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.
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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.

Common causes of conductive hearing loss include

a) Otitis media with effusion--- commonest cause in children

b) Wax impaction--- common in all age groups
c) Acute and chronic otitis media
d) Ossicular chain discontinuity (post trauma or secondary to infection)
e) Otosclerosis--- Second most common cause in Caucasian adults (after wax impaction)

Common causes of sensorineural hearing loss include

a) Presbycusis---usually secondary to ischaemia of the Organ of Corti
b) Noise induced hearing loss
c) Ototoxicity (aminoglycosides, loop diuretics, cytotoxic agents e.g. Cisplatin, quinolones)
d) Meningitis
e) Viral infections (Measles, Mumps, Herpes Zoster etc)
Presbycusis – progressive, bilaterally symmetrical perceptive hearing loss occurring with age usually at
the higher frequencies

Sensorineural Hearing Loss in Childhood

a) 50 % thought to be of 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)

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 Audiological Testing

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
• Give an indication of 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
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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.

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.

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
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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)
……………………………………………………
……….
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 fixation Nystagmus not influenced by visual 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.

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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 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).

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

Chronic suppurative otitis media: This condition is 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 otorrhoea
diminution of otalgia.
No mucus in otorrhea Discharge is mucopurulent
Very mild hearing loss Mild to moderate hearing loss
Pressure on the tragus and movement of the Pain unrelated to movement of pinna
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:

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• 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 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.

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 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 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.

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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
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)
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 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 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
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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 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
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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.

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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:

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 β-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
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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 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

15
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
• and 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 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

16
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:

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
17
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.
o Intravenous aminoglycosides used to be the main antibiotic therapy.

o 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
18
 malignant otitis externa provides a good medium for the growth of anaerobic organisms.

o 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.

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.

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
19
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

Examples of 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.

Examples of general causes

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:

20
 • Selective depression of the megakaryocytes by drug toxicity (cotrimoxazole,
phenylbutazone, thiazides, tolbutamide) or viral infections.
• Generalised bone marrow failure: plastic anaemia, leukaemia, marrow infiltration or
myelosclerosis.
• Ineffective platelet production: megaloblastic anaemia.

2) Increased platelet destruction:

• Idiopathic thrombocytopaenic purpura

• Secondary immune thrombocytopaenia ( post-infection, SLE, chronic lymphocytic
leukaemia)
• Disseminated intravascular coagulation
• 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 whether the epistaxis is predominantly an anterior or posterior bleed and
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

21
passing around the border of the septum). It is important to ask about any syncopal sensation, which
may be indicative of cardiovascular decompensation. The patient should be asked to give an 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. One should ask about nasal trauma( including nose-
picking), upper respiratory tract infections, recent medications, history of bleeding diathesis and any
significant medical illness.

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

The patient's 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 suctioning the clots, local anaesthetic and
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 resuscitation of the circulatory volume
with intravenous fluid and blood transfusion (if necessary) is carried out. 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 tamponade of the nasal vessels between the fingers,
nasal cautery, nasal packing, and 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.
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. Silver nitrate, trichloro-acetic acid
and electrocautery are highly effective. Electrocautery is the more effective than chemical cautery in the
22
presence of active bleeding, but would require general anaesthesia in children
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.

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 to facilitate 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 the 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.
23
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
well 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 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
24
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 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
25
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)

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.

26
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 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
27
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 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.
28
 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 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.
29
Complications of Sinusitis

Local
1. Chronicity and irreversible mucosal change
2. Mucocele
3. Osteomyelitis especially of the diploic anterior wall of frontal sinus

Orbital complications

(1) Dacrocystitis because of obstruction of the Naso-Lacrimal Duct.

(2) Conjunctivitis
(3) Subperiosteal abscess
(4) Periorbital cellulitis
(5) Orbital Cellulitis
(6) Orbital abscess
(7) Ophthalmoplegia
(8) Blindness

Intracranial Spread

Epidural Abscess
Meningitis
Subdural Abscess
Frontal lobe Abscess
Cavernous sinus thrombosis

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
30
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, glottic
muscles and cricoarytenoid joints.

CAUSES OF HOARSENESS

Intrinsic lesions of larynx

Acquired lesions
Vocal cord nodules
Vocal cord polyps
Reinke's oedema (marked oedema in the submucosa of the true cords)
Acute and chronic laryngitis
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

Congenital lesions

Vocal cord palsy

Vocal cord webs
Laryngeal cysts
Laryngocoele
Haemangioma or lymphangiomas

Recurrent laryngeal nerve palsy

This may be secondary to a lesion of the vagus or a direct lesion of the recurrent laryngeal nerve.

Supranuclear lesions of the vagus

Cerebrovascular accident
Nuclear lesion
Bulbar poliomyelitis
Motor neuron disease
Lateral medullary syndrome
31
Posterior fossa lesions
Acoustic neuroma
Meningioma
jugular foramen lesions
Glomus jugulare
Metastatic carcinoma of the nasopharynx

Cervical lesions
Penetrating neck injuries
Carotid body surgery
Radical neck dissection

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
32
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, 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.

Dyspnoea and stridor may be the presenting features in patients with advanced laryngeal cancer.
These symptoms may be present without hoarseness in the patient with a supraglottic or subglottic
tumour.

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
33
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 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
34
into the trachea.

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 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.

35
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)
• 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
36
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 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
37
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
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
38
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

a) Facial nerve palsy

b) Haemorrhage from retromandibular vein, postauricular artery, superficial temporal artery, maxillary
artery ordirectly from the external carotid artery

c) Parasthesia in the distribution of the greater auricular nerve

d) Neuroma of the greater auricular nerve

e) 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.

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:

39
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.

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

1) Malignant lesions such as carcinoma of the tongue and the floor of the mouth

2) Inadequate salivation e.g. post radiotherapy and Sjogren's syndrome

Pharyngeal lesions

1) Malignant lesions of the oropharynx and hypopharynx

2) 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)

40
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
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

41
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.

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.
42
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.

3. Achalasia. The best treatment is division of all the muscle layers at the oesophagogastric junction
43
 (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
44
(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.

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

45
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
Acts quickly, but 1% incidence of permanent hypoparathyroidism and recurrent laryngeal nerve palsy.
Generally in thyrotoxicosis, surgery is usually done for large goitres, compression syì¥Á_7???????

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

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.
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.

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.

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.

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
46
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”.

Hoarseness, secondary to vocal cord palsy that occurs on the same side as a 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.

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
47
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.

THYROID SCAN
The most common isotopes used in radionuclide imaging are I131 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

48
“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 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
49
 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

a) extrathyroidal or metastatic disease

b) gross bilateral lobar involvement

c) residual tumour after previous resection

d) history of significant radiation to the head and neck

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
50
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:

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 tracheostì¥Á_7 1??????_

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.
51
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.

Possible investigations include:

1) CBC, urea and electrolytes, cross match
2) Neck x-rays (including lateral view of cervical spine) and chest x-rays
52
 3) Doppler ultrasound or angiography
4) 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

53
 3. Obstruction to the airway which may result in snoring, mouthbreathing, obstructive sleep
apnoea, cor pulmonale

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

b) Palatine branch of the facial artery

c) Lingual artery

d) Palatine branches of the maxillary 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

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

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

1) Protection of the tracheobronchial tree:

2) Coma due to Drug Overdose, CVA
3) Bulbar Poliomyelitis
4) Guillain-Barre Syndrome
5) Trauma- surgical or accidental with bleeding into upper airways
6) Respiratory Failure… Requiring prolonged intubation,
7) 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.
55
Positioning: Supine with neck in extension (place sandbag under shoulders)

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

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

Complications of tracheostomy

Perioperative Complications

1. Haemorrhage from the anterior jugular veins, inferior thyroid veins, brachiocephalic veins and
rarely thyroidea ima artery
2. Injury to the recurrent laryngeal nerve
3. Injury to the oesophagus 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

Early Complications

8. Obstruction to the tracheostomy tube

9. Accidental decannulation

Late Complications

10. Granulation tissue formation in the trachea

11. Tracheal stenosis
12. Erosion into the innominate artery
13. Tracheo- cutaneous fistula
14. Keloid formation at the tracheostomy site

56