotoxic aminoglycosides (2)? Which are the cochleotoxic aminoglycosides
(3)?
309. What agents potentiate the effects of aminoglycosides (3)?
310. Which antibiotics can cause reversible hearing loss (2)? Which of these most commonly
manifests as loss in conversational frequencies?
311. What type of hearing loss is seen in cisplatin ototoxicity? What is the proposed mechanism of
action (2)?
312. What is the mechanism of action for ototoxicity secondary to loop diuretics?
313. For tinnitus or hearing loss caused by aspirin, is this reversible an if so, what is the recovery
time?
314. What special investigation(s) are available for early detection and monitoring of ototoxicity?
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Cerebellopontine Angle Tumours
315. What are the anatomic boundaries of the CPA (5)?

316. Which segment of the eighth nerve do acoustic neuroma (AN) arise?
317. What are the histologic types of schwannomas (2)?
318. What is the first and second most common symptom of AN? What are other symptoms (5)?
319. Tumour originating from which nerve is most likely to spread into the inner ear?
320. What is Hitselberger’s sign? What is its significance?
321. What is the most sensitive and specific audiologic test in the diagnosis of AN?
322. What audiometric findings are seen in AN (5)?
323. What abnormalities can be seen on ABR (4)?
324. An interaural difference in latency of wave V with a delay of more than ___ ms is considered
abnormal.
325. Involvement of which nerve will demonstrate hypofunction on ENG testing? Will this be a
favourable or unfavourable prognosis for hearing preservation and why?
326. What modification can improve diagnostic yield of AN with CT?
327. What is the appearance of AN with regards to signal intensity on MRI (3)?
328. What are the surgical approaches for excision of AN (3)? What are the indications for each
approach? What are the advantages and disadvantages of each approach?
329. When is stereotactic radiosurgery used (2)?
330. Which cells do meningiomas arise from (1)?
331. On CT, how can you differentiate a meningioma from an AN (3)?
332. What are the MRI characteristics of a CPA epidermoid (3)?
333. What are other CPA angle tumours (5)?
334. What is the MRI characteristics of a cholesterol granuloma (3)?
Sensorineural Hearing Loss (Cumming’s)
335. What are the risk factors that would prompt screening for sensorineural hearing loss (10)?
336. In a child with newly diagnosed sensorineural hearing loss, what non-audiological investigations
and consultations are ordered and why (12)?
Genetic Hearing Loss
337. What percentage of childhood SNHL is due to genetic factors, acquired factors and unknown
factors?
338. What percentage of genetic causes of SNHL is due to syndromes? What percentage are
autosomal recessive, autosomal dominant, X-linked, and mitochondrial?
339. What percentage of congenital hearing loss is due to membranous labyrinthine malformations
versus bony and membranous labyrinthine malformations?
340. What is Michel aplasia? At what gestational age does an insult cause this malformation?
341. What is Mondini aplasia? At what gestational age does an insult cause this malformation?
342. What is the most common form of inner ear aplasia?
343. What malformation is due to aplasia of the cochlear duct?
344. What malformation is due to complete membranous labyrinthine dysplasia?
345. What is the most common cause of congenital SNHL seen on radiographic evaluation? What
are the CT findings that make this diagnosis (2)?
346. What are the key features of Waardenburg syndrome?
347. What are the key features of Stickler syndrome?
348. What are the key features of Branchiotorenal syndrome?
349. What are the key features of Treacher Collins syndrome?
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350. Which type of neurofibromatosis is associated with bilateral acoustic neuromas?
351. What are the key features of Usher syndrome? How are Ush 1 and Ush 2 different clinically?
352. What are the key features of Pendred syndrome?
353. What ECG abnormality is seen in Jervell and Lange-Nielsen syndrome?
354. What are connexions? Which connexions can be tested for?
355. What is are the key features of Alport’s syndrome?
356. With regards to non-syndromic SNHL, how does autosomal dominant and recessive hearing
loss differ in terms of occurrence, degree of loss, familial variability, and audiogram
characteristics?
Sudden Sensory Hearing Loss
357. What percentage of sudden sensory hearing loss is defined versus idiopathic?
358. What are some of the defined causes of SSHL (10)?
359. What are the four theories of idiopathic SSHL?
360. What is seen on temporal bone histopathology following viral infection (1)?
361. What are some investigations in the workup of SSHL (6)?
362. What is the main treatment used for SSHL? What other proposed treatments have been
described (5)?
363. What proportion of patients recover spontaneously from SSHL?
364. What are the poor prognostic factors for SSHL (5)?
Tinnitus
365. What is the definition of tinnitus?

366. What are some of the objective causes of tinnitus (8)?
367. What are some of the subjective causes of tinnitus (8)?
368. What percentage of the populations will experience tinnitus?
369. What are some of the treatments for tinnitus?
370. What are the theories for the pathophysiology of tinnitus (3)?
Autoimmune Inner-Ear Disease
371. Which part of the inner ear contains immunocompetent cells?

372. What is thought to be site of the immune response in the inner ear?
373. What are four autoimmune disorders associated with cochlear injury?
374. Western blot analysis is positive for what protein in 89% of patients with autoimmune
progressive bilateral SNHL?
375. What other investigations can be ordered for the work-up of autoimmune inner ear disease (3)?
376. What is the mainstay of treatment? What other medications can be used (2)?
Aging and the Auditory and Vestibular System
377. What are the four types of presbycusis and what is the pathophysiology?
378. What are the age related changes seen in the auditory (3) and vestibular system (3)?
379. What are the five main classes of drugs used to control acute vestibular and autonomic
symptoms?
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Cochlear Implants and Other Implantable Auditory Prostheses
380. What are the essential components of a cochlear implant (4)?

381. What is the selection criteria for adults and children?
382. What are the three groups of cochlear implant recipients? Which group tends to have the least
success with cochlear implants? Who tends to have the best performance?
383. What investigations are required prior to cochlear implantation (3)?
384. What are two CT findings are absolute contraindications to cochlear implants?
385. What are the complications of cochlear implants (6)?
386. Who is at risk of a CSF gusher?
387. Where is the electrode array implanted?
Hearing Aids and Assistive Listening Devices
388. What are the components of a hearing aid (3)?

389. What is gain? What is the advantage of nonlinear gain?
390. What is saturation sound pressure level?
391. What are the advantages of digital hearing aids over analogue?
392. What are the different types of hearing aids (7)? What are the advantages and disadvantages
of each?
393. What is the indication for bone-anchored hearing aids? What is the maximum threshold that
can be serviced?
394. What are the advantages of binaural amplification over monaural amplification (4)?
395. What is the “half-gain” rule?
396. What are some assistive listening devices (3)?
Peripheral Vestibular Disorders
397. What are some causes of:

-sudden-onset unilateral vestibular dysfunction?
-sudden-onset bilateral vestibular dysfunction?
-gradual-onset unilateral vestibular dysfunction?
-gradual-onset bilateral vestibular dysfunction?
398. What is Alexander’s law?
399. What is oscillopsia?
400. Which vestibular nerve is affected if hyporeactivity is seen on ENG?
401. Describe the Dix-Halpike test.
402. Describe the Hamalgyi (head-thrust) test.
403. What is the differential diagnosis for vertigo lasting:
-seconds (1)?
-minutes to hours (5)?
-days (1)?
-variable duration (2)?
404. What is the proposed pathophysiology of Meniere’s disease (3)?
405. What are the classic symptoms of Meniere’s disease?
406. Approximately what percentage of patients with Meniere’s will vertigo resolve at 2 years and at 8
years?
407. What is the crisis of Tumarkin?
408. What is the Lermoyez variant of Meniere’s?
409. What is cochlear hydrops?
410. What are some investigations that help confirm Meniere’s disease (4)?
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411. Describe the three phases of nystagmus in Meniere’s disease.
412. What percentage of patients with Meniere will have profound hearing loss?
413. What are the conservative, medical and surgical treatment options for Meniere disease?
414. What is delayed endolymphatic hydrops? What are potential causes (4)?
415. What are the features of Cogan syndrome? What is the treatment?
416. What is recurrent vestibulopathy? What is the natural history of this condition?
417. What are the features of benign positional vertigo (6)?
418. What are the surgical treatment options for BPV (2)?
419. What is the fistula test? What is considered a positive fistula test?
420. What is the treatment of an inner ear fistula (5)?
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REVIEW QUESTIONS IN PEDIATRIC OTOLARYNGOLOGY
Airway Imaging in Children
1. In children with croup, what is seen in the hypopharynx and subglottic area on inspiration and
expiration?
2. Where do subglottic hemangiomas most commonly occur?
3. Where are foreign body ingestions most commonly seen?
4. Under which circumstance can there be a false positive for retropharyngeal abscess on lateral
neck views?
5. What is the most common cause of neonatal nasal obstruction?
Pediatric Sleep-Disordered Breathing
6. What is the most common cause of pediatric obstructive sleep apnea?

7. What are other anatomic causes of sleep disordered breathing?
8. What is the usual treatment of pediatric obstructive sleep apnea?
9. What are some differences between adult and childhood sleep disordered breathing?
10. What are potential sequelae of childhood sleep disordered breathing?
11. What is the “gold standard” for diagnosis of sleep disordered breathing?
12. What are the criteria for an abnormal sleep study?
Laryngeal Stenosis
13. In terms of size, what proportion is the pediatric larynx compared to the adult?
14. What is the vocal process to vocal cord ratio in the pediatric larynx? in the adult?
15. At what level is the cricoid of an infant’s larynx compared to an adult’s?
16. What is the narrowest part of an infant’s airway?
17. Subglottic stenosis is considered when the diameter of the airway is less than ____?
18. Compare the signs and symptoms of supraglottic, glottic and subglottic obstruction in terms of
quality of voice, characteristic of stridor, feeding, and cough.
19. What is the most popular theory concerning the etiology of congenital subglottic stenosis?
20. What are the different types of congenital subglottic stenosis (3)?
21. What is the Cotton-Myer grading scale for subglottic stenosis (4)?
22. Where do laryngeal webs arise from?
23. What is the incidence of post-intubation subglottic stenosis?
24. What are the risk factors that predispose to subglottic stenosis post-intubation (5)?
25. What is the pathophysiology of post-intubation subglottic stenosis (4)?
26. What are the surgical treatment options for Grade I or II unilateral stenosis?
27. What are the surgical treatment options for failed extubation stenosis?
28. What are the surgical treatment options for Grade III and IV stenosis?
29. What are the criteria for anterior cricoid split (7)?
Stridor, Aspiration and Cough
30. How does the phase of stridor help in determining the location of airway obstruction?
31. What is the most common cause of stridor in infancy?
32. What are the different types of laryngomalacia (6)?
F.Ling - Pediatric ENT Review (1)
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33. What are the indications for a supraglottoplasty (4)?
34. What are three different types of supraglottoplasty?
35. What is the most common cause of bilateral vocal cord paralysis in children?
36. What are some vascular anomalies that can cause tracheal compression?
37. What organism causes croup? What is the classic sign seen on x-ray? What is the treatment?
38. What is the organism that causes epiglottitis? What is the classic sign seen on x-ray? What is
the management for a child with epiglottitis and impending airway compromise?
39. What is the organism that causes bacterial tracheitis? What is the management?
Pediatric Tracheotomy
40. What are the intraoperative complications of tracheotomy (4)?

41. What are the early postoperative complications (3)?
42. What are the late postoperative complications (10)?
43. What are the steps required for pediatric tracheotomy tube decannulation?
Caustic Ingestion and Foreign Bodies in the Aerodigestive Tract
44. What are the different categories of agents that can cause injury to the esophagus if ingested
(3)?
45. Which of the above is the most worrisome and why?
46. When should endoscopy ideally be performed?
47. How are caustic esophageal injuries graded?
48. What is the management of caustic esophageal injuries based on this grading system?
49. What is the most common morbidity resulting from alkaline ingestion?
50. What are other complications of caustic ingestions (8)?
51. What type of radiographs should be done for suspected foreign body aspiration?
52. What are the different types of foreign body obstruction and what would their corresponding
radiographs look like (4)?
53. What medical management should be included in organic foreign body aspirations?
54. When performing bronchoscopy, what anaesthetic consideration is important to discuss with the
Anesthetist?
55. In adults, the right mainstem bronchi is the most common area for aspiration. Why (4)?
56. What is the most common type of foreign body aspirated in children?
57. What is the most common type of foreign body ingested in children?
58. What locations are foreign bodies in the esophagus most likely found (3)?
Congenital Anomalies of the Nose
59. What is the fonticulus nasofrontalis?

60. Where is the prenasal space?
61. Where is the foramen cecum?
62. What are the contents of a nasal dermoid?
63. What embryological tissues are found in a nasal dermoid? How is this different from a
teratoma?
64. Where can nasal dermoids be found? What percentage of them are intracranial?
65. What evaluation is required before contemplating surgical management? Why?
66. What are some CT findings that suggest deep intracranial involvement of a nasal dermoid (5)?
67. What are the surgical approaches to excision of a nasal dermoid (3)?
68. What is the difference between a glioma and an encephalocele? How do they differ clinically?
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69. Histologically, what is the make-up of a glioma (2)?
70. What are the three broad categories of encephaloceles? Which is the most common?
71. What are the types of sincipital encephaloceles (3)? Where are the masses located?
72. What are the types of basal encephaloceles (4)? Where are the masses located?
73. How can one clinically differentiate a intranasal encephaloceles from polyps based on location
within the nasal cavity?
ENT Manifestations of CHARGE Association
74. What does CHARGE stand for?

75. What CT scan finding of the temporal bones is almost pathognomonic of CHARGE?
Congenital Neck Masses and Cysts
76. List the congenital neck masses that are in the lateral neck (3), midline neck (5), and that involve
the entire neck (2).
77. What are the nerve, muscle, skeletal and artery derivatives of the branchial arches?
78. What are the derivatives of the pharyngeal pouches?
79. What is the most common type of branchial arch anomaly?
80. What is the most common type of first branchial arch anomaly? What is its course?
81. What is the course of a second branchial arch fistula?
82. What is the course of a third branchial arch fistula?
83. What is the course of a fourth branchial arch fistula?
84. What infectious condition may be diagnostic of a fourth branchial arch anomaly?
85. What is a pseudotumour of infancy? How is it diagnosed? How is it treated?
86. Describe the pathogenesis of a thyroglossal duct cyst.
87. What procedure is required for removal of a thyroglossal duct cyst?
88. What congenital neck mass causes immediate respiratory symptoms in the newborn period?
Congenital Malformations of the Nose
89. With regards to nasal embryology, what ruptures at 6 weeks to form the posterior choana?
90. Choanal atresia has a male or female preponderance?
91. Which is more common, unilateral or bilateral choanal atresia?
92. What percentage of bilateral choanal atresia is associated with CHARGE?
93. What other syndromes are associated with choanal atresia?
94. What are the frequency of bony versus membranous choanal atresia?
95. What are the CT findings for choanal atresia (3)?
96. What are the various theories of choanal atresia (4)?
97. Clinically, how do unilateral and bilateral atresias differ?
98. When are unilateral atresias repaired? Bilateral atresias?
99. What are the two main approaches for atresia repair? What are their advantages and
disadvantages?
100. What are the surgical approaches for repair of piriform aperture stenosis?
101. What is the significance of a single central incisor?
102. Briefly describe the prenasal space theory for the development of a nasal dermoid.
103. What are some signs of a nasolacrimal duct cyst (3)?
104. What are the indications for surgery of nasolacrimal duct cysts (3)
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Pediatric Rhinosinusitis
105. In terms of time frame of symptoms, how is sinusitis differentiated from URTI?
106. What are some of the signs and symptoms of pediatric rhinosinusitis (6)? Are these symptoms
diagnostic for sinusitis?
107. Nasal polyps in the pediatric population is associated with which condition?
108. What are the indications for CT scan in pediatric rhinosinusitis (4)?
109. What etiologic factors are responsible for the development of rhinosinusitis (5)?
110. What bacteria are involved in acute rhinosinusitis (3)?
111. What bacteria are involved in chronic rhinosinusitis (8)?
112. What are the potential routes for expansion of infection for the ethmoid to the orbit (4)?
113. Describe Chandler’s classification for orbital complications secondary to sinusitis (5)?
114. What are the intracranial complications of sinusitis (4)?
Cleft Lip and Palate: Evaluation and Treatment of the Primary Deformity
115. What is the incidence of CL(P)? With regards to ethnicity, which populations are most
susceptible and least susceptible? What is the M:F?
116. What is the incidence of CL? What is the M:F?
117. During development, which weeks are crucial for the development of the upper lip, nose and
primary palate? Which weeks are crucial for the development of the secondary palate?
118. What do the frontonasal process form (3)? What do the maxillary processes form (2)?
119. With regards to fusion of the secondary palate, in which direction does this occur?
120. What are the main features of a submucous cleft (3)? How is this best diagnosed?
121. What is the first priority in the management of cleft lip and palate deformities?
122. What are some of the anatomic deformities seen in a unilateral cleft lip (3)?
123. What are some of the anatomic deformities seen in a bilateral cleft lip (3)?
124. In a cleft palate, where do the muscle fibers run and where do they insert?
125. In terms of timing of surgery, when are the lip adhesion, lip repair and palatal repair performed?
126. What are some postoperative complications of cleft palate repair?
127. Why is middle ear disease common in children with cleft palate?
128. What are the treatment options for VPI (3)?
129. What are some causes of cleft lip palate (3)?
Tonsillitis, Tonsillectomy and Adenoidectomy
130. What is the blood supply of the adenoids (3)?

131. Which two cranial nerves supply sensation to the adenoids?
132. What three types of epithelium is seen in adenoids?
133. What is the blood supply of the tonsils (5)? Which artery is the main supply of the tonsil?
134. Which nerves supply the tonsils (2)?
135. Briefly describe the histology of the tonsils (4)?
136. Which organisms are usually seen in acute tonsillitis (4)?
137. What is the clinical classification of adenoids and tonsils based on temporal profile (4)?
138. What is the clinical classification of tonsil size (4)?
139. For recurrent acute tonsillitis, what is the minimum number of infections for which tonsillectomy
will prove efficacious according to a RCT (3)?
140. What are significant rare complications of GABHS (2)?
141. What type of resistant organisms are seen in recurrent or chronic cases of adenotonsillitis?
142. What are some indications and contraindications for adenoidectomy?
143. What are some complications of adenoidectomy (2)?
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144. What is the first line treatment of acute tonsillitis?
145. For chronic tonsillitis, what can obviate the need for tonsillectomy in 15% of children?
146. What are the absolute (5) and relative (5) indications for tonsillectomy?
147. What are the contraindications for tonsillectomy (3)?
148. What is the pathogenesis of a peritonsillar abscess?
149. What are complications of tonsillectomy (8)?
150. What is Grisel’s syndrome?
151. What are some indications for observation post-T+A (5)?
152. What are the risks in Down syndrome children with regards to tonsillectomies (2)?
Congenital Anomalies of the Aerodigestive Tract
153. List some common congenital anomalies affecting the nose/nasopharynx, oral/oropharynx,
larynx, trachea and esophagus.
154. A newborn infant with high-pitched inspiratory stridor is most likely to have a lesion in which
anatomic location?
155. A 3-week old infant presents with circumoral pallor and occasional cyanosis. In addition to a
thorough evaluation of the upper airway, what other investigation should be done?
156. What investigation should be done for a newborn that presents with severe respiratory distress
and bilateral vocal cord paralysis?
157. What percentage of subglottic hemangiomas are associated with cutaneous ones?
158. Describe the four types of laryngeal clefts.
159. What are the 5 types of tracheoesophageal fistulas?
160. List vascular anomalies that can cause airway and/or esophageal compression (5).
Recurrent Respiratory Papillomatosis
161. Which types of HPV are commonly implicated in laryngeal papillomatosis (2)?
162. What is the histology of papillomatosis?
163. Which are the common sites of involvement (6)?
164. What are the risk factors for developing laryngeal papillomatosis (5)?
165. What are the two clinical types of RRP? How do they differ?
166. What is the risk of transmission of HPV to an infant from a mother with condylomata?
167. What is the main treatment modality of RRP?
168. What protective precautions are required for laser treatment (8)?
169. Other than airway fire, what are the disadvantages of jet ventilation (7)?
170. What are some adjuvant treatment options for RRP (6)?
171. What are risk factors for malignant transformation of RRP (4)?
172. What are the adverse side effects of interferon-alpha treatment (6)?
The Syndromal Child
173. What are the three types of Usher syndrome?

174. Name the syndrome:
-heterochromia irides, white forelock SNHL
-glossoptosis, micrognathia and cleft palate
-external and middle ear anomalies, zygomatic and mandibular hypoplasia,
downslanting palpebral fissures, lower lid colobomas, and cleft palate
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-almond shaped palpebral fissures, deficient nasal alae, tubular nose with bulbous nasal
tip, small mouth, VPI
-bilateral acoustic neuroma, meningioma, spinal cord schwannomas
-café-au-lait spots and cutaneous neurofibromas
-mental retardation, prominent ears, large jaw, long face, jocular speech
-preauricular pits, branchial cleft abnormalities, renal abnormalities
-craniosynostosis, hypertelorism, syndactyly, cervical vertebral fusion
-short-limb dwarfism
Pediatric Malignancies
175. Excluding retinoblastoma and neoplasms of the CNS, what is the most common pediatric
malignancy of the head and neck?
176. What is the most frequent soft-tissue malignancy of childhood?
177. What is the most common malignancy in infants under 1 year of age?
178. What is the most common presenting sign in Hodgkin disease?
179. What is a Reed-Sternberg cell?
180. What is the Ann Arbor staging system for lymphoma?
181. What is the treatment of early versus late stage Hodgkin disease?
182. What is the treatment for lymphoma causing airway, nervous or vascular compromise?
183. What are the top two locations for rhabdomyosarcoma in the head and neck?
184. What are the histologic types of rhabdomyosarcoma (3)? Which type is most common in
children? Adolescents? Adults?
185. What is the treatment of rhabdomyosarcoma?
186. What is the most common type of thyroid malignancy in children?
187. At what time should children with MEN IIA and IIB have thyroidectomies?
188. What are the late complications in the treatment of pediatric malignancies (4)?
Otitis Media with Effusion
189. Define AOM, recurrent AOM, OME, CSOM.

190. Which age group has the overall highest incidence of AOM?
191. What is the mean duration of OME after AOM?
192. What are the risk factors for developing AOM (10).
193. What is the pathophysiology of AOM?
194. In cleft palate, deficiency of which muscle increases the risk of OME?
195. What are the most common pathogens in AOM and COM?
196. What percentage of H. influenzae and M. catarrhalis are beta-lactamase producing?
197. What is the spontaneous resolution rate of AOM?
198. When should surgical intervention be considered for MEE?
199. What are the treatment options for AOM?
200. What are the treatment options for recurrent AOM?
201. What are preventative measures for AOM (3)?
202. What are the indications for tympanostomy tubes (4)?
203. What are the complications of tympanostomy tubes (6)?
204. What are factors related to persistent TM perforation (2)?
205. What percentage of children will have OME after AOM in 4 weeks, 8 weeks and 12 weeks?
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Eustachian Tube Function and Middle Ear Aeration
206. What are the differences between the ET of adult and child (4)?
207. Which muscle dilates the ET? What innervates this muscle?
208. What closes the ET?
209. What are the functions of the ET (3)?
210. What is the Polizter and Toynbee test?
211. Describe the 9-step tympanometric inflation-deflation test.
212. What are the indications for tympnoscentesis
213. What is the “watch and wait” method for treatment of AOM?
Pediatric Audiology
214. What are the risk indicators that would warrant further hearing investigations in children (11)?
215. What are the behavioural test techniques and approximately what age are they employed (4)?
216. ABR provides threshold estimate in what frequency range?
217. What is the frequency range tested in OAEs?
218. What is the definition of central auditory processing disorders?
219. What are the signs of CAPD (4)?
Pediatric Facial Fractures
220. What are the most common facial fractures in children?

221. What is the most common facial fracture in children requiring hospitalization?
222. How do pediatric facial fractures differ from adult facial fractures?
223. Injuries to which part of the mandible will cause facial deformities?
224. What is the main principle of rigid fixation in children?
225. What are the five basic incision for surgical access to facial fractures?
226. What is the management of nasal fractures?
227. What is the management of mandibular fractures in children younger than 2 years versus
children 6-12 years?
228. What are the important steps needed to repair traumatic telecanthus (4)?
229. What is the general management of condylar fractures?
230. How do orbital fractures differ in children less than 5 years of age versus children older than 7
years of age?
Congenital Vascular Lesions
231. What are the clinical (2) and histological (2) differences between hemangioma and vascular
malformation?
232. What are the three clinical stages of hemangioma growth?
233. What are the three clinical types of hemangioma?
234. What is Kasabach-Merritt syndrome?
235. What are the indications for immediate treatment of hemangiomas (3)?
236. What are the treatment options for hemangiomas (4)?
237. Differentiate fast flow versus slow flow malformations.
238. What are potential complications of hemangiomas (5)?
239. What is the natural history of hemangiomas?
240. How are subglottic hemangiomas managed?
1400
241. What is the basic histology of capillary, venous and lymphatic malformations? How are they
treated?
242. What is Sturge-Weber syndrome?
243. Differentiate the two different types of lymphatic malformations based on location and ease of
resectability.
Juvenile Nasopharyngeal Angiofibroma
244. Where do JNAs originate?

245. Where can JNA extend to (5)?
246. What are the symptoms (4) and signs (4) of JNA?
247. What is the differential diagnosis of a nasopharyngeal tumour (8)?
248. What are the histopathologic features of JNA (2)?
249. What is the staging of JNA according to Sessions? Fisch?
250. What treatment modalities are available for JNA?
251. What are the various surgical approaches for JNA?
Velopharyngeal Insufficiency
252. What are the nasal phonemes (3)?

253. What are the causes of VPI (8)?
254. What muscles comprise the velopharyngeal sphincter (6)?
255. What methods can be used to diagnose VPI (4)?
256. What are the four types of pharyngeal closure patterns (4)?
257. What are the treatment options for VPI (4)?
258. Of the surgical options, what are the 3 methods of improving VPI?
259. What are the complications of surgery to correct VPI (6)?
1401
REVIEW QUESTIONS IN RHINOLOGY
Olfactory Function and Dysfunction
1. List the six different cell types within the olfactory neuroepithelium?
2. Define anosmia, hyposmia and dysosmia.
3. What are some of the causes of olfactory loss?
4. What is the link between olfaction and neurodegenerative disease such as Alzheimer’s disease?
5. What is the UPSIT?
Nasal Function and Evaluation
6. What are the major physiologic functions of the nasal airways?

7. What are the three areas of nasal resistance? Which area is the narrowest segment?
8. What is the nasal cycle?
9. What are the effects of the autonomic system on the nasal mucosa?
10. What are the anatomic boundaries of the nasal valve?
11. What are the three broad categories for the etiology of nasal obstruction?
12. What are two objective ways to measure nasal obstruction?
13. On an acoustic rhinogram, what does the first (I notch) and second (C notch) depression
represent?
Nonallergic Rhinitis
14. Which viruses can be involved in infectious rhinitis?

15. How does estrogen cause rhinitis?
16. What is NARES?
17. What is rhinitis medicamentosa?
18. What is ozena?
19. What are the primary causes of atrophic rhinitis? What are the secondary causes?
20. What is seen histologically in atrophic rhinitis?
21. What is the most common cause of unilateral rhinorrhea in children?
22. How does nasal cytology differentiate between an infectious versus an allergic etiology for
rhinitis?
23. List 5 categories of medications used in the treatment of rhinitis.
Allergic Rhinosinusitis
24. Briefly describe the management of allergic rhinosinusitis.

25. What are the mechanisms of action of steroids?
26. What are the adverse local effects of topical steroids?
27. What are the criteria for immunotherapy (4)?
Nasal Obstruction
28. What are physiologic functions of the nose (7)?

29. What some of the cells seen in nasal mucosa?
30. Where is the olfactory epithelium located in the nose?
F.Ling - Rhinology Review (1)
1402
31. According to Poisseuille’s equation, what variable most contributes to resistance?
32. What are the boundaries of the nasal valve?
33. What is the Cottle maneuver?
34. What are the causes of nasal obstruction?
35. What is Samter’s triad?
36. What disease is suspected if one sees polyps in children?
37. What are the mechanisms of action of topical steroids?
38. What is the most common pathogen in a septal abscess?
39. What are the causes of septal perforation?
Midline Nasal Masses
40. What is Rathke’s pouch?

41. What is a Tornwaldt cyst? From what structure is it derived?
42. What is the fonticulus frontalis?
43. What is the prenasal space?
44. What is required before surgical excision of a midline nasal mass and why?
45. What is the difference between a glioma and an encephalocele?
46. What is the Furstenberg test?
47. What is the bacterium involved in rhinoscleroma?
48. What are the stages of rhinoscleroma?
49. What is the malignant potential of an inverting papilloma?
50. What is the most common malignant neoplasm of the sinonasal tract?
51. What are risk factors for SCCa fo the nose?
52. What is the most common malignant salivary gland tumour of the nasal cavity?
53. What is the second common malignancy in the nose?
Sinus Anatomy and Function
54. What is the approximate order of paranasal sinus development?

55. Ethmoturbinals begin formation as ridges on the lateral nasal wall during the 9th and 10th week of
gestation. Which ethmoturbinals form the uncinate process? bulla ethmoidalis? middle
turbinate?
56. Describe the Keros classification of the ethmoid roof.
57. What are agger nasi cells? What are their significance?
58. What is a concha bullosa? What is its significance?
59. What is an Onodi cell? What is its significance?
60. What is a Haller cell? What is its significance?
61. What are the boundaries of the frontal recess?
62. At what distance does the anterior wall of the sphenoid lie from the nasal spine?
63. Describe Congdon’s classification of sphenoid pneumatization.
64. What are the theoretical functions of the sinuses (7)?
65. What are the four basic cell types in the sinus epithelium?
66. Describe the mucociliary blanket.
67. What the molecules that are found in nasal secretions that serve an immunologic purpose (5)?
Sinus Imaging
68. What are some anatomic variations that can contribute to sinus disease (6)?
69. What is a radiographic hallmark of granulomatous involvement of the sinuses?
1403
70. What is the radiographic appearance of fungal sinusitis on CT scan? MRI?
71. What is the radiographic appearance of polyps on CT scan? MRI?
72. What is the radiographic appearance of an inverted papilloma?
73. What is the radiographic appearance of a juvenile nasopharyngeal angiofibroma?
Rhinosinusitis: Current Concepts and Management
74. What are the components of the osteomeatal complex (8)?

75. What are the three pathophysiological factors in the etiology of sinus disease?
76. Define acute, subacute and chronic sinusitis.
77. What are the histological characteristics of allergic fungal sinusitis (3)?
78. What are the diagnostic criteria for Allergic Fungal Sinusitis (AFS) according to Bent and Kuhn
(6)?
79. What is the treatment of AFS?
80. What are the organisms found in a fungus ball?
81. What are the indications for CT scan in sinusitis?
82. What are the pathogens involved in acute (community acquired) sinusitis?
-what are their approximate percentages?
-what are their approximate resistance rates to penicillin?
83. What are the pathogens involved in acute (hospital acquired) sinusitis?
84. What are the pathogens involved in chronic sinusitis?
85. What is first line therapy for acute sinusitis? Second line therapy?
86. What antibiotics are generally used for orbital or intracranial complications of sinusitis?
87. What therapy is used for nosocomial sinusitis?
88. How long does one treat acute sinusitis?
89. What other concurrent treatments are helpful in the treatment of acute sinusitis?
90. What are the risk factors for recurrence (4)?
91. What are the complications of sinusitis (10)?
92. What is the minimum duration of antimicrobial therapy for chronic sinusitis?
Sinus Surgery
93. What are the indications for the Calwell-Luc operation (6)?
94. What are complications of the Calwell-Luc operation?
95. What are the indications for an external ethmoidectomy (4)?
96. What type of incision is used for external ethmoidectomy?
97. In relation to the lacrimal crest, how far back is the anterior ethmoid artery? posterior ethmoid
artery? optic nerve?
98. The anterior and posterior ethmoid arteries are important landmarks for what?
99. What are the complications of external ethmoidectomy?
100. What are two other non-endoscopic methods to surgically manage the ethmoid sinuses?
Endoscopic Sinus Surgery
101. What separates anterior from posterior ethmoidal cells?

102. What is the incidence of clinical bony dehiscence of the cavernous portion of the carotid canal?
103. List the preoperative checklist for evaluating the CT scan of the sinuses according to Lanza and
Kennedy (8).
104. What are the relative indications for endoscopic surgery (14)?
105. What are the relative contraindications for endoscopic surgery (5)?
1404
106. What are the four consistent landmarks from anterior to posterior used in endoscopic surgery?
107. Where is the base of skull thinnest?
Approaches to the Sphenoidal Sinus
108. What are the three patterns of sphenoid pneumatization according to Congdon? Which pattern
is the most common?
109. What are the contents of the cavernous sinus?
110. Which nerve travels in close association with the carotid artery in the cavernous sinus?
111. What is the main contraindication to a transnasal intracranial procedure?
112. List the various approaches for transsphenoidal hypophysectomy (5).
113. List the various approaches for sphenoid inflammatory disease (3).
114. List the various approaches to access sphenoid tumours (4).
115. What are the possible complications of sphenoid surgery?
Sphenoid Sinus Disease
116. What are the risk factors for acute bacterial sphenoiditis (4)?
117. What organisms are involved in invasive fungal sinusitis (4)?
118. What are the boundaries of Bolger’s parallelogram? What is the safe entry point into the
sphenoid sinus in relations to this parallelogram?
Complications of Sinus Surgery
119. Endoscopically, what structure is 5 cm from the nasal spine?

120. Endoscopically, what structures are 6 cm from the nasal spine (3)?
121. Endoscopically, what structures are 7 cm from the nasal spine (4)?
122. What are the complications of frontal sinus surgery with osteoplastic flap?
123. What are the orbital complications of endoscopic sinus surgery (5)?
124. What is the management of a retrobulbar hematoma?
125. What methods are used to identify a CSF leak?
126. What other bodily fluids is B2-transferrin found in?
127. What is the most common complication of functional endoscopic sinus surgery?
128. What is the most common complication of external sinus surgery?
Epistaxis
129. Which branch of the internal carotid artery supplies the nasal cavity (1)?
130. From this branch, which arteries arise (2)?
131. Which branches of the external carotid artery supplies the nasal cavity (2)?
132. What are the subsequent branches that supply the nasal cavity (6)?
133. There are two plexus of arteries within the nasal cavity, what are they?
134. Which arteries make up the anastomosis in Little’’s area (4)?
135. What are some local (10) and systemic (10) causes of epistaxis?
136. Name two autosomal dominant vascular disorders in which epistaxis is prominent.
137. What are the non-medical treatments of epistaxis (6)?
138. What are the surgical treatments of epistaxis (6)?
139. What are possible complications of nasal packing (10)?
1405
Manifestations of Systemic Diseases of the Nose
140. What are the three histologic features of Wegener’s granulomatosis?

141. What are the drugs used to treat Wegener’s granulomatosis (5)?
142. What is lupus pernio?
143. What enzyme correlates with clinical activity of sarcoidosis?
144. What electrolyte abnormality may be seen with sarcoidosis?
145. What are the features of Churg-Strauss syndrome?
146. Which organism is involved in rhinoscleroma?
147. What other organ system in the head and neck that can be involved in rhinoscleroma?
148. What are the four stages of rhinoscleroma?
149. What is classically seen on histopathology for rhinoscleroma (2)?
150. What is lupus vulgaris?
151. Which drug is used to treat disseminated histoplasmosis?
152. What is the management of rhinosporidiosis?
153. What are the treatment options for mucormycosis (2)?
154. What is the treatment of choice for localized T-cell lymphoma?
CSF Leaks
155. What are the two broad categories of CSF rhinorrhea? Which category is the most common?
156. What is the most common cause of CSF otorrhea?
157. Which type of temporal bone fracture results more frequently with CSF leaks?
158. Where do CSF rhinorrheas most commonly occur?
159. Which congenital anomalies are associated with CSF otorrhea (2)?
160. What are the signs and symptoms of CSF rhinorrhea (5) and otorrhea (5)?
161. What is the incidence of CSF otorhinorrhea after acoustic neuroma surgery?
162. What are the most common locations for spontaneous CSF otorrhea (3)?
163. List 5 methods that can be used to diagnose CSF leaks.
164. List 4 methods that can be used to localize CSF rhinorrhea.
165. Which tissue fluids is B2 transferrin found in (3)?
166. Which type of CSF leaks are likely to resolve with conservative management?
167. Which type is likely to require surgical exploration?
168. What is involved in the conservative management of CSF leaks (5)?
169. If using a lumbar drain to manage CSF leak, when is this instituted and how much fluid is
drained per day?
170. What are the surgical approaches for repair of CSF rhinorrhea (3)?
171. What material can be used to repair dura (4)?
172. For grafting, what materials are generally used and how?
1406
REVIEW QUESTIONS IN TRAUMA
Auricular Trauma
1. What is the blood supply to the external ear (2)?

2. What is the nerve supply to the external ear (5)?
3. An auricular hematoma occurs between which two layers?
4. What is the sequelae of an untreated auricular hematoma? What is this deformity called?
5. How long is a pressure dressing applied post-evacuation of an auricular hematoma?
6. What are the options for reconstruction a totally avulsed ear (4)? Which yields the best results?
7. What is the pocket principle technique?
8. What options are available for helical rim defects less than 2 cm? More than 2 cm?
9. What options are available for defects of the upper and middle third of the ear?
10. What is the most important contour to reconstruct? What is the least important?
Laryngeal Trauma
11. What are two serious sequelae of a “clothesline” injury?

12. Compared to the adult, how are laryngeal injuries in a child different (3)?
13. What are the signs and symptoms of laryngeal trauma (10)?
14. When is a CT scan used in the assessment of laryngeal trauma?
15. Draw out an algorithm for the management of laryngeal trauma.
16. How should the airway be managed in the case of impending obstruction in laryngeal trauma?
17. How is the airway managed in a child?
18. What injuries do not need exploration or repair (4)?
19. What injuries require open laryngeal exploration and repair (6)?
20. What injuries require stenting (4)?
21. If observation is indicated, what is involved in the medical management (5)?
22. What are the advantages and disadvantages of early versus late exploration?
23. What surgical approach is used for exploration (1)?
24. If mucosa cannot be reapproximated to cover exposed cartilage, what can be done?
25. Why is it important to cover exposed cartilage?
26. How long is a stent usually placed? What is the risk of leaving a stent in too long?
27. If the recurrent laryngeal nerve is severed, why does one attempt to repair it despite the
extremely low chance of regaining any vocal cord movement?
28. What are three long term complications of laryngeal trauma?
Management of Soft-Tissue Trauma
29. What is the leading cause of facial soft-tissue injuries?

30. What emergencies require immediate intervention (3)?
31. What emergencies require urgent intervention (4)?
32. What are the five layers of the scalp?
33. Which deep lacerations of the cheek require surgical exploration and repair of the facial nerve or
parotid duct?
34. Which branch of the facial nerve is potentially injured with parotid duct injuries?
35. How are parotid duct injuries repaired (2)?
F.Ling - Trauma Review (1)
1407
Mandibular Fractures
36. What are the anatomical components of the mandible (8)?

37. What are the inherent areas of weakness (3)?
38. What are the three most common areas of mandibular fracture?
39. Describe the horizontally unfavourable fracture. Describe the vertically unfavourable fracture.
40. Describe the insertion of the muscles of mastication to the mandible.
41. Along the body and angle, where are tension and compression forces distributed as a result of
the forces of the muscles of mastication?
42. Describe Angle’s classification of occlusion.
43. What are some physical signs of a mandibular fracture (8)
44. What is the single best radiographic evaluation for mandibular fractures?
45. Which type of fracture is associated with highest incidence of infection?
46. What are the indications for maxillomandibular fixation (MMF) (3)?
47. What is the general length of time for MMF in children, adults and the elderly?
48. What is the general management for coronoid, greenstick, unilateral nondisplaced fractures and
fractures in elderly edentulous patients with minimal displacement?
49. What is the general management of favourable, minimally displaced non-condylar fractures?
50. What are the indications for ORIF (8)? What are two relative contraindications?
51. What management options are available for displaced fractures of the body, symphysis, and
angle of the mandible (5)?
52. What are the management options for non-displaced condylar and displaced condylar fracture?
53. What are the absolute indications for open reduction of a condylar fracture (4)? What are
relative indications (4)?
54. When are teeth removed in the management of mandibular fractures (3)?
55. What are the indications for external fixation (2)?
56. What are the surgical approaches for ORIF (4)?
57. What are the complications of mandibular fractures (8)?
Maxillary and Periorbital Fractures
58. What are the vertical buttresses of the midface (4)?

59. What are the horizontal buttresses of the midface (7)?
60. Describe the LeFort classification of facial fractures.
61. What are the surgical approaches to maxillary and periorbital fractures (6)?
62. What is the tripod fracture? Which sutures does it involve (4)?
63. What is the Gilles operation? When is it used?
64. What is the general approach for reconstructing panfacial fractures (3)?
65. What are the complications of maxillary and periorbital fractures (10)?
Fractures of the Nasal and Frontal Sinuses
66. What is the sensory innervation to the external nose (4)?

67. When are the best times to reduce a nasal fracture (2)?
68. What are the indications for closed reduction (2)? What are indications for open reduction (4)?
69. With all nasal injuries, what should be ruled out in order to prevent a devastating complication?
70. How are nasal injuries in children different from adults (3)?
71. What is the normal intercanthal distance in infants? Adults?
72. What are the signs and symptoms of nasoethmoidal fractures (5)?
73. How are nasoethmoidal fractures managed?
74. What are the early and late complications of nasal fractures (10)?
1408
75. What are the complications of nasoethmoidal fractures (5)?
76. What is the most common cause of frontal sinus fractures?
77. What are the surgical approaches to frontal sinus fractures (4)?
78. What is the management of non-displaced and displaced anterior table fractures?
79. What is the management of non-displaced and displaced posterior table fractures?
80. What is the treatment of comminuted, contaminated or through-and-through fractures (2)?
81. What are the options for frontonasal duct damage (2)?
82. What are the complications of frontal sinus fractures (8)?
Penetrating Face and Neck Trauma
83. What defines a penetrating neck injury?

84. What are the mechanisms of GSW injuries (5)?
85. What is Chen’s classification of facial injuries (3)?
86. When are arteriograms indicated in penetrating facial injuries?
87. When do you explore and repair a facial nerve injury?
88. What are the complications of facial injuries (8)?
89. What are the complications of neck injuries (6)?
90. What are the neck zones classification in penetrating neck injuries? What structures are most at
risk for each zone?
91. What is the most common cause of death in penetrating neck injuries?
92. What are the signs and symptoms of vascular injury (6)?
93. What are the signs and symptoms of laryngotracheal injury (6)?
94. What are the signs and symptoms of pharyngoesophageal injury (3)?
95. What are the indications for immediate surgical exploration (2)?
96. What is the general management of penetrating neck injuries based on zone-type injuries?
97. What are the two alternatives of treating asymptomatic zone II injuries?
98. How do you treat penetrating pharyngoesophageal injuries superior to the arytenoids and inferior
to the arytenoids?
1409

Dr. F. Lings Otolaryngology Notes

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Dr. F. Lings Otolaryngology Notes

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Arranged by:

Dr. Fouad Shamsan

The contents is according to:

Bailey's Head and Neck Surgery - Otolaryngology (2001)

Cumming's Otolaryngology - Head and Neck Surgery (1999)

The arrangement is according to :

Bailey's Head and Neck Surgery - Otolaryngology (2006)

II Rhinology & Allergy:

III General Otolaryngology:

IV Airway & Swallowing:

VII Pediatric Otolaryngology:

VIII Head & Neck Surgery:

X Facial Plastic & Reconstructive Surgery:

IX OTOLARYNGOLOGY FACTS AND POINTS……………………………………….………………1345

IIX Review Questions:

ACUTE OTITIS MEDIA

Microbiology Primary Alternatives

-Streptococcus pneumoniae (25%) -amoxicillin or clavulin -cefpodoxime, cefdinir

ACUTE BULLOUS MYRINGITIS and ACUTE SUPPURATIVE OTITIS MEDIA

PERSISTENT OTITIS MEDIA WITH EFFUSION

Microbiology Primary Alternatives

-Streptococcus pneumoniae -vancomycin IV plus ceftriaxone -levofloxacin IV

F.Ling - Antimicrobial Therapy (1)

Microbiology Primary Alternatives

-Pseudomonas aeruginosa -ototopicals: -adjunctive therapy

ACUTE (DIFFUSE) OTITIS EXTERNA

Microbiology Primary Alternatives

-Pseudomonas aeruginosa -alcohol/acid mixtures -neomycin/polymyxin/

ACUTE LOCALIZED OTITIS EXTERNA (FURNUCULOSIS)

Microbiology Primary Alternatives

-S. aureus -cephalexin -clindamycin

Microbiology Primary Alternatives

-Aspergillus niger -clotrimazole solution -acetic/citric acids in alcohol

F.Ling - Antimicrobial Therapy (2)

Microbiology Primary Alternatives

-Pseudomonas aeruginosa -topical ciprofloxacin

PLUS added intravenous

Microbiology Primary Alternatives

F.Ling - Antimicrobial Therapy (3)

F.Ling - Antibiotics (1)

F.Ling - Antibiotics (2)

F.Ling - Antibiotics (3)

BONY LESIONS OF THE SKULL

F.Ling - Degenerative and Idiopathic Diseases (1)

age <30 yr >40 yr

presentation monostotic polyostotic

most commonly affected bones ribs, femur lumbar sacrum

most commonly affected head and neck region maxilla skull

treatment curettage calcitonin

RECURRENT PAROTID SWELLING DIFFERENTIAL

-sialographic appearance of recurrent parotid swelling:

Autoimmune Parotid Swelling

F.Ling - Degenerative and Idiopathic Diseases (2)

MIDLINE DESTRUCTIVE DISEASES

“Lethal midline granuloma”

Lymphomatoid Granulomatosis (T-Cell Lymphoma)

F.Ling - Degenerative and Idiopathic Diseases (3)

Allergic Granulomatosis and Vasculitis

NONNEOPLASTIC NONTRAUMATIC SUBGLOTTIC STENOSIS

-Wegener’s, amyloidosis, sarcoidosis, relapsing polychondritis

F.Ling - Degenerative and Idiopathic Diseases (4)

F.Ling - Degenerative and Idiopathic Diseases (5)

F.Ling - Degenerative and Idiopathic Diseases (6)

-SLE -anti-native DNA, Anti-Sm