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CASE DISCUSSION

NASOPHARYNGEAL CARCINOMA

Supervisor
dr. H. Oscar Djauhari, Sp. THT-KL

Presentants
Satyadharma Michael Winata 2010.061.022
Natharina Yolanda 2010.061.023
Stella 2011.061.094

Clinical Rotation
Otolaryngology, Head and Neck Department
Medical Faculty of Unika Atma Jaya–Syamsudin, S.H. Regional General
Hospital, Sukabumi
Period of 6 August 2012 – 8th September 2012
th

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CASE DISCUSSION

A 60-years-old male came to ENT clinic with a complaint of sensation of blocked right nose
and bloody nasal discharge for 7 past days.

A. PATIENT’S IDENTITY
Name : Mr. N
Gender : Male
Age : 60 years old
Occupation : Industrial worker
Address : Sukabumi

B. HISTORY
 Chief Complaint : sensation of blocked right nose and bloody nasal discharge
since 7 past days.
 Additional Complaint : right ear fullness, neck mass, and weight loss
 History of Present Illness
A 60-years-old male came to ENT clinic with a chief complaint of sensation
of blocked right nose and bloody nasal discharge since 7 past days. The bloody
discharge was intermittent and in a small amount. The discharge was only in the right
nose. He also felt right ear fullness.
He also noticed a mass at his right upper neck. The mass was single, round,
not enlarging in the past 7 days, and painless. In the past 6 months, he lost weight
dramatically despite of regular meal.
History of fever and malaise was denied. He didn’t have any other ear or eye
complaint. There was no ear discharge, ear pain, tinnitus, or hearing loss. Complaint of
swallowing pain and cough were also denied.

 History of Past Illness


History of previous illness was denied

 History of Family Illness


His father had a enlargement of the neck, which known as a ca KGB

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C. PHYSICAL EXAMINATION
General condition : Appear calm
Body weight : 55 kg
Height : 160 cm
Blood pressure : 110/80 mmHg
Pulse : 88 beat per minute
Respiratory rate : 20 times per minute
Temperature : 37oC

ENT Examination
 Ear
Right ear
- Auricle : normal
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (-)
- Tymphanic membrane:
Intact, hyperemic (-), bulging (+), light reflex ↓

Left ear
- Auricle : normal
- External auditory canal:
hyperemic (-), edema (-), mass (-), laceration (-) secretion (-) , cerumen (-)
- Tymphanic membrane:
Intact, bulging (-), light reflex (+)

 Nose
Right nose
- Mucous membrane:
hyperemic (-), edema (-), blood-stained discharge (+), mass (-), laceration (-),
crust (-)
- Inferior conchae : eurtrophy
- Septum : no deviation
- Air passage : decreased

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Left nose
- Mucous membrane:
hyperemic (-), edema (-), secretion (-), mass (-), laceration (-), crust (-)
- Inferior conchae : eurtrophy
- Septum : no deviation
- Air passage : normal

 Oropharynx
- Posterior pharynx : hyperemic (-)
- Palatine tonsils : T2 / T2, hyperemic (-), detritus (-)
- Uvula : symmetrical
- Dental : no abnormatlities

 Maxillofacial : symmetrical

 Neck : single right upper jugular lymphadenopathy, diameter of 2 cm,


painless

D. WORKING DIAGNOSIS
Suspect of nasopharyngeal carcinoma

E. DIFFERENTIAL DIAGNOSIS
Nasal polyp
Turbinate hypertrophy

F. WORK-UP
Laboratory:
- Complete blood count
- Liver function test
Head and neck CT-scan
Nasopharyngoscopy + biopsy

G. TREATMENT

Radiotherapy ± chemotherapy

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NASOPHARYNGEAL CARCINOMA

Epidemiology

NPC is a relatively rare disease in the west, but is endemic in the Far East. The highest
incidence reported is from the Guangdong Province of Southern China, where it is the third
most common malignancy among men, with an incidence rate of between 15 to 50 per
100,000.[33] High incidences are also seen among Hong Kong and Singapore Chinese, with
intermediate incidences in Alaskan Eskimos and in the Mediterranean basin. Emigration from
high to low incidence areas such as the United States and Canada reduces the incidence of
NPC in first-generation Chinese but still remains at seven times the rate in whites.[19] The
incidence in most other countries is low, with an age-adjusted incidence rate of less than 1
per 100,000.[77]

The geographic distribution of the disease suggests a multifactorial pathogenesis, resulting


from a unique interaction between genetic susceptibility, environmental factors, and
migration patterns. Chromosomal abnormalities in chromosomes 1, 2, 3, 4, 5, 6, 9, 11, 13, 14,
16, 17, 22, and the x chromosome have been implicated in its pathogenesis. Chan[7] recently
published a hypothesis for the development of NPC. Early dysplastic changes are associated
with allelic losses on the short arms of chromosomes 3 and 9, resulting in the inactivation of
tumor suppressor genes p14, p15, and p16.[6][37][62] Latent infection by the Ebstein-Barr virus
(EBV) is crucial in the progression to severe dysplasia, and gains on chromosome 12 and
allelic losses on 11q, 13q, and 16q lead eventually to invasive carcinoma. Mutations in p53
and aberrant expression of cadherins propagate the further development of metastases.[38]
Specific haplotypes in the human lymphocyte antigen (HLA), located on the short arm of
chromosome 6, have also been found to increase the risk of NPC.[107] Dietary factors have
focussed mainly on preserved foods, and salted fish, in particular, has been found to have a
strong relation to the development of NPC.[106] There is also an increased risk with diets
deficient in fresh fruits, carotene, or fiber intake; vegetables do not provide protection against
NPC.[68]

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Pathology

Although the nasopharyngeal mucosa consists of a variety of surface epithelium and soft
tissue components that include respiratory-type pseudostratified columnar and transitional
epithelium, lymphoid stroma, and mucous glands, squamous epithelium predominates in
adult life. NPC is by far the most common epithelial malignancy arising from the
nasopharynx.

Three histopathologic types are described in the World Health Organization (WHO)
classification.[87] Type I consists of keratinizing squamous cell carcinoma, having features of
squamous differentiation that include intercellular bridges and abundant keratin production.
They may be further graded as well, moderately or poorly differentiated. Although the type I
variety may account for 20% to 30% of cases seen in North America,[72] true well-
differentiated squamous cell carcinoma is rare in the Asian context, accounting for 1% to 3%
of all NPC.[88]

WHO type II consists of nonkeratinizing carcinoma and essentially encompasses all tumors
that do not fall into either the type I or type III categories. Type III consists of
undifferentiated carcinoma, historically termed lymphoepithelioma because of an intimate
admixture of undifferentiated epithelial and lymphoid cells. Types II and III exhibit a wider
degree of cellular pleomorphism than the keratinizing variety and include microscopic
patterns of spindle, transitional, clear and anaplastic cells, lymphoepitheliomas, or a
combination of these. The commonalties in these ultrastructural features make it difficult to
make clear-cut histologic distinctions and their similar clinical behavior had led to the
suggestion that these two entities should be considered as a single entity, undifferentiated
cancer of the nasopharyngeal type (UCNT).[67][69][81] Indeed, an increasing body of evidence
supports this distinction of squamous and nonsquamous carcinoma of the nasopharynx both
in their clinical behavior and prognosis. WHO types II and III are typically more
radiosensitive and exhibit better local control rates than keratinizing squamous cell carcinoma
but have also been shown to have higher rates of distant metastases.[67][81]

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Clinical Presentation

NPC affects a relatively younger group of patients than the garden-variety squamous cell
cancer of the head and neck. The incidence begins to rise in the second decade of life, and
peaks in the forth and fifth decades of life. The male/female ratio is approximately 3:1.[90]

Early symptoms and signs are subtle and variable and often are neglected by both patient and
physician. Cervical lymphadenopathy is the most common presentation and can be seen in
between 50% and 90% of patients. A rich lymphatic plexus drains the nasopharynx, and up to
a third of these patients may have bilateral cervical involvement. Involvement of the upper
jugular and jugulodigastric nodes occur first, and spread occurs in a fairly organized fashion
to the lower neck and supraclavicular nodes.[85] This pattern of spread has been shown to be
of prognostic significance.[84] Lymphatic spread to the first echelon nodes, the
retropharyngeal nodes of Rouviere, may only, however, be detected radiologically. In areas
where NPC is endemic, it is important to exclude NPC in any young patient who has
asymptomatic cervical lymphadenopathy.

Nasal symptoms are seen in half of presenting patients and usually consist of blood-stained
nasal discharge and unilateral nasal obstruction. Aural symptoms most commonly consist of
unilateral hearing loss, although tinnitus and otalgia may occasionally be present. Hearing
loss is due to tumor producing a physiologic and/or an anatomic obstruction of the eustachian
tube, causing a serous otitis media. NPC should always be considered in high incidence
regions in patients with unilateral serous otitis media.

Neurologic symptoms, usually in the form of cranial nerve paralysis and occasionally
headaches, are seen in a fifth of patients. Unimpeded superior extension of tumor through the
foramen lacerum to the cavernous sinus results in multiple cranial nerve involvement. Cranial
nerve VI is the most commonly involved, resulting in diplopia, followed by cranial nerve V,
which results in facial or high neck pain or paresthesia. Eye signs may further be complicated
by involvement of cranial nerves III and IV. Tumor eroding into the jugular foramen and
hypoglossal canal results in any combination of cranial nerve IX, X, XI, and XII nerve
paralysis, resulting in the jugular foramen syndrome (IX, X, XI) or the Collet-Sicard
syndrome (IX, X, XI, XII).

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Approximately 5% of all patients have systemic metastases, most commonly to the bone
(thoracolumbar vertebrae, pelvis, and femoral heads) followed by the lungs and liver.[86]

Diagnostic Evaluation
Clinical Evaluation

A detailed history and clinical examination should be taken, and although symptoms may be
trivial, a high index of suspicion must be present in evaluating patients within the geographic
endemic areas of the disease. A thorough visualization and examination of the nasopharynx is
also required, either with a rigid (0-, 30-, or 70-degree Hopkins rod) or flexible endoscope.
Rigid endoscopes provide excellent visualization but have limited maneuverability within the
confines of the nasopharynx or when anatomic variations in the nasal cavity preclude the
introduction of a rigid instrument. Flexible fiberoptic nasopharyngeal endoscopes are
relatively atraumatic and provide greater maneuverability at the expense of a slightly inferior
image. Biopsy is required for definite diagnosis and can be done through the biopsy channel
of a flexible scope if one is present or with a separate biopsy forceps like a Takahashi or
Halyard cup forceps. The most common sites of origin are the fossa of Rosenmüller and the
nasopharyngeal roof, keeping in mind that in up to 10% of patients the disease may be
entirely submucosal. Biopsy of the nasopharynx is usually performed in the outpatient setting
under local anesthesia. Transnasal biopsies may be endoscopically directed, performed
through indirect nasopharyngoscopy or blind. If performed with separate instruments, the
forceps and endoscope may be placed through the same or through different nostrils. It may
sometimes be necessary to take biopsies with the patient under general anesthesia, either in
patients with suspected recurrent submucosal disease that may require deep biopsies or in
patients with a strong suspicion of disease with repeated negative biopsies. Nasopharyngeal
curettage may also be performed at the time as a last resort.

Biopsy is sometimes necessary from a cervical node for diagnosis. Fine-needle aspiration
cytology (FNAC) is the safest and most expeditious method for tissue diagnosis. [8] Open
biopsies, either in the form of an incisional or excisional biopsy, should be avoided, because
there is evidence to suggest that it may adversely affect survival.[36]

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Serology

Latent EBV infection seems to be crucial in the pathogenesis of NPC. EBV infection is
prevalent and occurs in early life, especially during weaning. Once infected, the virus remains
latent in epithelial cells and B lymphocytes and in NPC expresses one of six possible nuclear
proteins, EBNA 1 to 6 and three membrane proteins LMP-1, LMP 2A, and 2B.[9] Latent to
replicative infection is triggered by BamH1 Z EBV replication activator (ZEBRA) protein,
resulting in extensive transcription of the viral genome and expression of the early (EA,
nonstructural) and late (VCA, structural) antigens.[9] High antibody titers to these EBV
antigens serve an important function as diagnostic markers. An elevated IgA anti-VCA titer is
highly sensitive (sensitivity 95%, specificity 80%–95%), and an elevated IgA anti-EA is
highly specific (specificity >95%, sensitivity 80%).[49] Both tests collectively provide a useful
index for detecting early occult disease or in raising the degree of suspicion of an abnormal
clinical examination or radiologic finding. It is interesting to note that although WHO types II
and III exhibit between 82% to 100% positivity with respect to the antibody titers, WHO type
I showed only a 38% and 19% positivity to IgA EA and VCA, respectively. [74] EBV titers
may be useful in posttreatment surveillance.[66]

EBV DNA titers, on the other hand, seem to be an important index for prognostication. Lo, in
a series of publications, found that EBV DNA titers correlate with stage, treatment response,
relapse, and survival.[63][64] Lin also found a correlation of EBV DNA titers with overall,
metastasis-free, and progression-free survival.[58]

Radiology

MRI with gadolinium and fat suppression is the diagnostic imaging modality of choice in that
it provides multiplanar views, excellent delineation of soft tissue and fascial planes, and
better tissue specificity. Coronal views are helpful in determining tumor spread through the
petroclinoid fissure or foramen lacerum to the cavernous sinus, as well as through the
foramen ovale, rotundum, or spinosum. Axial views display extension into the
retropharyngeal, paranasopharyngeal, and pterygomaxillary space and into the infratemporal
fossa. CT, however, provides better definition of bone involvement, especially skull base
erosion, and may be more accurate in assessing cervical lymphadenopathy, especially in the
presence of extracapsular spread[14] ( Figure 73-3a and Figure 73-3b ). Indeed, both imaging
modalities are complementary and may be required collectively to obtain maximal

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information about the extent of disease. Imaging also provides important information about
the state of the retropharyngeal nodes of Rouvière, which are a common site of drainage but
are not evaluable by clinical examination.

When tumor extends beyond the confines of the nasopharynx, NPC can spread along several
defined ways. Lateral spread is the most common, through the pharyngobasilar fascia,
resulting in lateral displacement or effacement of the fat-filled parapharyngeal space.
Anterolateral extension leads to the pterygoids, the muscles of mastication and causes
trismus. Posterolateral spread into the carotid sheath or jugular foramen results in cranial
nerve IX, X, XI, and XII palsies.[13]

Anterior extension is to the nasal fossa and through the sphenopalatine foramen into the
pterygopalatine fossa (PPF). The PPF may also be involved by direct invasion of the
pterygoid process or through the masticator space. The earliest sign of PPF involvement is
the obliteration of normal fat content. The maxillary nerve may then be involved and lead to
spread to the cavernous sinus through the foramen rotundum.[14]

Superior spread results in skull base or sphenoid sinus erosion, with or without intracranial
extension. Superolateral extension involves the petrous apex and foramen lacerum, from
which the tumor may gain the cavernous sinus and cause cranial nerve III, IV, V, and VI
cranial nerve palsies.[12]

Positron emission tomography scans are becoming an essential diagnostic tool in the
management of residual or recurrent disease. A study on its usefulness compared with CT in
36 patients evaluated for posttreatment disease reported a 100% sensitivity, 96% specificity,
and 97% accuracy in diagnosis.[47]

Staging

There exists to date no universally accepted staging classification for NPC. The classification
proposed by John Ho[34] has been widely used in Asia since his classic publication in 1978.
Ho's system is composed of three T- and N-stages individually and five overall stages, I to V,
instead of the usual practice of four. Despite this departure from international staging
systems, there are several strengths to Ho's classification. Ho recognized that the limits of the
primary tumor within the nasopharynx were not easy to define, especially with the possibility

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of submucosal extension, and, therefore, defined all tumors within the nasopharynx as T1
regardless of subsite. Ho's T stage takes into consideration lateral spread into the
parapharyngeal space, a factor of considerable prognostic implication.[93] In addition, Ho's
staging of the neck was into upper, middle, and lower neck disease, which has since been
shown to correlate well with prognosis, with lower neck involvement portending a poorer
prognosis.[19] Ho's classification has withstood the test of time and has been prognostically
validated.[73][94]

The UICC/AJCC staging classification is more widely used in the United States and the West
and since 1992 has been incorporated into one. The staging systems before 1992
distinguished T1 from T2 disease by the number of subsites involved within the nasopharynx.
As mentioned, clearly defining tumor extent within the nasopharynx is not always exact, and
it has been shown that this designation into T1 and T2 has no correlation with survival. T
classification did not take into account parapharyngeal spread, and N staging was more
traditionally based on other staging systems that took into account nodal size and the number
of nodes involved rather than node levels. In 1997, a new UICC/AJCC classification was
formulated that took into account these and other significant prognostic variables. The current
system has been validated in both the Asian[52] and Western context.[17]

Management
Primary Disease
Radiation

The management of NPC is unique for two reasons. The first is that the tumor is in a
relatively inaccessible location, making surgical extirpation difficult and morbid, especially if
the tumor has extended beyond the confines of the nasopharynx. The second is that these
tumors are particularly radiosensitive. For these reasons, radiotherapy has been the
cornerstone of the definitive treatment for NPC for close to half a century.

Effective radiotherapy requires careful simulation and treatment planning. All patients must
be referred for dental clearance before instituting therapy to reduce the development of

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xerostomia-related osteomyelitis and osteoradionecrosis and continue with meticulous dental
care and flouride prophylaxis.

Radical radiotherapy may be delivered several ways. External beam radiotherapy is most
commonly delivered by opposed lateral fields to encompass the primary tumor and upper
neck. A third anterior matched field may be used to irradiate the lower cervical and
supraclavicular neck nodes with protection of midline structures such as the spinal cord and
larynx. Conventional delivery is from a linear accelerator and consists of tumoricidal
radiation doses of 70 to 76 Gy in fractions of 1.8 to 2.0 Gy per day to the primary and
anatomic structures at risk within the vicinity of the nasopharynx. Radiation boosts in the
form of intracavitary brachytherapy for T1 to T2 lesions have been used to improve local
control rates.[51][79] Stereotactic radiosurgery boosts may also be given for T3 and T4 lesions.
Le reports a 100% local control rate in 45 patients with T3 and T4 primary tumors treated with
a stereotactic boost at a median of 4 years follow-up.[50] Because there is a high incidence of
subclinical neck disease, radiation doses between 50 and 60 Gy are used to electively treat the
neck. The shrinking field technique is used to provide a range of doses to various regions,
reducing the portals in subsequent deliveries to attain tumoricidal doses eventually only to the
primary tumor and involved neck nodes.

Advances in radiation technology have resulted in the advent of three-dimensional conformal


(3DCRT) and IMRT, which have replaced conventional two-dimensional techniques as the
standard of care since the early 1990s. With better delineation of gross tumor volume (GTV)
by coregistration of images from CT and MRI scans, 3DCRT and IMRT can result in a much
lower incidence of "geographic misses" at the same time providing better sparing of vital
structures in the vicinity. The clinical target volume (CTV) includes all adjacent structures at
risk of subclinical disease, and the planning target volume (PTV) should ideally include a
further safety margin that takes into consideration systematic errors and day-to-day positional
variability.

Overall survival with the use of conventional radiotherapy alone in the treatment of NPC is in
the range of 50% to 76%. The use of 3DCRT has improved both tumor coverage and dose
delivery[57] but has not improved local control or long-term complications.[104] The data for
IMRT seem more convincing in terms of improvement in tumor coverage, dose delivery,
locoregional control, and tissue sparing.[11][40][56]

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In addition to improved planning and delivery techniques, altered fractionation to shorten the
treatment time (acceleration) or increase total dosage (hyperfractionation) has been used to
improve local control. Although of proven efficacy in squamous cell head and neck cancers
in other sites,[26] a phase III trial comparing conventional radiotherapy to an aggressive course
of accelerated hyperfractionated radiotherapy had to be terminated early because of excessive
neurologic complications, without improvement in local control rates.[95] Accelerated
fractionation, however, seems to be efficacious in local control. Lee, in a recent retrospective
analysis of more than 300 patients, reported on improved local control rates with the use of
six fractions per week instead of the usual five, without a significant increase in toxicity.[53]
Accelerated fractionation with small fraction sizes is currently being studied in a phase III
randomized trial of patients with locally advanced disease.

Chemotherapy

Because the results of radiation alone in stages I and II are excellent, radiation continues to be
the mainstay of treatment for early stage NPC.[1] For locally advanced disease (stage III and
IV), however, despite good initial response, local recurrence and subsequent systemic failure
are significant problems. Single and combination chemotherapy have been used as an adjunct
to radiation in an attempt to achieve better local and systemic control. Combination
chemotherapy produces better responses, and combination cisplatin/5-flurouracil is the most
widely used and studied. Nonrandomized studies that used induction, adjuvant, concomitant,
or combinations of these chemotherapy delivery methods have shown an improvement in
survival ( Table 73-3 ). To date, 10 phase III randomized trials have compared radiation
therapy alone with radiation and chemotherapy. The method of delivery differed significantly
between the various studies, and two did not use the cisplatin-5FU combination. Only two
studies achieved a significant difference in 5-year progression-free and overall survival. The
Head and Neck Intergroup Study reported by Al-Sarraf, which used a combination of
concurrent chemoradiation followed by adjuvant chemotherapy,[2] achieved a significant
difference in 5-year overall and progression-free survival ( Table 73-4 ). The results of the
radiation only arm, however, are sufficiently poor to question the validity of the study. More
recently, however, Jin in a study of 284 patients receiving concurrent chemotherapy
consisting of cisplatin-5FU administered during weeks 1 and 5 of radiation therapy also
reported a significant improvement in progression-free and overall survival.[59] This study is
the first to demonstrate a significant benefit of concurrent chemoradiation in the Asian

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population. An improvement in regional and distant control rates was also seen, although the
difference did not reach statistical significance. A meta-analysis of more than 1500 patients
from six of the randomized trials comparing combination chemotherapy with radiation alone
found that progression-free survival and overall survival increased by 34% and 21%,
respectively at 4 years for the chemotherapy arm.[39] Since publishing the results of the
Intergroup Study, Al-Sarraf has reversed the sequence of chemotherapy delivery to
neoadjuvant chemotherapy followed by concomitant chemoradiation, and reports, from
unpublished data, a 90% overall survival.[1] The results of concomitant chemoradiation seem
promising but need to be further validated. Two ongoing phase III trials, NPC 9901 and 9902
studying further the benefits of chemotherapy, will hopeful shed new light on its efficacy in
the management of locally advanced NPC.

Table 73-3 -- SURVIVAL IN NONRANDOMIZED STUDIES OF THE USE OF


CHEMOTHERAPY IN THE TREATMENT OF NASOPHARYNGEAL CANCER
Therapy No. of Series Range % Survival (Ave)

RT only 18 26–62 45

CT + RT 10 35–78 62

RT + CT 3 50–77 66

CT/RT + CT 3 70–80 77

CT + CT/RT 2 83–94 88

From Al-Sarraf M: Cancer Control 9:387, 2002.

Recurrent Disease
Radiotherapy

Locoregional recurrences without distant metastases are treated with radical external beam
radiation, brachytherapy, or by surgical resection. If detected early, they are potentially
curable and therefore should be treated aggressively.[99] Because recurrent tumors are likely
to be more radioresistant, doses exceeding 60 Gy may be required for tumor eradication.
Five-year local control rates approach 50% to 60%, and survival ranges from 16% to 45% (

14
Table 73-5 ). Small recurrences <5 cm in diameter may be treated with interstitial
brachytherapy with gold grain (138Au) implants.[15][97] The implants may be inserted under
endoscopic guidance or under direct vision by use of a split palatal approach. Despite
significant sparing of vital structures in the vicinity by the inverse square law, morbidity in
the form of headache, nasopharyngeal radiation necrosis, skull base necrosis, and palatal
fistula are not uncommon. The use of chemotherapy in both locally recurrent and systemic
disease is on a protocol basis and has not been validated by a prospective randomized study.

Surgery

The role of surgery in NPC is largely confined to the treatment of residual or recurrent
disease either in the nasopharynx or in the neck. Neck dissection for postradiation residual or
recurrent nodal disease is the most common indication for surgery, although it should be
mentioned that unlike other squamous cell cancers of the head and neck, large bulky neck
disease of up to 8 cm can be effectively controlled with radiation. The extent and level of
nodal dissection is often more extensive than suspected and is complicated further by
posttreatment changes and fibrosis. A classical radical neck dissection is often required,
consisting of a comprehensive clearance of all neck levels, including sacrifice of cranial
nerve XI, the internal jugular vein, and the sternocleidomastoid.[48][100] If the skin of the
lateral neck is involved by recurrent disease, it should be incorporated in the neck dissection
specimen. The defect should then be closed by nonirradiated healthy tissue, usually in the
form of a pedicled local myocutaneous flap like a pectoralis major flap.

There are a variety of approaches to the nasopharynx. Because surgery is very much
intracavitary, important considerations are tumor extent, access for exposure, and control of
the internal carotid artery. The transpalatal, transmaxillary, and transcervical approaches are
preferred, because they provide the most accessible routes.[23] The transpalatal approach
involves a U-shaped incision along the mucosa of the hard palate approximately 5 mm from
the maxillary dentition. This may be extended around the maxillary tuberosity into the
gingival buccal sulcus if access to the pterygopalatine fossa is necessary. Mucoperiosteal
flaps are raised based on the greater palatine neurovascular pedicle, and bone is removed
from the palatine bone and posterior hard palate ( Figure 73-5 ). Division or resection of the
soft palate may also be required for better exposure. The transmaxillary approach to the
pterygopalatine space is gained by way of the posterior maxillary sinus wall. Ligation of the
internal maxillary artery then permits entry into this space. The transcervical approach
15
identifies cranial nerve IX and lateralizes the internal carotid artery to access the
parapharyngeal space. Lateralization of the internal carotid necessarily protects cranial nerves
X, XI, and XII also. Resection then proceeds cranially through the oral cavity. A Le Fort I
osteotomy by means of a mid-face degloving procedure has also been described.[96]

The lateral infratemporal approach advocated by Fisch provides excellent exposure for
tumors extending into the infratemporal fossa and parapharyngeal space but at the expense of
limited access to the contralateral nasopharynx.[24] It requires transecting the auditory canal
and zygoma, a radical mastoidectomy rerouting cranial nerve VII and displacing the internal
carotid artery.

An anterolateral approach by means of a "maxillary swing" has also been proposed, by Wei
that involves detaching the maxilla from its bony buttresses inferior to the orbit and swinging
the entire osteocutaneous complex laterally based on the cheek flap.[101] This provides wide
exposure of the nasopharynx, paranasopharyngeal space, and the internal carotid artery below
the skull base.

Five-year local control rates range from 43% to 67%. For early disease (rT1), the Stanford
experience is of 67% survival at 5 years.[22] Surgery, therefore, offers reasonable control and
survival in carefully selected patients with residual or recurrent disease.

16

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