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Figure 48.1. Adenoid mass after removal with curette. Note ridges
of lymphoid tissue separated by deep clefts.
SECTION IV — Diseases of Pharynx
Figure 48.4. Enlarged adenoids (arrows) in a 7-year-old girl. There is
very little breathing space in the nasopharynx.
Figure 48.2. Adenoid tissue is seen on MRI in all infants by age of
5 months, gradually it increases in size and is at its maximum on 6–7
years. Starts regressing at puberty and disappears by the age of 15 years.
Persistence of tissue may be seen beyond 15 years in cases of allergy or
infection. Symptoms of adenoid disease depend on the comparative
size of nasopharynx.
DIAGNOSIS
Examination of postnasal space is possible in some young
children and an adenoid mass can be seen with a mirror.
A rigid or a flexible nasopharyngoscope is also useful to
see details of the nasopharynx in a cooperative child.
Soft tissue lateral radiograph of nasopharynx will reveal
the size of adenoids and also the extent to which nasopharyngeal air space has been compromised (Figure 48.4).
Detailed nasal examination should always be conducted
to exclude other causes of nasal obstruction.
TREATMENT
When symptoms are not marked, breathing exercises,
decongestant nasal drops and antihistaminics for any
co-existent nasal allergy can cure the condition without
resort to surgery.
When symptoms are marked, adenoidectomy is done.
Indications and details of the operation are discussed in
the section on operative surgery.
ACUTE NASOPHARYNGITIS
AETIOLOGY
Acute infection of the nasopharynx may be an isolated
infection confined to this part only or be a part of the
generalized upper airway infection. It may be caused by
viruses (common cold, influenza, parainfluenza, rhino or
adenovirus) or bacteria (especially streptococcus, pneumococcus or Haemophilus influenzae).
Figure 48.3. Adenoid facies. Patient is a mouth breather.
CLINICAL FEATURES
Dryness and burning of the throat above the soft palate
is usually the first symptom as is commonly noted in
common cold. This is followed by pain and discomfort
localized to the back of nose with some difficulty on swallowing. In severe infections, there is pyrexia and enlarged
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cervical lymph nodes. Examination of nasopharynx reveals congested and swollen mucosa often covered with
whitish exudate.
TREATMENT
Mild cases clear up spontaneously. Some analgesic may be
required for relief of pain and discomfort. In severe cases
with general symptoms, systemic antibiotic or chemotherapy may be necessary. In children, there is associated
adenoiditis which causes nasal obstruction and requires
nasal decongestant drops.
CHRONIC NASOPHARYNGITIS
AETIOLOGY
It is often associated with chronic infections of nose,
paranasal sinuses and pharynx. It is commonly seen in
heavy smokers, drinkers and those exposed to dust and
fumes.
CLINICAL FEATURES
Postnasal discharge and crusting with irritation at the
back of nose is the most common complaint. Patient has
a constant desire to clear the throat by hawking or inspiratory snorting (forcefully drawing nasal secretions back
into the throat).
Examination of nasopharynx reveals congested mucosa and mucopus or dry crusts. In children, adenoids are
often enlarged and infected (chronic adenoiditis).
TREATMENT
Chronic infections of the nose, paranasal sinuses and oropharynx should be attended to. Excessive smoking and
drinking should be corrected. Preventive measures should
be taken to avoid dust and fumes. Alkaline nasal douche
helps to remove crusts and mucopus. Steam inhalations
are soothing.
THORNWALDT’S DISEASE (PHARYNGEAL
BURSITIS)
It is infection of the pharyngeal bursa which is a median recess representing attachment of notochord to
endoderm of the primitive pharynx. Pharyngeal bursa is
located in the midline of posterior wall of the nasopharynx in the adenoid mass.
CLINICAL FEATURES
1. Persistent postnasal discharge with crusting in the nasopharynx.
2. Nasal obstruction due to swelling in the nasopharynx.
3. Obstruction to eustachian tube and serous otitis media.
4. Dull type of occipital headache.
5. Recurrent sore throat.
6. Low-grade fever.
Examination would reveal a cystic and fluctuant
swelling in the posterior wall of nasopharynx. It may
also show crusts in the nasopharynx due to dried up
discharge.
TREATMENT
Antibiotics are given to treat infection and marsupialization of the cystic swelling and adequate removal of its
lining membrane.
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Chapter 49
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Tumours of Nasopharynx
BENIGN TUMOURS
Benign and malignant tumours of the nasopharynx are
listed in Table 49.1 .
NASOPHARYNGEAL FIBROMA (JUVENILE
NASOPHARYNGEAL ANGIOFIBROMA)
It is a rare tumour, though it is the commonest of all benign tumours of nasopharynx.
Aetiology
The exact cause is unknown. As the tumour is predominantly seen in adolescent males in the second decade
of life, it is thought to be testosterone dependent. Such
patients have a hamartomatous nidus of vascular tissue
in the nasopharynx and this is activated to form angiofibroma when male sex hormone appears.
Site of Origin and Growth
The site of origin of the tumour is still a matter of dispute.
Earlier it was thought to arise from the roof of nasopharynx or the anterior wall of sphenoid bone but now it is believed to arise from the posterior part of nasal cavity close
to the superior margin of sphenopalatine foramen. From
here the tumour grows into the nasal cavity, nasopharynx
and into the pterygopalatine fossa, running behind the
posterior wall of maxillary sinus which is pushed forward
as the tumour grows. Laterally, it extends into pterygomaxillary fossa and thence to infratemporal fossa and cheek.
Pathology
Angiofibroma, as the name implies, is made up of vascular and fibrous tissues: the ratio of the two components
may vary. Mostly, the vessels are just endothelium-lined
spaces with no elastic or muscle coat. This accounts for
the severe bleeding as the vessels lose the ability to contract; also the bleeding cannot be controlled by application of adrenaline (Figure 49.1). Though benign, angiofibromas do not have a capsule.
Extensions of Nasopharyngeal Fibroma
Nasopharyngeal fibroma is a benign tumour but locally
invasive and destroys the adjoining structures. It may extend into:
1. Nasal cavity causing nasal obstruction, epistaxis and
nasal discharge.
2. Paranasal sinuses. Maxillary, sphenoid and ethmoid
sinuses can all be invaded.
3. Pterygomaxillary fossa, infratemporal fossa and
cheek.
4. Orbits giving rise to proptosis and “frog-face deformity.” It enters through the inferior orbital fissure and
also destroys apex of the orbit. It can also enter the
orbit through superior orbital fissure.
5. Cranial cavity. It can extend into:
(a) Anterior cranial fossa through roof of ethmoids or
cribriform plate.
(b) Middle cranial fossa through erosion of floor of
middle cranial fossa or indirectly by invading the
sphenoid sinus and sella turcica. In the former
case, tumour lies lateral to internal carotid artery
and in the latter case medial to the artery.
Clinical Features
1. Age and sex. Tumour is seen almost exclusively in
males in the age group of 10–20 years. Rarely, it may
be seen in older people and females.
2. Profuse, recurrent and spontaneous epistaxis. This is
the most common presentation. Patient may be markedly anaemic due to repeated blood loss.
3. Progressive nasal obstruction and denasal speech. It
is due to mass in the postnasal space.
4. Conductive hearing loss and otitis media with effu-
sion. It occur due to obstruction of eustachian tube.
5. Mass in the nasopharynx. Tumour is sessile, lobulated or smooth and obstructs one or both choanae.
It is pink or purplish in colour. Consistency is firm but
digital palpation should never be done until at the time of
operation.
6. Other clinical features like broadening of nasal bridge,
proptosis, swelling of cheek, infratemporal fossa or involvement of IInd, IIIrd, IVth and VIth cranial nerves
will depend on the extent of tumour (Figure 49.2 ).
TABLE 49.1 BENIGN AND MALIGNANT TUMOURS
OF THE NASOPHARYNX
Benign Malignant
• Angiobroma
• Choanalpolyp
• Squamouspapilloma
• Thornwaldt’scyst
• Pleomorphicadenoma
• Craniopharyngioma
• Paraganglioma
• Hamartoma
• Congenitaltumours
• Hairy polyp
• Teratoma
• Epignathi
Scan to play Benign Tumours of Nasopharynx.
• Carcinomanasopharynx
• Lymphoma
• Rhabdomyosarcoma
• Chordoma
• Plasmacytoma
• Haemangiopericytoma
• Malignantsalivarygland
tumours
• Melanoma
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SECTION IV — Diseases of Pharynx
Figure 49.1. Angiofibroma. Section shows multiple dilated vessels surrounded by fibrous stroma. (A) H&E, ×100. (B) H&E, ×200.
Figure 49.2. (A) Specimen of an extensive angiofibroma in a 32-year-old male. (B&C) CT scans of the same. Note destruction of bone and
extension into pterygopalatine fossa.
Scan to play Nasopharyngeal Fibroma.
Diagnosis
It is mostly based on clinical picture. Biopsy of the tumour
is attended with profuse bleeding and is, therefore, avoided. If it is essential to differentiate it from other tumours,
biopsy can be done under general anaesthesia with all arrangements to control bleeding and transfuse blood.
Investigations
1. Computed tomography (CT) scan of the head with
contrast enhancement is now the investigation of
choice (Figure 49.3). It has replaced conventional radiographs. It shows the extent of tumour, bony destruction or displacements. Anterior bowing of the poste-
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281
Figure 49.3. Embolization of angiofibroma to decrease vascularity: (A) & (B) pre-embolization and (C) after embolization.
rior wall of maxillary sinus, often called antral sign or
Holman-Miller sign, is pathognomic of angiofibroma.
2. Magnetic resonance imaging (MRI) is complementary
to CT scans and shows any soft tissue extensions present intracranially in the infratemporal fossa or in the
orbit.
3. Carotid angiography shows the extent of tumours, its
vascularity and feeding vessels which mostly come
from the external carotid system. In very large tumours
or those with intracranial extension vessels may also
come from internal carotid system. Embolization of
vessels can be done at this time to decrease bleeding at
operation. Feeders from only the external carotid system can be embolized. Resection of tumour should not
be delayed beyond 24–48 h of embolization to avoid
revascularization from the contralateral side.
4. Arrangement for blood transfusion. Though blood
may not be required during surgery if successful
embolization is done, 2–3 units of blood should be
available and kept in reserve after grouping and crossmatching.
Treatment
surgery. Surgical excision is the treatment of choice
though radiotherapy and chemotherapy singly or in
combination have also been used. Spontaneous regression of the tumour with advancement of age, as thought
previously, does not occur and no wait and watch policy
should be adopted. Surgical approaches used to remove
angiofibroma, depending on its origin and extensions,
are listed below.
1. Transpalatine (Figure 49.4)
2. Transpalatine + Sublabial (Sardana’s approach)
3. Lateral rhinotomy with medial maxillectomy
(a) Via facial incision
(b) Via degloving approach
4. Endoscopic removal
5. Transmaxillary (Le Fort I) approach
6. Maxillary swing approach or facial translocation approach, or Wei’s operation
7. Infratemporal fossa approach
8. Intracranial–extracranial approach
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Figure 49.4. Nasopharyngeal fibroma as seen after transpalatal
exposure.
SECTION IV — Diseases of Pharynx
Transpalatal approach is used for tumours confined to
the nasopharynx. It can be extended into Sardana’s approach if the tumour extends laterally. These days such
tumours can be removed endoscopically. Wide access to
pterygomaxillary fossa can also be obtained by removing
the anterior wall of maxillary sinus along with parts of
pyriform aperture of nose through osteotomies and later
reconstruction at the end of operation with plates. This
avoids depression and deformity of the face (Table 49.2).
Transmaxillary Le Fort I approach has also been used
to give a wider access to remove tumours which extend
into maxillary and ethmoid sinuses and pterygopalatine
fossa. For tumours of infratemporal fossa maxillary swing
approach also called facial translocation has been used.
Here an osteoplastic flap with entire cheek and maxilla is
raised as a single unit, which is later reconstructed. Most
of the intracranial extensions are extradural and can be
removed easily with the extracranial approaches but tumours extending intradurally or to the cavernous sinus
require help of the neurosurgeon.
Preoperative embolization of the tumour reduces its
blood supply and causes less bleeding, if tumour removal is performed within 24–48 h of embolization before
collaterals have time to develop. Preoperative angiography also helps to find any feeders from internal carotid
system.
Before the era of tumour embolization, oestrogens
were used systemically to reduce blood supply. Similarly
cryotherapy was also used.
Recurrence of juvenile angiofibroma is not uncommon
and has been reported in up to 35%.
ManageMent oF recurrent tuMour. Various options
used are:
(a) Observation. The tumour may spontaneously regress.
(b) Revision surgery and removal. If it recurs even after revi-
sion surgery, radiotherapy may be considered.
(c) Radiation. Reduces the blood supply and the tumour
subsides over time. It is also used when tumour recurrence is surgically inaccessible.
raDiotheraPy. Radiotherapy has been used as a primary mode of treatment, thus avoiding surgery. A dose
of 3000 to 3500 cGy in 15–18 fractions is delivered in
3–3.5 weeks. Response is not immediate. Tumour regresses slowly in about a year, sometimes even up to 3 years.
Radiotherapy is also used for intracranial extension of
disease when tumour derives its blood supply from the
internal carotid system.
Recurrent angiofibromas have also been treated by radiotherapy. Intensity modulated radiotherapy—a newer
mode of treatment—may be employed.
Treatment with radiotherapy is controversial. Some
believe that all large tumours with intracranial extension
should be treated with radiation while others reserve it
for recurrent inoperable tumours. Radiation to nasopharynx in the young has the risk of development of malignancy at a later age.
horMonaL theraPy. Since the tumour occurs in young
males at puberty, probably activated by testosterone, hormonal therapy as the primary or adjunctive treatment
has been used. Diethylstilbestrol and flutamide (an androgen blocker) have been used in the past to arrest the
TABLE 49.2 EXTENT OF JUVENILE NASOPHARYNGEAL ANGIOFIBROMA AND SURGICAL APPROACH
Location Approach
A. Nose and nasopharynx Transpalatal or endoscopic
B. Nose, nasopharynx maxillary antrum and pterygopalatine fossa Lateral rhinotomy with medial maxillectomy
C. As in B + Infratemporal fossa Extended lateral rhinotomy
D. As in C + Cheek extension Extended lateral rhinotomy
E. As in B + C + Intracranial Combined intracranial and extracranial approach (craniotomy + one
F. Residual or recurrent disease (extracranial) Observation OR repeat surgery or radiation if inaccessible
G. Intracranial residual or recurrent Stereotactic radiation (X or gamma knife)
OR
Endoscopic
OR
Le Fort I
OR
Infratemporal fossa approach
OR
Maxillary swing approach
of the extracranial approaches)
OR
Radiation if intracranial part is inaccessible
Chapter 49 — Tumours of Nasopharynx
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growth but no significant regression has been observed
in practice.
cheMotheraPy. Very aggressive recurrent tumours
and residual lesions have been treated by chemotherapy.
Doxorubicin, vincristine and dacarbazine have been used
in combination.
Chemotherapy and radiotherapy can arrest the growth
and cause some tumour regression but not total tumour
eradication.
OTHER BENIGN TUMOURS
OF NASOPHARYNX
They are very rare and arise from the roof or lateral wall
of nasopharynx. They include:
1. Congenital tumours. They are seen at birth and are
six times more common in females than males. Vari-
ous types include:
(a) Hairy polyp. A dermoid with skin appendages.
(b) True teratoma. Having elements derived from all
the three germ layers.
(c) Epignathi. Having well-developed fetal parts.
2. Pleomorphic adenoma.
3. Chordoma. Derived from the notochord.
4. Hamartoma. Malformed normal tissue, e.g. haeman-
gioma.
5. Choristoma. Mass of normal tissues at an abnormal
site.
6. Paraganglioma.
MALIGNANT TUMOURS
NASOPHARYNGEAL CANCER
Epidemiology and Geographic Distribution
Nasopharyngeal cancer is a multifactorial disease. Its incidence and geographic distribution depends on several
factors such as genetic susceptibility, environment, diet
and personal habits.
Nasopharyngeal cancer is most common in China particularly in southern states and Taiwan.
Its incidence in North American whites is 0.25% of all
cancers, while it is 18% in American Chinese. Chinese
born in America have lesser incidence than those born
in China. Burning of incense or wood (polycyclic hydrocarbon), use of preserved salted fish (nitrosamines) along
with vitamin C deficient diet (vitamin C blocks nitrosification of amines and is thus protective) may be other
factors operative in China.
Nasopharyngeal cancer is uncommon in India and
constitutes only 0.41% (0.66% in males and 0.17% in
females) of all cancers except in the North East region
where people are predominantly of Mongoloid origin.
People in Southern China, Taiwan and Indonesia are
more prone to this cancer.
Aetiology
The exact aetiology is not known. The factors responsible
are:
1. Genetic. Chinese have a higher genetic susceptibility
to nasopharyngeal cancer. Even after migration to oth-
er countries they continue to have higher incidence.
2. Viral. Epstein–Barr (EB) virus is closely associated
with nasopharyngeal cancer. Specific viral markers are
being developed to screen people in high-incidence
areas. EB virus has two important antigens: viral cap-
sid antigen (VCA) and early antigen (EA). IgA anti-
bodies of EA are highly specific for nasopharyngeal
cancer but have sensitivity of only 70–80% while IgA
antibodies of VCA are more sensitive but less specific.
AgA antibodies against both EA and VCA should be
done for screening of patients for nasopharyngeal
cancer.
3. Environmental. Air pollution, smoking of tobacco
and opium, nitrosamines from dry salted fish, smoke
from burning of incense and wood have all been
incriminated.
Pathology
Squamous cell carcinoma in various grades of its differentiation or its variants such as transitional cell carcinoma and lymphoepithelioma is the most common (85%).
Lymphomas constitute 10% and the rest 5% are rhabdomyosarcoma, malignant mixed salivary tumour or malignant chordoma.
On the basis of histology, as seen on light microscopy,
WHO has lately reclassified epithelial growths into three
types (see Table 49.3).
TABLE 49.3 WHO CLASSIFICATION BASED ON HISTOPATHOLOGY
Type I (25%) Keratinizing carcinoma Squamous cell carcinoma
Type II (12%) Nonkeratinizing differentiated
Type III (63%) Nonkeratinizingundifferentiated
Note: All the types are squamous cell carcinoma when seen under electron microscope. Special stains for epithelial and lymphoid markers are required to
differentiate them from lymphomas.
Present WHO terminology Former terminology
• Transitionalcellcarcinoma
carcinoma
carcinoma
• Intermediatecellcarcinoma
• Lymphoepithelialcarcinoma(Regaudtypeistumourwithmalignant
tissues in nests)
• Anaplasticcarcinoma
• Clearcellcarcinoma
• Lymphoepithelialcarcinoma(Schminketypeistumourwithdiffusely
distributed malignant tissue)
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SECTION IV — Diseases of Pharynx
Grossly, the tumour presents in three forms:
1. proliFeratiVe. When a polypoid tumour fills the nasopharynx, it causes obstructive nasal symptoms.
2. ulceratiVe. Epistaxis is the common symptom.
3. inFiltratiVe. Growths infiltrate submucosally.
Spread of nasopharyngeal carcinoma
(see Figure 49.5 )
local spread. Commonest site of origin in the nasopharynx is the fossa of Rosenmüller. Anterior spread
causes blockage of choana and nasal cavity and inferior
spread is towards oropharynx and hypopharynx, lateral
spread involves parapharyngeal space and infratempo-
ral fossa through the sinus of Morgagni, upward spread
is towards intracranial structures. Foramen lacerum and
foramen ovale provide direct routes of spread to middle
cranial fossa causing diplopia or ophthalmoplegia. VIth
cranial nerve is the first to be involved. Spread along
the posterior skull base involves jugular foramen (CN
IX, X, XI), hypoglossal canal (CN XII) or sympathetic
nerve (Horner syndrome). These structures can also
be involved secondary to involvement of parapharyngeal space. Involvement of pterygoid muscles causes
trismus.
lymphatic spread. Nasopharynx is rich in lymphatics
and an early lymphatic spread is seen in cervical nodes.
Ipsilateral nodes are involved more often but contralateral or bilateral nodes can also get involved. Lymphatic
spread may be direct to these nodes or indirectly through
involvement of retropharyngeal or parapharyngeal
nodes. Involvement of retropharyngeal nodes also causes
neck stiffness and torticollis.
distant metastases. Lung, bone and liver are the most
common sites involved.
Clinical Features
• Age. It is mostly seen in fifth to seventh decades but
may involve younger age groups. It is not uncommon
to see cancer of nasopharynx in twenties and thirties.
• Sex. Males are three times more prone than females.
Symptomatology is divided into four main groups:
1. nasal. Nasal obstruction, nasal discharge, denasal
speech (rhinolalia clausa) and epistaxis.
2. otologic. Due to obstruction of eustachian tube,
there is conductive hearing loss, serous or suppurative
otitis media. Tinnitus and dizziness may occur. Presence
of unilateral serous otitis media in an adult should raise
suspicion of nasopharyngeal growth. Rarely, tumour
grows up the tube into the middle ear.
3. ophthalmoneurologic. This occurs due to extension of tumour to the surrounding regions. Nearly all the
cranial nerves may be involved.
Squint and diplopia due to involvement of CN VI,
ophthalmoplegia (CN III, IV and VI), facial pain and reduced corneal reflex (invasion of CN V through foramen
lacerum) may occur. Tumours may directly invade the orbit leading to exophthalmos and blindness (CN II at the
apex of the orbit). Involvement of IXth, Xth and XIth
cranial nerves may occur, constituting jugular foramen
Figure 49.5. Routes of spread (green area) and clinical features (blue area) of nasopharyngeal cancer.
Scan to play Malignant Tumours of Nasopharynx.
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285
syndrome. Usually, this is due to pressure of enlarged lateral retropharyngeal lymph nodes on these nerves in the
neck. CN XII may be involved due to extension of growth
to hypoglossal canal. Horner syndrome may occur due to
involvement of cervical sympathetic chain.
Nasopharyngeal cancer can cause conductive deafness
(eustachian tube blockage), ipsilateral temporoparietal
neuralgia (involvement of CN V) and palatal paralysis
(CN X)—collectively called Trotter’s triad.
4. cerVical nodal metastases. This may be the only
manifestation of nasopharyngeal cancer. A lump of nodes
is found between the angle of jaw and the mastoid and
some nodes along the spinal accessory in the posterior
triangle of neck. Nodal metastases are seen in 75% of the
patients, when first seen, about half of them with bilateral nodes.
5. distant metastases. involve bone, lung, liver and
other sites. Distant metastases may be present at the time
of diagnosis.
Presenting symptoms and signs of nasopharyngeal
cancer in order of frequency are:
• Cervical lymphadenopathy (most common) (60–90%)
• Hearing loss
• Nasal obstruction
• Epistaxis
• Cranial nerve palsies. CN VI paralysis is the most com-
mon of these
• Headache
• Earache
• Neck pain
• Weight loss
Diagnosis
1. Endoscopic evaluation. This can be done under local
anaesthesia using rigid or flexible endoscopes. Growth
may be proliferative, ulcerative or infiltrative submu-
cosal. Biopsy can be taken.
2. Imaging studies
(a) CT scan/MRI nasopharynx and neck. High-reso-
lution, contrast-enhanced CT of neck and nasopharynx is the study of choice. It reveals primary
growth, erosion of skull base and clivus, extensions to parapharyngeal, retropharyngeal and intracranial regions. Neck nodes can also be seen.
MRI is better for soft-tissue extension.
(b) X-ray/CT chest for secondaries lung.
(c) CT abdomen or ultrasound abdomen for secondar-
ies liver.
(d) Positron emission tomography scan. It is getting
popular to show metastases anywhere in the body.
3. Biopsy. It can be done under local or general anaes-
thesia using endoscopes. In case growth is not visible,
but highly suspected because of metastatic nodes,
blind biopsies from multiple sites in nasopharynx can
be taken. A strip of mucosa from fossa of Rosenmüller
or posterior wall of nasopharynx can be taken. It may
require transpalatal exposure of nasopharynx. General
anaesthesia is preferred if occult primary is suspected.
4. Audiogram. A baseline audiogram is important. It not
only establishes diagnosis of serous otitis media but is
also important for side effects of radiation and chemotherapy which can cause sensorineural hearing loss.
Classification (see Table 49.4)
WHO classified nasopharyngeal carcinoma on histopathological basis into three types (Table 49.3). Type III
is the most common in North America. However, the
frequency of different histopathological types may differ
from country to country. These types have also been correlated to titres of EB virus and also in their response to
radiotherapy. It is observed that type II and type III are
associated with higher titres of EB virus and have higher
local control rates with radiotherapy.
Treatment
1. Radiotherapy. It is the treatment of choice for na-
sopharyngeal cancer. Stage I and II are treated by
radiotherapy alone while stage III and IV require concomitant radiation and chemotherapy or radiation followed by chemotherapy. External beam radiation of
6000–7000 cGy can be delivered by linear accelerator
to the primary and both sides of neck. More advanced
techniques of radiotherapy such as three-dimensional
conformal radiotherapy and intensity modulated radiotherapy (IMRT) are now being used more and more.
They allow higher dose delivery to the tumour with reduced damage to the adjacent normal structures such
as spinal cord, brainstem and parotid glands. IMRT has
also been used for recurrent disease where conventional radiotherapy produces more serious side effects such
as transverse myelitis.
2. Chemotherapy. Some stage III and IV cancers of naso-
pharynx can be cured by radiotherapy alone but cure
rate is doubled when chemotherapy is combined with
radiotherapy. Chemotherapy can be given concomitantly or postradiotherapy. Cisplatin or cisplatin with
5-FU have been used. Chemotherapy has also been
found useful to control metastases from lymphoepithelioma and undifferentiated carcinoma of nasopharynx. Goal of chemoradiotherapy in nasopharyngeal
carcinoma is to improve local control of tumour and
to treat distant metastases.
3. Treatment of recurrent and residual (persistent) dis-
ease. This can occur in neck nodes or in the nasopharynx.
(a) Positive nodes in the neck. They require radical neck
dissection with removal of sternocleidomastoid
muscle, CN XI and internal jugular vein. Modified
neck dissection is not preferred as extensive disease has been seen on histopathology even when
only a single node was present. Bilateral neck
disease may require bilateral neck dissection but
with preservation of internal jugular vein to avoid
cerebral and facial oedema.
(b) Recurrent or residual (persistent) disease in the naso-
pharynx. First it should be evaluated by CT and
MRI to see the size, location and regional extent or
infiltration. More recently, PET-CT has been used
to find any regional or systemic metastases. It can
be treated by:
(i) Second course of external radiation. IMRT has
been used. Second course of radiation is more
hazardous and causes injury to brainstem, eye,
ear, pituitary gland and temporal lobe.
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