NASOPHARYNGEAL CARCINOMA

INTRODUCTION
Nasopharyngeal carcinoma is a tumour of epidermoid origin that is endemic in certain ethnic
groups. It constitutes 90% of all malignancies found in the nasopharynx. Nasopharyngeal carcinoma is
prevalent in the Cantonese Chinese in Southern China, Hong Kong and Singapore. The age-adjusted
incidence in males in Hong Kong is 26: 100,000. In Jamaica it is found in 1.4: 100,000 males and 0.5:
100,000 females. This cancer is uncommon among Caucasians. In North America the incidence is 1:
100,000. In Northern China nasopharyngeal carcinoma has an incidence of only 3 per 100,000. There is a
moderately high incidence in the Malays, Indonesians, Thais and Filipinos. In North African countries
such as Tunisia, Algeria and Sudan the incidence is less than that in South-east Asia but still appreciably
higher than in North America and Europe. The Eskimos in Alaska have an incidence that is 15 times that
of the general USA population. The aetiology is multifactorial and includes genetic, viral and
environmental factors.
Although this carcinoma has its highest incidence in particular racial groups, it occurs universally.
Clinicians must have a high index of suspicion in order not to miss this lesion since the presentation can
be subtle and varied.
Nasopharyngeal carcinoma is more commonly found in males. The male to female ratio is 2-3: 1.
In high risk regions the incidence of nasopharyngeal carcinoma rises from the end of the second decade to
reach a peak in the fourth decade and then remains at a plateau. In low risk countries such as Jamaica, a
high proportion of cases have their onset in the second decade of life with a second peak occurring in the
sixth decade.
Aetiology
Nasopharyngeal carcinoma is an interesting tumour that demonstrates the interaction of several
factors in carcinogenesis. The important aetiologic factors are viral, genetic and environmental. Exciting
data has been collected from the continued research into the aetiology of this carcinoma.
The role of the Epstein-Barr virus
The Epstein-Barr virus has been associated with Burkitt's lymphoma, infectious mononucleosis,
non-Hodgkin's lymphoma in immunosuppressed individuals, some cases of Hodgkin's lymphoma and
nasopharyngeal carcinoma. Antibodies to the Epstein-Barr virus have been strongly associated with
nasopharyngeal carcinoma. In high risk regions there is a rise in the titres of certain antibodies to the
Epstein-Barr virus prior to the onset of the malignancy. The association of the Epstein-Barr virus and
nasopharyngeal carcinoma was subsequently confirmed by demonstrating that the DNA of this virus (
EBV DNA) was present in biopsy material from nasopharyngeal carcinoma
In situ hybridisation is considerably more sensitive for the detection of EBV-encoded RNA than it
is for EBV DNA because of the high levels of the former in specimens from nasopharyngeal
tumours.

Genetic factors
The high incidence of nasopharyngeal carcinoma among certain ethnic groups strongly suggests a
genetic link, which possibly interacts with environmental factors.
The major histocompatibility gene complex on the short arm of chromosome six comprises six
recognised loci called HLA-A, -B, -C, -DR, -DQ, -DS. There are now well-established associations
between HLA (human leukocyte antigen) and nasopharyngeal carcinoma.
Deletion of the short arm of chromosome 3 (3p) has been noted in these cancers and this may
reflect the loss of a tumour suppressor gene.
Environmental factors
Ingestion of Cantonese- style salted fish, especially in childhood, has been linked to
nasopharyngeal carcinoma. It is known that carcinogenic nitrosamines are present in such salted fish.
Histopathology
The World Health Organisation Classification recognises three histologic types
a) Keratinising squamous cell carcinoma (WHO-1) -30-50 % of the cases in non-endemic regions but
only 5 % in endemic areas.
b) Non- keratinising squamous cell carcinoma (WHO-2)
c) Undifferentiated carcinomas that have abundant non-neoplastic, lymphocytic infiltrate (WHO-3). This
latter histologic type has often been called lymphoepitheliomamost 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.
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
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.
True vocal cords

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

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
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 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
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.

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

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 p_7?????
Almost exclusive of the parotid gland,, it cause a smooth swelling in the tail of the gland that may feel
cystic
Aetiology
Malignant lesions
The only well-documented risk factor for salivary gland cancer is ionizing radiation.
Benign lesions
Radiation-induced neoplasms in the salivary glands are usually benign. The commonest associated
tumour is the pleomorphic adenoma. The increasing incidence of Warthin's tumour, especially in women,
has been linked to cigarette smoking .
Presentation
Mass
The majority of patients with parotid neoplasms present with painless masses typically in front of or
below the ear.
Pain
Pain is generally found with inflammatory conditions rather than neoplasms. Advanced malignant parotid
lesions may however present with intractable pain. 12 to 24 percent of malignant tumours of the salivary
glands present with pain.
Facial nerve palsy
A parotid lesions that is associated with facial nerve weakness should be assumed to be malignant until
proven otherwise. However only 10 to 15 percent of malignant lesions present with facial nerve palsy.
Skin involvement and cervical lymphadenopathy
Skin ulceration occurs in 9 percent of malignant lesions. Cervical nodal metastases may be found in
malignant parotid tumours of epithelial origin or primary lymphomas.
DIAGNOSIS
A thorough history and physical examination are essential components of the assessment but are
most useful in the patient with bilateral parotid enlargement. Sjgren'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
the capillary network of the salivary glands. The presence of a hot mass is usually indicative of Warthin's
tumour or oncocytoma. However, hot masses may occasionally be malignant and therefore
radiosialography is unreliable and is not recommended.
Since the advent of contrast CT, sialography and ultrasonography are rarely indicated in the
investigation of the patient who has parotid disease. Sialography is helpful in suspected cases of ductal
stricture, calculi or sialectasia.

The role of fine needle aspiration cytology

Fine needle aspiration (FNA) has revolutionised the management of many head and neck lesions. The
thyroid gland has been a fruitful area for the cytopathologist. The results in the salivary glands have been
far less impressive. While a diagnostic accuracy of greater than 90% is sometimes quoted, this has not
been the experience in most centres.
.
Neck Dissection and Radiotherapy
 Patients who have clinically apparent cervical nodal metastases should undergo parotidectomy,
radical neck dissection and radiotherapy. Patients who have aggressive histologic types such as
high-grade mucoepidermoid carcinoma, malignant mixed tumour, high-grade adenocarcinoma and
squamous cell carcinoma should have prophylactic neck dissections and radiotherapy. This also
applies to T3 lesions and lesions associated with facial nerve palsy.
Complications of parotidectomy
Facial nerve palsy
Haemorrhage from retromandibular vein, postauricular artery, superficial temporal artery, maxillary artery
ordirectly from the external carotid artery.
Parasthesia in the distribution of the greater auricular nerve
Neuroma of the greater auricular nerve
Frey's Syndrome : this is characterized by sweating over the parotid region when the patient thinks about
food or eats. It is thought to be due to aberrant regrowth of parasympathetic secretomotor nerves which
end up supplying the sweat glands.

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

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

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

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

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

CLASSIFICATION OF DYSPHAGIA

The discussion will predominantly focus on the oesophagus

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

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

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

2. Tumours: malignant and benign

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

4. Schatzki's ring with hiatus hernia

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

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

Lesions outside the wall of the oesophagus

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

Neural and Neuromuscular disorders

1. Bulbar Palsy
2. Myasthena Gravis
3. Tetanus

The commoner conditions are:

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

DIAGNOSIS AND MANAGEMENT

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

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

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

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

Pain
Retrosternal or back pain following oesophagoscopy or dilatation suggests oesophageal perforation.

Regurgitation
This is characteristic of long-standing achalasia, a sliding hiatus hernia and pharyngeal pouch formation.
Regurgitation of offensive, undigested food, or a feeling of a bulge in the neck suggests Zenker's
diverticulum.

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

Special tests
Barium swallow, barium meal and oesophagoscopy are most frequently helpful.
Barium swallow
1. Pharyngeal pouch may be visualized as a rounded pouch
2. Achalasia of the cardia produces
a) Dilatation of the oesophagus
b) The distal oesophagus tapers to a smooth point.

3. Carcinoma of the oesophagus will appear as an irregular filling defect. An oesophago-bronchial fistula
may be demonstrated.

Barium meal
May demonstrate associated gastric disorders such as carcinoma of the cardia extending into the stomach,
hiatus hernia or peptic ulceration.
Oesophagoscopy
Flexible fibreoptic endoscopy is the preferred method for diagnostic oesophagoscopy. Suspicious lesions
should be biopsied.

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

Curative treatment

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

2. Corrosive stricture.
Oesophagoscopy should be done within 36 hours to determine the extent of injury and to guide further
management. Initially broad-spectrum antibiotics and corticosteroids are prescribed. Subsequently
oesophageal strictures may require repeated dilatation but ultimately bypass, usually with gastic
transposition or a gastric tube flap may be necessary. If the stomach is not suitable, colonic interposition
is an alternative option.

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

Carcinoma of the oesophagus

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

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

SWELLINGS OF THE THYROID GLAND

Identification: - The thyroid is surrounded by the pretracheal fascia and is firmly attached to the trachea
by the ligaments of Berry and thus moves upwards on swallowing.
When a patient presents with a thyroid mass, the doctor will need to ascertain the following:

(1) The functional status of the thyroid

(2) Whether or not there is a neoplastic process going on
(3) Whether or not the mass is causing a local functional problem, by compression or invasion
(4) Whether there is an inflammatory or infiltrative process going on.
(5) Whether or not the thyroid mass presents a cosmetic problem to the patient.

Patients with thyroid swellings can be classified clinically as having

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

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

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

Thyroiditis

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

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

Treatment
a) Medical Therapy with antithyroid drugs( usually carbimazole plus B-Blocker)
Often used in young patients, pregnant women, patients with cardiac complications. The disadvantages
include a 50% recurrence rate after 2 years of therapy, drug rashes and leucopaenia.

b) Radioiodine 131
Can be given as a simple drink. Avoids the risk of surgery and the complications of medical therapy.
There are theoretical risks of carcinogenesis and teratogenicity. Therefore generally given to men and
women over age 40 years. The onset of its effect is slow.
c) Surgery
Acts quickly, but 1% incidence of permanent hypoparathyroidism and recurrent laryngeal nerve palsy.
Generally in thyrotoxicosis, surgery is usually done for large goitres, compression sy_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
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
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
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
c) is associated with a higher recurrence rate and lower survival rate in the case of malignant nodules.

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

There is considerable controversy on the extent of surgical resection necessary for the unilateral and
grossly intrathyroidal, differentiated carcinoma of the thyroid. The most important rationale for total
thyroidectomy is that it facilitates the use of radioactive iodine in the detection and treatment of any local
or metastatic lesions. Normal thyroid tissue has a 100-fold greater affinity for iodine than papillary or
follicular carcinoma of the thyroid. The presence of residual thyroid tissue can therefore significantly
impair the uptake of radioactive iodine by metastatic lesions.

Histologic sections have demonstrated microscopic foci of carcinoma in the contralateral lobe in up to
85% of cases of papillary carcinoma. Total thyroidectomy would eliminate these foci, which are potential
sources of recurrence. The lowest recurrence rate has been found in patients who have had a combination
of total thyroidectomy, radioactive iodine and TSH suppression using exogenous thyroxine.

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

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

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

1) Age and sex

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

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

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

3) Regional nodal and distant metastases

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

4) Residual tumour after surgery

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

5) Histologic type and degree of differentiation.

The following histologic variants of papillary carcinoma tend to run an aggressive clinical course:
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 Hrthle cell carcinoma should have a total thyroidectomy unless
the patient is unfit for surgery or the primary is not resectable. Follicular carcinoma and the Hrthle 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 tracheost_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.
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:

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

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

Tonsils and adenoids

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

Indications for tonsillectomy and adenoidectomy

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

B. Obstruction
1. Obstruction to the eustachian tube resulting in otitis media with effusion or recurrent acute otitis
media

2. Obstruction to the drainage of the nose and paranasal sinuses resulting in recurrent or chronic
rhinosinusitis
 3. Obstruction to the airway which may result in snoring, mouthbreathing, obstructive sleep apnoea,
cor pulmonale

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

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
Protection of the tracheobronchial tree:
Coma due to Drug Overdose, CVA
Bulbar Poliomyelitis
Guillain-Barre Syndrome
Trauma- surgical or accidental with bleeding into upper airways
Respiratory Failure Requiring prolonged intubation,
Reduction of dead space

Outline of Tracheostomy Technique

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

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

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

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

Incision with size 15 blade 2cm below the cricoid cartilage or midway between the sternal notch and the
cricoid cartilage
Blunt dissection and retraction of strap muscles laterally

Elevate or transect thyroid isthmus

Control bleeding. Change sucker from rigid type to flexible suction tube.
Incise trachea and hold cartilage to be resected with Allis forceps. Suction trachea and insert tracheostomy
tube. Inflate bulb with air. Secure tracheostomy tube with tapes or 2/0 silk sutures.

Complications of tracheostomy

Perioperative 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