CASE REPORT

ACUTE DIFFUSE OTITIS EXTERNA

Moderator: dr. Bondan
Presenter:
Tharanrajh Arumuam !"#$%&'())$*U$+%#,)-
Prad.ta Sr. M.tasar. !"#$%(/%/"$*U$+%(#(-
Na0aneethan A1 2e3a4a5an !"#$%&'&"%$*U$+%,'&-
M. Fa6hru5 7usman !"#$%()#"%$*U$+%("#-
8anda3an. E6a Pus9.ta Sar. !"#$%()//,$*U$+%/&%-
Des3 Pus9a Putr. !"#$%&%(,&$*U$+%#/)-
A:a5.3a Pranjasdh.ta !"#$%(),&,$*U$+%(%&-
Department oI Otorhinolaryngology-Head and Neck Surgery
Medical Faculty Gadjah Mada University DR.Sardjito Hospital
Yogyakarta
2013
C8APTER I
INTRODUCTION
Acute otitis externa (AOE) is deIined as diIIuse inIlammation oI the external ear canal,
which may also involve the pinna or tympanic membrane.A hallmark sign oI diIIuse AOE is
tenderness oI the tragus,pinna, or both, that is oIten intense and disproportionate towhat might be
expected based on visual inspection.Also known as 'swimmer`s ear or 'tropical ear, AOEis
one oI the most common inIections encountered by clinicians.
The annual incidence oI AOE is between 1:100 and1:250 oI the general population,with
regional variationsbased on age and geography; liIetime incidence is up to10.The direct cost oI
AOE is unknown, but the ototopicalmarket in the United States is approximately 7.5 million
annual prescriptions with total sales oI $310 million (IMS/Verispan 2004, personal
communication). Additional medicalcosts include physician visits and prescriptions Ior
analgesicsand systemic medications, such as antibiotics,steroids, or both. The indirect costs oI
AOE have not beencalculated but are likely to be substantial because oI severeand persistent
otalgia that limits activities.
The usual pathogens responsible Ior acute otitis externa are Pseudomonas aeruginosa,
Proteus mirabilis, staphylococci, streptococci, and various gram-negative bacilli. For the mild or
uncomplicated inIection, culture oI the canal is ordinarily not taken, because it will usually
demonstrate a mixed pattern oI growth. For recalcitrant inIections, culture may identiIy a
predominant organism and assist in the choice oI antibiotic therapy.
Topical antimicrobials are beneIicial Ior AOE, but oralantibiotics have limited
utility.Nonetheless, about 20 to40 oI patients with AOE receive oral antibiotics, oIten
inaddition to topical therapy.The oral antibiotics selectedare usually inactive against P
aeruginosaand Saureus, may have undesirable side eIIects, and, becausethey are widely
distributed, serve to select out resistantorganisms throughout the body.Bacterial resistance isoI
Iar less concern with topical antimicrobials, because thehigh local concentration oI drug in the
ear canal will generallyeradicate all susceptible organisms plus those withmarginal resistance.
Strategies to prevent AOE are aimed at limiting wateraccumulation and moisture
retention in the external auditorycanal, and maintaining a healthy skin barrier.
C8APTER II
1ITERATURE RE;IE<
II.+. Anatom3 and Ph3s.o5o3
The external ear is composed oI the auricle and external auditory canal. Both contain
elastic cartilage derived Irom mesoderm and a small amount oI subcutaneous tissue, covered by
skin with its adnexal appendages
1,2
. There is Iat but no cartilage in the lobule. The auricle is
derived Irom six hillocks, three each Irom branchial arches I and II (Fig. 1). During normal
gestation, the cartilaginous hillocks merge to Iorm the auricle, and with selective growth oI the
mandible, the auricle rises Irom its original position near the lateral commissure oI the mouth to
the temporal area.
The external auditory canal is derived Irom the Iirst ectodermal branchial groove between
the mandibular (I) and hyoid (II) arches
2,3
. The epithelium lining this groove contacts the
endoderm oI the Iirst pharyngeal pouch, thus Iorming the tympanic membrane, the most medial
extent oI external auditory canal. Connective tissue oI mesodermal origin is Iound between
ectoderm and endoderm and becomes the Iibrous layer oI the tympanic membrane
2
. Because oI
its origin, the external auditory canal, including the lateral surIace oI the tympanic membrane, is
derived Irom ectoderm and is lined by squamous epithelium.
The process oI canalization is complete by about week 12 oI gestation, at which time the
canal Iills with epithelial tissue. The canal ordinarily recanalizesby about week 28 oI Ietal liIe
3
.
The external auditory canal may be thought oI in two sections. The outer 40 is
cartilaginous and contains a thin layer oI subcutaneous tissue between the skin and cartilage. The
inner 60 is osseous, is Iormed primarily by the tympanic ring, and contains very scant soIt
tissue between the skin, periosteum, and bone. The average length oI the adult external auditory
canal is 2.5 cm. Because oI the oblique position oI the tympanic membrane, the posterosuperior
part oI the canal is about 6 mm shorter than the anteroinIerior portion
1
. The junction oI the
cartilaginous and bony portions oI the canal is a narrowed section termed the isthmus.
Figure 1. The auricle is Iormed Irom six auricular hillocks, three each Irom branchialarchesI and
II
The tragus and antitragus Iorm a partial barrier to the entrance oI macroscopic Ioreign
bodies. Laterally to medially, the canal curves slightly superiorly and posteriorly in a gentle S
shape. The canal can be thought oI as pointing toward the nose; thus, the auricle needs to be
pulled gently upward, outward, and backward to straighten the canal Ior examination. Three
macroscopic deIense mechanisms protect the external auditory canal and lateral surIace oI the
tympanic membrane: the tragus and antitragus, the skin with its cerumen coat, and the isthmus oI
the canal.
The skin oI the cartilaginous canal contains many hair cells and sebaceous and apocrine
glands such as cerumen glands. Together, these three adnexal structures provide a protective
Iunction and are termed the apopilosebaceous unit. Glandular secretions combine with sloughed
squamous epithelium to Iorm an acidic coat oI cerumen, one oI the primary barriers to inIection
oI the canal. An invagination oI the epidermis Iorms the outer wall oI the hair Iollicle, and the
hair shaIt Iorms the inner wall. The Iollicular canal is the space between these two structures.
The alveoli oI the sebaceous and apocrine glands empty into short, straight excretory ducts,
which drain into Iollicular canals. Obstruction oI any part oI the ductal system predisposes to
inIection.
The canal is normally a selI-protecting and selI-cleansing structure. The cerumen coat
gradually works its way past the isthmus to the lateral part oI the canal and sloughs externally.
Instrumentation and excessive cleansing oI the canal disturb this primary protective barrier and
may lead to inIection. Individual variations in the anatomy oI the canal or the consistency oI the
cerumen produced may predispose some people to wax accumulation.
The canal interIaces on all but its lateral surIace. Medially, it is bound by the tympanic
membrane and squamosa oI the temporal bone, which when intact is a good barrier to the spread
oI inIection. In the presence oI a tympanic membrane perIoration, inIection may spread back and
Iorth Irom the middle ear cleIt to the external auditory canal. The horseshoe-shaped tympanic
ring and squamosa separate the canal Irom the middle cranial Iossa. Rarely is this the direct
mechanism oI intracranial extension oI inIection. The posterior bony canal serves as the anterior
boundary oI the mastoid cavity. Several vessels penetrate
the canal, especially along the tympanomastoid suture. These may be involved in the
hematogenous extension oI inIection Irom the canal to the mastoid segment. Posterior to the
cartilaginous canal lies dense connective tissue overlying the mastoid, which may become
secondarily inIected.
Superiorly, the canal is bound by the inIratemporal Iossa and base oI the skull. InIections
extending through the rooI oI the canal may extend into these structures. Anteriorly, the canal is
bordered by the temporomandibular joint and the parotid gland.
The lymphatic drainage oI the canal is an important channel Ior the spread oI inIection.
Anteriorly and superiorly, the canal drains to the preauricularlymphatics in the parotid gland and
the superior deep cervical nodes. The inIerior portion oI the canal drains into the inIra-auricular
nodes near the angle oI the mandible. Posteriorly, the lymphatics drain into the postauricular
nodes and the superior deep cervical nodes. The auricle and external auditory canal receive their
arterial supply Irom the superIicial temporal and posterior auricular branches oI the external
carotid artery (1). Venous drainage Irom the auricle and meatus is via the superIicial temporal
and posterior auricular veins. The Iormer joins the retromandibular vein, which usually divides
and joins both jugular veins; the latter joins the external jugular but may also drain to the
sigmoid sinus through the mastoid emissary vein (1).
Ta45e +
E5ements o= the d.anos.s o= d.==use a>ute
ot.t.s e?terna
1. Rapid onset (generally within 48 hours) in
the past 3 weeks. AND
2. Symptoms oI ear canal inIlammation that
include :
Otalgia (oIten severe), itching, oI
Iullness,
WITH or WITHOUT hearing loss or
jaw pain, AND
3. Signs oI ear canal inIlammations that
include :
Tenderness oI the tragus, pinna, or
both
OR diIIuse ear canal edema, erythema,
or both
WITH or WITHOUT otorrhea,
regional lymphadenitis, tympanic
membrane erythema, cellulitis oI the
pinna and adjacent skin
Sensation to the auricle and external auditory canal is supplied Irom cutaneous and
cranial nerves, with contributions Irom the auriculotemporal branches oI the trigeminal (V),
Iacial (VII), glossopharyngeal (IX), and vagus (X) nerves and the greater auricular nerve Irom
the cervical plexus (C2-C3). The vestigial extrinsic muscles oI the ear, anterior, superior, and
posterior auricular, are supplied by the Iacial nerve (VII)
1
.
II.%. A>ute Ot.t.s E?terna
II.%.+. De=.n.t.on
Acute otitis externa (AOE) is deIined as diIIuse inIlammation oI the external earcanal,
which may also involve the pinna or tympanic membrane.A diagnosis oI diIIuse AOE requires
rapid onset(generally within 48 hours) in the past 3 weeks oI symptomsand signs oI ear canal
inIlammation as detailed in Table 1.A hallmark sign oI diIIuse AOE is tenderness oI the
tragus,pinna, or both, that is oIten intense and disproportionate towhat might be expected based
on visual inspection.
Although commonly called swimmer's ear, acute otitis externa may be caused by
anything that results in the removal oI the protective
lipid Iilm Irom the canal, allowing bacteria or Iungal
organisms to enter the apopilosebaceous unit. It
usually begins with itching in the canal and is
commonly caused by instrumenting the canal with a
cotton swab or Iingernail. This temporarily relieves
itching but allows proliIeration oI bacteria in locally
macerated skin and sets up an itch-scratch cycle. The
warm, dark, moist setting oI the canal is now a
perIect medium Ior rapid bacterial growth. Later,
pain ensues as the swollen soIt tissues oI the canal
distract the periosteal lining oI the bony canal. As the
disease progresses, purulent discharge begins, and the
auricle and periauricular soIt tissues may become
involved.
II.%.%. Et.o5o3
AOE is a cellulitis oI the ear canal skin and subdermis,with acute inIlammation and
variable edema. Nearly all(98) AOE in North America is bacterial. The most
commonpathogens are Pseudomonas aeruginosa(20 to 60prevalence) and Staphylococcus
aureus(10 to 70 prevalence),oIten occurring as a polymicrobial inIection. Otherpathogens
are principally gram negative organisms (otherthan P aeruginosa), which cause no more than 2
to 3 oIcases in large clinical series.Fungal involvement isdistinctly uncommon in primary AOE
but may be more common in chronic otitis externa or aIter treatment oI AOE with topical, or less
oIten systemic, antibiotics.
The cause oI AOE is multiIactorial. Regular cleaning oI the ear canal removes cerumen,
which is an important barrier to moisture and inIection.Cerumen creates a slightly acidic pH that
inhibits inIection (especially by P aeruginosa) but can be altered by water exposure, aggressive
cleaning, soapy deposits, or alkaline eardrops.Debris Irom dermatologic conditions may also
encourage inIectionsas can local trauma Irom attempts at selI-cleaning, irrigation, and wearing
hearing aids.Other Iactors such as sweating, allergy, and stress have also been implicated in the
pathogenesis oI AOE.
II.%.'. E9.dem.o5o3
AOE is more common in regions with warmer climates, increased humidity, or increased
water exposure Iromswimming.Most, but not all, studies have Iound an association with water
quality (in terms oI bacterial load)and the risk oI AOE. The causative organisms are present in
most swimming pools and hot tubs; however, even those that comply with water quality
standards may still contain AOE pathogens.Some individuals appear more susceptible to AOE
on a genetic basis (those with type A blood group) and the subspecies oI Pseudomonas causing
AOE may be diIIerent Irom those causing other Pseudomonas inIections.
II.%.). 8.stor3
The history and Iunctional inquiry should include inIormation regarding the length oI
time, the number oI occurrences, the nature and severity oI pain, antecedent otologic disease,
previous auricular instrumentation or trauma (especially the use oI cotton-tipped applicators or
IorceIul aural irrigation), and any predisposing Iactors such as diabetes or radiotherapy or any
condition causing immunosuppression. Any previous otologic or head and neck surgery is noted.
Pain, Iullness, itching, and hearing loss are the Iour major symptoms oI external otitis, although
not every patient has each symptom
4
. Throughout the examination, the examiner should
remember the innervation oI the external auditory canal and recall that pain Irom other areas oI
the upper aerodigestive tract may be reIerred to the ear.
II.%./. Ph3s.>a5 E?am.nat.on
On initial inspection, look at the ear itselI and then at its relation to the head. Is it red,
swollen, protruding? Is there obvious discharge? Are the auricle and periauricular tissues normal
in appearance or licheniIied, with a heaping up oI the normal epidermal architecture? Is there
erythema or cellulitis spreading to the periauricular tissues, Iace, and neck? A gentle tug upward
and backward will usually conIirm the clinical suspicion. Although not an inIallible rule, the
patient with acute otitis externa usually will not tolerate this maneuver; patients with acute otitis
media oIten will.
To make the correct diagnosis oI inIections oI the external canal and to Iollow the clinical
response to treatment, clean the canal thoroughly and examine it under good illumination. A
hand-held otoscope will oIten suIIice Ior a quick examination, but all instrumentation oI the ear
is best done under the microscope with the patient lying supine in the chair, in anticipation oI a
possible vasovagal response mediated by Arnold nerve, a branch oI cranial nerve X.
Figure 2. Otitis externa, acute inIlammatory stage. Mild erythema and edema oI the canal
skin are seen. Clear secretions may be viewed in the canal. (From Senturia BA, Marcus MD,
Lucente FE. Diseases oI the external ear, 2nd ed. New York: Grune& Stratton, 1980, with
permission.)
Although topical and local anesthesia may be tried beIore cleansing, they are usually oI
little eIIect in hyperemic macerated tissue and no substitute Ior reassurance and patience. Using
graduated specula will oIten ease the patient into a complete examination. The canal may be
cleaned with suction, a cerumen loop, or alligator Iorceps. The choice oI instruments is
unimportant. Gentleness and thoroughness are very important.
II.%.(. D.==erent.a5 D.anos.s
The diIIerential diagnosis oI conditions that are similar to external otitis is large and
includes necrotizing otitis externa, bullous external otitis, granular external otitis, perichondritis,
chondritis, relapsing polychondritis, Iurunculosis, and carbunculosis, as well as many
dermatoses, such as psoriasis and seborrheic dermatitis. All have Ieatures in common with acute
and chronic external otitis yet have enough dissimilarities to be considered distinct clinical
entities.
Carcinoma involving the external auditory canal may present as inIection, and in its
earliest stages is oIten mistaken Ior inIection and treated inappropriately. The most common
malignant neoplasm oI the external ear is squamous cell carcinoma, although other primary
carcinomas, such as basal cell carcinoma, malignant melanoma, ceruminous adenoma or
adenocarcinoma, adenoid cystic and metastatic carcinomas to the temporal bone with extension
to the external auditory canal such as breast, prostatic, small (oat) cell, and renal cell carcinomas,
have been described. The occurrence oI pain in an old previously stable mastoid cavity is the
hallmark oI carcinoma and must be excluded by biopsy and other investigations.
II.%.&. Natura5 8.stor3
The natural history oI untreated acute otitis externa is one oI increasing pain, swelling,
and discharge Irom the canal. The inIection may spread to the adjacent periauricular soIt tissues,
Iace, and neck. In an immunocompromised patient, what began as an isolated superIicial
inIection oI the apopilosebaceous unit oI the external auditory canal may progress to
perichondritis, chondritis, cellulitis, and erysipelas. Rich lymphatic and hematogenous drainage
pathways Iavor the spread oI inIection to local and regional sites in the head and neck. Few
patients progress to such an advanced stage beIore seeking medical attention.
II.%.#. Med.>a5 Treatment
The Iour Iundamental principles in the treatment oI acute external otitis in are Irequent
and thorough cleaning, judicious use oI appropriate antibiotics, treatment oI associated
inIlammation and pain, and recommendations regarding the prevention oI Iuture inIections. In
any stage oI inIection, thorough cleaning is a priority. Meticulous debridement oI exIoliated
debris, purulence, and cerumen will do as much iI not more than simply placing the patient on
ear drops. In the preinIlammatory stage, a complete cleaning may be all that is required. In the
absence oI purulence, a brieI course oI an acidiIying drop such as aluminum sulIate calcium
sulIate (Domeboro) is eIIicacious in discouraging bacterial or Iungal growth.
Treatment oI the acute inIlammatory stage varies with the extent oI disease. In the
mildest Iorm, cleaning as described previously is indicated. An antibiotic otic drop is
recommended to cover what is probably a Pseudomonas inIection. There is an emerging body oI
evidence that the Iluoroquinolone preparations with or without steroids (ciproIloxacin, oIloxacin,
dexamethasone, hydrocortisone (Cipro HC, Ciprodex, Floxin)| may have advantages over the
neomycin/polymyxin/hydrocortisone preparations (Cortisporin or Coly-Mycin S Otic)
6,7
.At this
time, no signiIicant antibiotic resistance has been shown to emerge due to the use oI the
Iluoroquinaloneototopic medications
8
.
At this stage, edema oI the external auditory canal should not be severe, and the patient
should be able to instill drops into the ear by tilting the head to the side or by lying down with
the involved ear upright.
In the moderate stage oI inIlammation, edema oI the canal may interIere with the
instillation oI drops. The physician should then insert a wick into the canal and instill drops on it.
OIten the canal may accommodate two or even three wicks. As the wick expands, it presses the
soIt tissues and periosteum toward the nondistended position; this alone may relieve pain. All
instrumentation oI the ear is best done under the microscope. The wick is removed by the
physician at the time oI reexamination. II the edema has not been signiIicantly reduced,
repacking is indicated. Antibiotic drops should be continued Ior at least 2 to 3 days aIter the
cessation oI pain, itching, and drainage, so that complete eradication oI inIection may be
ensured.
In the moderate stage, an oral analgesic is oIten prescribed because pain can be
pronounced. Caution the patient to avoid manipulation oI the canal. Teach swimmers to towel
dry the concha and lateral canal, to shake water out oI the canal, or to instill an acidiIying drop
aIter swimming. II the inIection has not spread beyond the boundaries oI the external canal, the
use oI oral antibiotics will be oI little iI any value. A Iinal oIIice visit is important to ensure that
the inIection has completely resolved and the canal is back to its normal state.
In the severe stage, inIection usually extends beyond the limit oI the canal. In addition to
the cleaning, packing, and use oI antibiotic drops as discussed previously, attend to any soIt-
tissue involvement by using an oral antibiotic with broad-spectrum coverage. Successive
generations oI the cephalosporins widen gram-negative coverage at the expense oI gram-positive
coverage.
In addition to anti-Pseudomonas eardrops, common choices oI oral antibiotics are
antistaphylococcalpenicillins, Iirst-generation cephalosporins, or one oI the
antipseudomonalIluoroquinolones such as ciproIloxacin or levoIloxacin. The Iluoroquinolone
antibiotics are eIIective against Pseudomonas species but at present are not approved Ior use in
patients under age 18 because oI the risk oI arthropathy Iormation
6
. Multiple reports over the last
10 years have indicated the saIe use oI ciproIloxacin in the pediatric patient with little iI any
increased development oI arthopathy over adults. The Iluoroquinolones remain contra-indicated,
however, except in extraordinary circumstances, such as in the treatment oI respiratory disease in
children with cystic Iibrosis
9
.
Warm soaks (normal saline or diluted aluminum sulIate calcium acetate solution) are also
useIul in the treatment oI the crusting and edema involving the auricle and surrounding skin.
Culture oI the canal is indicated only Ior the severe stage or Ior patients who have previously
been treated without resolution. Treatment is generally continued Ior 10 to 14 days iI there is a
good response. In rare patients who do not respond to this regimen, hospitalization, vigorous
daily local care, repeat culturing, and intravenous antibiotics are indicated.
In all cases oI acute or chronic external otitis, instruct the patient to avoid Iuture
inIections by not placing any object or instrument into the canal. These oIten excoriate the canal
skin and push debris Iurther into the canal rather than remove it. Patients who have repeated
inIections despite adhering to these measures are best advised to use an acidiIying drop
composed oI equal measures oI vinegar and water, or ethyl alcohol and water, when exposed to
high humidity. Alternatively, an acidiIying power such as boric acid may be used. Custom-made
ear molds are useIul Ior these patients.
C8APTER III
CASE REPORT
A. IDENTITI7
Name : RH
Age : 19 years old
Gender : Female
Address : Banyumas
Occupation : Student
Religion : Islam
Date oI visit : June 20th 2013
B. ANAMNESIS
Ma.n >om95a.nt : Pain in the right ear
8.stor3 o= 9resent .55ness :
o Patient presents with dull right ear pain Ior the past 3 days with a decrease in hearing,
and also Iullness sensation. No itching and discharge were complained. Patient oIten
uses the cotton bud to clean her ears. No history oI swimming or water clogging. No
history oI trauma.
o Complaints like Iever, cough, and common cold were denied. She does not have any
complaints regarding nose or throat
8.stor3 o= 9ast .55ness :
o Same symptoms beIore (-)
o History oI Ioreign body insertion (-)
o History oI allergy (-)
o History oI trauma (-)
8.stor3 o= .55ness .n the =am.53 mem4ers :
o History oI similar complaints (-)
o History oI allergy (-)
C. P8S7ICA1 EXAMINATION
General status : conscious, well nourished, non anemic
Vital signs :
o Blood pressure : 120/80 mmHg
o Pulse : 110x/min
o Respiration : 30x/menit
o Temperature : aIebrile
SpeciIic/Local Physical Examination (ENT Examination)
i. Ear examination :
R.ht 1e=t
Sha9e Normal Normal
Aur.>u5ar Normotia Normotia
Preaur.>u5ar
Tragus pain ()
edema (-)
Hyperemia (-)
Fistula (-)
Tragus pain (-)
Edema (-)
Hyperemia (-)
Fistula (-)
Right LeIt
Ear Cana5 Narrow (edema) Wide
Co5our Hyperemia Not hyperemia
D.s>hare @ -
Cerumen (-) (-)
Mem4ran
T.m9an.
Cannot be visualized Intact, cone oI light ()
ii. Nose examination :
Anterior rhinoscopy :
Within normal limit
Posterior rhinoscopy
Intact tymphanic membrane, cone of
light visible
Tymphanic membrane is not
AD: Tragus pain (+), Swelling an
reness in !A"
AS: #ithin normal
Within normal limit
iii. Mouth and throat examination :
Within normal limit
Indirect Laryngoscopy
Within normal limit
Tuning Fork Examination:
Right Ear LeIt Ear
Rinne BC ~ AC AC ~ BC
Weber Lateralization to the right
Swabach Increase Same with examiner
Conclusion Conductive hearing loss oI right ear
D. DIAANOSIS
Based on anamnesis and physical examination, the patient is diagnosed with Acute
DiIIuse Otitis ExternaAurisDextra.
E. TREATMENT
Medication :
SoIratule tampon
Na DikloIenac
Patient education :
o Keep the ears in a dry condition
o Do not remove the tampon beIore 3 days
o Do not clean the ears with cotton bud by yourselI.
F. PROANOSIS
Dubia ad bonam
A. PROB1EM
Do we need to use systemic antibiotic therapy?
C8APTER I;
DISCUSSION
According to Ong and Chee, 2005, otitis externa reIers to a spectrum oI inIections oI
external auditory canal and auricle. It is a common condition and aIIects between 5 - 20 oI
the patients attending ENT clinics. Otitis externa can be classiIied to diIIuse otitis externa, acute
localized otitis externa, chronic otitis externa, otomycosis, herpes oticus, dermatoses and
malignant otitis externa.
Bailey, et al. (2006) stated that acute otitis externa is an inIection oI the canal caused by a
break in the normal skin or cerumen protective barrier, oIten occurring in the milieu oI elevated
humidity and temperature. Although commonly called swimmer's ear, acute otitis externa may be
caused by anything that results in the removal oI the protective lipid Iilm Irom the canal,
allowing bacteria or Iungal organisms to enter the apopilosebaceous unit. Trauma Irom cleaning
the ears with Iingernails or cotton bud has been identiIied as the most common predisposing
Iactor locally
11
. On this patient, her habits oI cleaning her ear using cotton bud can be the
predisposition Iactor Ior the acute diIIuse otitis externa disease.
Based on a clinical guide by RosenIeld, et al. 2006, acute diIIuse otitis externa is
characterized by sign oI ear canal inIlammation, such as tenderness oI the tragus (when pushed),
pinna (when pulled up and back), or both and symptom oI ear canal inIlammation including
otalgia. Otorrhea might be observed on some patients, but this sign doesn`t necessarily mark the
inIlammation oI outer ear. There can be itching, or Iullness sensation, with or without hearing
loss or ear canal pain on chewing. The diagnosis oI acute diIIuse otitis externa requires rapid
onset (generally within 48 hours) in the past 3 weeks oI symptoms and sign oI ear canal
inIlammation$ During anamnesis with the patient, she complained oI the pain she Ielt in the
right ear, Iullness sensation in the past 3 days. There is also a complaint oI decrease in hearing
acuity.
In ear examination, we can Iind that there was pain and tenderness in the tragus when we
palpated the auricle. We couldn`t visualize the tymphanic membrane using otoscope during
examination because there was swelling and redness in the ear canal that blocked the view oI the
eardrum. This corresponds with the theory that otoscopy will reveal diIIuse ear canal edema,
erythema or both, either with or without otorrhea or material in the ear canal.
10
Anniko et al.
2010, also explained that the cartilagenous part oI the external ear canal is oedematous and the
size oI its lumen is reduced.
The therapy that was given to the patient is antibiotic tulle tampon that was inserted to the
external ear canal and planned to be removed aIter 3 days. The tulle contains Iramycetin sulIate,
an aminoglycoside antibiotic. The patient was also prescribed with Na-dicloIenac to reduce the
pain.
According to RosenIeld, et al. 2006
10
, Ior the initial therapy oI diIIuse and uncomplicated
AOE, clinicians should use topical preparations. Systemic antimicrobial therapy should not be
used unless there is extension outside the ear canal or the presence oI speciIic host Iactors that
would indicate a need Ior systemic therapy. Topical antimicrobials are beneIicial Ior AOE, but
oral antibiotics have limited utility. The oral antibiotics selected are usually inactive against P
aeruginosa and S aureus, may have undesirable side eIIects, and, because they ae widely
distributed, serve to select out resistant organism throughout the body. Bacterial resistance is oI
Iar less concern with topical antimicrobials, because the high local concentration oI drug in the
ear canal will generally eradicate all susceptible organism plus those with marginal resistance.
The statement was also reinstated by Anniko et al., 2010, which proposed that oral
antibiotics are indicated only in cases oI severe external otitis with cellulitis or lymphadenitis,
and always in diabetic patients. HajioII and Mackeith, 2010, stated that there are no clinically
important results Irom RCTs about whether oral antibiotics are better than topical antibiotics
against otitis externa.
RosenIeld
10
also stated Irom the meta-analyses oI topical antimicrobials that used Ior
treating acute otitis externa, there was no signiIicant diIIerences Irom the clinical outcomes oI
antiseptic compare to antibiotic. But there was a signiIicance oI bacteriologic cure oI the
quinolone compared to non-quinolone, thus ciproIloxacin or oIloxacin are still in the Iirst line Ior
treating otitis externa. However, in deciding drug oI choice, we also need about the cost oI the
therapy. Aminoglycoside is also widely used in treating otitis externa because it is cheaper than
those other agents. Despite reports on ototoxicity with the aminoglycoside agents
12
, it only
happens in patients whose tymphanic membranes are unintact or perIorated. This Iactor also
contributes in deciding when to use quinolone or aminoglycoside.
Education plays important role in acute otitis externa patients. We as clinicians need to
ensure patient not to selI-cleaning the ear using cotton bud or Iingernails or other tools. Patients
need to keep their ears in dry condition, by using hair cap while showering, using earplugs while
swimming or bathing to decrease the amount oI moisture entering the ear.
C8APTER ;
CONC1USION
It has been reported this Iemale patient, aged 19 years old, with diagnosis oI Acute DiIIuse
Otitis Externa on the right ear and has been given treatment with antibiotic tulle tampon and
Natrium dicloIenac. Education that need to be given to patient is that she needs to keep the ear
dry, do not use cotton bud to clean the ear, and can use earplugs when swimming or bathing.
REFERENCES
1. Hollinshead WH. Anatomy Ior surgeons: the head and neck, 3rd ed. Vol. 1. Philadelphia:
Harper & Row, 1982 : 159-163.
2. Anson BJ, Donaldson JA. Surgical anatomy oI the temporal bone, 3rd ed. Philadelpia: W.B.
Saunders, 1981 : 28.
3. Hughes GB, Pensak ML. Textbook oI clinical otology. New York: Thieme-Stratton, 1997.
4. Senturia BA, Marcus MD, Lucent FE. Diseases oI the exernal ear, 2nd ed. New York:
Grune&Stratton, 1980.
5. Lucente FE. External otitis. In: Gates GA, ed. Current therapy in otolaryngology-head and
neck surgery, 6th ed. New York: Elsevier science, 1997.
6. Roland PS, Pien FD, Henry DC, et al. EIIicacy and saIety oI topical ciproIloxacin
/dexamethasone versus neomycin/polymyxin B/ hydrocortisone Ior otitis externa. Curr Med
Res Opin 2004;8: 1175-1183.
7. Myer CM III. Ear Nose Throat J. 2004;83(Suppl):9-11.
8. Weber PC, Roland PS, Hannley M, et al. The development oI antibiotic resistant organisms
with the use oI ototopical medications.Otolaryngol Head Neck Surg. 2004;130(3 Suppl)S89-
S94.
9. Gendrel D, Chalumeau M, Moulin F, et al. Fluoroquinolones in paediatrics: a risk Ior the
patient or Ior the community? Lancet InIect Dis 2003;9:537-546.
10. RosenIeld, RM, et al. Clinical practice guideline: Acute otitis externa. OtolaryngologyHead
and Neck Surgery (2006) 134, S4-S23.
11. Ong, YK, Chee G. Review Article: InIections oI the External Ear. Ann Acad Med Singapore
2005; 34:330-4.
%&$ Nierengarten, MB. 2009. http://www.enttoday.org/details/article /497005/Swimmers Ear Be
on the Alert For Complications.html$
13. Bailey BJ, Johnson JT. Head and neck surgery-otolaryngology. Lippincot Williams and
Wilkins, 2006.
14. Anniko M, et al. Otorhinolaryngology, head and neck surgery. New York: Springer, 2010.
15. HajioII, D, Mackeith, S. Clinical evidence otitis externa. BMJ Publishing Group
2010:8:510-531.