ORL Department

The Pharynx
Mansoura University

Anatomy
The pharynx is a funnel shaped fibro-muscular tube which extends from the base of the skull
(basi-sphenoid) to the lower border of the cricoid cartilage at the lower border of 6th cervical
vertebra (at which point it becomes the esophagus). Portions of the pharynx lie posterior to the
nasal cavity (naso-pharynx), oral cavity (oro-pharynx) and larynx (laryngo-pharynx or
hypopharynx). Pharynx lie anterior to the upper six cervical vertebrae. Its length is about 5
inches in adults.

naso-pharynx: extends from the base of the skull (basi-sphenoid) to the lower border of soft
palate, lies infront of 1st cervical vertebra. It communicates anteriorly with the nasal fossa
through the choana, and inferiorly, with the oropharynx by the velo-pharyngeal isthmus. Its
lateral wall contains: pharyngeal orifice of Eustachian tube (1cm behind the posterior end of
inferior turbinate), with the tubal tonsils around it and fossa of Rossenmuller just above and
behind it. Nasopharyngeal tonsils lies at the junction of the roof and posterior wall

oro-pharynx: extends from the lower border of soft palate to the upper border of the epiglottis,
lies infront of 2nd and 3rd cervical vertebrae. Its lateral wall contains: anterior (contains the
palatoglossus muscle) and posterior (contains the palatopharyngeus muscle) pillars and palatine
tonsil in-between.

laryngo-pharynx: extends from the upper border of the epiglottis to the upper end of the
esophagus, lies infront of 4th, 5th, and 6th cervical vertebrae. It consists of the post-cricoid area
behind the cricoid, and two pyriform fossae on eithr sides of the larynx, and the posterior
pharyngeal wall.

Figure 1. Semischematic mid-sagittal section through the nose, mouth, end pharynx to illustrate
the approximate position of the three groups of "tonsils".
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Structure of the pharynx: Its wall consists of five layers; from within outwards:
1. Mucous membrane: Lined by stratified squamous epithelium, except upper part of the nasopharynx which is lined by pseudo-stratified ciliated columnar epithelium.
2. Sub-epithelial lymphoid tissues: It forms a ring of lymphoid tissues called Waldeyer's ring.
This ring includes: palatine (faucial) tonsils, lingual tonsils ( in tongue base),

nasopharyngeal tonsil at the junction between roof and posterior wall of the naso-pharynx
(named adenoids when enlarged), tubal tonsils (around pharyngeal orifice of eustachian
tube), lateral pharyngeal band, and scattered lymphoid tissues in posterior pharyngeal wall.
The Waldeyer's ring have efferent (No afferent) lymph vessels drains into the
retropharyngeal and upper deep cervical lymph nodes.
3. Pharyngeal aponeurosis: A layer of loose connective tissues, contain abundant lymphoid
tissues. It is continous above with the pharyngo-basilar fascia.
4. Muscular layers.
5. Bucco-pharyngeal fascia: A thin connective tissue surrounds the pharynx. It is loosely
attached to the prevertebral fascia by the median raphe.

Figure 2. Side view illustrating the 3 constrictors of the pharynx and their attachments. From
Basmajian, Grant's Method of Anatomy, p. 501.
Nerve supply of the pharynx: (pharyngeal plexus of neves:9th, 10th, and 11th)
1. Motor: the motor nerve supply for the muscular layers is derived from the cranial accessory
nerve, and distributed via vagus nerve, excluding the stylopharyngeus muscle which is
supplied by the glossopharyngeal nerve.
2. Sensory: glossopharyngeal and vagus nerves supply all the pharynx except the upper part of
the naso-pharynx which is supplied by twigs from the trigeminal nerve like the rest of the
nose.
NB. Upper part of the naso-pharynx: The closest area of the pharynx to the nose, is covered by
respiratory epithelium., and takes sensory nerve supply from the trigeminal nerve.
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Arterial supply of the pharynx:

1.
2.
3.
4.
5.

Ascending pharyngeal artery: from the external carotid artery.

Ascending palatine artery: from facial artery.
Tonsillar artery (main artery of the tonsils): from facial artery.
Dorsalis liguae artery: from lingual artery.
Descending palatine artery: from maxillary artery.

Venous drainage of the pharynx:

Veins of the pharynx collect to form the pharyngeal plexus of veins which communicates with
the pterygoid plexus of veins to drain into the common facial and internal jugular veins.
Lymphatic drainage of the pharynx:
1. Upper deep cervical lymph nodes: drain the whole pharynx. Palatine tonsils drains into the
uppermost node of the upper deep cervical group, which lies at the site of crossing of internal
jugular vein with the posterior belly of digastric, and so it is named Jugulo-digastric Lymph
node.
2. Retropharyngeal lymph nodes: add drainage to naso-pharynx.
3. Lower deep cervical lymph nodes: add drainage to laryngo-pharynx.
Functions of the Pharynx
The muscular layers of the pharynx are comprised of an outer muscular layer made up of 3
circularly disposed muscles, the constrictors. Figure 2 below shows the arrangement and
attachments of the pharyngeal constrictors similar to 3 stacked flower pots.
The inner muscular layer of the pharynx is made up of 3 small longitudinally oriented muscles:
the stylopharyngeus, palatopharyngeus, and salpingopharyngeus.
Action of the pharyngeal muscles: Pharyngeal phase of swallowing:
During swallowing, successive contraction of the superior, middle, and inferior constrictor
muscles helps to propel the bolus (ball) of food down into the esophagus. In addition, contraction
of the 3 longitudinal muscles of the pharynx helps to raise the pharynx, effectively aiding it in
engulfing the bolus of food.
In between acts of swallowing, the lowest fibers of the inferior constrictor are thought to act as a
sphincter, guarding the entrance to the esophagus and preventing the entry of air into the
digestive system.

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Anatomy of the palatine "faucial" tonsils:

Sub-epithelial lymphoid tissue collection with prominent germinal centers concerned in
production of lymphocytes and plasma cells. Tonsils are located laterally in either sides of the
oropharynx. The tonsils are bordered by the following tissues:
1. Lateral (Deep): Capsule, Peritonsillar space, Superior constrictor muscle, Buccopharyngeal
fascia, parapharyngeal space, medial pterygoid muscle, and the inner surface of the angle of
the mandible.
2. Anterior: Palatoglossus muscle (anterior pillar)
3. Posterior: Palatopharyngeus muscle (posterior pillar)
4. Superior: Soft palate
5. Inferior: Lingual tonsil
6. Medial surface: is covered by stratified sqamous epithelium, and is penetrated by 12-15
crypts that open on this surface, the largest one is called crypta magna
Function: formation of specific antibodies, and B&T cell activities in response to a variety of
antigens. The antigen is captured by an epithelial cell lining the crypts called M cells, which in
turn transport the antigen to the sub-epithelial lymphoid tissues, which stimulate production of Ig
G, and Ig M. Repeated attacks of acute tonsillitis lead to shedding of these M cells
Arterial supply is through the external carotid artery and its branches:
Superior pole: is usually supplied from:
1. Ascending pharyngeal artery
2. Tonsillar branch of the facial artery (chief artery of the tosnils)
3. Descending palatine artery of the maxillary artery
Inferior pole: is usually supplied from:
1. Ascending palatine artery of facial artery.
2. Tonsillar branch of the facial artery (chief artery of the tosnils)
3. Dorsal linguae artery of lingual artery
Venous outflow is handled by the plexus around the tonsillar capsule, and the paratonsillar vein,
the lingual vein, and the pharyngeal plexus.
Lymphatic drainage involves the upper deep cervical nodes and the jugulodigastric nodes.
Sensory supply is provided by the glossopharyngeal nerve and the lesser palatine nerve.
Important structures deep to the inferior pole include the glossopharyngeal nerve, the lingual
artery, and the internal carotid artery.

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Pharyngitis
Inflammation of the mucous lining of the pharynx (mucous membrane, and sub-epithelial
lymphoid tissues)
Acute Pharyngitis
Acute pharyngitis represents one of the most common reasons for children to be seen by a
physician.
1. Non-Specific: Acute simple pharyngitis.
2. Specific:
a. Bacterial: Streptococcal (GABHS) pharyngitis, Scarlet fever, Diphtheria, and Vincent's
angina.
b. Viral: Infectious mononucleosis, Measles, Chickenpox, Herpes, AIDS.
c. Fungal: Moniliasis (Candidiasis or Thrush)
3. Pharyngeal manifestations of systemic diseases:
a.
b.
c.
d.
e.

Blood diseases: Agranulocytosis, Acute leukemia.

Skin disease: pemphigus and lichen planus
Deficiency disease:Vit C deficiency (Scurvy)
Drug intoxication: Lead, mercury, and anti-depressants
Diseases of unknown aetiology: Recurrent aphthous ulcers, Behcet's disease.
Chronic Pharyngitis

1. Non Specific:
a.
b.
c.
d.

Chronic simple pharyngitis,

Chronic hypertrophic pharyngitis
Chronic atrophic pharyngitis
Chronic superficial pharyngo-oesophagitis (Plummer-Vinson Syndrome).

2. Specific: Scleroma, TB, and Syphilis

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Acute simple pharyngitis

Predisposing factors:
1. General: as low resistant, bad hygiene and overcrowding.
2. Local: as rhinitis, sinusitis, adenoiditis, stomatitis, dental caries, excessive alcohol intake or
tobacco or spicy food and abuse of voice.
Causative organisms:
1. Mostly primary viral (70%):
a. In course of coryza (rhinovirus, corona virus adenovirus, RSV) or
b. Influenza (influenza and para-influenza virus)
2. Bacterial (15-30%): May be primary, or following viral infections.
a. The commonest is streptococcus pyogens (GABHS), followed by
b. Streptococcus pneumoniae, moraxella catarrhalis, and haemophilus influenza.
Special concern will be given to GABHS (group A beta haemolytic streptococci) pharyngitis.
Mode of transmission: droplet infection.
Symptoms:
1. General: Rapid onset of fever, malaise, headache and anorexia, and flushed face..
2. Local: Rapid onset of sorethroat, dysphagia, and referred otalgia.
Signs:
1. Diffuse congestion of mucosa of the pharynx, non-adherent yellowish true membrane may
be formed.
2. Enlarged tender upper deep cervical lymph nodes.
Complications: Otitis media, and laryngitis.
Treatment:
1. Antibiotics
2. Supportive measures: Warm drinks, analgesic antipyretics, gargles.

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Streptococcal (GABHS) pharyngitis

It is an acute pharyngitis with inflammation of the mucous membrane and lymphoid tissue of the
pharynx, caused by group A beta haemolytic streptococci (GABHS).
Its diagnosis is based on laboratory findings. Therefore, during the course of acute simple
pharyngitis, the clinician should identify GABHS, because it may lead to serious complications.
Still there are some major points of debate among clinicians:
1. Which children should be tested for streptococcal pharyngitis?
2. How should children be tested for streptococcal pharyngitis?
3. What treatment approach should be used for suspected streptococcal pharyngitis?
Children with streptococcal pharyngitis do not have cough, rhinorrhea, or symptoms of viral
upper respiratory infection.
Symptoms: may be
1. Same as acute simple pharyngitis, but
a. Some patients may be toxic, with high fever, malaise, headache, and severe pain on
swallowing.
b. Sub-clinical infection: The symptoms may pass unrecognized.
2. Vomiting and abdominal pain may be prominent early symptoms simulating gastroenteritis
or even acute appendicitis.
Signs:
1. Diffuse congestion of mucosa of the pharynx, non-adherent yellowish true membrane may
be formed. A red edematous uvula, palatal petechiae.
2. Enlarged tender upper deep cervical lymph nodes.
Group A beta-hemolytic Streptococcus pyogenes (GABHS) and Epstein-Barr virus (EBV) can
cause tonsillitis that may be associated with the presence of palatal petechiae. GABHS
pharyngitis usually occurs in children aged 5-15 years.
Complications:
Attributed to an antibody reaction against the antigen of (GABHS):
1. Rheumatic fever: arthritis, carditis, chorea, etc
2. Acute glomerulo-nephritis.
3. Subacute bacterial endocarditis.

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Investigations:
1. Rapid Antigen Detection Test (RADT): It is a rapid test to detect the streptococcus
carbohydrate wall. It takes two hours. It is expensive.
2. Throat culture remains the criterion standard for the diagnosis of streptococcal pharyngitis. It
takes two hours
3. An increase in antistreptolysin O titers can be observed but is a late finding and usually of
value only in retrospect.
NB:
1. If a rapid streptococcal test result is positive, a culture is not necessary.
2. If a rapid streptococcal test result is negative, a culture is mandatory.
3. A positive culture unfortunately cannot be used to differentiate between acute infection and
asymptomatic carriage.
Treatment:
1. Rest, fluids, analgesics, and antipyretic.
2. Antibiotics ( penicllins or amoxicillins) for 10 days.
3. Gargles. Lozenges containing antibiotics are not recommended as they encourage growth of
monilia.

Scarlet Fever
It is caused by spread of toxins from streptococcal infections of the pharynx and tonsils.
Scarlet fever is an infection caused by exotoxin-producing (GABHS) found in secretions and
discharge from the nose, ears, throat, and skin. It may follow streptococcal wound infections or
burns, as well as upper respiratory infections.
Clinical Pictures:
General:
1. Sudden onset of fever, malaise, headache, and vomiting.
2. Characteristic rash appears within the first two days of onset, mainly on trunk and limbs, but
rarely of the face which is flushed with ring area of circumoral pallor.
Local:
1. Sore throat, and enlarged tender cervical lymph nodes.
2. Congested pharynx, yellow slough on the tonsils that can be wiped easily
3. Strawberry and cream tongue (yellowish tongue coat through which the papillae projects).
Later the coat disappear leaving a strawberry tongue.

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Treatment:
1. Rest, fluids, analgesics, and antipyretic.
2. Antibiotics ( penicllins or amoxicillins) for 10 days.

Diphtheria
Definition:
It is an acute specific infectious disease caused by corynebacterium diphetheria (Gram positive),
which produce a powerful exotoxin responsible for the general toxaemia (circulatory failure,
peripheral neuritis and local sloughing).
Incidence:
It is very rare nowadays because of the compulsory vaccine program.
Age: in children 2-10 years.
Mode of infection:
Direct contact: Droplet infection.
Indirect contact: Through articles of a patient or a carrier(source).
Incubation period: 2-5 days.
Pathology & Sites of infection:
Pharynx: is the commonest site resulting in faucial diphtheria 60%.
The tonsils are commonly affected , and there is superficial ulceration with the formation of a
false membrane which may spread to the soft palate and uvula. The exudate is greyish white ,
firmly adherent , and appears to have been laid on the surface rather than laid in as in case of
Vincent's angina. Its removal is difficult and leaves a bleeding area.
Larynx: 10%. See the larynx.
Nose: 5%. See the nose.
Symptoms:
General: insidious onset of low grade fever , malaise , and headache.
Local: Sore throat. Foul breath with sweetish odour (an important diagnostic feature). Bull neck.
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Signs:
General: Severe toxaemia, and pallor.
1. Temperature: low grade fever up to 38.0 C.
2. Pulse: is rapid, weak and not synchronous with the temperature.
Local:
1. Pseudo-membrane which is characterized by:
a. Greyish white to yellow in colour.
b. Formed of: thick fibrinous exudate , dead leucocytes and bacteria as well as sloughed
mucosa.
c. Usually unilateral and extends beyond the margin of the tonsil to the pharynx and even
to the larynx.
d. Has a thick curved edge because it contain fibrin.
e. Not wiped easily (adherent) and leaves a raw bleeding area on removal and recurs rapidly
after removal.
f. Offensive in odour.
2. Enlarged tender upper deep cervical lymph nodes resulting in Bull neck.
Investigations: Laboratory finding:
1. A swab from the membrane:
a. Direct film for diphtheria like organisms (Chinese letter appearance).
b. Culture on Loffler's serum or Tellurite agar for diphtheria bacilli.
2. Urine analysis: Albuminuria.
Differential Diagnosis: see membrane on tonsils
Complication:
They result from spread of infection and membrane causing respiratory obstruction or
pneumonia , and from the action of exotoxin that has an affinity for neuromuscular junction and
myocardium, for this reason early diagnosis and treatment are necessary.
I. Cardiovascular:
Heart failure may be central and early (during 1st week) due to toxic myocarditis or peripheral
and late (during the 3rd week) due to vagal nerve neuritis .
II. Renal:
Acute nephritis is early and common, causing albuminuria.
III. Paralytic complication: usually occurs on 3rd or 4th week.
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1. Palate: palatal paralysis is the earliest and the commonest resulting in nasal tonation (hypernasality or rhinolalia aperta) of voice, and regurgitation of fluid and the uvula is deviated to
the normal side.
2. Eye muscles: intrinsic and extrinsic muscle are effected resulting in: diplopia due to 6th nerve
paralysis. loss of accommodation due to 3rd nerve paralysis.
3. Pharynx: resulting in dysphagia for fluids.
4. Larynx: resulting in hoarseness of voice and ineffective cough that predisposes to
bronchopneumonia.
5. Chest muscle: diaphragm and intercostals causing suffocation
6. Limb muscles are very rarely paralyzed
IV. Respiratory complications:
1. Laryngeal obstruction due to extension of the membrane to the larynx, or by laryngeal
oedema
2. Lung collapse due to bronchial obstruction by an inhaled piece of membrane
3. Bronchopneumonia
Management:
A.

Curative: Hospitalization

1. Rest for 3 weeks to avoid heart failure.

2. Isolation in fever hospital till 3 negative successive daily swabs.
3. Antitoxic serum (Anti-Diphtheretic Serum= ADS)
A. IM 40000-100000 I.U is given once diphtheria is suspected without waiting the culture
results. It is usually horse-serum, preliminary skin test is mandatory.
B. But if the patient is sensitive to horse-serum, either:
Rapid desensitization (gradual increasing dose): 1/2 cc SC, 1/2 hour 1/2 o the dose IM.
1/2 hour rest of the dose IM. Or
Substitute horse-serum by Cow's serum.
C. Anti-shock measures should be available : adrenaline, cortisone, calcium and
antihistamines.
4. Antibiotics: Penicillin for 10 days.
5. Treatment of complications: Tracheostomy for stridor, stomach tube for dysphagia.
Tonsillectomy is advised for diphtheria carrier
B.

Prophylactic:

1. Active Immunization: DPT (triple vaccine: Diphtheria toxoid, Pertusses killed, and Tetanus
toxoid) is compulsory in Egypt: One cc IM three doses (2nd, 4th, and 6th month of age), and a
booster dose of DPT at 18 months and another DT at school age (5 years).

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2. Passive Immunization: For contacts 3000-10000 IU of anti-toxic serum. It give 3 weeks

immunity.
3. Tonsillectomy for diphtheretic carrier.

Vincent's Angina
Definition: Acute necrotizing ulcerative gingivitis: ANUG.
Predisposing factors: bad oral hygiene, and carious teeth.
Causative organisms: Two anaerobic organisms act in symbiosis:
1. Spirochaeta denticola (Borellia Vincenti), and
2. Fusiform bacilli
Symptoms:
1. General: M ild fever, malaise, headache and anorexia.
2. Local: Severe sorethroat, odynophagia, referred otalgia, and marked foetor (Halitosis)
Signs:
1. Deep punched out ulcer covered by dirty grayish false membrane. It affects the tonsillar,
pharyngeal, and buccal mucosa especially at the gingival margins.
2. Enlarged tender upper deep cervical lymph nodes.
Investigations: Swab from the membrane to be examined by a direct film.
Treatment:
1. Antibiotics: Penicillins ( specific for spirochetes), Clindamycin, and metronidazole (specific
for being anaerobes).
2. Hydrogen peroxide mouth wash and gargles to change the media of organisms.
Infectious mononucleosis
Synonyms: Mononucleosis, "Mono", or Glandular fever.
Definition: Acute specific viral infection characterized by swollen lymph glands and conatant
fatigue.
Causative organism: Epstein-Barr virus (EBV).
The incubation period of EBV infectious mononucleosis is 1-2 months
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Pathophysiology:
EBV is transmitted via intimate contact with body secretions, primarily oropharyngeal
secretions.
EBV infects the B cells in the oropharyngeal epithelium.
Circulating B cells spread the infection throughout the entire reticular endothelial system (RES),
ie, liver, spleen, and peripheral lymph nodes.
EBV infection of B lymphocytes results in a humoral and cellular response to the virus.
Symptoms:
1. General: Rapid onset of fever, malaise, headache, anorexia, Constant fatigue.
2. Local: Rapid onset of sorethroat, dysphagia, and referred otalgia.
Signs:
1. General: Generalized lymphadenopathy, splenomegally, and hepatomegally.
2. Local:
a. Diffuse congestion of phargyneal and tonsillar mucosa, shallow ulcers covered by false
membrane, similar to that of diphtheria (but is bilateral).
b. Palatal petichae appear in early stages. Rubelli skin rash may appear after ampicillin
therapy.
Mononucleosis usually lasts for one to two months.
Once a person has had mononucleosis, the virus remains dormant in the throat and blood cells
for the rest of that persons life. Once a person has been exposed to the Epstein-Barr virus, a
person is usually not at risk for developing mononucleosis again, as he is already has the virus.
Investigations: Diagnosis can be confirmed with:
1. White blood cell count: Monocytosis, lymphocytosis with atypical lymphocytes.
2. EBV infection induces specific antibodies to EBV and a variety of unrelated non-EBV
heterophile antibodies:
a. These heterophile antibodies react to antigens from animal RBCs.
Sheep RBCs agglutinate in the presence of heterophile antibodies and are the
basis for the Paul-Bunnell test.
o Agglutination of horse RBCs on exposure to heterophile antibodies is the basis of
the Monospot test.

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Mono spot is up to 95% sensitive in children and less than 60% sensitive in
infants.
False-positive Monospot test results include toxoplasmosis, rubella, lymphoma,
and certain malignancies, particularly leukemias and/or lymphomas.
A false-negative Monospot test result may occur if testing is performed too early
in the course of the illness or in very young children (<2 y) and occasionally in
elderly patients.
b. Specific antibodies to EBV: IgM and IgG antibodies directed against the VCA of EBV:
o Confirming the diagnosis of EBV.
o Differentiating acute and/or recent infection from previous infection.
EBV IgM VCA titers decrease in most patients after 3-6 months but may persist
in low titer for up to 1 year. EBV IgG VCA antibodies rise later than the IgM
VCA antibodies but remain elevated with variable titers for life
Treatment:
1. Rest for about one month, analgesics, gargles.
2. Corticosteroids may be used to reduce swelling of the throat and tonsils
3. Antibiotics may be used to guard against secondary bacterial infections, but avoid ampicillin
that proven to produce skin rash in such cases.

Measles
It is a viral infection and serious particularly in young due to possible complications.
Membranous pharyngitis may occurs.
Symptoms: The prodroma stage lasts for 3-4 days with severe coryza (Conjunctivitis, nasal catarrh,
diarrhea, and vomiting) and laryngitis (laryngeal croup)
Signs:
1. Prodroma stage: Koplik's spots (small white spots surrounded by an area of erythema) o the buccal
mucosa opposite the molar area. This stage is followed by:
2. Typical measles rash: (behind the auricles, on the face, and trunk) and fading of the Koplik's spots.
Complications:
1. Acute necrotizing otitis media
2. Bronchitis, pneumonia

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Treatment:
1. Supportive treatment
2. Gamma globulin may be given.
3. Antibiotics may minimize the complications.

Chickenpox
It is a varicella virus infection infection (this virus causes chickenpox if it affects children, and
causes herpes zoster if it affects adults).
The lesion may affect buccal and pharyngeal mucosa.
Clinical picture:
1. Short prodroma: malaise and fevr, followed by
2. Typical chickenpox rash: macules (red spot) or maculopapules. Centripetal in distribution
(Trunk is more). The eruption occurs over a period of 2-3 days so fresh lesions appear while
the older ones become superficial vesicles or pustules (pleomorphic ie different stages at the
same time). Usually the have no permanent effects as they are superficial.
Treatment:
1. Supportive treatment: analgesic antipyretics
2. Local soothing paints.
Herpes
Herpes Simplex:
It may occur in pharynx giving rise to small vesicles that rupture and form superficial painful ulcers. They
are commonly seen in the hard palate round the palatal gingival especially when teeth are present. HSV
pharyngitis presents with red swollen tonsils that may have aphthous ulcers on their surfaces. Herpetic
gingival stomatitis, herpes labialis, and hypopharyngeal and epiglottic lesions may be observed.
Herpes Zoster:
It occasionally affects the pharynx in the distribution of the 9th and 10th cranial nerves. Vesicles appear
unilaterally and intensely painful.

Acquired Immuno Deficiency Syndrome (AIDS)

Causative organism: Human Immuno-deficiency Virus (HIV). It binds to T lymphocytes
causing impaired immunity.
Transmission: Sexual contact, and parentral injections.

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Clinical Picture:
1. General: Poor general condition.
2. Local:
a.
b.
c.
d.

Hypertrophy of nasopharyngeal tonsils (Adenoids)

Recurrent severe candidiasis, viral pharyngitis, and aphthous ulcers
Hairy leukoplakia: White mucosal patches.
Kaposi's sarcoma: Red plaque or nodule. It is a malignant mesenchymal tumour. It
consists of aberrant slit-like vascular spaces surrounded by dense atypical spindle cells.

3. Enlarged deep cervical lymph nodes.

Investigation:
Enzyme-linked immuno-sorbent assay (ELISA) to detect the antibody to HIV.
Treatment:
Notification, and referral to a specialized hospital.
Moniliasis (Candidiasis or Thrush)
Causative organism: Candida albicans.
Predisposing factors:
1. Debilitating diseases (AIDS, malignancy, DM), and
2. Drugs: Cyto-toxic drugs, prolonged use of systemic broad spectrum antibiotics and steroids.
Symptoms:
1. No General symptoms.
2. Local: Mild sorethroat.
Signs:
1. Diffuse hyperemia of oral and pharyngeal mucosa, which may be covered by multiple small
milky white patches.
2. Removal of these patches reveals superficial mucosal ulcers.
Investigation:
Swab from the white patches to be examined by a direct film by using KOH showing the fungus
hyphae.

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Treatment:
1. Local antifungal: Miconazole and nystatin. Systemic anti-fungal is rarely used except in
severe extensive cases.
2. Treatment of the cause.

Agranulocytosis
Depression of the bone marrow
Aetiology:
1. Dugs: antibiotics (chloramphenicol), anti-thyroid (neomercazole), anti-mitotic
(methotrexate), and anti-emetic (chloropromazine). Irradiation.
2. Idiopathic
Clinical Pictures:
1. Recurrent infections due to leucopenia
2. Local: Sorethroat, referred otalgia, and extensive necrotic ulceration & false membrane
formation on the pharyngeal mucosa. The ulcers are not surrounded by red inflammatory
reaction.
Investigations:
1. Blood picture: marked leucopenia, particularly the granulocytes.
2. Bone marrow aspirate (sternal puncture)
Treatment:
1. Immediate withdrawal of the drug
2. Hospitalization, isolation and systemic antibiotics to prevent secondary infections, and
Vitamin B12 injection.
3. Repeated fresh blood transfusion

Acute leukemia
Aetiology:
Neoplastic proliferation of the precursors of white blood cells in bone marrow.
Clinical Picture:
1. General:
a. Pallor due to anaemia
b. Bleeding tendency due to thrombocytopenia
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c. Recurrent infection because most leucocytes are non-functiong and immature.

d. Sternal tenderness
2. Local
a. Sorethroat and referred otalgia
b. Extensive necrotic ulceration & false membrane on the pharyngeal mucosa.
c. Multiple haemorrhagic petechiae on pharyngeal mucosa.
Investigations:
1. Blood picture: marked leucopenia, with many immature blast cells, anaemia, and
thrombocytopenia.
2. Bone marrow aspirate (sternal puncture)
Treatment: Hospitalization
1.
2.
3.
4.

Chemotherapy: eg Corticosteroid, Vincristine,

Bone marrow transplantation
Isolation and systemic antibiotics to prevent secondary infections.
Repeated fresh blood transfusion

Aphthous ulcers
The commonest cause of oral and pharyngeal ulcerations
Aetiology:
1. Idiopathic
2. It may be due to vitamin deficiency, or immunological disturbance or stress
Clinical Picture:
1. Recurrent, multiple (rarely it may be single), variable-sized, painful oral and pharyngeal
ulcers which are surrounded with marked hyperaemia.
2. They heal spontaneously within 1-2 weeks
Treatment:
1. Local steroids.
2. Local cautery with silver nitrate sticks is tried to fasten healing.

Behcet's syndrome
Aetiology:
1. Idiopathic
2. It may be due to auto-immune disease
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Clinical Picture:
1. Iridocyclitis, genital ulcers, recurrent multiple small painful oral and pharyngeal ulcers,
which occur in groups.
2. Progressive sensori-neural hearing loss.
Treatment:
1. Local, and
2. Systemic steroids.

Chronic Pharyngitis
Chronic inflammation of the pharyngeal mucosa and submucosal lymphoid tissues.
Aetiology:
1. Recurrent attacks of acute pharyngitis.
2. Persistence of the predisposing factors of acute simple pharyngitis rhinitis, sinusitis,
adenoiditis, smoking, alcohol intake, etc
3. Mouth breathing due to nasal obstruction.
4. GERD "gastro-oesophageal reflux disease"
Symptoms:
1. Sense of throat irritation
2. Frequent hawking and hemming to clear the throat.
Signs:
1. Catarrhal pharyngitis: Mild hyperaemia of the pharyngeal mucosa
2. Hypertrophic pharyngitis: Enlarged lateral pharyngeal wall, and scattered small nodules on
the posterior pharyngeal wall (due to hypertrophy of the subepithelial lymphoid tissues)
leading to granular appearance.
3. Atrophic pharyngitis: associated with atrophic rhinitis with crustation. The pharyngeal
mucosa appears pale, and glazed.
Treatment:
1. Treatment of the predisposing factors.
2. Cautery of the prominent lymphoid follicles.

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Chronic superficial pharyngo-oesophagitis

"Paterson-Brown-Kelly Syndrome"
"Plummer-Vinson's Syndrome"
Definition: It is a chronic inflammation of the mucous membrane of the hypopharynx and inlet
of the oesophagus leading to: atrophic glazed mucosa, and submucosal fibrosis with the
formation of a fibrous web at the pharyngo-oesophageal junction.
Aetiology: Unknown, but may be due to iron and or vitamin deficiency.
Clinical Pictures: usually seen on female at forties.
1. Gradual progressive dysphagia.
2. General signs:
a. Pallor (anaemia)
b. Spoon-shaped nails (Koilonychia)
c. Splenomegally.
3. Local signs:
a. Angular stomatitis fissured mouth angles.
b. Glossitissmooth tongue due to loss of papillae.
c. Atrophic glazed mucosa of the hypopharynx and inlet of the oesophagus.
Investigations:
1. Blood Picture: Hypochromic anaemia.
2. Gastric secretions: Achlorohydria due to atrophy of the gastric mucosa.
Complications:
1. Stenosis at the pharyngo-oesophageal junction. Due to the fibrous web formation.
2. Malignant changes: Post-cricoid carcinoma and cancer oesophagus.
Treatment:
1. Iron and vitamin supply.
2. Repeated endoscopic dilatation when stenosis occurs.
3. Regular follow-up to detect early malignant transformation.

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Pharyngo-scleroma
Aetiology: Most commonly secondary to rhinoscleroma.
Clinical Pictures:
1. Atrophic form: Glazed, atrophic dry pharyngeal mucosa.
2. Nodular form: painless, pinkish, non-ulcerating indurated nodules.
3. Fibrotic stage: Submucosal fibrosis, and shortening of the soft palate.
Treatment: of rhinoscleroma.

Tuberculous Pharyngitis
Aetiology: Most commonly secondary to pulmonary TB.
Clinical Pictures:
1. Pallor of pharyngeal mucosa.
2. Painful shallow ulcer, with undermined edge and caseous pale yellowish floor.
Treatment: Anti-tuberculous.

Syphilitic Pharyngitis
Aetiology: Congenital or acquired.
Clinical Pictures:
1. Primary Syphilis (Chancre); very rare: single pailess indurated papule.
2. Secondary Syphilis: hyperaemia of the pharyngeal mucosa with multiple painless white
mucous patches. These patches may ulcerate forming snail track ulcers.
3. Tertiary Syphilis (Gumma): single or multiple painless pinkish rubbery ulcerating swellings.
The ulcers have deep punched-out edges and necrotic dirty yellow floor (wash-leather
appreance).
Treatment: Anti-syphilitic.

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Ulcers of the Pharynx

(Oropharyngeal Ulcers)
Traumatic Ulcers:
FB, Caustics, burns, rough teeth, ill-fitted dentures: Superficial, serrated edge.
Inflammatory Ulcers:
1. Acute non specific:
a. Dyspeptic ulcers: yellowish, painful, shallow, recurrent ulcers
2. Acute specific:
a.
b.
c.
d.

Viral: Herpes (simplex, zoster), Measles (Koplik's spots)

Diphtheria
Vincent's angina: deep punched out, necrotic base
Fungal ulcers (moniliasis)

3. Chronic specific:
a. Syphilis: deep punched-out edges
b. TB: bluish cyanotic undermined edges
Pharyngeal Ulcers associated with systemic diseases:
1.
2.
3.
4.
5.

Blood diseases: acute leukaemia,

Skin disease: pemphigus and lichen planus
Deficiency disease:Vit C deficiency (Scurvy)
Drug intoxication: Lead, mercury, and anti-depressants
Diseases of unknown aetiology: Recurrent aphthous ulcers, Behcet's disease.

Malignant Ulcers: everted edge, indurated wide base

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Acute Tonsillitis
Definitions
An acute inflammation of the palatine tonsils and the surrounding pharyngeal mucosa.
The inflammation usually extends to the adenoids and the lingual tonsils; therefore, the term
pharyngitis, pharyngo-tonsillitis, and adenotonsillitis may be used interchangeably.
Age: Tonsillitis most often occurs in children:
The commonest age is 5-6 years of age, however (rarely younger than 2 years).
Streptococcus tonsillitis typically occurs in children aged 5-15 years.
Causes: : Most episodes are caused by viruses. Bacteria cause 15-30%
1. Viral: HSV, EBV, Adenovirus, RSV, Rhinovirus, influenza, and para-influenza
2. Bacteria: GABHS causes most bacterial tonsillitis. Other bacteria includes, Streptococcus
pneumoniae., Staphylocossus., Haemophilus influenza.
Clinical Pictures:
Symptoms: Acute onset of:
1. Fever, headache, malaise, sore throat, foul breath,
2. Dysphagia (difficult swallowing), Odynophagia (painful swallowing), Otalgia, Arthralgia,
and Myalgia.
3. Airway obstruction may manifest as mouth breathing, snoring, sleep apnea, and voice change
(thicker voice) result from obstructive tonsillar enlargement.
Signs:
1. Fever may reach 40C with proportionate tachycardia. Febrile convulsions may occur.
2. Clinical forms: usually acute tonsillitis presents in on of the following forms:
a. Acute catarrhal tonsillitis: congestion of the tonsils and surrounding mucosa with little or
no enlargement of the tonsils.
b. Acute follicular tonsillitis: whitish yellow spots on the red inflamed surface.
c. Acute parenchymatous tonsillitis: uniformly enlarged and congested tonsils (phlegmon)
d. Acute membranous tonsillitis: exudates coalesce to form a confluent membrane over the
surface.
3. Enlarge tender jugulodigastric lymph nodes and neck stiffness.

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Fate:
1. Symptoms usually resolve in 3-4 days but may last up to 2 weeks despite adequate therapy.
2. Recurrent tonsillitis: 7 infections in 1 year, 5 infections in 2 consecutive years, or 3 infections
each year for 3 years consecutively.
3. Chronic tonsillitis:chronic sore throat, halitosis, persistent tender cervical nodes.
Complications:
1. Local:
a. Chronic tonsillitis (chronicity may be due to inadequate antibiotic, or virulent organism)
b. Suppuration around the pharynx: peritonsillar abscess, parapharyngeal abscess, and retropharyngeal abscess.
c. Descending infection: acute otitis media, laryngitis, bronchitis, and bronchopneumonia.
2. Systemic: (Ag-Ab reaction to GABHS):
a. Rheumatic fever: arthritis, carditis, chorea, etc
a. Acute glomerulo-nephritis.
b. Subacute bacterial endocarditis.
Differential Diagnosis: membrane on tonsils
Investigation:
1.
2.
3.
4.

Throat swab from the tonsil for culture and antibiotic sensitivity.
Blood picture: leucocytosis.
High ESR.
Elevated ASO titre.

Treatment:
1. Rest, fluids, analgesics, and antipyretic.
2. Antibiotics
3. Gargles. Lozenges containing antibiotics are not recommended as they encourage growth of
monilia.

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Differential Diagnosis of Acute Tonsillitis

Differential Diagnosis of membrane on tonsils
Differential Diagnosis of membrane on pharynx
1. Infectious Mononucleosis:
Consider infectious mononucleosis (MN) due to EBV in an adolescent or younger child with
acute tonsillitis, particularly when tender cervical, axillary, and/or inguinal nodes; splenomegaly;
severe lethargy, malaise, Constant fatigue; and low-grade fever accompany acute tonsillitis.
a. A grey membrane may cover tonsils (usually bilateral). This membrane can be removed
without bleeding.
b. Palatal mucosal petechiae of the hard palate may be observed.
c. Monocytosis, lymphocytosis with atypical lymphocytes.
d. Heterophile antibody test or monospot test or Paul-Bunnell's test.

2. Scarlet fever:
a. Characteristic rash appears within the first two days of onset, mainly on trunk and limbs,
but rarely of the face.
b. The face is flushed with ring area of cirumoral pallor
c. Congested pharynx, yellowish exudate on the tonsils that can be wiped easily.
d. Strawberry and cream tongue (yellowish tongue coat through which the papillae
projects). Later the coat disappear leaving a strawberry tongue.

3. Vincent's angina:
a. Marked foetor (Halitosis)
b. Deep punched out ulcer covered by dirty grayish false membrane (usually unilateral).
c. Swab from the membrane to be examined by a direct film by using KOH for the
causative organisms.

4. Diphtheria:

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5. Acute membranous Tonsillitis:

Diphtheria
Organism

Corynebacterium Diphtheriae

Age

Children (school age is the

commonest)
Insidious
Toxic Pale
38-38.5 C

Onset
General Look
Temperature
Pulse

Membrane

Cervical LN

Feeble, weak, and rapid,

asynchronous with
temperature.
Usually unilateral, exceeds
tonsil margin, adherent
leaving bleeding raw surface
when removed (slough): false
Bull's neck (marked
enlargement), unilateral or
bilateral.

Acute membranous
Tonsillitis
Commonly viral, Bacteria (1530%) GABHS (the commonest)
Any age but mostly children
Rapid
Flushed irritable
May reach 40.5 C Febrile
convulsion may occur
Full, bounding, and rapid,
synchronous with
temperature.
Usually bilateral, limited to
the tonsils, non-adherent,
removed easily without
bleeding (exudates): true
Moderate enlargement,
usually bilateral.

6. Moniliasis:
Mild sorethroat, diffuse hyperemia of oral and pharyngeal mucosa, which may be covered by
multiple small milky white patches. Removal of these patches reveals superficial mucosal ulcers.
Swab from the white patches to be examined by a direct film by using KOH showing the fungus
hyphae.
7. Agranulocytosis:
8. Acute leukemia:
Both Agranulocytosis, and Acute leukemia are charaterized by necrotic ulcerations, and false
membrane formation on the mouth, pharyngeal mucosa, and tonsils without surrounding
inflammatory exudates.
Blood picture: marked leucopenia, particularly the granulocytes (Agranulocytosis). Marked
leucopenia, with many immature blast cells, anaemia, and thrombocytopenia (Acute leukemia).
9. Traumatic ulcer
10. Ulcerative stomatitis
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Chronic tonsillitis
Aetiology: Recurrent acute attacks with inadequate antibiotic.
Symptoms:
1.
2.
3.
4.

Persistent sore throat with frequent hawking, and hemming.

Foeter oris (Halitosis) due to accumulation of pus and food debris in the crypts.
Dysphagia, snoring, and obstructive sleep apnea: Chronic hypertrophic tonsillitis.
Septic focus: anorexia, arthralgia , and myalgia.

Signs of chronicity:
1.
2.
3.
4.
5.

Inequality of size.
Irregularity of shape.
Persistent congestion of the anterior pillar.
Pus comes from crypts on pressing the tonsils
Persistent tender cervical nodes (JDLN).

Complications:
1. Local infection: acute otitis media, sinusitis, laryngitis, bronchitis.
2. Systemic: (Ag-Ab reaction to GABHS):
a. Rheumatic fever: arthritis, carditis, chorea, etc
b. Acute glomerulo-nephritis.
c. Subacute bacterial endocarditis.
Treatment: Tonsillectomy.

Tonsillectomy
Definition:
Surgical excision of the palatine tonsils. It is still an extremely common operation and
considered the most common major surgical procedure performed in children.
Indications: Otolaryngology textbooks list a variety of indications for tonsillectomy. The
American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) publishes clinical
indicators for surgical procedures as follows:

185

Absolute indications:
1. Enlarged tonsils that cause upper airway obstruction, severe dysphagia, sleep disorders, or
cardiopulmonary complications
2. Peritonsillar abscess that is unresponsive to medical management and drainage documented
by surgeon, unless surgery is performed during acute stage
3. Tonsillitis resulting in febrile convulsions
4. Tonsils requiring biopsy to define tissue pathology
Relative indications:
1. Three or more tonsil infections per year despite adequate medical therapy
2. Persistent foul taste or breath due to chronic tonsillitis that is not responsive to medical
therapy
3. Chronic or recurrent tonsillitis in a streptococcal carrier not responding to beta-lactamaseresistant antibiotics
4. Unilateral tonsil hypertrophy that is presumed neoplastic
NB: Other indications not documented by (AAO-HNS):
1.
2.
3.
4.

Impacted FB in the tonsil

Diphtheria carrier
TB cervical lymphadenitis
As a step for other operations:
a. UPPP
b. IX neurectomy in IX neuralgia
c. Fracture, and excision of the elongated styloid process (Eagle's syndrome)

Contraindications:
Absolute contraindications:
Bleeding diathesis: Haemophilia, purpura, leukaemia
Relative contraindications:
1.
2.
3.
4.

Poor anesthetic risk or uncontrolled medical illness: DM, HTN, Anemia

Acute infection: Acute tonsillitis, or URTI.
Active systemic disease: Rheumatic fever, pulmonary TB
Coagulation defect:
a. Drugs: Salicylates, NSAIDs, anticoagulants.
b. Menstruation.
5. Epidemics of poliomyelitis.
6. Children under 3 years old.

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NB: Enlarged tonsils interfering with airway and deglutition, in a child with purpura, or
haemophilia. What can you do?
Complications:
1. Anaesthesia:
a. Idiosyncracy or overdosage,
b. Prolonged succinyl choline apnea
c. Injury of teeth, pharynx, or larynx.
d. Aspiration: blood or vomitus
e. Laryngeal and bronchial spasam
f. Respiratory and cardiac arrest
2. Haemorrhage:
Primary: During operation.
a. Causes: Improper selection of patient, Incompetent surgeon.
b. Treatment: Haemostasis of the bleeding BV (ligation or diathermy), removal of remnants.
Reactionary: During first 24 hours after operation.
a. Causes: slipped ligature or dislodged clot, or regaining the blood pressure that may open
collapsed BV.
b. Treatment: Readmission to the theatre for haemostasis of the bleeding BV (ligation or
diathermy)
Secondary: During 3rd -10th day after operation.
a. Causes: Secondary infection.
b. Treatment: Antibiotics, compression of the tonsillar bed by a gauze pack impregnated
with antibiotic ointement, and kept in place by suturing the pillars. The tonsillar bed is
soft and friabale from infection and can not withstand sutruring or ligation.
NB: in severe blood loss.
a. Blood transfusion is mandatory.
b. External carotid ligation may be need if the bleeding is uncontrolled.
3. Respiratory complications:
Laryngeal obstruction:
a. Intubation oedema
b. Extubation spasm
c. Falling back of the tongue
d. Inhaled FB: cotton, blood clot, vomitus.
Bronchial obstruction (atelectasis): Inhaled FB: cotton, blood clot, vomitus.
Bronchopneumonia:
4. Injury: Teeth, palate, pharynx.
5. Infection: OM, DNS infection, and bacteraemia that may activate rheumatic lesions and
cause subacute bacterial endocarditis.
6. Incomplete removal:

187

Adenoids
Definition: Hypertrophy of the nasopharyngeal tonsil sufficient to obstruct nasal respiration. It
has no capsule and is covered by pseudostratified columnar ciliated epithelium.
Aetiology:
1. Physiological
2. Recurrent URTI
Age: It occurs in children between 2 to 8 years
Symptoms: are largely due to persistent efforts at nasal breathing
1. Nasal:
a. Nasal obstruction: mouth breathing, snoring, nasal tone of speech (rhinolalai clausa) and
noisy breathing.
b. Nasal discharge: mucoid or mucopurulent.
c. Epistaxis: due to congestion that may result from stasis of secretions.
2. Aural:
a. Deafness due to Eustachian tube obstruction causing secretory otitis media
b. Repeated attacks of acute otitis media
Presentations:
1. In Infants: difficult suckling
2. In children: sinusitis or retardation in school due to deafness
Signs:
1. Nose: Full of mucoid or mucopurulent discharge.
2. Nasopharynx:
a. Adenoid mass is seen by posterior rhinoscopy, and telescope (digital palpation was used
in the past)
b. A gummy egg-white secretion is seen behind the palate
3. Ear:
a. Retracted drum or secretory otitis media,
b. Conductive deafness

188

Complications:
A. Of obstruction:
I. Adenoid Facies ( Idiot Look): dull apathic child with the following look:
1.
a.
b.
c.
2.
a.
b.
c.
d.
e.
3.

Nose:
Narrow pinched nostrils,
Inactive atrophic alae nasi
Flat naso-labial fold
Mouth:
Open mouth,
Short upper lip.
Overcrowded protruding upper incisors,
High arche palate.
Receding mandible and enlarged lower lip
Chest:

a. Retracted lower costal margin ( Harrison's sulcus)

b. Pigeon chest (Tapering anteriorly)
II. Obstructive Sleep Apnea: see later
B. Of Infection:
1.
2.
3.
4.
5.
6.

Nose: Rhinitis and sinusitis

Mouth: Dryness, pyorrhea, and caries.
Ear: Otitis Mesia
Pharyngitis, laryngitis, and bronchitis.
Gastro-intestinal disturbances.
Malaise and physical fatigue
C. Reflex:

1. Nocturnal enuresis.
2. Laryngismus stridulous.
3. Irritative choking cough.
Investigations: Plain X-ray: Lateral view for the nasopharynx shows the soft tissue shadow
narrowing the air column.
Treatment: Adenoidectomy

189

Adenoidectomy
Definition:Curettage of the hypertrophied nasopharyngel tonsil.
Indications: Adenoids causing symptoms, or complications.
Contraindications: Same as tonsillectomy + Cleft palate
Complications: Same as tonsillectomy +
1. Injury of pharyngeal orifice of the ET may occour, and
2. Injury of the cervical spine may occur if the head is hyperextended during curettage of
adenoids.
3. Incomplete removal is a common cause of haemorrhage
4. Diathermy is the effective way of haemostasis, as there is no space for suturing or ligation of
the bleeding BV.
Suppuration related to the Pharynx
Peritonsillar abscess (PTA) (Quinsy)
Definition: Collection of pus in the peritonsillar space.
Peritonsillar space is bounded by the tonsil medially and the superior constrictor laterally. The
anterior and posterior tonsillar pillars form the remaining borders.
Incidence:
1. Peritonsillar abscesses are the most common deep neck space abscess.
2. It usually affects young adults although acute tonsillitis is a disease of children.
3. It is almost always unilateral.
Aetiology:
Tonsillar infections pass through one of the crypts, and usually the crypta magna.
Clinical Pictures:
Symptoms: Individuals with peritonsillar abscesses typically exhibit:
General: Fever, headache, anorexia, and malaise.
Local:
1. Trismus (caused by inflammation of the pterygoid muscles),
2. Sever sore throat, pain becomes throbbing when pus forms.
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3. Dysphagia (difficult swallowing), odynophagia (painful swallowing), and referred otalgia,

4. Drooling, and
5. A "hot potato" voice (causeed by pharyngeal edema and trismus). The voice change with
acute tonsillitis usually is not as severe as that associated with PTA.
Signs: They demonstrate: pharyngeal swelling in soft palate above and lateral to the tonsil with:
1.
2.
3.
4.

Uvular deviation, to the opposite side causing palatal asymmetry.

Displacement of the tonsil inferiorly and medially.
Tonsillar erythema and exudates may be mild despite the presence of an abscess.
Torticollis and decreased range of motion of the neck caused by inflammation of the
paraspinal muscles
5. Enlarged tender upper deep cervical lymph nodes (JDLN).
Investigations:
Inferior pole PTA: is difficult in diagnosis, and CT scan with contrast is helpful.
Complications:
1.
2.
3.
4.

Parapharyngeal abscess.
Laryngeal oedema.
Broncho-pneumonia may occur if abscess is ruptured and pus is aspirated.
Septicaemia and pyaemia.

Differential Diagnosis:
1. Tumours (no acute symptoms)
2. Aneurysm of the carotid artery (Pulsation of the internal carotid artery)
3. Parapharyngeal abscess. See table.
Treatment:
Massive antibiotics in the peritonsillitis stage.
Once abscess forms (throbbing pain, pitting palatal oedema, pointing or pus on aspiration)
incision and drainage are mandatory.
Surface anaesthesia (Xylocaine spray 10%), in sitting position, needle aspiration is done first to
be sure that it is an abscess, and not an aneurysm. Incision is the done with quinsy (or shielded)
knife, by using Hilton's method (introduce forceps closed and withdraw it open), at one of the
following points:
1. Most pointing point.
2. Midway between the last upper molar tooth and uvula base.

191

3. 1/2 cm lateral to the meeting point of: a. horizontal line at uvula base, b. vertical line along
the anterior pillar.
4. Crypta magna.
Most commonly, interval tonsillectomy is performed 4-12 weeks after resolution of the infection
to avoid recurrence. Some surgeons do abscess tonsillectomy, but this is hazardous due to
defective haemostasis, and spread of infection which may supervens in acute inflammation.
Patients who have had their tonsils removed effectively lose this space, but they can still develop
peritonsillar pathology.
Parapharyngeal Abscess
Definition: Collection of pus in the parapharyngeal (lateral pharyngeal) space.
Parapharyngeal space is an inverted pyramidal area.
a. The inferior limitation is the lesser horn of the hyoid bone.
b. The superior margin is the skull base.
c. Its medial boundary is the visceral layer of the deep cervical fascia (buccopharyngeal fascia)
around the superior constrictor muscle.
d. Laterally, the space is defined by the deep cervical fascia (superficial layer) that overlies the
mandible, medial pterygoids, and parotid.
The parapharyngeal space is subdivided into two compartments the styloid process.
1. Prestyloid (anterior) compartment: contains internal maxillary artery, inferior alveolar nerve,
lingual nerve, and auriculotemporal.
2. Poststyloid (posterior) compartment: contains the carotid sheath (carotid artery, internal
jugular vein, vagus nerve) and the glossopharyngeal, accessory nerve, hypoglossal nerves,
sympathetic chain, and lymphatics.
Aetiology:
Infections can arise from the tonsils (tonsillitis, PTA, tonsillectomy), pharynx, dentition,
salivary glands, nasal infections, or Bezold abscess (ie, mastoid abscess).
NB: The parapharyngeal space connects posteromedially with the retropharyngeal space. The
carotid sheath courses through this space into the chest.
Clinical Pictures:
Beck's Triad
1. Medial displacement of the lateral pharyngeal wall and tonsil is a hallmark of a
parapharyngeal space infection.
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2. Trismus (inflammation of the pterygoid muscles), drooling, dysphagia, and odynophagia also
are observed commonly.
3. External neck swelling: tender, firm swelling just below the angle of the mandible
Differential diagnosis: The most consistent signs of parapharyngeal space infection are fever,
leucocytosis, and tenderness. This can differentiate infections from any other lesions like
tumours arising from the parapharyngeal space (schwannoma, mixed salivary tumour of the deep
lobe of parotid gland).
Beck, 1947 compare peritonsillar and parapharyngeal spaces infection as follow:

Trismus
Parotid involvement

Peritonsillar
Not as pronounced
Minimal

Sepsis (Fever)
Soft palate
Tonsil

Low-grade fever
Edematous
Acute exudate

Parapharyngeal
Marked
More commonly affected
(deep lobe)
More common
Often normal
Often normal

Complications:
1. Spread of infection:
a. Upwards causing meningitis.
b. Downwards along the carotid sheath, causing mediastinitis and empyema.
c. Posteriorly to paraspinal muscles, causing torticollis and decreased range of motion of the
neck.
2. Spread of infection to compromise the contents of the parapharyngeal space:
a. Great vessels: leading to internal jugular vein thrombosis, and subsequent pulmonary
emboli, carotid artery thrombosis, and fatal haemorrhage, due to erosion of the carotid
vessles.
b. Cranial nerves: hoarseness due to vagal involvement.
c. Horner syndrome from involvement of the cervical sympathetic chain
3. PPA alone may cause airway obstruction at the level of the pharynx
4. Septicaemia, and pyaemia.
Investigations:
1. CT and MRI for pharynx and neck are diagnostic.
2. Leucocytosis.
Treatment:
1. Massive antibiotic.
2. Incision and drainage of the abscess along the anterior border of the sternomastoid muscle at
the level of the hyoid bone

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Acute Retropharyngeal Abscess

Definition: Collection of pus in the retropharyngeal space.
It lies between the visceral layer of the deep cervical fascia (buccopharyngeal fascia) around the
pharyngeal constrictor muscle, and the alar division of the deep cervical fascia posteriorly. It
extends from the skull base to the tracheal bifurcation around T2 where the visceral and alar
divisions strongly fused.
It primarily contains retropharyngeal lymphatics (one lymph node in each space: lymph node of
Henle). Retropharyngeal lymph nodes tend to regress by about age 5 years, making infection in
this space much more common in children than adults.
Retropharyngeal space: is sometimes considered a third medial compartment within the
parapharyngeal space because the 2 communicate laterally.
Aetiology:
1. Infection may enter this space directly, as with traumatic perforations of the posterior
pharyngeal wall or esophagus, or indirectly, from the parapharyngeal space.
2. More than 60% of retropharyngeal abscesses in children are caused by URIs,
3. Other common sources of infection in the retropharyngeal space are the nose, adenoids
(infections after adenoidectomy), nasopharynx, and sinuses.
Clinical Pictures:
Symptoms:
1.
2.
3.
4.

Sever sore throat, pain becomes throbbing when pus forms.

Dysphagia (difficult swallowing), odynophagia (painful swalloing), and referred otalgia,
Drooling, and
Dyspnea from nasal obstruction (pus behind the nasopharynx), laryngeal obstruction and
stridor (pus behind the laryngopharynx).

Signs:
1. Abscess in the space may push forward, occluding the airway at the level of the pharynx.
2. It may appear as anterior displacement of one or both sides of the posterior pharyngeal wall
because of involvement of lymph nodes, which are distributed lateral to the midline fascial
raphe.
3. Torticollis and decreased range of motion of the neck caused by inflammation of the
paraspinal muscles. The patient flex his neck towards the abscess side to avoid muscle stretch
that may press on the abscess ensuing pain.
4. The most consistent signs of a retropharyngeal space infection are fever, leucocytosis, and
tenderness. This can differentiate infections from any other lesions like tumours arising from
the retropharyngeal space.
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Complications:
1. Infections of this space may drain into the prevertebral space and follow that space into the
chest. Mediastinitis and empyema ensue.
2. Bronchopneumonia due to rupture of the abscess, and aspiration of pus.
3. RPA alone may cause airway obstruction at the level of the pharynx
4. Septicaemia, and pyaemia.
Investigations:
1. Radiological: Plain x-ray, and CT of the pharynx and neck showing widening of the prevertebral space with normal vertebral bodies.
2. Leucocytosis.
Treatment:
1. Massive antibiotic.
2. Incision and drainage of the abscess along the posterior pharyngeal wall through an intra-oral
approach with the patient in trendlenberg's position (supine with head lower than the chest to
avoid aspiration of pus).
3. Tracheostomy if required.
Chronic Retropharyngeal Abscess
(Cold abscess of the pre-vertebral space or Pott's disease of the spines)
Pre-vertebral space:
The prevertebral space is located anterior to the vertebral bodies and posterior to the prevertebral
division of the deep layer of the deep cervical fascia. It lies just posterior to the danger space (see
below). Laterally, it is bounded by the fusion of the prevertebral fascia with the transverse
processes of the vertebral bodies. It extends from the skull base to the coccyx.
Danger space:
The danger space is immediately posterior to the retropharyngeal space and immediately anterior
to the pre-vertebral space, between the alar and pre-vertebral divisions of the deep layer of the
deep cervical fascia. It extends from the skull base to the posterior mediastinum and diaphragm.
Laterally, it is limited by the fusion of the alar and pre-vertebral division with the transverse
processes of the vertebrae. Some authors consider the danger space a component of the prevertebral space.
Aetiology:
TB caries of the cervical vertebrae (Pott's disease). It starts as a cold abscess in the pre-vertebral
space. It reaches the retro-pharyngeal space when the abscess ruptures through the pre-vertebral
fascia.
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Clinical Pictures: Adults showing:

Symptoms: TB toxaemia: night fever, night sweat, anorexia, and loss of weight.
1. Mild sore throat.
2. Limited painful neck movements.
Signs:
1. Abscess in the space may push forward, occluding the airway at the level of the pharynx.
2. It may appear as midline anterior displacement of the posterior pharyngeal wall.
3. Tender cervical spines.
Investigations:
Radiological: Plain x-ray, and CT of the pharynx and neck showing widening of the prevertebral space with destruction of the vertebral bodies.
Treatment:
1. Anti-tuberculous chemotherapy.
2. Drainage of the abscess by a vertical cervical incision along the posterior border of the
sternomastoid muscle (No intra-oral approach to avoid aspiration of TB materials and bacilli
into the lung) .
3. Orthopedic management of the cervical spines.
Ludwig's Angina
Diffuse cellulites of the mouth floor. Suppuration rarely occurs.
Mouth floor is a connective tissue space, subdivided by the mylo-hyoid muscle into sublingual
space above it, and submandibular space below it.
Aetiology:
Infection of this space may come from:
1. Lower teeth infection or extraction(commonest): The roots of the second and third molar
teeth reach downward to the level of the attachment of the mylohyoid muscle, and usually
below it, while most of those of the first molar teeth, and usually all of those anterior to this,
are located above this level
2. Mandible, tongue, submandibular or sublingual salivary glands.
3. Acute pharyngitis.

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Clinical Pictures:
Symptoms: Individuals with Ludwig's angina typically exhibit:
General: Fever, headache, anorexia, and malaise.
Local:
1.
2.
3.
4.
5.

Sever throat Pain.

Sever dysphagia (difficult swallowing) and odynophagia (painful swalloing), referred otalgia,
Drooling, and
Trismus (caused by inflammation of the pterygoid muscles),
Muffled voice (causeed by oropharyngeal edema and trismus).

Signs: They demonstrate:

1. A swelling in the floor of the mouth, with extreme hardness, "brawny", "indurated" swelling
pushing the tongue upwards and backwards, obstructing the food and air passages.
2. Tender indurated brawny swelling of the submandibular regions. Suppuration rarely occurs.
Complications:
Spread of infections:
1.
2.
3.
4.

to the lateral pharyngeal space and then may enter

the retropharyngeal space and even descend to
the mediastinum.
Laryngeal oedema: spread of infection into the larynx.

Death from Ludwig's angina occurs as a result of:

1.
2.
3.
4.

Suffocation due to edema of the mouth, tongue, and the glottis,

Mediastinitis due to spread, or
Septicemia or
Pneumonia

Treatment:
1. Massive antibiotics. Bed rest in semi-sitting position to avoid airway obstruction.
2. Incision and drainage : A horizontal submandibular incision. To relieve the tension and
resolve the oedema, even if no pus comes out.
3. Tracheostomy if required.

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