ENT NOTES

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 OTOLOGY
The Physiology Of Hearing
Sound is a waveform of mechanical energy, which exerts pressure throughout the medium in
which it is transmitted. Hearing (the perception of sound) is essential for speech and language
development, and is thus a prime prerequisite for communication.
The pinna functions as a funnel that collects sound and transmits it to the external auditory canal.
We can tell the direction of sound by the fact that sound will tend to be louder in the ipsilateral ear
and will also arrive earlier at that ear. The external auditory canal amplifies sound in the frequency
range 3-4 kHz. This is due to the resonating properties of the external auditory canal.
For hearing to occur, sound needs to pass from air in the external canal into the fluid medium of
the cochlea, wherein lie the pressure sensors – the hair cells. If sound should pass directly into the
cochlea, over 99% of sound energy would be reflected at the interface. To match the impedance
(resistance to sound transmission) of air to that of the cochlear fluid, we need an intervening
mechanism for sound transmission. The tympanic membrane and the ossicular chain (malleus,
incus and stapes) are responsible for "impedance matching”.
A much greater pressure is required to transmit sound through liquid as compared to transmission
by air. Pressure equals force divided by area. By the Hydraulic Principle, the same force that is
exerted on the tympanic membrane, when exerted on the footplate of the stapes, will exert a
pressure at the footplate that is 13 times greater than that at the tympanic membrane. This occurs
because the ratio of the functional area of the tympanic membrane to that of the footplate of the
stapes is 13 to 1.
The pressure at the footplate of the stapes is further increased by the mechanical advantage gained
by the lever system of the malleus and the incus. The relative lengths of the handle of the malleus
to that of the long process of the incus is 1.3 to 1.0.
The tympanic membrane and ossicular chain therefore increase the pressure at the footplate of the
stapes 18 fold (1.3 times 14).
A requirement for maximum sensitivity of the tympanic membrane to sound pressure is equality of
pressure in the external auditory canal to that in the tympanic cavity. The Eustachian tube is
responsible for maintaining the middle ear pressure close to atmospheric pressure. This ensures
that energy is not wasted in overcoming any pressure differential across the tympanic membrane.
The middle ear is a balanced system i.e. it moves about a fulcrum and the moments about that
fulcrum are equal. The ossicles are suspended in the tympanic cavity by very tenuous ligaments.
These provide minimal frictional force and resistance to movement.
Sound pressure that reaches the inner ear produces travelling waves in the liquid of the cochlear
duct and eventual movement of the basilar membrane. The sensitive receptor hair cells lie in the
organ of Corti on the basilar membrane. We can identify the frequency of sound heard by the
place on the basilar membrane that best responds (resonates) to that sound (Place Theory). High
frequencies mainly stimulate the basal turn of the cochlea.
The intensity of sound is predominantly detected by the rate of production of action potentials in
the auditory nerve.

Hearing loss
Hearing loss can be broadly classified into conductive and sensorineural hearing loss. Conductive
hearing loss occurs when conditions of the external ear or middle ear prevent efficient transfer of
sound pressure to the inner ear. Conditions affecting the inner ear or the auditory nerve will lead
to sensorineural hearing loss.

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 Common causes of conductive hearing Common causes of sensorineural
loss hearing loss

a) Otitis media with effusion--- a) Presbycusis---usually secondary to

commonest cause in children ischaemia of the Organ of Corti
b) Noise induced hearing loss
b) Wax impaction--- common in all age
groups

c) Acute and chronic otitis media c) Ototoxicity (aminoglycosides, loop

diuretics, cytotoxic agents e.g. Cisplatin,
quinolones)
d) Meningitis
d) Ossicular chain discontinuity (post
trauma or secondary to infection)

e) Otosclerosis--- Second most e) Viral infections (Measles, Mumps,

common cause in Caucasian adults Herpes Zoster etc)
(after wax impaction)

Presbycusis – progressive, bilaterally symmetrical perceptive hearing loss occurring with age
usually at the higher frequencies

Sensorineural Hearing Loss in Childhood

a) 50%--- genetic origin ---majority autosomal recessive
e.g.
 Usher's Syndrome ---Sensorineural hearing loss (SNHL) and retinitis pigmentosa
 Pendred's Syndrome (SNHL and hypothyroidism)

b) 25-30%---Environmental factors
 Rubella and other members of TORCHS (toxoplasma, rubella, cytomegalovirus, herpes, HIV,
hepatitis, and syphilis) group
 Meningitis
 Kernicterus
 Hypoxia perinatally

c) Idiopathic (Unknown cause)

Audiological Testing

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a) Free field testing using whispered voice, conversational voice and loud voice
b) Tuning fork tests –Rinne's, Weber and Absolute Bone Conduction Test

50% of patients with a conductive hearing loss of 20 dB will have a negative Rinne's (bone
conduction better than air conduction). 90% of patients with a 40 dB conductive hearing loss will
have a negative Rinne's. A negative Rinne's test therefore usually indicates a substantial conductive
hearing loss. A false negative Rinne's test is associated with profound hearing loss. In such cases,
no significant perception of sound occurs when the tuning fork is placed beside the ipsilateral ear.
When the tuning fork is placed on the ipsilateral mastoid, bone conduction allows detection of the
sound by the opposite cochlea.

In the Weber's test, sound typically lateralizes to the ear with a conductive hearing loss. In a patient
with a false negative Rinne's test, sound lateralizes to the good ear.

The Absolute Bone Conduction Test is useful in the bilateral, equal sensorineural loss, when the
Rinne would be positive and the Weber not lateralized. Here a doctor (who has normal hearing)
compares his bone conduction with the patient's.

c) Pure Tone Audiometry

Here the patient's Air and Bone Conduction are tested for different frequencies in a sound proof
environment. The threshold for each frequency is charted. One can detect and quantify both
conductive and sensorineural hearing loss. Children 2-4 years will not be suitable for this test.
Instead Behavioural Audiometry is used. In the latter test, sound is introduced while the child is
occupied playing and one expects alteration of behaviour if the sound is heard.

d) Impedance Audiometry used to elucidate:

 Middle Ear Pressure
 Compliance of Conductive system
 Acoustic Reflexes, indirectly giving an idea of the threshold of hearing
 Type of lesion in sensorineural loss
Patients with middle ear effusions usually have Type B tympanograms (flat tracings) while those
with negative middle ear pressures will have Type C curves (peak in the negative range)

e) Otoacoustic emissions test

This is a very important objective tool in neonatal hearing screening. The test is quickly
administered and it does not require highly trained personnel to operate and interpret the test.
Sound is introduced into the ear and sound emanating from the cochlea is detected in patients with
hearing better than 30 dB.

f) Auditory Brain Stem Response or Evoked Response Audiometry

This is another objective test that is useful in neonates, in infants and in people who cannot or will
not cooperate for hearing tests (malingerers) .An auditory stimulus is introduced into the ear and
this will result in electrical activity sequentially in the cochlear nerve, the cochlear nucleus, the
superior olivary nucleus, the lateral lemniscus and the inferior colliculus. The test is repeated while
a computer subtracts the background EEG activity leaving behind the response to the sound
stimulus. Thus one can objectively follow the stimulus throughout the auditory system, and can
detect problems therein.

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 VERTIGO AND THE PHYSIOLOGY OF BALANCE
The maintenance of equilibrium at rest and in motion is achieved by a complex interaction of
peripheral receptors and the central coordinating areas in the brain. The whole balance mechanism
serves to orient the individual in space.

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 The peripheral sensory systems are
1. Vestibular system (semicircular canals, utricle and saccule)
2. Visual Pathway
3. Proprioceptive system

Central coordination occurs in the cerebellum and the vestibular nuclei. There are also important
inputs from the cerebral cortex, limbic system, red nucleus and substantia nigra that modulate
these centres. Usually a positive activity in one side of the body is balanced by a negative activity
on the contralateral side. Disequilibrium occurs when the inputs from one system does not match
with those from the other systems.
The cerebellum has a mainly dampening effect on vestibular nuclear activity, inhibiting excessive
electrical activity of the vestibular nuclei. The midbrain nuclei have a less negative effect and can be
regarded as a finer adjuster of vestibular nuclear activity. The cerebrum has a positive or negative
effect on vestibular nuclear activity and maybe under voluntary control.
Vertigo is an abnormal sensation of rotation relative to one's environment or “a hallucination
of movement”. Vertigo is specifically associated with the disorders of vestibular system.
The vestibular receptors for the detection of angular acceleration are located in the
semicircular canals. The semicircular canals lie at right angles to each other, occupying the three
planes of space. Thus, in the semicircular canals, we have sensors to monitor circular movement in
the three planes of space. The utricle and the saccule contain receptors oriented at right angles to
each other for the detection of linear acceleration and tilt. A gelatinous matrix called the otoconial
membrane covers these receptors. Embedded in the otoconial membrane are dense calcific bodies
called, otoconia, which exert pressure on the hair cells. Since the otoconia and hair cells have
different inertia, they will move differently if there is accelerating or decelerating force acting on
them. This gives us the ability to sense linear movement with gravity or against gravity.
The vestibular nerve carries information from these receptors to the vestibular nuclei. There are
important connections between the vestibular system and the visual system via the medial
longitudinal fasciculus. This accounts for the vestibulo-ocular reflex and for nystagmus in
vestibular disorders. Patients who have disorders of the peripheral vestibular system are initially
vertiginous, nauseous (and often vomit) and sweaty. In three to four weeks significant
compensation occurs predominantly in the cerebellum so that the patient becomes much less
symptomatic.

Diagnostic pointers in the assessment of the dizzy patient

Patients should be initially classified into one of the following groups:
a) Patients with true vertigo (problem lies in the peripheral or central vestibular system)
b) Patients with syncopal sensation or actual syncope (inadequate cerebral blood flow, oxygenation,
or nutrition)
c) Miscellaneous group of patients who experience imbalance, but no syncope or vertigo. This may be
secondary to almost any medical disorder.

Peripheral vestibular disorder/ Central

vestibular disorder
Nausea, vomiting, sweating with initial attack Nausea and vomiting occurs late (often
with raised intracranial pressure)

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 Nystagmus only present when patients have Nystagmus often noted in the absence of
significant systemic symptoms systemic symptoms
Nystagmus is usually in the horizontal plane Nystagmus may occur in any plane

Nystagmus worsened by the loss of visual Nystagmus not influenced by visual

fixation fixation
Compensation occurs in three to four weeks Compensation may not occur as the lesion
is central

If one has determined by the symptoms and signs that this is a peripheral vestibular disorder, one
will next need to decide whether it is the left or right vestibular system that has been affected.

The vestibular system and the hearing mechanism are closely related. If the patient has unilateral
hearing loss it is reasonable to assume that the vestibular problem originates from the ipsilateral
side. The caloric test is a good method of testing each vestibular system individually. The
mnemonic “COWS” is useful in remembering the responses. Infusion of Cold water causes
nystagmus to the Opposite side
Infusion of Warm water causes nystagmus to the Same side.

The commonest cause of vertigo in elderly patients is vertebrobasilar ischaemia. Some of the
conditions that result in vertebrobasilar ischaemia are
 atherosclerosis,
 cervical spondylosis
 cardiac dysfunction including arrhythmias.
Benign paroxysmal positional vertigo, labyrinthitis, vestibular neuronitis, eustachian tube
dysfunction are important in all the age groups.

Menière's Disease
This disorder has stimulated much interest. It is however an uncommon cause of vertigo. It is
characterized by recurrent episodes of vertigo, sensorineural hearing loss and tinnitus. The attacks
last 1/2 hour to 12 hours and are often preceded by a sensation of aural fullness. This is a
peripheral vestibular disorder and patients usually experience significant nausea and vomiting.

The aetiology is unknown but the salient histopathologic finding is endolymphatic hydrops with
marked increase in the volume of endolymphatic fluid. It is believed that symptoms occur when
the endolymphatic compartment is so distended that Reissner's membrane ruptures. This results in
the mixing of endolymphatic and perilymphatic fluid.

In severe attacks, patients are admitted to hospital for intravenous hydration, anti-emetics and
sedation. Most patients will never need surgical intervention. Patients who have frequent, disabling
vertigo and very poor hearing in the affected ear are best managed by labyrinthectomy. This
procedure is followed by compensation within three to four weeks. If the hearing is good,
vestibular neurectomy is one useful surgical option.

Benign paroxysmal positional vertigo

This condition is thought to be due to cupulolithiasis. Calcium deposits from the otoconial
membrane become dislodged and travel in the endolymphatic fluid to the posterior semicircular

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canal. Transient vertigo is induced by certain head positions that place the posterior semicircular
canal in the dependent position.
After appropriate head positioning (Dix-Hallpike test), there is a latent period of 5-10
seconds. This is followed by vertigo and nystagmus that lasts 15-30 seconds. Nystagmus is rotary
with the fast component in the direction of the dependent ear.
Most cases of benign paroxysmal positional vertigo will resolve in 18 to 24 months. Many
cases respond well to vestibular exercises. Occasionally surgery is necessary and this entails
transection of the nerve to the posterior semicircular canal (the singular nerve).

Otitis Media and Otitis Externa

Definitions:
Acute suppurative otitis media:
Acute inflammation of the mucosal lining of the middle ear cleft [tympanic cavity,
eustachian tube and the mastoid air cell system]. The features of acute inflammation are present.

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Acute suppurative otitis media may be complicated by perforation of the tympanic membrane.
These perforations will generally heal within four weeks.

Otitis media with effusion

Presence of liquid behind an intact tympanic membrane, in the absence of the features of
acute inflammation.

Chronic suppurative otitis media:

Characterized by the presence of a persistent (> 4 weeks) perforation of the tympanic
membrane.

Otorrhoea

Otorrhoea may be secondary to a primary pathology in the external auditory canal or in the middle
ear. Base of skull fractures involving the temporal bone may present with CSF otorrhoea.

In some cases, visualization of the tympanic membrane is difficult because of exudate in the
external auditory canal. Without seeing the tympanic membrane one can often still distinguish
between acute otitis externa and acute otitis media. (Unfortunately the two sometimes co-exist)

Otitis Externa Otitis Media

Otalgia often severe. Severity of otalgia varies.
Onset of otorrhoea not associated with Otalgia markedly reduced at onset of
diminution of otalgia otorrhoea
No mucus in otorrhea Discharge is mucopurulent
Very mild hearing loss Mild to moderate hearing loss
Pressure on the tragus and movement of Pain unrelated to movement of pinna
the pinna cause significant pain

Pathogenesis of middle ear infections

The pathogenesis of middle ear infections is strongly linked to disorders of the eustachian tube.
The eustachian tube has the following functions:
 Ventilation of the middle ear
 Equalization of the pressure in the middle ear with that of atmospheric pressure
 Drainage of middle ear secretions into the nasopharynx
 Protection of the middle ear from nasopharyngeal secretions and organisms

Dysfunction of the eustachian tube is generally secondary to obstruction and or infection.

Acute suppurative otitis media and otitis media with effusion are most commonly associated with
children. Adenoidal hyperplasia is the commonest source of obstruction to the eustachian tube in
this age group. The adenoids are an important source of ascending infection into the middle ear
via the eustachian tube. Congenital cysts such as Thornwaldt's cysts can also obstruct the ostium of
the eustachian tube. In male teenagers angiofibroma is an important cause of otitis media with
effusion and severe epistaxis.
One must always be on the alert for cases of nasopharyngeal carcinoma since this tumor

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 frequently presents with otologic complaints. The nasopharyngeal carcinoma directly obstructs the
ostium of the eustachian tube but also has the effect of obstructing the lymphatic drainage of the
eustachian tube, further perpetuating the otitis media with effusion.
Infections of the nose, paranasal sinuses and the nasopharynx result in edema of the ostium
of the eustachian tube and subsequent obstruction. These infections are more common in patients
who have obstructive lesions in the nose such as nasal polyps, hypertrophied turbinates and
marked septal deviation. Allergic rhinitis and vasomotor rhinitis produce obstruction of the nose
and of the paranasal sinuses with subsequent frequent infections.
Children who attend nurseries have a high incidence of upper respiratory tract infections
and, consequently, frequent otitis media with effusion or acute suppurative otitis media.
Passive smoking impairs mucociliary function by damaging the cilia. Otitis media with
effusion occurs more frequently and is more difficult to eradicate in children who are exposed to
smoking.
Patients with cleft palate, those with cystic fibrosis and patients who are immunocompromised will
obviously get frequent ear infections.

Acute otitis media

Chronic Suppurative Otitis Media

This condition is characterized by the presence of a persistent (> 4 weeks) perforation of the
tympanic membrane.
Chronic suppurative otitis media can be divided into:
a) Cholesteatoma or squamous disease ---- presence of keratinising squamous
epithelium in the middle ear cleft.
b) Tubotympanic or mucosal disease.

Genesis of cholesteatoma

1. Retraction pocket---- commonest mechanism

The external auditory canal is lined by squamous epithelium, which extends onto the tympanic
membrane to form the external layer of the drum. Long-standing eustachian tube dysfunction can
produce persistent negative pressure in the tympanic cavity. This can result in the weakest parts of

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the tympanic membrane being pulled medially to form retraction pockets. Classically this affects
the pars flaccida (which lacks a fibrous layer) or the postero-superior aspect of the pars tensa. These
retraction pockets are lined by keratinising squamous epithelium and an accumulation of keratin
occurs if the opening of the retraction pocket is relatively small. Secondary infection in the
retraction pocket results in the production of collagenases and phosphatases that ultimately erodes
surrounding bone and ligaments.

2. Squamous epithelial growth at the edge of a perforation

In cases of long-standing perforation of the tympanic membrane, squamous epithelium can
overgrow the edge of the perforation and extend into the middle ear. This is especially likely to
occur if, in the region of the perforation, there is loss of mucosa from the medial aspect of the
tympanic membrane.

3. Implantation cholesteatoma
Squamous epithelium can be implanted by a penetrating injury to the tympanic membrane, or this
can occur during surgery.

4. Squamous Metaplasia of the middle ear mucosa

5. Congenital cholesteatoma
In this case congenital squamous epithelial rests are trapped in the middle ear.

Chronic suppurative otitis media can be active or inactive. Cholesteatoma, by its very nature, is
always considered active.

Cholesteatoma is important because of the complications associated with this disorder.

These include:
1. Hearing loss secondary to adhesions, granulation tissue, perforation of the tympanic
membrane, exudate in the middle ear, and ossicular chain discontinuity
2. Facial nerve palsy
3. Acute and chronic mastoiditis
4. Sub periosteal abscess
5. Bezold's abscess-- along the sternomastoid

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 6. Citelli's Abscess-- along the digastric muscle
7. Perilabyrinthitis and labyrinthitis
8. Gradenigo's syndrome-- lateral rectus palsy, pain in the distribution of the fifth cranial
nerve and a discharging ear. These features are noted when chronic suppurative otitis
media involves the apex of the petrous temporal bone (petrous apicitis)
9. Sigmoid sinus thrombosis which can extend into the internal jugular vein
10. Meningitis
11. Extradural abscess
12. Subdural abscess
13. Temporal lobe or cerebellar abscesses are usually secondary to chronic suppurative otitis
media
14. Benign intracranial hypertension

It is clear that cholesteatoma is a serious disorder with the risk of life-threatening complications.
Cholesteatoma is a surgical disease and all patients who are medically fit to undergo surgery
should be given this option.

Prior to surgery, an ear swab should be sent for culture and sensitivity and the condition of the ear
optimized by using
 topical ear drops,
 aural suctioning plus or minus systemic antibiotics.
The commonest organisms grown are Gram-negative organisms such as Pseudomonas and
Proteus. Often the infection is a mixed infection involving anaerobes and gram negatives. Failure to
control the ear discharge with medications should hasten rather than delay the surgical procedure .
The actual surgery is usually a form of a modified radical mastoidectomy. In this procedure, the
squamous lining in the mastoid cavity and middle ear is removed, the posterior wall of the external
auditory canal is usually removed and the external auditory canal is widened (meatoplasty). At the
end of the procedure, the mastoid cavity and middle ear can easily be visualised and cleaned
through the external auditory canal. The ear would have been converted from an "unsafe ear" to a
"safe ear". Once the cholesteatoma is controlled, the hearing mechanism can be reconstructed or a
hearing aid can be utilised.

OTITIS MEDIA WITH EFFUSION: AETIOLOGY AND MANAGEMENT IN CHILDREN

INTRODUCTION
Otitis media with effusion is defined as the presence of liquid behind an intact tympanic
membrane, without any of the symptoms or signs of acute inflammation. It is thought to be the
commonest cause of hearing loss in children. Otitis media with effusion is predominantly a disease

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of children 1-9 years old. The peak incidence is found in children 6 months to 2 years old but as the
diagnosis in this age group is difficult and the condition often asymptomatic, the peak incidence in
children attending otolaryngology clinics is in the age group 3-6 years. In many developed countries,
otitis media with effusion is the commonest indication in children for admission to hospital for
elective surgery. In these countries, sixty percent of children will experience otitis media with
effusion by the age of 2 years and 80% prior to school entry. The prevalence falls from 38 % at age 2
years to 1 % at 11 years. In Jamaica, the prevalence rate in children 5-7 years is 2 %
There is a high incidence in North American Indians and Eskimos. OME is generally thought to be
more common in Caucasians than in Blacks, even though most studies do not define the racial
composition of the study group. Males are more frequently affected than females. There is a
seasonal variation with the highest incidence in January, February and March and the lowest
incidence in August, September and October.

AETIOLOGY
The major underlying factors are related to eustachian tube dysfunction and infection. The
classic example of eustachian tube dysfunction occurs in cleft palate where the tensor palati muscle
is abnormal and thus active opening of the eustachian tube is impaired. Patients with cleft palate
also have a direct pathway for the passage of vomitus, sputum and drinks to gain access to the
pharyngeal opening of the eustachian tube. The result is secondary infection. Otitis media with
effusion is also very common in patients with a submucous cleft palate.
Obstruction to the eustachian tube can either be intrinsic or extrinsic.
In the intrinsic type, oedema and secretions associated with inflammation cause
obstruction of the eustachian tube. This occurs in upper respiratory infections. The nose, sinuses
and the adenoids can act as reservoirs for infection producing repeated intrinsic obstruction of the
eustachian tube. A distinct possibility is that the lymphatic drainage of the eustachian tube
becomes obstructed by peritubal inflammation and this causes otitis media with effusion. In the
child who is less than 7 years old, abnormal compliance of the eustachian tube, due to a relative
reduction in the amount and stiffness of the cartilage, can cause collapse of the eustachian tube
with resultant obstruction.
Extrinsic obstruction of the eustachian tube is seen in patients with adenoidal hyperplasia
or nasopharyngeal tumours that compress the eustachian tube. In patients with craniofacial
abnormalities such as Down's, Hunter's and Hurler's syndromes, there is a relative disproportion
of the adenoidal size to the nasopharyngeal space which predisposes to obstruction of the
eustachian tube. When obstruction to the eustachian tube occurs, the air in the middle ear is
gradually utilised or absorbed, leaving a vacuum. The result is transudation of fluid from the
mucosa to the tympanic cavity. The situation is much more complex than mere obstruction to the
eustachian tube.
Infection plays a significant role. Cultures of aspirates from middle ear effusions have grown
organisms in 30-60% of cases. The organisms that have been found are the same as those associated
with acute suppurative otitis media. The most frequent organisms found are Streptococcus
pneumoniae, Haemophilus influenzae, and Moraxella (Branhamella) catarrhalis. Although the
adenoids can cause obstruction of the eustachian tube, it appears that the main role of the adenoids
is as a source of sepsis. Ascending infection up the eustachian tube causes oedema and exudate
with eventual obstruction.
It is likely that otitis media with effusion and acute suppurative otitis media are different
ends of a spectrum of manifestations of obstruction and inflammation of the eustachian tube. In
patients with otitis media with effusion, the host mechanisms and the organisms have created a
balance so that a latent infection is maintained. In acute suppurative otitis media, the host

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mechanisms have been temporarily overwhelmed. It is known that otitis media with effusion can
be a sequel to acute suppurative otitis media.
In chronic otitis media with effusion, there is hyperplasia of the goblet cells and an increased
number of mucous glands in the middle ear cleft. This will tend to perpetuate the effusion.
Some patients have an inefficient mucociliary system, which predisposes them to otitis media
with effusion. These include patients with the immotile cilia syndrome, Kartagener's syndrome and
cystic fibrosis. Viral and bacterial infections can adversely alter the mucociliary system.
The role of allergy in otitis media with effusion is uncertain. A true causal relationship has not been
established. Some studies have found an increased incidence of atopic disease in children with
otitis media with effusion. The adenoids have been shown to have a large number of mast cells and
these can bind IgE with the resulting release of histamine. However, antihistamines and
decongestants have not altered the course of otitis media with effusion. This casts doubts on the
significance of allergy in these patients.

CLINICAL FEATURES

Otitis media with effusion is usually asymptomatic or presents with symptoms related to hearing
loss. In the infants and young children, parents may complain that the child has delayed or
impaired speech development. In the older child, his teacher may report that his academic
performance is poor, that the child does not pay attention or that he has general behavioural
problems. Excessive shouting and increasing the volume of the television may be subtle signs of
hearing loss.
Otalgia is uncommon in a pure otitis media with effusion. However some patients get recurrent
acute suppurative otitis media and otalgia often heralds the onset of this complication. Disorders of
balance may also occur.

DIAGNOSIS
The diagnosis is based on the clinical findings and audiological investigations.
 If the tympanic cavity is filled with fluid, the colour of the drum may suggest underlying liquid.
 Many patients have evidence of retraction of the tympanic membrane (horizontal handle of the
malleus, fore-shortened malleus, and prominent lateral process of the malleus).
 If the fluid is opaque, the middle ear structures will be obscured.
 When the eustachian tube is partially patent or functioned recently, air bubbles or air-liquid
levels may be identified.
 The most useful clinical signs are the reduction in the mobility of the tympanic membrane that
is found on pneumatic otoscopy.
 The tuning fork tests may show features of a conductive hearing loss depending on the severity
of deafness.
Impedance tympanometry and pure tone audiogram are then performed. The impedance
tympanometry is an objective assessment. It is the most sensitive audiological test for the presence
of middle ear effusions. There is a high correlation between a Type B tympanogram and the
presence of otitis media with effusion but this is not specific and clinical correlation is necessary.
The pure tone audiogram can be performed in children older than 5 years. It assesses the severity of
the hearing loss and is thus useful in the management of this disorder.

TREATMENT
Treatment can be divided into the following categories

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a) Management of predisposing factors
b) Medical treatment of otitis media with effusion
c) Surgical management of otitis media with effusion
It is important that identifiable predisposing factors are adequately addressed. Parental smoking
has been linked to otitis media with effusion. The control of recurrent acute suppurative otitis
media is important, as otitis media is frequently a sequel. Nasal or sinus infections must be treated.
Although considerable controversy exists, in patients who are known to have allergies to inhaled or
ingested allergens, appropriate measures should be taken in managing these allergens. Frequent
hand washing and wearing an extra layer of clothing in winter can reduce the incidence of viral
infections that may predispose the patient to secondary bacterial infection and otitis media with
effusion.
Medical management of otitis media with effusion
Since 90% of the cases of otitis media with effusion will resolve within three months surgery is not
indicated in this period. Medical therapy should be undertaken while the patient is being observed.
Unfortunately, no medications have given long lasting results.
Antibiotics
In 30-60% of cases, cultures of middle ear effusions have grown organisms similar to those that
cause acute suppurative otitis media. Antibiotic therapy should incorporate drugs that are effective
against these bacteria. A -lactamase-stable antibiotic should be prescribed for patients who have
persistent otitis media with effusion despite therapy with one of the medications above.

Other medications
Antihistamines, decongestants and non-steroidal anti-inflammatory drugs have efficacy
comparable to placebo and are therefore not recommended. Systemic steroids have been used alone
or in combination with antibiotics in the treatment of otitis media with effusion. The results have
been inconsistent and, with the risk of significant complications, they should not be recommended.

Surgical management of otitis media with effusion

Surgery is indicated in cases that fulfil all of the following criteria:
a) Hearing loss secondary to otitis media with effusion
b) Persistence of the effusion for greater than 3 months
c) Failed medical therapy

Surgical management aims to

1) Reverse hearing loss and the associated disability
2) Prevent recurrent suppurative otitis media
3) Prevent complications such as cholesteatoma

Surgery entails the insertion of grommets and adenoidectomy.

Surgery may be required to eliminate potential causes of recurrent otitis media with effusion. This
may include repair of cleft palate, antral washouts, turbinectomies and polypectomies.

OTITIS EXTERNA
The external ear consists of the external auditory canal and the pinna. The squamous lining of the
external canal extends unto the tympanic membrane to form the lateral surface of the drum.
Inflammation of the external canal is therefore commonly associated with hyperaemia of the

15
tympanic membrane. The skin of the external auditory canal is firmly adherent to the
perichondrium laterally and to the periosteum medially. Infection involving the lining of the
external auditory canal is therefore often extremely painful.

Infection of the external canal occurs in three forms:

a) Diffuse otitis externa
b) Localized otitis externa (furuncle or carbuncle)
c) Malignant otitis externa

Diffuse otitis externa

Normal skin is a good protective organ. Otitis externa is usually initiated by secondary infection of
skin that has been traumatized by scratching, macerated in persistently moist conditions or affected
by particular skin disorders.

Factors commonly associated with diffuse otitis externa include:

 Seborrhoeic dermatitis
 Frequent swimming
 Hot, humid climates
 Repeated trauma to the external auditory canal (frequently produced by excess cleaning of the
external auditory canal).
 Hypersensitivity reaction to otologic topical preparations

The typical features of acute otitis externa include otalgia, pruritus, scant exudate, oedema and
hyperemia of the external auditory canal wall. In the more severe cases, cellulitis of the peri-
auricular soft tissue occurs and this is usually accompanied by pyrexia.
The management of acute otitis externa aims to
 remove debris and exudate from the external auditory canal,
 eradicate the infective organism,
 remove predisposing conditions
 return the skin of the external auditory canal to normal.
Ear swabs should be sent for culture and sensitivity prior to initiating antibiotic therapy. The
commonest organisms associated with acute otitis externa are Pseudomonas, Proteus and
Staphylococcus aureus. In severe cases the external canal can be virtually occluded by oedema. In
such a case, a wick soaked in glycerine and ichthammol should be inserted. This can be changed 48
hours later. After the oedema has lessened significantly, treatment can be continued with topical
drops containing a fluoroquinolone or gentamycin and a corticosteroid.
 Systemic antibiotics are generally unnecessary except in cases with cellulitis.
 Analgesic therapy is an important part of the treatment of this painful condition. Non-
steroidal anti-inflammatory drugs are usually effective.
 Regular aural toilet, preferably by suctioning, is the most important treatment modality in
these patients.
In chronic otitis externa, Pseudomonas and Fungi are most commonly isolated. Treatment
consists of aural toilet, topical gentamycin/steroid drops or anti-fungals (eg clotrimazole drops and
ketoconazole orally). One should always search for predisposing conditions and identify cases of
immnuosuppression in recurrent acute or chronic otitis externa.

Furuncles are most commonly located in the superior aspect of the cartilaginous canal. They are

16
treated with topical and systemic antibiotics. It is usually unnecessary to incise and drain these.
Incision and drainage can be complicated by perichondritis of the pinna.

MALIGNANT OTITIS EXTERNA

Malignant otitis externa is a progressive, necrotising infection of the external auditory canal, which
is most commonly found in elderly diabetics. Most of the morbidity associated with malignant
otitis externa is secondary to osteomyelitis of the temporal bone and the skull base which, when
inadequately treated, result in cranial nerve palsies and intracranial complications. Chandler
coined the term “malignant external otitis” in 1968 when he reported his experience with his first
thirteen cases. Six of these cases died from this disease or underlying medical problems.
Malignant otitis externa is an aggressive form of infection of the external auditory canal,
which is most frequently detected in immuno-suppressed patients. Classically, it is found in elderly
diabetics. Pseudomonas aeruginosa is the responsible organism in most cases. Males are affected
twice as frequently as females. Malignant otitis externa has now been diagnosed in patients on
cytotoxic therapy, acquired immune deficiency syndrome and in malnourished infants.
The pathogenesis is an infection by a virulent organism in an immunosuppressed host. The
organisms produce exotoxins that cause tissue necrosis at the advancing edge of the infection or
produce substances that encapsulate the infection from host defences and from systemic antibiotics.
Of importance in the diabetic is the microangiopathy, which makes the tissues ischaemic and
impairs the effect of systemic therapy. The infection spreads in the base of skull predominantly as
an osteomyelitis and periosteitis. It involves the cranial nerves as they exit the skull via their
various foramina. The facial nerve is most frequently affected in an abscess cavity close to the
stylomastoid foramen. The ninth, tenth and eleventh cranial nerves are affected close to the jugular
foramen, while the hypoglossal nerve is affected at the hypoglossal canal. The osteitis and
periosteitis spreads along the petrous temporal bone to involve the sixth cranial nerve close to the
petrous apex.

CLINICAL FEATURES
Typically, the patient is an elderly diabetic who has purulent otorrhoea with otalgia
disproportionate to the clinical signs. The otalgia is worse at nights and is associated with hearing
loss. The discharge is usually yellow or green. Characteristically, granulation tissue is noted in the
external auditory canal at the osseo-cartilaginous junction. The granulation tissue marks the site of
abscess formation beneath the tympanic plate.
Conductive hearing loss is found in almost fifty percent of patients. This hearing loss is secondary
to obstruction to the ear canal or to otitis media with effusion. The inflammation at the skull base
causes obstruction to the lymphatic and venous drainage of the eustachian tube and this will
predispose the patient to otitis media with effusion.
Marked tenderness is invariably present on palpation between the mastoid process and the
ascending ramus of the mandible, just below the floor of the external auditory canal. In advanced
cases, there may be trismus and tenderness over the temporo-mandibular joint.
Cranial nerve palsies are common in advanced lesions.

Investigations
Blood:

17
A complete blood count and blood film should be requested. Neutrophilia represents the host
response to bacterial infection but neutropaenia or abnormal white cells can be important clues to
underlying immunosuppression, leukaemia or lymphoma.
ESR: The ESR is usually markedly elevated. The ESR can be used to monitor the response to
therapy.
Urea and electrolytes must be monitored as patients may be placed on nephrotoxic drugs or
diabetic nephropathy may be present.
Glucose profile --- as most cases are found in diabetics.
Pure tone audiogram --- as a baseline study, since the patient may be treated with ototoxic drugs.

Ear Swab
Microscopy and culture and sensitivity tests are done to guide antibiotic therapy. Cultures for
aerobic, anaerobic and acid fast bacteria should be done.
Histology
Multiple biopsies are sent to rule out malignancy. The histopathologist should look for any
evidence of fungal infection.
Nuclear Scanning:
Nuclear scanning of the temporal bone and the base of skull will show increased uptake.
Technetium 99 (Tc 99) is commonly used. Technetium is absorbed by osteoblasts and osteocytes.
Unfortunately, the Technetium scan may be positive for an indefinite period. The Technetium scan
is therefore not useful in the follow-up of the patient. Gallium 67 citrate scan reverts to normal
when active inflammation ceases and this scan can be done six-weekly to assess the patient's
response to therapy
CT Scans
CT scans are less sensitive than nuclear scans in assessing the involvement of the temporal bone.
CT however, is far more sensitive than plain x-rays

TREATMENT
The treatment of malignant otitis externa has undergone considerable changes as the pathogenesis
of this disorder became clearer.
Surgical management is limited to regular suction clearance of the ear, biopsy of the granulation
tissue, drainage of abscesses and debridement of necrotic bone and cartilage. Patients who are
deteriorating despite adequate medical therapy should be considered for debridement.
Medical management is the mainstay of therapy. It is important to control underlying medical
problems. The diabetes should be controlled. Anaemia and malnutrition should be treated. The
patient's fluid and electrolyte status must be monitored.
Intravenous aminoglycosides used to be the main antibiotic therapy.
Ceftazidime is a useful parenteral cephalosporin that can be used empirically with oral
fluoroquinolones in the initial management of the patient. This combination avoids the
nephrotoxicity and ototoxicity of the aminoglycosides. The tissue necrosis seen in malignant otitis
externa provides a good medium for the growth of anaerobic organisms.
Daily suction toilet of the ear is performed and a gentamycin wick used or gentamycin drops
administered.
Treatment should continue for six to sixteen weeks. Treatment is discontinued when the external
canal has returned to normal, the white blood cell count and ESR are normal, and the Gallium scan
(if available) shows no evidence of active inflammation.

18
 THE MANAGEMENT OF EPISTAXIS

Epistaxis can be defined as bleeding emanating from the internal nose. Epistaxis is a frightening
experience for the patient. Most cases are easily controlled and can be managed on an outpatient
basis. On the other hand, epistaxis can be a life-threatening problem. It is important that the
clinician has a logical approach to the management of epistaxis. Management will include the
establishment of haemostasis, identification and treatment of hypovolaemia or circulatory shock
(when present) and the specific management of any aetiologic factor.

19
BLOOD SUPPLY OF THE INTERNAL NOSE
The nose is supplied by both the external carotid and internal carotid arterial systems and
there are multiple anastomoses between these systems in the nose. The major blood supply is via
the maxillary branch of the external carotid artery.
Venous drainage
The venous drainage of the central parts of the lateral nasal wall is to the pterygoid venous plexus.
The anterior areas drain to the facial vein while posteriorly the drainage is to the pharyngeal
venous plexus.

The specific blood supply to the septum must be reviewed, as this is the commonest source of
epistaxis.

The blood supply of the nasal septum

The major source of arterial blood to the nasal septum is the sphenopalatine branch of the
maxillary artery. The ascending branch of the greater palatine artery passes through the incisive
canal to anastomose with the sphenopalatine, the superior labial and the anterior ethmoidal arteries
at Little's area on the antero-inferior portion of the septum. The plexus of arteries at this site is
called Kiesselbach's plexus. The commonest site for epistaxis is Little's area. The posterior
ethmoidal artery gives a small contribution to the antero-superior aspect of the septum.

Venous drainage
The septum drains anteriorly to the facial vein, posteriorly to the pterygoid venous plexus
and superiorly via ethmoidal veins to the ophthalmic veins. In 1% of individuals, the nasal veins
are connected to the superior sagittal sinus by a vein that passes through the foramen caecum in
front of the crista galli. The retrocumellar vein is an important source of venous bleeding in
children and young adults.
There are important anastomoses across the midline between the two anterior ethmoidal
vessels and also occurring in the nasopharynx. This can explain some of the cases in which arterial
ligation fails to control epistaxis.

Causes of epistaxis
Local causes
a) Trauma: trivial or major injuries, nasal fracture, surgical trauma, foreign body, excessive
sneezing or coughing (with increased pressure in the nasal vessels).
b) Inflammation, infection and allergy: e.g. acute and chronic, specific and non-specific rhinitis.
c) Neoplasms (and tumour- like masses) of the nose, nasopharynx and sinuses:
1) Benign - angiofibroma, haemangioma, inverted papilloma, pyogenic granuloma (tumour-
like), other granulomas.
2) Malignant - squamous cell carcinoma, adenocarcinoma, salivary gland tumours,
melanocarcinoma, midline lethal granuloma (generally considered a lymphoma).
d) Drugs - cocaine abuse.
e) Congenital vascular malformation.

In many cases of epistaxis the actual aetiology is never elucidated. These cases are often labelled as
“spontaneous epistaxis” but a careful clinical assessment will often reveal contributory factors such
as minor trauma and inflammation.

General causes

20
Abnormal bleeding may result from a defective coagulation pathway, thrombocytopaenia, platelet
function defects and vascular abnormalities.
A) Congenital coagulopathies e.g. haemophilia, Christmas disease, von Willebrand's disease.
B) Acquired defects in the coagulation pathway: heparin or warfarin therapy; hepatic or obstructive
biliary diseases.
C ) Thrombocytopaenia
1) Platelet production failure
i) Selective depression of the megakaryocytes by drug toxicity (cotrimoxazole,
phenylbutazone, thiazides, tolbutamide) or viral infections.
ii) Generalised bone marrow failure: plastic anaemia, leukaemia, marrow infiltration or
myelosclerosis.
iii) Ineffective platelet production: megaloblastic anaemia.
2) Increased platelet destruction:
i) Idiopathic thrombocytopaenic purpura
ii) Secondary immune thrombocytopaenia ( post-infection, SLE, chronic lymphocytic
leukaemia)
iii) Disseminated intravascular coagulation
iv) Drug- induced immune thrombocytopaenia (sulphonamides, quinine, PAS, rifampicin
digitoxin).
3) Splenic pooling in patients with splenomegaly.
4) Massive transfusion of old blood: dilutional thrombocytopaenia
D) Abnormal platelet function
Aspirin therapy, hepatic and renal disease, multiple myeloma and Waldenstrom's
macroglobulinaemia are all acquired causes of platelet dysfunction .
E) Vascular abnormalities: Hereditary haemorrhagic telangiectasia, steroid-induced vascular
weakness, scurvy, Monckeberg's sclerosis.

Hypertension and anxiety tend to cause prolongation of epistaxis but the incidence of
epistaxis is not increased in these patients. Hypertension is associated with vascular changes, which
inhibit vasoconstriction thus prolonging epistaxis. The increased arterial pressure will also increase
the severity of the epistaxis. Thus hypertensive patients are more frequently admitted to hospital
for the control of epistaxis. The control of hypertension is an essential part of the management of
epistaxis in the hypertensive patient.

Management of active epistaxis

History
A brief history is obtained from the patient or a relative while preparations are being made to
control the epistaxis. It is useful to inquire:
1. Whether the epistaxis is predominantly an anterior or posterior bleed
2. Whether the epistaxis is unilateral. If the bleeding is reported as bilateral, one should still
inquire as to the side that initially bled (often blood is entering the opposite nasal passage at
the posterior choanae by passing around the border of the septum).
3. Syncopal sensation, which may be indicative of cardiovascular decompensation.
4. Estimate of the blood loss in terms of common utensils such as cups or tablespoonfuls.
Patients tend to exaggerate the blood loss, but often have containers with them that they have
used to collect the blood and these can be very helpful in estimating the blood loss.
5. Nasal trauma( including nose-picking), upper respiratory tract infections, recent medications,
history of bleeding diathesis and any significant medical illness.

21
 It should be clear that the thoroughness of the initial history would depend on the clinical
status of the patient. The patient who is in hypovolaemic shock will require emergency
resuscitation while attempts are made to control the bleeding. The patient whose cardiovascular
system is stable but who is bleeding heavily is best managed by controlling the bleeding and then
completing the history.

Examination
1. Pulse and blood pressure should be taken. If the cardiovascular system is
stable the patient should be examined sitting up or in the semi-recumbent position.
Strong suction and a good headlight are prerequisites for an adequate assessment of the
patient with epistaxis. It is useful to attempt a preliminary assessment of the nose without
vasoconstriction because this can sometimes stop the bleeding and prevent identification of the
bleeding point. After
2. Suction the clots, local anaesthetic & vasoconstrictive nasal drops or sprays
will facilitate examination of the nose and assist with haemostasis in patients who are not bleeding
profusely. Cocaine is a very potent vasoconstrictor and local anaesthetic and is therefore frequently
used in this setting. The maximum dose should be 1.5mg/kg. An alternative preparation is a
mixture of 0.1% xylometazoline and lignocaine.
While local measures are being undertaken, it is important that
3. Resuscitation of the circulatory volume with intravenous fluid and blood
transfusion (if necessary) is carried out.
4. Sedation should be prescribed as this relieves the patient's anxiety, reduces the
blood pressure and facilitates nasal cautery and packing.

Anterior epistaxis
Effective treatment for anterior epistaxis includes:
1. Tamponade of the nasal vessels between the fingers,
2. Nasal cautery,
3. Nasal packing, and
4. Surgery with ligation of the anterior ethmoidal artery.
Most patients who are being assessed by an otolaryngologist will have already attempted to
tamponade the nasal vessels between the fingers, but may not have applied pressure properly and
so the otolaryngologist should give the relevant instructions. The patient can attempt to tamponade
the nasal vessels while preparations are being made to examine the nose.
If the source of an anterior epistaxis is identified, the treatment of choice is nasal cautery. This
treatment is usually successful unless the bleeding is profuse. The commonest site of epistaxis is
Little's area on the antero-inferior nasal septum. The immediate area around the focus of bleeding
should first be cauterised before cautery to the actual bleeding site is attempted, otherwise there
would be a significant risk of aggravating the epistaxis. Successful nasal cautery has the advantage
of avoiding nasal packs.
Silver nitrate, trichloro-acetic acid and electrocautery are highly effective. Electrocautery is the
more effective than chemical cautery in the presence of active bleeding, but would require general
anaesthesia in children
Patients who have not had major bleeds with cardiovascular decompensation can often go
home after a short period of 20- 30 minutes of observation for recurrent bleeding.
There is a risk of septal perforation when unilateral cautery is overzealously performed.
Bilateral nasal cautery at equivalent sites on the nasal septum should be avoided, as this is
associated with a high incidence of perforations.

22
Nasal packs will be required in cases of profuse anterior epistaxis and in cases where the focal
bleeding point cannot be identified. A half- inch petrolatum gauze-strip soaked in antibiotic
ointment or bismuth iodoform paraffin paste (BIPP) packing is commonly used. The nasal packing
should be applied meticulously, in loops, from the nasal floor to the nasal roof and extending as far
posteriorly as is feasible. Patients often find the insertion and the removal of these packs very
uncomfortable. Adequate local anaesthesia and analgesia should be administered. Merocel sponges
can be inserted easily and are better tolerated. These are especially useful in children. Experience
with Merocel sponges suggest that they are less effective than BIPP or gauze strip packs. They are
most useful in mild epistaxis. Gauze strip packs, BIPP and Merocel all adhere to the nasal mucosa
to varying degrees and epistaxis may resume on removal of the nasal packs.
Nasal balloons are easy to insert and to remove, but are slightly less effective than traditional nasal
packs in controlling epistaxis because they do not adapt very well to the irregularity of the lateral
nasal wall.
Anterior nasal packs should be left in situ for 24-48 hours. During this period the patient
should be on antibiotics and should be nursed propped up so that that the head is elevated.
.
Nasal endoscopy
Nasal endoscopy has increased the frequency with which the actual bleeding point is identified.
This has facilitated both chemical and electro-cautery. Nasal endoscopy has been particularly
helpful in epistaxis that is relatively posterior in location. The 0 and the 30 degrees rigid telescopes
or the flexible fibreoptic scopes can be used. The flexible fibreoptic scope is particularly useful in
identifying bleeding points that are posterior to septal deviations.
Occasionally septoplasty (operation to straighten the septum) must be performed to facilitate
access to a bleeding point so that cautery or effective nasal packing can be accomplished.

Treatment options for posterior epistaxis

Posterior epistaxis can be very difficult to manage. Identification of the bleeding point is sometimes
impossible and one has to rely on post- nasal packs or balloon tamponade initially if significant
active bleeding is occurring. Sometimes the patient presents with mild posterior epistaxis. In these
cases the nose should be:
 Decongested and
 Topical anaesthesia applied
This facilitates examination endoscopically or microscopically. It is worthwhile to attempt a
preliminary nasal examination without the use of vasoconstriction as the latter occasionally stops
the bleeding and prevents identification of the bleeding point. If the bleeding point is identified, the
site should be cauterised. In cases where heavy posterior bleeding is occurring, the initial
management should be:
 Insertion of a double-lumen balloon to apply nasal as well as postnasal tamponade since one
would not be certain of the exact source of the bleeding. This method also increases the
efficiency of the tamponade.
Under local anaesthesia, nasal balloons can be inserted quickly and easily with minimal discomfort
to the patient. Nasal balloons are tolerated much better than the traditional anterior and posterior
nasal packs. The nasal balloons should remain in situ for 48 - 72 hrs.
If bleeding persists despite the insertion, or on the removal, of the nasal balloons, endosopic or
microscopic examination of the nose should be performed. If the epistaxis is not controlled by
posterior endoscopic microscopic cautery, then a Foley's catheter should be inserted and the
balloon inflated with 15 ml of air or saline. Saline does carry with it the tiny theoretical risk of

23
aspiration but has the advantage that it does not leak as easily as air. Bilateral anterior nasal packs
(petrolatum gauze strips) should also be inserted to maximise the tamponade effect.
When posterior endoscopic cautery (under local anaesthesia) and nasal packs fail to control
epistaxis, or epistaxis recurs on removal of the packs, the nasal passages and the postnasal space
should be examined under general anaesthesia. Any bleeding point that is identified should be
cauterised. Identification of the bleeding point may require fracturing the turbinates to allow access
to the meati. If the bleeding site cannot be identified, the maxillary artery should be ligated. The
alternative is to insert firm anterior and posterior nasal packs under general anaesthesia, leave
these in situ for 72- 96 hrs and to proceed to ligate the maxillary artery if bleeding recurs on
removal of the packs. It is perhaps a better choice to avoid two general anaesthesias and to proceed
with ligation of the maxillary artery at the first general anaesthesia.
Ligation of the maxillary artery is effective in 95% of cases. Embolization of the maxillary artery
using gelfoam, has been successful in controlling epistaxis, but has a higher failure rate than
ligation of the maxillary artery and its sphenopalatine and greater palatine branches. It is rarely
necessary to ligate the anterior ethmoidal vessels when adequate ligation of the maxillary arteries
and its main branches has been performed.

Special conditions
There are many possible causes for epistaxis. In the management of epistaxis one
should be careful not to miss a malignancy of the nose, sinuses or the nasopharynx. Careful clinical
assessment and radiologic studies will identify these malignancies. The male teenager may have an
angiofibroma requiring angiography and CT scanning to plan the surgical approach to be utilised
after embolization of the major feeding vessels. Patients who have hereditary haemorrhagic
telangiectasia are difficult to manage. Septodermoplasty has produced transient success but
telangiectactic vessels tend to grow into the split skin graft with resultant recurrent epistaxis.
Oestrogens and local radiotherapy have been useful in some cases. Recurrent bleeding from the
edges of a septal perforation can be controlled with cautery.

NASOPHARYNGEAL CARCINOMA

INTRODUCTION
Nasopharyngeal carcinoma is a tumour of epidermoid origin that is endemic in certain ethnic
groups. It constitutes 90% of all malignancies found in the nasopharynx. Nasopharyngeal
carcinoma is prevalent in the Cantonese Chinese in Southern China, Hong Kong and Singapore.
The age-adjusted incidence in males in Hong Kong is 26: 100,000. In Jamaica it is found in 1.4:
100,000 males and 0.5: 100,000 females. This cancer is uncommon among Caucasians. In North
America the incidence is 1: 100,000. In Northern China nasopharyngeal carcinoma has an incidence
of only 3 per 100,000. There is a moderately high incidence in the Malays, Indonesians, Thais and

24
 Filipinos. In North African countries such as Tunisia, Algeria and Sudan the incidence is less than
that in South-east Asia but still appreciably higher than in North America and Europe. The Eskimos
in Alaska have an incidence that is 15 times that of the general USA population. The aetiology is
multifactorial and includes genetic, viral and environmental factors.
Although this carcinoma has its highest incidence in particular racial groups, it occurs universally.
Clinicians must have a high index of suspicion in order not to miss this lesion since the
presentation can be subtle and varied.
Nasopharyngeal carcinoma is more commonly found in males. The male to female ratio is 2-3: 1. In
high risk regions the incidence of nasopharyngeal carcinoma rises from the end of the second
decade to reach a peak in the fourth decade and then remains at a plateau. In low risk countries
such as Jamaica, a high proportion of cases have their onset in the second decade of life with a
second peak occurring in the sixth decade.
Aetiology
Nasopharyngeal carcinoma is an interesting tumour that demonstrates the interaction of several
factors in carcinogenesis. The important aetiologic factors are viral, genetic and environmental.
Exciting data has been collected from the continued research into the aetiology of this carcinoma.
The role of the Epstein-Barr virus
The Epstein-Barr virus has been associated with Burkitt's lymphoma, infectious mononucleosis,
non-Hodgkin's lymphoma in immunosuppressed individuals, some cases of Hodgkin's lymphoma
and nasopharyngeal carcinoma. Antibodies to the Epstein-Barr virus have been strongly associated
with nasopharyngeal carcinoma. In high risk regions there is a rise in the titres of certain antibodies
to the Epstein-Barr virus prior to the onset of the malignancy. The association of the Epstein-
Barr virus and nasopharyngeal carcinoma was subsequently confirmed by demonstrating that the
DNA of this virus ( EBV DNA) was present in biopsy material from nasopharyngeal carcinoma
In situ hybridisation is considerably more sensitive for the detection of EBV-encoded RNA
than it is for EBV DNA because of the high levels of the former in specimens from nasopharyngeal
tumours.
Genetic factors
The high incidence of nasopharyngeal carcinoma among certain ethnic groups strongly suggests a
genetic link, which possibly interacts with environmental factors.
The major histocompatibility gene complex on the short arm of chromosome six comprises
six recognised loci called HLA-A, -B, -C, -DR, -DQ, -DS. There are now well-established
associations between HLA (human leukocyte antigen) and nasopharyngeal carcinoma.
Deletion of the short arm of chromosome 3 (3p) has been noted in these cancers and this may
reflect the loss of a tumour suppressor gene.
Environmental factors
Ingestion of Cantonese- style salted fish, especially in childhood, has been linked to
nasopharyngeal carcinoma. It is known that carcinogenic nitrosamines are present in such salted
fish.
Histopathology
The World Health Organisation Classification recognises three histologic types
a) Keratinising squamous cell carcinoma (WHO-1) -30-50 % of the cases in non-endemic regions but
only 5 % in endemic areas.
b) Non- keratinising squamous cell carcinoma (WHO-2)
c) Undifferentiated carcinomas that have abundant non-neoplastic, lymphocytic infiltrate (WHO-3).
This latter histologic type has often been called “lymphoepithelioma”most commonin endemic
areas. It is squamous cell ( cytokeratin is present)

25
Anatomy
The nasopharynx has dimensions of 4 cm x 4 cm x 3 cm. The anterior “wall” is really the
posterior choanae separated by the posterior border of the nasal septum. The floor consists of the
superior surface of the soft palate and the nasopharyngeal isthmus. The roof and the posterior wall
form one continuous sloping surface formed by the body of the sphenoid, the basiocciput and the
first two cervical vertebrae. The prevertebral fascia and muscles separate the adenoids from the
vertebrae. The lateral wall contains the pharyngeal end of the eustachian tube, the tubal tonsils and
the Fossa of Rosenmuller.
Most cases of nasopharyngeal carcinoma seem to arise in the region of the Fossa of
Rosenmuller. In the adult this cleft-like space may be as deep as 1.5 cm. Its base lies superomedial
to the pharyngeal opening of the eustachian tube and it extends posterolaterally to its apex which
reaches the petrous apex and the anterior margin of the carotid canal. The foramen ovale and the
foramen spinosum lie lateral to the apex of the Fossa of Rosenmuller. Lateral to the fossa lie the
mandibular division of the trigeminal nerve, the tensor palatini, the parapharyngeal space with the
internal carotid artery, the internal jugular vein and the lower four cranial nerves. Above the
superior border of the superior constrictor muscles (at the sinus of Morgagni), the nasopharynx is
separated from the parapharyngeal space by the pharyngobasilar fascia and the pharyngeal
mucosa only, allowing easy spread of tumour in the parapharyngeal space.
Clinical features
Symptoms may be due to the local effects of the tumour mass in the nasopharynx, direct
spread into contiguous structures (including erosion of the skull base), regional or distant
metastases, cranial nerve involvement or paraneoplastic syndromes.
Sixty percent of patients present with palpably enlarged cervical nodal metastases.
CT scans have detected nodal metastases in 75% to 90% of nasopharyngeal carcinomas of
histologic types WHO 2 and WHO 3. The initial spread of nasopharyngeal carcinoma is to the
retropharyngeal nodes (nodes of Rouviere) but the first palpable nodes are the jugulodigastric
nodes followed by apical nodes deep to the superior aspect of the sternomastoid. Metastases to
submandibular and parotid nodes are relatively common. The tumour can directly invade the deep
lobe of the parotid. Bilateral cervical nodal metastases frequently occur. Fifty percent of
undifferentiated carcinoma of the nasopharynx will present with bilateral cervical
lymphadenopathy.
Nasal symptoms are common but may be quite subtle. Nasal obstruction along with bloodstained
postnasal discharge is common. Epistaxis may only occur after hawking. Secondary infection or
obstruction to the drainage of the paranasal sinuses can cause the symptoms of sinusitis.
Aural symptoms are frequently present. The tumour obstructs the eustachian tube or infiltrates the
tensor or levator palati muscle, interfering with the function of the eustachian tube. Otitis media
with effusion is commonly the end result. Recurrent acute suppurative otitis media may also be
found. One must always be suspicious of nasopharyngeal carcinoma in any teenager or adult who
has unilateral otitis media with effusion (although this lesion can also cause bilateral otitis media
with effusion). Other aural symptoms include otalgia and tinnitus.
Cranial nerve palsies are found in 15-20 % of patients. At the University Hospital of the West
Indies, cranial nerves VI and XII are most commonly involved.
Nasopharyngeal carcinoma can easily invade the fifth cranial nerve since the foramen ovale
lies lateral to the apex of the Fossa of Rosenmuller. Cranial nerves V and VI can both be affected at
the petrous apex. Nasopharyngeal carcinoma can spread superiorly through the foramen lacerum
and along the internal carotid artery to the cavernous sinus. In this way cranial nerves III, IV, Va,
Vb and VI may be invaded or compressed. Spread to the parapharyngeal space, the jugular
foramen and/or the hypoglossal canal can cause cranial nerve palsies involving the last four cranial

26
nerves. The tumour can spread anteriorly to the pterygopalatine fossa and the maxillary sinus with
subsequent involvement of the orbit and the optic nerve. It is conceivable that the olfactory nerve
may rarely be affected by further spread into the roof of the nose or the anterior cranial fossa. All
cranial nerves except for 7 and 8 can be involved
The fossa of Rosenmuller is where most of the nasopharengeal carcinomas arise.
Other symptoms and signs include trismus due to invasion of the pterygoid muscles and severe
headaches resulting from erosion of the skull base or secondary sinusitis.
Distant metastases can be detected in 20- 30 % of nasopharyngeal carcinomas. Skeletal metastases
(especially to the thoracolumbar spine) account for 50 % of these lesions. Intracranial spread has
been found in 3-12 % of cases.

Diagnosis
The nasopharynx can be assessed by nasopharyngeal mirrors or by endoscopes in the
Outpatients' Department. The diagnosis is confirmed by the histology of nasopharyngeal biopsies
under local or general anaesthesia.
One must stress that the lesion may be almost entirely submucosal and deep biopsies may be
required to obtain adequate samples. These cases are best biopsied under general anaesthesia. The
CT scan or MRI can often alert one of the need for deep biopsies.
Assessment of the extent of the tumour
Clinical and radiological studies are the main methods of assessing the tumour extent. CT scans of
the base of the skull and the neck should be the minimum investigations. Plain X-ray can
demonstrate erosion of the skull base and the foramina but is too insensitive a method to accurately
assess the extent of the lesion. Plain X-rays of the head and neck are only indicated when CT or
MRI is unavailable. Chest X-rays are used in the general evaluation of the patient and also to detect
pulmonary metastases ( CT scan more accurate for the latter).
Immuno-cytochemistry used to determine what the cancer developed from

TREATMENT
Nasopharyngeal carcinoma is predominantly treated with radiotherapy. The use of Cobalt 60 and
megavoltage linear accelerator has decreased the incidence of complications while at the same time
improving the results. Imaging studies have allowed better delineation of the tumour extent and
therefore better planning of radiotherapy. Doses of 65-70 Gy are now given. Hyperfractionation is
being utilised but there are no well-controlled, prospective studies assessing the efficacy of this
technique, in nasopharyngeal carcinoma, when compared to that of traditional radiotherapy.
Intracavitary and interstitial radiotherapy may be particularly useful in recurrent lesions.
Surgery is generally limited to biopsies and radical neck dissections for residual tumour following
radiotherapy. In patients with massive lymphadenopathy, surgery to reduce the tumour mass, is
sometimes advocated prior to radiotherapy. The rational for this is that radiotherapy is less
effective in these cases since the centre of the lesion is likely to be hypoxic. When there is recurrent
tumour in the nasopharynx, intracavitary radiotherapy or surgery may be initiated. Grommets
have been inserted to treat the otitis media with effusion that is often associated with
nasopharyngeal carcinoma

Prognosis
Major prognostic factors adversely influencing the outcome of treatment include large size
of the tumour, higher T stage, and the presence of involved neck nodes (especially nodes > 8 cm
diameter and supraclavicular nodes). Cranial nerve palsies, bone invasion and intracranial spread
significantly affect survival. Small cancers of the nasopharynx are highly curable by radiotherapy

27
 with survival rates of 80%-90%. Moderately advanced lesions without clinical evidence of spread to
cervical lymph nodes are often curable with survival rates of 50%-70%. The overall 5-year survival
is 57 %.
Patients with advanced lesions, especially those associated with clinically positive cervical
lymph nodes, cranial nerve involvement, and bone destruction, are poorly controlled locally by
radiotherapy with or without surgery and often develop distant metastases despite local control.
Most present very late in Jamaica.

MANAGEMENT OF SINUSITIS

Acute sinusitis is defined as an acute inflammation of the paranasal sinuses, which resolves
without residual mucosal change following appropriate medical therapy. Children who meet the
following criteria are categorised as having chronic sinusitis:
a) Persistent symptoms and signs for twelve weeks
or six episodes per year of recurrent acute sinusitis
b) in association with persistent mucosal change on CT scan four weeks after medical therapy
(International Conference on Sinus Disease: terminology, staging, therapy ---- 1993)
The paranasal sinuses develop as outgrowths from the lateral wall of the nose starting at the
40th gestational day. At birth, only the maxillary and the ethmoidal sinuses are readily identifiable.
Most of the subsequent growth of the maxillary sinus depends on the eruption of the dentition. The

28
 frontal sinus usually develops from anterior ethmoidal air cells called the frontal recess. The
majority of the paranasal sinuses drain into the middle meatus. Normal physiology of the
paranasal sinuses depends on the patency of the ostia of the sinuses, good mucociliary function and
adequate immune function.
Sinusitis is often initiated by obstruction of the ostiomeatal complex, which results in
hypoxia of the sinus mucosa and ciliary dysfunction. This produces stasis of the sinonasal
secretions and multiplication of bacteria. The inflammatory response perpetuates the obstruction of
the ostia. Thus patients may have a primary lesion obstructing the ostia or inflammation may
produce secondary obstruction of the ostia. Chronic sinusitis develops if the obstruction is not
relieved. Persistent disease in the sinuses is usually secondary to disease in the anterior ethmoids
and the ostiomeatal complex (middle meatus and adjoining areas). Medical and surgical
management must attempt to correct the abnormalities in these key areas.
A thorough history and a full examination are essential in each patient. However it is often
difficult to examine the middle meatus without the use of nasal endoscopes. When the middle
meatus is not seen and symptoms and signs of purulent rhinorrhoea, postnasal discharge and nasal
obstruction persist for more than ten days a presumptive diagnosis of rhinosinusitis should be
made. It is also reasonable to make a diagnosis of rhinosinusitis in the patient who has nasal
symptoms associated with pain in the region of the sinuses.
In the past we relied heavily on plain X-rays in the investigation of the sinuses. Mucosal
thickening, sinus opacification and fluid levels are often indicative of sinusitis. It is now possible to
assess the sinuses with great precision. The state of the art techniques in the assessment of the
sinuses are nasal endoscopy and high resolution computerised tomography. Nasal endoscopy has
allowed us to examine areas that were previously inaccessible without general anaesthesia.
Patients with suspected complications of sinus disease (e.g. orbital and intracranial
complications) and those with persistent symptoms and signs despite adequate medical therapy
require computerised tomography. This will allow precise planning of the surgical approach in
each patient.

Complications of Sinusitis
Local Orbital complications Intracranial Spread
1. Chronicity and 1.Dacrocystitis because of 1. Epidural Abscess
irreversible mucosal change obstruction of the Naso- 2. Meningitis
2. Mucocele lacrimal Duct. 3. Subdural Abscess
3. Osteomyelitis 2.Conjunctivitis 4. Frontal lobe
especially of the diploic 3.Subperiosteal abscess Abscess
anterior wall of frontal sinus 4.Periorbital cellulitis 5. Cavernous sinus
5.Orbital Cellulitis thrombosis
6.Orbital abscess
7.Ophthalmoplegia
8.Blindness

29
Note that the paranasal sinuses are the commonest source of frontal lobe abscess.

Medical therapy of Sinusitis aims to control infection, establish patency of the ostia, relieve
symptoms and treat predisposing conditions. Streptococcus pneumoniae and Haemophilus
influenzae are responsible for 76% of cases of community-acquired sinusitis. Anaerobes, other
streptococcal species, Moraxella catarrhalis and Staphylococcus aureus each account for 3-7% of
cases. Amoxicillin plus Clauvulanic acid, and Cefuroxime are considered as good first line
antibiotics.

True vocal cords

During phonation the true vocal cords are adducted. When the expiratory respiratory
muscles contract, the subglottic air pressure increases. The subglottic air pressure will eventually be
high enough to force the true vocal cords apart allowing the egress of expiratory air. The resultant
fall in the subglottic pressure, the elastic recoil of the tissue and the Bernoulli effect will restore the
true vocal cords to their original adducted position. Once again, the cycle of increasing subglottic
pressure and separation of the true vocal cords will begin again. Studies have demonstrated that
throughout the cycle of phonation, the vocal cord ligaments remain in an adducted position.
Adduction and separation predominantly involves the mucosa. Thus we can speak about a
mucosal wave of vibration. This explains the marked deterioration of the voice that is associated
with disease of the mucosa of the true vocal cords.
Normal vocal cord mobility requires intact recurrent laryngeal nerves, neuromuscular junction,

30
glottic muscles and cricoarytenoid joints.

CAUSES OF HOARSENESS
Intrinsic lesions of larynx

Acquired lesions Congenital lesions

Vocal cord nodules Vocal cord palsy
Vocal cord polyps Vocal cord webs
Reinke's oedema (marked oedema in Laryngeal cysts
the submucosa of the true cords) Laryngocoele
Acute and chronic laryngitis Haemangioma or lymphangiomas
Granulomas of the vocal cords:
intubation granulomas, pyogenic
granulomas, and tuberculosis
Myxoedema: a dry waxy type of
swelling (non pitting oedema) with
abnormal deposits of mucin in the
skin and other tissues associated with
hypothyroidism the facial changes
are distinctive with swollen lips and
thickened nose
Benign tumours: Laryngeal
papillomatosis
Malignant tumours: Squamous cell
carcinoma (95%)
Trauma with haematoma and oedema
Foreign bodies at the glottis

Recurrent laryngeal Supranuclear lesions of Posterior fossa lesions

nerve palsy the vagus Acoustic neuroma
20 lesion of the vagus or Cerebrovascular accident Meningioma
directly

Nuclear lesion Jugular foramen lesions Cervical lesions

Bulbar poliomyelitis Glomus jugulare Penetrating neck injuries
Motor neuron disease Metastatic carcinoma of Carotid body surgery
Lateral medullary the nasopharynx Radical neck dissection
syndrome

31
 Thoracic lesions
Carcinoma of esophagus
Tuberculous or metastatic
nodes
Aortic aneurysm or
aneurysmal surgery

Lesions of the recurrent laryngeal nerve in the neck

 Invasion by malignancies of the thyroid, cervical oesophagus, pyriform sinus. (Carcinoma of
the larynx typically causes vocal cord palsy by infiltration of the intrinsic laryngeal muscles)
 Thyroidectomy
 Pharyngeal pouch surgery
 Repair of tracheal stenosis or tracheo-oesophageal fistula

Viral infections and disorders such as vasculitis (e.g. associated with diabetes and autoimmune
disorders) can affect either the vagus or the recurrent laryngeal nerve.

Hoarseness can also occur because of:

Disorders at the neuromuscular junction: myasthena gravis
Muscular disorders: muscular dystrophies
Cricoarytenoid joint dysfuntion: Perichondritis, arthritis, post-traumatic adhesions

The assessment of the patient would require a thorough history and examination,
special radiologic studies and blood investigations. It is essential that the vocal cords be
visualised if hoarseness persists beyond two weeks.

CARCINOMA OF THE LARYNX

Carcinoma the larynx usually presents in the sixth or seventh decades of life. It
is strongly associated with cigarette smoking and alcohol intake. Polycyclic aromatic
hydrocarbons derived from cigarette smoking are converted by aryl hydrocarbon
hydroxylase to epoxides, which bind DNA and are the true carcinogens. Other
associated factors include human papilloma virus types 16 and 18, nickel and asbestos,
mate tea in Latin America, and prior radiation. Genetic factors may be important, as
there is a higher incidence of laryngeal cancer in some families than the incidence found
in the general population.
Men are affected five times as frequently as women are. In the United States of
America 10,000 to 12,000 cases of laryngeal cancer are reported annually. In men,

32
laryngeal carcinoma occurs in 9 per 100,000 while women have a reported incidence of
1.5 per 100,000. In Jamaica, the incidence is 4 per 100,000 males annually. Worldwide,
ethnic differences have been noted in the incidence of laryngeal cancer. Blacks are
affected more often than Caucasians, while Japanese and the Chinese have lower
incidences than both groups. There is a higher incidence in urban than in rural
populations. This may be related to urban pollution.
Ninety-five percent of cases are squamous cell carcinomas. Most are moderate to
well differentiated. In Jamaica, United States, and Great Britain sixty percent of cases
arise at the glottis, thirty-five percent at the supraglottis and the five percent in the
subglottis. Wine producing countries such as Italy, Spain and France have a higher
incidence of supraglottic than glottic cancers and patients tend to present in middle age
at the time of diagnosis.
Glottic cancers tend to present early with persistent hoarseness, which becomes
progressively worse. Any adult patient who has persistent hoarseness for more than
two weeks must be assumed to have malignancy until proven otherwise. Examination
of the larynx is mandatory. Early laryngeal cancer can be treated with minimal
morbidity and good preservation of voice. Late diagnosis on the other hand may result
in a relatively uncomfortable and unpleasant death. Hoarseness/change in voice
Foreign body sensation
Dyspnoea and stridor may be the presenting features in patients with advanced Dyspnea
Dysphagia
laryngeal cancer. These symptoms may be present without hoarseness in the patient Stridor (due to airway narrowing)
Aspiration while eating or drinking
with a supraglottic or subglottic tumour. Can have referred ear pain.

Cervical nodal metastases are common in supraglottic cancers but are uncommon in
glottic cancers until the late stages. This is a reflection of the poor lymphatic drainage of
the mucosa of the true vocal cords.

The larynx can be examined by a number of methods in the clinic:

 Indirect laryngoscopy using a mirror
 Flexible fiber-optic nasolaryngoscopy
 Rigid telescope (70 degree)

The lesion usually arises in the anterior one-third of the vocal cords. Often it appears
as warty excrescences on the true vocal cords. Areas of leukoplakia may be present.
Vocal cord palsy may be present in the more advanced lesion. In cases where the
diagnosis has been greatly delayed, tumour may extend from the supraglottis to extend
across the glottis into the subglottis (transglottic tumour). These patients often present
with stridor because of the compromised airway. Deep jugular chain cervical
lymphadenopathy may be present. This is especially likely in supraglottic tumours
where 30% of patients present with palpable nodes (often bilaterally). The lymphatic
drainage tends to follow the arteries. (Superiorly along the superior laryngeal vessels to
pass through the thyrohyoid membrane to mid deep jugular chain nodes and inferiorly
along the inferior laryngeal and inferior thyroid vessels to jugulo-omohyoid nodes).
There is also anterior lymphatic spread to prelaryngeal (Delphian node) and pretracheal
nodes.

Once the diagnosis is suspected the patient should be assessed for his/her fitness for
surgery and for the possibility of metastatic spread. Chest Xray and CT examination of
the neck and chest should be done. If a CT scan cannot be done because of cost

33
 constraints, ultrasound examination of the neck can be substituted.

The diagnosis is confirmed by biopsies at direct laryngoscopy or

microlayngoscopy. Prior to taking biopsies, the extent of the tumour must be assessed
endoscopically and also by palpation of the base of the tongue. There is a 10% incidence
of an associated second primary tumour in the head and neck or bronchus.
Panendoscopy (laryngoscopy, tracheobronchoscopy, oesophagoscopy and
nasophayngoscopy) is often performed. Fine needle aspiration cytology should be
perfomed if nodal enlargement is present. However, even if FNA is negative, the neck
must still be treated in patients with cervical lymphadenopathy since there is a small
false negative rate and all nodes may not have been adequately sampled.

Treatment
Early laryngeal cancer is best treated with radiotherapy.
When the lesion is confined to one vocal cord and there is no impairment of cord
mobility, the ten-year survival is 90%. Partial laryngectomy is the second choice for
early lesions but results in a poorer voice than when radiotherapy is the treatment
modality. Advanced lesions may require total laryngectomy and radiotherapy.

Metastases to cervical nodes are treated by neck dissection. The radical neck dissection
entails resection of all the lymph nodes in the anterior and posterior triangles of the
neck along with the sternomastoid muscle, the accessory nerve and the internal jugular
vein. A functional neck dissection spares the non-lymphatic structures. Extranodal
spread (into non-lymphoid tissue) is more common in patients with nodes> 3 cm
diameter and in patients with multiple nodes. Functional neck dissection would not be
advisable in these patients.

Chemotherapy is still experimental---- 30-50% respond but no increase in survival rate

has been demonstrated. 30 % also become resistant to the treatment.

Voice Rehabilitation
There are a number of methods of achieving speech after total laryngectomy:
a) Oesophageal speech b) Electronic larynx c) Tracheo-oesophageal puncture and insertion
of Blom- Singer or Provox valve d) Neoglottic techniques

The tracheo-oesophageal puncture with insertion of a one- way valve is now most
popular. The valve allows air to go into the oesophagus while the patient is expiring but
will not allow food or drinks to get into the trachea.

34
 SALIVARY GLAND TUMOURS
The major salivary glands are the parotid, submandibular and sublingual glands.
Hundreds of minor salivary glands are found in the palate, buccal mucosa, tongue,
vallecula, larynx, trachea and paranasal sinuses.
The parotid gland is the largest of the salivary glands.
Relations
The parotid gland is a serous gland, which has three surfaces: anteromedial,
posteromedial and lateral or superficial. The anteromedial surface embraces the
ascending ramus of the mandible, which is sandwiched between the masseter externally
and the medial pterygoid muscle medially.
Posteromedial surface is related to the mastoid with the associated attachments of the
sternomastoid and the posterior belly of the digastric. The external carotid artery
grooves this surface before entering the gland. The styloid process and its associated

35
muscles separate the internal carotid artery and the internal jugular vein from this
surface of the gland.
This superficial or lateral surface is covered by skin and superficial fascia.
The gland extends superiorly to the level of the zygomatic arch.
Inferiorly the gland extends into the neck, overlapping the superior aspect of
sternomastoid. Anteriorly it extends to overlap the masseter muscle.
The facial nerve traverses the gland and the portion of the gland superficial to the
nerve is called the superficial lobe while that lying deep to the nerve is called the deep
lobe of parotid. The parotid gland has a true capsule formed by condensation of the
investing layer of the deep cervical fascia. This explains why acute inflammatory
conditions of the parotid are so painful. The greater auricular nerve supplies the skin
overlying the parotid and its posterior branch supplies the ear lobe. This posterior
branch can sometimes be saved during parotidectomy but the anterior branch has to be
sacrificed.

The submandibular gland is a mixed salivary gland; which is divided into superficial
and deep lobes by the mylohyoid muscle. The marginal mandibular branch of the facial
nerve is a lateral relationship to the gland. The lingual and the hypoglossal nerves are
closely related to the medial aspect of the gland. The submandibular duct (Wharton's
duct) emerges from the deep lobe and courses anteriorly between the hyoglossus and
mylohyoid muscles. While occupying this plane the duct is crossed twice by the lingual
nerve, once on its lateral aspect near its origin and again on the medial aspect of the
duct near its termination at the lingual frenulum. The facial artery and vein supplies the
gland and are intimately linked to the submandibular gland.
Tumours of the salivary glands
The diversity of histopathologic lesions that are expressed in the salivary glands make
these tissues truly unique. Salivary gland tumours constitute 3-6 % of all head and neck
tumours. Sixty-five to eighty-five percent of all salivary gland tumours occur in the
parotid gland. The majority (80 %) of parotid tumours are benign; while 50% to 60% of
submandibular tumours and 40% of sublingual and minor salivary gland tumours are
benign. Parotid neoplasms are slightly more common in females. There is a slight racial
predilection for African - Americans over Caucasians. In Kingston, Jamaica, the
incidence of malignant tumours of the salivary gland is 1.2 per 100 000 males and 0.5
per 100 000 females. Salivary gland tumours have an annual incidence of 1 per 100 000
in the United States of America. The majority of patients present in the age range 30 to
70 years.

CLASSIFICATION
Parotid tumours can be classified as tumours of epithelial or non-epithelial origin. The
tumours may be benign or malignant. The malignancies may be primary or
metastastatic parotid tumours.

Tumours of epithelial origin

Benign:
 Mixed tumour (pleomorphic adenoma)

36
  Papillary cystadenoma lymphomatosum (Warthin's tumour)
 Oncocytoma
 Monomorphic tumours
e.g. Basal cell adenoma and Myoepithelioma

Primary Malignant Parotid Tumours:

 Mucoepidermoid carcinoma (low, intermediate and high grade): 15 % of all

salivary gland tumours
 Adenoid cystic carcinoma: 10 % of all salivary gland tumours
 Adenocarcinoma: 8% of all salivary gland tumours
 Carcinoma ex pleomorphic adenoma (carcinoma arising in a mixed tumour) and
Malignant mixed tumour (biphasic tumour): 6% of all salivary gland tumours
 Acinous cell (acinic cell) carcinoma: 3% of all salivary gland tumours
 Oncocytic carcinoma

Secondary or Metastatic Parotid tumours

Tumour-like swellings of the parotid

 Sjogren's syndrome
 Benign lympho-epithelial lesion
 Sialosis

The malignant tumours can also be classified into low and high-grade carcinomas
according to their aggressiveness. Acinic cell carcinoma is a good example of a low-
grade carcinoma. The malignant mixed tumour is usually a high-grade carcinoma.
There are also aggressive subtypes of mucoepidermoid and adenoid cystic carcinoma.
Pleomorphic adenoma
This is the commonest benign tumour of the parotid, submandibular and sublingual
glands. It is responsible for 70 percent of parotid tumours. It occurs slightly more
frequently in females (female to male ratio of 3: 2). It occurs most commonly in the 5th
decade of life. The tumour is slow growing with occasional growth spurts. Facial nerve
palsy is extremely rare and the presence of any facial weakness should suggest
malignant transformation. Pleomorphic adenomas that have been present for greater
than 10 years undergo malignant transformation in 2-10 percent of cases (carcinoma ex-
pleomorphic adenoma).
Grossly the tumour is firm and grey-white with variegated myxoid and blue translucent
areas of chondroid.
The tumour is pleomorphic in a number of ways.
 The stroma may show chondroid, osteoid, myxomatous or fibrous features
 the ratio of stroma to epithelial component varies from tumour to tumour and
from site to site within any one tumour.
 The epithelial cells may be polygonal, cuboidal or columnar and may form nests
or cords of cells

The tumour has an incomplete capsule with pseudopodial projections extending

through the capsule. This explains the high recurrence rate if lumpectomy is

37
performed.

Most of the tumours arise in the superficial lobe and the treatment is superficial
parotidectomy with preservation of the facial nerve. While paresis of the facial nerve
branches occasionally occurs, permanent facial nerve palsy is rare in the hands of the
otolaryngologist. The recurrence rate after superficial parotidectomy is approximately
five percent. When lumpectomy is performed, the recurrence rate can vary from 20- 35
percent

Warthin's tumour
This is also called adenolymphoma or papillary cystadenoma lymphomatosum. It is
the second most common benign neoplasm of the parotid. Warthin's tumour comprises.
4-8 pì¥Á_7?????
Almost exclusive of the parotid gland,, it cause a smooth swelling in the tail of the
gland that may feel cystic
Aetiology
Malignant lesions
The only well-documented risk factor for salivary gland cancer is ionizing radiation.
Benign lesions
Radiation-induced neoplasms in the salivary glands are usually benign. The commonest
associated tumour is the pleomorphic adenoma. The increasing incidence of Warthin's
tumour, especially in women, has been linked to cigarette smoking .

Presentation
Mass
The majority of patients with parotid neoplasms present with painless masses typically
in front of or below the ear.

Pain
Pain is generally found with inflammatory conditions rather than neoplasms. Advanced
malignant parotid lesions may however present with intractable pain. 12 to 24 percent
of malignant tumours of the salivary glands present with pain.
Facial nerve palsy
A parotid lesions that is associated with facial nerve weakness should be assumed to be
malignant until proven otherwise. However only 10 to 15 percent of malignant lesions
present with facial nerve palsy.
Skin involvement and cervical lymphadenopathy
Skin ulceration occurs in 9 percent of malignant lesions. Cervical nodal metastases may
be found in malignant parotid tumours of epithelial origin or primary lymphomas.

DIAGNOSIS
A thorough history and physical examination are essential components of the
assessment but are most useful in the patient with bilateral parotid enlargement.
Sjögren's syndrome, diabetes mellitus, alcoholism, malnutrition, AIDS and drug
hypersensitivity are important causes of bilateral (and less frequently unilateral) parotid
enlargement.

Diagnostic Imaging

38
The imaging options available include plain X-rays, sialography, radiosialography,
ultrasound, CT and MRI. Plain X-rays are only useful in the detection of radio-opaque
calculi. They should not be recommended in the assessment of parotid masses as less
than 20% of parotid duct calculi are radio-opaque. However, 80% of submandibular
calculi are radiopaque.
CT/ MRI are routine investigations in some centres. CT and MRI are unlikely to
influence the management of well-defined, freely movable tumours. CT and MRI are
valuable in the evaluation of patients presenting with palatal or tonsillar swellings in
order to distinguish between deep lobe parotid tumours and other lesions of the
parapharyngeal space.
Radiosialography: The salivary gland striated ductal epithelium can extract Tc99m
(pertechnetate) from the capillary network of the salivary glands. The presence of a hot
mass is usually indicative of Warthin's tumour or oncocytoma. However, hot masses
may occasionally be malignant and therefore radiosialography is unreliable and is not
recommended.
Since the advent of contrast CT, sialography and ultrasonography are rarely indicated
in the investigation of the patient who has parotid disease. Sialography is helpful in
suspected cases of ductal stricture, calculi or sialectasia.
The role of fine needle aspiration cytology
Fine needle aspiration (FNA) has revolutionised the management of many head and
neck lesions. The thyroid gland has been a fruitful area for the cytopathologist. The
results in the salivary glands have been far less impressive. While a diagnostic accuracy
of greater than 90% is sometimes quoted, this has not been the experience in most
centres.
.
Neck Dissection and Radiotherapy
Patients who have clinically apparent cervical nodal metastases should undergo
parotidectomy, radical neck dissection and radiotherapy. Patients who have aggressive
histologic types such as high-grade mucoepidermoid carcinoma, malignant mixed
tumour, high-grade adenocarcinoma and squamous cell carcinoma should have
prophylactic neck dissections and radiotherapy. This also applies to T3 lesions and
lesions associated with facial nerve palsy.
Complications of parotidectomy
 Facial nerve palsy
 Haemorrhage from retromandibular vein, postauricular artery, superficial
temporal artery, maxillary artery or directly from the external carotid artery
 Parasthesia in the distribution of the greater auricular nerve
 Neuroma of the greater auricular nerve
 Frey's Syndrome : this is characterized by sweating over the parotid region
when the patient thinks about food or eats. It is thought to be due to aberrant
regrowth of parasympathetic secretomotor nerves which end up supplying the
sweat glands.

39
 DYSPHAGIA

SURGICAL ANATOMY AND PHYSIOLOGY

The pathway for swallowing involves the oral cavity, the pharynx and oesophagus.
Three anatomical areas of narrowing occur in the oesophagus:

1. At the level of the cricoid cartilage (at the cricopharyngeus )

2. In the midthorax, from compression by the aortic arch and the left main stem
bronchus
3. At the level of the oesophageal hiatus of the diaphragm

Deglutition can be divided into three phases: oral, pharyngeal and oesophageal phases.

40
The oral phase is a voluntary phase during which the bolus is formed and prepared for
transfer into the pharynx. Tongue mobility and adequate salivary flow are very
important in this phase. The pharyngeal phase is the most complex phase, as it requires
the safe transfer of the bolus across a pathway that is also used for respiration. During
the pharyngeal phase the nasopharynx is separated from the oropharynx by the actions
of the tensor palatini and the levator palatini muscles. Respiration temporarily stops at
the end of inspiration. The larynx is elevated and pulled anteriorly under the base of the
tongue. The laryngeal inlet, the false cords, and true cords are closed as a three tiered
protective mechanism. All of this activity requires a finely coordinated neurological
system that is also responsible for relaxation of the cricopharyngeus muscle, allowing
transfer of food from the pharynx to the esophagus. Neurological disorders will often
manifest themselves with dysphagia associated with episodes of aspiration. During the
oesophageal phase the bolus is transferred by a series of peristaltic waves that are
preceded by waves of relaxation. Liquids are predominantly transferred by gravity
when the patient is in the upright position.

CLASSIFICATION OF DYSPHAGIA
The discussion will predominantly focus on the oesophagus

Oral lesions
Malignant lesions such as carcinoma of the tongue and the floor of the mouth
Inadequate salivation e.g. post radiotherapy and Sjogren's syndrome

Pharyngeal lesions
Malignant lesions of the oropharynx and hypopharynx
Pharyngeal webs and strictures

Oesophageal lesions
Lesions in the lumen of the oesophagus
Foreign bodies (commonly coins in children; bones or meat bolus in adults)
Lesions in the wall of the oesophagus
1. Benign Strictures
a. Gastro-oesophageal reflux with reflux oesophagitis
b. Corrosives
c. Post-irradiation
d. Post-traumatic

2. Tumours: malignant and benign

3. Plummer-Vinson-Paterson-Kelly syndrome (usually occurs in middle aged
women but can also occur in men though rarely. It is associated with iron
deficiency anaemia and the development of a postcricoid web. The features of
iron deficiency (glossitis, angular stomatitis and microcytic anemia) will by
present and the web will by demonstrated by barium swallow)
4. Schatzki's ring with hiatus hernia

5. Motility disorders
a. Achalasia of the cardia
b. Cricopharyngeal spasm

41
 c. Diffuse oesophageal spasm
6. Scleroderma
7. Dermatomyositis
8. Crohn's disease
9. Congenital atresia (tracheo-oesophageal fistulae) or stenosis

Lesions outside the wall of the oesophagus

1. Retrosternal goitre
2. Para-oesophageal hiatus hernia
3. Pharyngeal pouch ( Zenker's diverticulum)
4. Mediastinal tumours or mediastinal lymph nodes
5. Aortic aneurysm
6. Dysphagia lusoria

Neural and Neuromuscular disorders

1. Bulbar Palsy
2. Myasthena Gravis
3. Tetanus

The commoner conditions are:

1. Carcinoma of the oesophagus
2. Reflux oesophagitis with stricture formation
3. Achalasia of the cardia

DIAGNOSIS AND MANAGEMENT

The diagnosis is made after a careful consideration of the history, examination and
special tests.
These tests may include barium or gastrografin swallow, endoscopy, videofluoroscopy
and manometry.

History
Age
Achalasia occurs most frequently in patients 30 to 40 years old.
Patients 50-70 years old, with gradual, progressive dysphagia have oesophageal
carcinoma until proven otherwise.

Sex
Paterson-Kelly syndrome occurs almost exclusively in females. Postcricoid carcinoma is
an important complication of Paterson- Kelly syndrome. Apart from this carcinoma,
malignant lesions of the pharynx and oesophagus are predominantly founded in males.

Symptoms
Dysphagia.
1. A sudden onset may suggest foreign body obstruction. Occasionally foreign
body impaction may be the first evidence of carcinoma of the oesophagus.
2. A slow onset is more likely with carcinoma of the oesophagus, achalasia and
stricture formation.

42
 Pain
Retrosternal or back pain following oesophagoscopy or dilatation suggests oesophageal
perforation.
Regurgitation. This is characteristic of long-standing achalasia, a sliding hiatus hernia
and pharyngeal pouch formation. Regurgitation of offensive, undigested food, or a
feeling of a bulge in the neck suggests Zenker's diverticulum.

Signs
Malignancy may be evidenced by weight loss, palpable cervical lymph nodes,
hepatomegaly or ascites. Glossitis and koilonychias may be indicatice of oesophageal
webs.

Special tests
Barium swallow, barium meal and oesophagoscopy are most frequently helpful.

Barium swallow
1. Pharyngeal pouch may be visualized as a rounded pouch
2. Achalasia of the cardia produces
a) Dilatation of the oesophagus
b) The distal oesophagus tapers to a smooth point.
3. Carcinoma of the oesophagus will appear as an irregular filling defect. An
oesophago-bronchial fistula may be demonstrated.

Barium meal
May demonstrate associated gastric disorders such as carcinoma of the cardia extending
into the stomach, hiatus hernia or peptic ulceration.

Oesophagoscopy
Flexible fibreoptic endoscopy is the preferred method for diagnostic oesophagoscopy.
Suspicious lesions should be biopsied.

Manometry
This is most beneficial in the investigation of motility disorders.

Curative treatment
1. Pharyngeal pouch. Cricopharyngeal myotomy is an important component of the
treatment and may suffice for small pouches. The gold stardard is excision of the pouch
via an external approach and cricopharyngeal myotomy. Endoscopic transection of the
partition wall between the pharyngeal pouch and the oesophagus is an alterative option
(Dohlman's procedure).

2. Corrosive stricture. Oesophagoscopy should be done within 36 hours to

determine the extent of injury and to guide further management. Initially broad-
spectrum antibiotics and corticosteroids are prescribed. Subsequently oesophageal
strictures may require repeated dilatation but ultimately bypass, usually with gastic
transposition or a gastric tube flap may be necessary. If the stomach is not suitable,
colonic interposition is an alternative option.

43
3. Achalasia. The best treatment is division of all the muscle layers at the
oesophagogastric junction (Heller's cardiomyotomy).

Carcinoma of the oesophagus

This occurs particularly in males over 60 years. There is a higher incidence in
females with Plummer-Vinson-Patterson-Kelly Syndrome. Longstanding achalasia and
corrosive strictures are predisposing factors. Southern Africa and China have high
incidences. Iron brewing pots and nitrosamines have been linked to oesophageal
carcinoma.
The lower third of the oesophagus is involved in 50% of cases and the middle third in
35%.
Most are non-keratinising squamous cell carcinomas. Metaplasia of the distal
oesophagus (“Barrett's oesophagus.”) may precede the development of an
adenocarcinoma.
The main modalities of spread are direct and via lymphatics.
Oesophageal mucosal skip lesions may also occur as the cancer spreads in the
sumucosal plane.
The mortality from oesophagectomy is still of the order of 15% and the average survival
time after operation is about 15 months.
Achalasia
Failure of relaxation of the lower oesophagus (achalasia) is considered to result from a
neuromuscular disorder, which may be associated with degeneration of Auerbach's
plexus. Similar changes have been noted in Trypanosoma cruzi infection (Chagas' disease).
The condition usually occurs in middle-aged.
The best treatment is division of all the muscle layers at the oesophagogastric junction
(Heller's cardiomyotomy).

Dysphagia lusoria
The oesophagus may be compressed by an anomalous right subclavian artey or a
double aortic arch.

SWELLINGS OF THE THYROID GLAND

Identification: - The thyroid is surrounded by the pretracheal fascia and is firmly

attached to the trachea by the ligaments of Berry and thus moves upwards on
swallowing.
When a patient presents with a thyroid mass, the doctor will need to ascertain the
following:
(1) The functional status of the thyroid
(2) Whether or not there is a neoplastic process going on
(3) Whether or not the mass is causing a local functional problem, by compression or
invasion
(4) Whether there is an inflammatory or infiltrative process going on.
(5) Whether or not the thyroid mass presents a cosmetic problem to the patient.

44
Patients with thyroid swellings can be classified clinically as having

Diffuse, non-toxic goitre e.g. physiologic goitre

Diffuse toxic goitre e.g. Grave's
Nodular goitre ----solitary or multiple and toxic or non-toxic
Most thyroid neoplasms present as solitary, non-toxic goitres

Most thyroid masses are multinodular goitres. If the thyroid is not producing
adequate amounts of thyroxine (as occurs when dietary iodine intake is poor), TSH
levels rise and the gland becomes hyperplastic. When thyroxine production is sufficient,
increased colloid stores are found. After several cycles, multinodular goitres develop
with areas of hyperplasia and other areas with colloid stores. Cystic degeneration,
calcification and haemorrhage may occur in these multinodular goitres.
In the early stage in the development of these goitres, thyroxine supplement should be
given to reduce TSH secretion. This can cause regression of hyperplastic areas but
would not be expected to affect areas of cystic change and large colloid nodules.
Surgery is recommended for lesions causing significant compression of the trachea,
oesophagus or recurrent layngeal nerves.

Thyroiditis

a) Grave's Disease (accounts for 85% of cases of thyrotoxicosis)

This is an autoimmune disorder characterised by a diffuse goitre, hyperthyroidism and
ophthalmic involvement. Thyroid-stimulating immunoglobulins (e.g. LATS, an IgG
antibody to TSH receptor) and thyroid growth-stimulating antibodies result in
hyperplasia and overactivity of the thyroid. The patient presents with features of a
hypermetabolic state as well as symptoms related to overactivity of the sympathetic
system (thyroxine facilitates sympathetic activity). Palpitations, excess sweating, weight
loss despite increased appetite; heat intolerance, nervousness, tremors and menstrual
disturbances are common. Cardiac arrhymias are most common in the elderly.
Exophthalmos, lid lag, lid retraction, ophthalmoplegia and chemosis are the ophthalmic
features. Lid lag and lid retraction are the result of increased activity in the smooth
muscle of the levator palpebrae superioris (supplied by sympathetics) Pretibial
myxoedema and gynaecomastia may occur. The T4 and T3 levels are elevated and the
TSH suppressed. Thyroid scan demonstrates diffuse increased uptake.

Treatment
a) Medical Therapy with antithyroid drugs(usually carbimazole plus B-Blocker)
Often used in young patients, pregnant women, patients with cardiac
complications. The disadvantages include a 50% recurrence rate after 2 years of
therapy, drug rashes and leucopaenia.
b) Radioiodine 131
Can be given as a simple drink. Avoids the risk of surgery and the complications
of medical therapy. There are theoretical risks of carcinogenesis and
teratogenicity. Therefore generally given to men and women over age 40 years.
The onset of its effect is slow.
c) Surgery

45
 Acts quickly, but 1% incidence of permanent hypoparathyroidism and recurrent
laryngeal nerve palsy. Generally in thyrotoxicosis, surgery is usually done for
large goitres, compression symptoms.

Thyroid nodules are common. Palpable thyroid nodules are present in 5% of the adult
population. Autopsy studies have found thyroid nodules in 50% of patients dying from
non-thyroidal disease. Of the nodules detected at autopsy, 75 % were multinodular
goitres and 25 % solitary nodules.
The surgeon must utilise his clinical skills along with the appropriate investigations to
identify the nodules that are malignant so that they can be treated appropriately.
Benign nodules may also require surgical management because of symptoms of
compression, hyperthyroidism with failed medical therapy or for cosmetic reasons.

The major forms of thyroid cancer are the papillary, follicular, medullary and anaplastic
carcinomas but lymphomas, sarcomas, carcinosarcomas and metastatic lesions can also
occur in the thyroid.

HISTORY AND PHYSICAL EXAMINATION

A careful history and a thorough physical examination are required before
embarking on special investigations of the thyroid. There is no symptom or sign that is
pathognomonic of carcinoma of the thyroid but some are more frequently associated
with malignancy. If the clinical features suggest malignancy, lobectomy and histologic
diagnosis are generally required even if the special investigations suggest a benign
lesion.

HISTORY
1. The patient's age and sex are important aspects of the history. While 80% of
thyroid nodules occur in women, nodules in men are three times more likely to be
malignant.
2. A history of exposure to low dose gamma radiation (0.06 to 20 Gy) increases the
incidence of both malignant and benign thyroid nodules for at least 30 years after
the exposure (Harvey 1990).
Most of these malignancies are papillary carcinomas.
3. A family history of thyroid carcinoma suggests the possibility of medullary
carcinoma of the thyroid although 80% of medullary carcinomas are sporadic
cases. Papillary carcinoma of the thyroid can also be familial.
4. Patients who have Gardner's syndrome and those who have Cowden's disease
have an increased risk of developing thyroid cancer. Cowden's disease is
characterised by mucocutaneous lesions and internal malignancy. The disorder is
autosomal dominant and is associated with breast cancer, cancer of the colon and
benign and malignant thyroid nodules.
5. A history of surgery for a previous thyroid carcinoma is important as any
recurrent thyroid nodule would have to be deemed malignant unless proven
otherwise by histology. Recurrence may occur because the lesion was multifocal.
Persistent carcinoma can remain in the thyroid when the original carcinoma is
inadequately treated and then enlarge to form a palpable “recurrent nodule”.
6. Hoarseness, secondary to vocal cord palsy that occurs on the same side as a

46
 thyroid nodule, is highly suggestive of malignancy. Large, benign thyroid nodules
can cause recurrent laryngeal nerve palsy but the presence of vocal cord palsy,
makes histologic diagnosis mandatory.
7. Dysphagia and dyspnoea are non-specific symptoms that are found in both benign
and malignant lesions. Pain is present in less than 10% of malignant thyroid
nodules. In fact, pain suggests thyroiditis or haemorrhage in an adenoma or
thyroid cyst.
The commonest cause of a rapid increase in the size of a thyroid nodule is
haemorrhage in a benign nodule. If aspiration or ultrasound does not suggest that
haemorrhage has occurred then the lesion should be considered malignant and
histologic assessment is required. It is worthwhile remembering that benign
thyroid lesions may undergo malignant degeneration. Anaplastic change may
occur in a long-standing multinodular goitre. Patients with Hashimoto's
thyroiditis have a 70 times higher incidence of lymphoma than the general
population.

PHYSICAL EXAMINATION
Nodules that are hard, gritty or fixed to the surrounding structures are highly likely to
be malignant. Malignancy is more common in solitary nodules than in multinodular
lesions. The incidence of malignancy in multinodular goitres has been reported to be
1%. Forty to seventy-five percent of clinically solitary thyroid nodules are found to be
multinodular on ultrasound examination. A dominant nodule in a multinodular goitre
should therefore be managed as if it was a solitary nodule because malignant
degeneration may occur in a multinodular goitre.
The presence of non-tender, cervical lymphadenopathy is a strong indicator of the
probability of thyroid malignancy. Recurrent laryngeal nerve palsy has already been
mentioned as evidence of malignancy until proven otherwise by histology. A solitary
thyroid nodule associated with an ipsilateral Horner's syndrome, though rare, can be a
useful pointer to malignancy with extra-thyroidal spread.

INVESTIGATION OF THE SOLITARY THYROID NODULE

When the history and physical examination findings are very suggestive of a
malignancy, then diagnostic studies such as ultrasound, thyroid scan and fine needle
aspirate are generally not indicated. Histologic diagnosis is mandatory and the most
cost-effective method is to proceed with thyroidectomy after radiologic assessment of
the extent of the lesion. However, ninety-five percent of all patients with malignant
thyroid nodules will be euthyroid and asymptomatic. Diagnostic screening methods are
therefore usually required to select the nodules that are likely to be malignant.

ULTRASOUND
Ultrasound examination of the thyroid can accurately assess the size of the thyroid
gland, the number and dimensions of nodules present, and distinguish between solid
and cystic lesions. Ultrasound is also useful in detecting cervical lymphadenopathy.
Thyroid ultrasound is non-invasive, repeatable without any special preparation and
does not expose the patient to radiation. It is especially useful in pregnant women and
in children as it avoids the radiation of a scan and the mild discomfort of a fine needle
aspirate.

47
THYROID SCAN
The most common isotopes used in radionuclide imaging are I 131 I123 and
Tc99 pertechnetate. Technetium-99m pertechnetate is trapped in the thyroid but unlike
iodine it is not organified by the thyroid. Technetium-99m pertechnetate and
radioactive iodine 123 (I-123) have replaced radioactive iodine 131 (I-131) in routine
thyroid scanning because of the higher radiation dose with the latter isotope. I-131 is
now mainly used therapeutically and in screening for metastases. Technetium-99m
pertechnetate offers the lowest radiation dose and can be given intravenously with the
test being performed on the same day and this is a distinct advantage over radioactive
iodine.
Nodules can be classified according to their ability to take up the radioisotope. Non-
functional nodules are labelled “cold”, normally functioning nodules are “warm” and
hyper- functioning nodules are “hot”. In Ashcraft and Van Herle's review of 22
series(1981) in which all patients underwent surgery regardless of the functional status
of the nodules, 84% were cold, 10.5% were warm and 5.5 % were hot. Malignancy was
found in 16% of the cold nodules, 9% of the warm nodules and 4% of the hot nodules.
Thyroid scans cannot distinguish between benign and malignant thyroid nodules but
rather give an indication of the probability of malignancy in a nodule. It is to be noted
that even “hot” nodules can be malignant.

FINE NEEDLE ASPIRATION CYTOLOGY

Fine-needle aspiration (FNA) cytology has revolutionised the assessment of the solitary
thyroid nodule.
The accuracy of the technique depends on adequate sampling of the thyroid and the
experience of the cytopathologist. The best results are obtained when the
cytopathologist takes the aspirate as well as interprets the sample. The sample is
satisfactory for a diagnosis to be made in 85% to 90% of aspirates in experienced
centres. Results can be classified as benign (75%), suspicious (20%) and malignant (5%).
The main limitation of the fine-needle aspirate is its inability to distinguish follicular
adenoma from the well-differentiated follicular carcinoma. Instead, a diagnosis of
“follicular neoplasm” is offered and a lobectomy with histologic diagnosis is required.
Vascular or capsular invasion is necessary for the histologic diagnosis of follicular
carcinoma to be made. Follicular neoplasms are responsible for the majority of aspirates
that are reported as “suspicious”. The reported incidence of false-negative results varies
from 8% to 10% in most series while false-positive results occur in approximately 2.5 %
of cases.

Lesions diagnosed as “malignant” and those labelled “suspicious” should undergo at

least a lobectomy unless the diagnosis is anaplastic carcinoma or the patient is unfit for
the procedure. Alternatively, “suspicious” lesions can be followed up with
ultrasonography and thyroid scan. Nodules labelled “benign” require follow-up with
observation for clinical features suggesting malignancy and the fine needle aspirate can
be repeated because of the incidence of false-negative aspirates. Fine needle aspiration
is useful in diagnosing and treating thyroid cysts. The cellular yield from aspiration of a
cyst is poor and an attempt should be made to aspirate the wall of the cyst after removal
of the fluid. Ultrasound can be useful in guiding the aspiration. Large thyroid cysts (> 4

48
cm diameter) and cysts that recur three times after repeated aspiration require
lobectomy and histology because they can represent cystic degeneration in a malignant
nodule.

X-RAYS, CT SCAN AND MRI

These radiologic studies are not generally used to differentiate benign and malignant
thyroid lesions. Plain X-rays can demonstrate tracheal deviation and compression as
well as any evidence of retrosternal extension. Pulmonary metastases are uncommon on
initial presentation but these are often found on follow-up X-rays. The CT scan can
accurately assess the extent of the primary lesion, cervical and pulmonary metastases.
Unfortunately CT scans often involve the use of significant amounts of iodine in
contrast reagents. This could interfere with subsequent radioactive iodine scan and
therefore MRI is to be preferred if this is available.

SPECIAL BLOOD INVESTIGATIONS

Patients with nodular goitres are almost always euthyroid. Free T4, free T3 and TSH
levels can be obtained as baseline studies in patients who will undergo surgery.
Thyrotoxicosis can usually be detected by a careful history and examination but one
should confirm the clinical findings because there is a risk of a thyroid storm when
surgery is performed on the thyrotoxic patient.
Serum calcitonin levels should be measured in patients with a family history of
medullary carcinoma and in those with intractable diarrhoea. Occasionally, features of a
multiple endocrine neoplasia syndrome (such as mucosal neuromas) may be discovered
and calcitonin levels should be obtained in these cases.

TOTAL VERSUS PARTIAL THYROIDECTOMY

Considerable debate exists on the surgical aspects of the treatment of thyroid cancer.
There is no large prospective, randomised clinical trial comparing the efficacy of
lobectomy and total thyroidectomy in the management of thyroid carcinoma.
With the exception of tumours localised to the isthmus, the minimum surgery that
should be performed in a case of a thyroid nodule is an ipsilateral lobectomy and
isthmusectomy. (Nodules confined to the isthmus can be excised with a 1 cm resection
margin of normal tissue from the medial aspect of each lobe).

Partial lobectomy should generally not be done because this

a) increases the risk of entering and disseminating tumour

b) risks a recurrence on the ipsilateral side and the recurrent laryngeal nerve and the
parathyroids would then be in considerable danger of injury at revision surgery
c) is associated with a higher recurrence rate and lower survival rate in the case of
malignant nodules.

There is general agreement that total thyroidectomy should be performed when there is
1) extrathyroidal or metastatic disease
2) gross bilateral lobar involvement
3) residual tumour after previous resection
4) history of significant radiation to the head and neck

49
There is considerable controversy on the extent of surgical resection necessary for the
unilateral and grossly intrathyroidal, differentiated carcinoma of the thyroid. The most
important rationale for total thyroidectomy is that it facilitates the use of radioactive
iodine in the detection and treatment of any local or metastatic lesions. Normal thyroid
tissue has a 100-fold greater affinity for iodine than papillary or follicular carcinoma of
the thyroid. The presence of residual thyroid tissue can therefore significantly impair
the uptake of radioactive iodine by metastatic lesions.
Histologic sections have demonstrated microscopic foci of carcinoma in the
contralateral lobe in up to 85% of cases of papillary carcinoma. Total thyroidectomy
would eliminate these foci, which are potential sources of “recurrence. The lowest
recurrence rate has been found in patients who have had a combination of total
thyroidectomy, radioactive iodine and TSH suppression using exogenous thyroxine.

A true total thyroidectomy eliminates the 1% risk of anaplastic change that occurs in
differentiated thyroid carcinomas. The use of thyroglobin levels as a tumour marker for
recurrent thyroid carcinoma is also greatly facilitated by total thyroidectomy.

The arguments in favour of a lobectomy include the reduced morbidity when this
operation is compared to total thyroidectomy. The incidence of recurrent laryngeal
nerve palsy and that of permanent hypoparathyroidism is increased in total
thyroidectomy compared to lobectomy.

Factors associated with a poor prognosis in differentiated carcinoma of the thyroid

1) Age and sex

Males greater than forty years old and females older than fifty years have a poor
prognosis.

2) Size of primary tumour and direct extra- thyroidal extension

Primary cancers 5 cm or larger and evidence of extra-thyroidal spread are factors
associated with a reduced survival.

3) Regional nodal and distant metastases

Distant metastases have a significant effect on the mortality rate of differentiated
carcinoma of the thyroid. In papillary carcinoma of the thyroid, cervical nodal
metastases seem to increase the incidence of recurrence in the neck but do not
significantly affect the mortality rate

4) Residual tumour after surgery

Incomplete resection of carcinoma of the thyroid is an independent prognostic factor
that has a negative effect on survival.

5) Histologic type and degree of differentiation.

The following histologic variants of papillary carcinoma tend to run an aggressive
clinical course:

50
a) Diffuse sclerosing
b) Tall cell

c) Columnar cell.
The degree of capsular and especially vascular invasion has an inverse relationship to
survival in follicular carcinoma of the thyroid .

RECOMMENDATIONS
Total thyroidectomy is a relatively safe operation in the hands of experts with a 2%
incidence of recurrent laryngeal nerve palsy and 3% permanent hypoparathyroidism
(Lore,1988). Total thyroidectomy facilitates radioactive iodine therapy and also
facilitates the use of thyroglobulin as a tumour marker for metastases, eliminates
multifocal disease, reduces local recurrence and prevents anaplastic change in any
tumour which would have remained in the thyroid had a lobectomy been performed. It
is difficult to argue against total thyroidectomy when this operation is performed with
minimal morbidity.

All patients with follicular carcinoma or Hürthle cell carcinoma should have a total
thyroidectomy unless the patient is unfit for surgery or the primary is not resectable.
Follicular carcinoma and the Hürthle cell carcinoma tend to have worse prognoses than
papillary carcinoma. Papillary carcinoma that is associated with any of the factors listed
above as indicators for a poor prognosis, should be managed by total thyroidectomy.
All other cases of papillary carcinoma can be treated by a lobectomy because this
reduces the surgical risks to the patient and gives equivalent recurrence and survival
rates to total thyroidectomy in these patients.

When nodal metastases are present, a modified radical neck dissection should be
performed and any paratrachael or superior mediastinal metastatic nodes resected. This
approach will reduce the local recurrence rate but will not significantly alter the
survival rate in papillary carcinoma.
Medullary carcinoma is best managed by total thyroidectomy and unilateral or bilateral
neck dissections.
Anaplastic carcinoma is usually not resectable at presentation and surgical management
is often limited to incisional wedge biopsy of the isthmus and tracheostomy.

51
 NECK INJURIES
Injuries that involve the anterior triangle of the neck have a greater potential for fatality.
The neck can also be divided into the Zones I-III.
Zone I: sternal notch to the cricoid cartilage
Zone II: cricoid cartilage to the angle of the mandible
Zone III: above the angle of the mandible
The platysma muscle covers the anterior triangle and a significant portion of the
posterior triangle. Traditionally it has been said that injuries that penetrate the
platysma require hospitalisation. Familiarity with the location of the platysma (just
deep to the skin) will make one realize that this policy would result in virtually all
patients being admitted to hospital.

The initial management follows the ABC's of the resuscitation of the patient with
multiple trauma. Of paramount importance is the establishment of adequate airway
control. Stridor, air escape via the neck wound, hoarseness, surgical emphysema and
haemoptysis are suggestive of injury to the airway. Adequate light and suctioning are
essential. If flexible endoscopy is available this should be utilised to assess the upper
airway and to facilitate intubation under direct vision. In patients with gunshot injuries
to the neck, tracheostomy is usually the best option as endotracheal intubation can
convert a partially transected trachea to complete transection. In many cases the site of
the wound facilitates the initial insertion of the tracheostomy tube.

One should always protect the cervical spine until cervical spinal injury can be ruled
out. It may therefore be necessary to perform tracheostomy with the neck in the neutral
position.

The adequacy or ventilation must be ensured. One should check for features of a
tension pneumothorax. Control of hemorrhage may be achieved by tamponade while
blood is taken to group and cross match the patient. The patient who is in shock but
has distended neck veins may have a tension pneumothorax or cardiac tamponade.

Clinical signs of significant injury in penetrating injuries to the neck

Airway injury
Stridor, dyspnea, hoarseness, subcutaneous emphysema
Vascular injury
Circulatory shock, expanding haematoma, active bleeding, thrill or bruit, absent or
reduced pulses
Oesophageal injury
Haemoptysis or haematemesis, dysphagia or odynophagia, subcutaneous emphysema
Neurologic signs
Deteriorating consciousness level
Contralateral neurologic signs: suggest carotid injury on the ipsilateral side
Ipsilateral neurologic signs with sensory level: suggests spinal injury
Specific features of injury to the brachial plexus, vagus, recurrent laryngeal,
hypoglossal, marginal mandibular or phrenic nerve may be present.

52
 Possible investigations include:
CBC, urea and electrolytes, cross match
Neck x-rays (including lateral view of cervical spine) and chest x-rays
Doppler ultrasound or angiography
Barium swallow and endoscopy

Neck exploration
Patients in circulatory shock, who cannot be stabilised, require urgent neck exploration.
Patients, who are stable, can be investigated prior to surgery. This is especially
important in patients with level I injury were the possibility of significant intra-thoracic
vascular injury exist. Access to the major vessels may be difficult in patients with level
III injuries and here; once again, investigations are helpful in locating the exact site of
injury. In assessing the patient, one should always bear in mind the trajectory since an
entry wound may be in level II but significant damage may still occur in level III or in
the superior mediastinum.

Tonsils and adenoids

The tonsils and adenoids are the largest members of Waldeyer's ring. They are
strategically located posterior to the oral cavity and the nasal cavity respectively. They
are able to sample foreign organisms and antigens and present the information to the
rest of the immune system so that an adequate immune response can be mounted.
Tonsillectomy and adenoidectomy may be necessary when the tonsils and adenoids are
causing significant obstructive problems or when they repeatedly become infected.
Tonsillectomy and adenoidectomy does not generally increase in the incidence of
infections. This may be partially due to the fact that the other members of Waldeyer's
ring can carry out the function of the tonsils and adenoids in their absence.

Indications for tonsillectomy and adenoidectomy

A. Infections
1. Recurrent acute tonsillitis of a frequency that significantly impairs the patient's
education or occupation. In children, 4 episodes of acute tonsillitis in one year would
warrant tonsillectomy.
2. Chronic tonsillitis---- characterized by persistent sore throats, small tonsils, and chronic
cervical lymphadenopathy.
3. Two episodes of peritonsillar abscesses (quinsy)
4. Frequent tonsilloliths (usually occurring in patients with large intra-tonsillar recesses)
5. Recurrent febrile convulsions due to tonsillitis
6. Carriers of Diphtheria in the tonsils
7. Recurrent attacks of acute rheumatic fever despite antibiotic prophylaxis
8. Atypical Mycobacterium infection of tonsils with cervical lymphadenopathy

B. Obstruction
1. Obstruction to the eustachian tube resulting in otitis media with effusion or recurrent
acute otitis media
2. Obstruction to the drainage of the nose and paranasal sinuses resulting in recurrent or
chronic rhinosinusitis
3. Obstruction to the airway which may result in snoring, mouthbreathing, obstructive
sleep apnoea, cor pulmonale

53
4. Obstruction to the oral pathway resulting in difficult eating

C. Miscellaneous
1. Unilateral enlargement of the tonsils (suggestive of malignancy)
2. Metastatic cervical lymph nodes of unknown origin
3. In the operation uvulopalatopharyngoplasty (used to treat severe snoring)
4. In the surgical approach to the glossopharyngeal nerve (in patients with
glossopharyngeal neuralgia)
5. In the surgical approach to the styloid process

The main complication of tonsillectomy is primary or secondary hemorrhage. The

blood supply to the tonsils consist of branches from
a) Tonsillar branch of the facial artery d) Palatine branches of the
b) Palatine branch of the facial artery maxillary artery
c) Lingual artery e) Ascending pharyngeal artery

STRIDOR
Stridor is the auditory manifestation of obstruction of the larynx or trachea. Often musical in
character. High or low pitched.
Glottic obstruction-----Inspiratory stridor
Subglottis and trachea----Inspiratory and expiratory

Always require prompt assessment, establishment of aetiology and if possible relief of

the obstruction

Common causes in adults

Upper aerodigestive cancers: Cancers of the larynx, hypopharynx, oesophagus, trachea
Thyroid cancers
Bilateral vocal cord palsy: Post thyroidectomy, Bulbar palsy
Blunt and penetrating cervical injuries

Common causes in children

Congenital: Laryngomalacia, subglottic stenosis, bilateral vocal cord palsy, subglottic
haemangiomas, laryngeal cysts and webs

Acquired: Laryngotracheobronchitis and epiglottitis, Foreign body aspiration, Laryngeal

papillomatosis, Caustic ingestion and steam inhalations. Diphtheria is now an
infrequent cause.
Croup
This is a condition of infants and children due to obstruction of the larynx by allwrgy
forign fg

Croup Syndrome
Laryngotracheobronchitis Acute Epiglottitis
6 months-2 years 3-7 years
Preceding URTI symptoms for 2-3 days Develop over hours rather than
days

54
 Low grade fever Marked pyrexia
Marked dysphagia and drooling
Drooling absent Haemophilus influenza

Parainfluenza virus

TRACHEOSTOMY
Creation of an opening (window) in the anterior wall of the trachea. In children a slit is
made and no cartilage resected (tracheotomy).

Indications
Upper airway obstruction----See causes of stridor
Protection of the tracheobronchial tree:
Coma due to Drug Overdose, CVA
Bulbar Poliomyelitis
Guillain-Barre Syndrome
Trauma- surgical or accidental with bleeding into upper airways

Respiratory Failure… Requiring prolonged intubation,

55
Reduction of dead space

Outline of Tracheostomy Technique

Tracheostomy should be performed, whenever possible as an elective procedure, with

an endotracheal tube in place. Adequate suction, lighting and oxygen should be
available. The operation is ideally performed in the Main Operating Theatre. Test the
competence of the valve to the tracheostomy tube's bulb. In adult patients, size 8.5 or 9
mm Portex tube is generally adequate for males. While in females size 7.5 –8 mm
should be selected. Alternate sizes should readily be available should there be
difficulty in inserting the tube.

Positioning: Supine with neck in extension (place sandbag under shoulders)

Inject with 1% lignocaine in adrenaline 1: 200,000

Incision with size 15 blade 2cm below the cricoid cartilage or midway between the
sternal notch and the cricoid cartilage
Blunt dissection and retraction of strap muscles laterally
Elevate or transect thyroid isthmus
Control bleeding. Change sucker from rigid type to flexible suction tube.
Incise trachea and hold cartilage to be resected with Allis forceps. Suction trachea and
insert tracheostomy tube. Inflate bulb with air. Secure tracheostomy tube with tapes or
2/0 silk sutures.

Complications of tracheostomy
Perioperative Early Complications Late Complications
Complications

56
1. Haemorrhage from the 1. Obstruction to the 1. Granulation tissue
anterior jugular veins, tracheostomy tube formation in the trachea
inferior thyroid veins, 2. Accidental 2. Tracheal stenosis
brachiocephalic veins decannulation 3. Erosion into the
and rarely thyroidea ima innominate artery
artery 4. Tracheo- cutaneous
2. Injury to the recurrent fistula
laryngeal nerve 5. Keloid formation at
3. Injury to the oesophagus the tracheostomy site
with the creation of a
tracheo- oesophageal
fistula
4. Injury to thoracic duct
leading to a chylous
fistula
5. Pneumothorax
6. Massive surgical
emphysema
7. Apnoea in the patient
who has had long-
standing upper airway
obstruction

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