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• Definitive (curative) radiotherapy: 66–74 Gy/33–37
• Postoperative radiotherapy for negative margins:
• Postoperative radiotherapy for positive margins:
• Hypofractionation or hyperfractionation schedules are
SECTION VIII — Recent Advances
fractions/6–7 weeks.
60 Gy/30 fractions/6 weeks.
66 Gy/33 fractions/6.3 weeks.
also being practiced in a few selected centres.
• Hypofractionation treatment is with higher dose per
fraction (2.5–3 Gy/fraction), so as to reduce the total
number of fractions and time of radiation.
• Hyperfractionation patients are treated with 2–3
fractions/day (1.2 Gy/fraction).
CONCURRENT CHEMOTHERAPY
IN HEAD AND NECK CANCER
Cisplatin is the most common agent used concomitantly with radiation. Other agents used are cetuximab, carboplatin, paclitaxel, 5-fluorouracil, hydroxyurea, etc.
BRACHYTHERAPY IN HEAD
AND NECK CANCER
Brachytherapy is a form of radiotherapy where a sealed
radiation source is placed inside or close to the tumour
(Figures 73.5 and 73.6). It can be used to provide a boost
to external beam radiotherapy in early T1 or T2 tumours
or to recurrences, for example, cancers of nasopharynx,
lip and tongue. Brachytherapy involves delivering radiation to the tumour via thin tubes called catheters. Earlier
low-dose brachytherapy was delivered, but nowadays,
high-dose brachytherapy is the main modality of treatment. Various radioactive materials have been used: gold
(198), seeds; pallidium (103) and radium (226), needles;
caesium (137), tubes and needles; and iridium (192),
wires and seeds.
Figure 73.6. Brachytherapy for tongue cancer (catheters visible
which transmit source to the tumour). (Courtesy Dr Vadhiraj BM, Senior
Consultant.)
UNUSUAL NEOPLASMS OF THE HEAD
AND NECK (TABLE 73.1)
Figure 73.5. Brachytherapy needles in lower lip cancer.
CP angle schwannomas (acoustic tumours): These
are benign tumours seen in the cerebellopontine
angle, near the brainstem. They arise from the Schwann
cells (schwannoma). Usual presentation is some form of
nerve compression (7th or 8th nerve complex) or compression of brainstem with symptoms such as vertigo,
dizziness, hearing loss or cerebellar gait. Smaller-size
tumours can be treated by SRS alone (with a dose of 12–
14 Gy in a single session), while larger tumours are operated first and then the residual parts are radiated with a
Chapter 73 — Radiotherapy in Head and Neck Cancers
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TABLE 73.1 TREATMENT OF SOME COMMON NEOPLAMS OF THE HEAD AND NECK
Tumour sites Histology Treatment modalities Radiation doses Related side effects
Ear pinna and
auditory canal
Nasal cavity and
PNS
Nasopharynx SCC, lymphoma,
Lip and oral
cavity
Oropharynx SCC,
Larynx and
hypopharynx
Salivary gland Mucoepidermoid,
BCC and SCC Early tumours: RT alone
Advanced tumours:
surgery + postoperative RT
SCC, adenoid
cystic carcinoma,
lymphoma,
melanoma
melanoma,
chordoma,
sarcoma
SCC, adenoid
cystic or
mucoepidermoid
carcinoma
adenocarcinoma,
adenoid cystic,
NHL
SCC, lymphoma If resectable:
adenoid cystic
carcinoma
If resectable: surgery alone
Advanced lesion: surgery + RT
Inoperable lesion: CCRT
CCRT, chemoradiotherapy
and RND for residual
nodes
Early tumours: surgery or RT
Advanced tumours:
surgery + RT
(brachytherapy/electron
therapy as boost) or CCRT
only
If resectable:
surgery + postoperative
RT or definitive RT or
CCRT
surgery + postoperative RT
or definitive RT or CCRT
Surgery ± RT 54–60 Gy/27–30
56–66 Gy/28–33
fractions/5–6 weeks
66–70 Gy/33–35
fractions/6–7 weeks
70 Gy/35 fractions/7
weeks along with
weekly chemotherapy
Definitive RT: 70 Gy/35
fractions/7 weeks
Postoperative RT: 56–
66 Gy ± chemotherapy
Postoperative RT:
56–66 Gy
CCRT: 66–70 Gy/33–35
fractions/7 weeks
Postoperative RT:
56–66 Gy
CCRT: 66–70 Gy/33–35
fractions/7 weeks
fractions/5–6 weeks
Necrosis of pinna,
osteoradionecrosis of temporal
bone (>70 Gy), CSOM, hearing
loss, xerostomia
Cataract, xerostomia, dryness of
eyes and nasal cavity, monitor
dose to brainstem and optic
chiasma
Erythema, dryness of eyes and
nasal cavity, xerostomia,
monitor dose to chiasma,
brainstem and spinal cord
Skin reactions (erythema),
mucositis, trismus, xerostomia,
dental caries, monitor spinal
cord dose
Mucositis, oral infections,
dysphagia, xerostomia, dental
necrosis, trismus
Mucositis, dysphagia, hoarseness,
tracheostomy tube care (if in
situ)
Xerostomia, erythema, mucositis
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BCC, Basal cell cancer; CCRT, concurrent chemoradiotherapy; CSOM, chronic suppurative otitis media; NHL, non-Hodgkin lymphoma; PNS, paranasal
sinuses; RND, radical neck dissection; RT, radiotherapy; SCC, squamous cell cancer.
conventional dose of 50 Gy in 5 weeks. Local control is
more than 95%–98%.
Chloromas: They are solid extramedullary tumours
consisting of early myeloid precursors cells associated with acute myeloid leukaemia. Usually seen in the
central nervous system or in the orbit. Radiotherapy is
the treatment of choice with a local control of more than
80%–90%.
Chordomas: They originate from primitive notochord; 50% occur in the sacrococcygeal area and 35% in
the base of skull. Maximal safe resection is followed by
postoperative radiotherapy. For very small tumours, SRS
can be done. There is a local control of 40%.
Esthesioneuroblastomas: They arise in the olfactory
epithelium of the nasal mucosa close to the cribriform
plate. Most common symptoms are epistaxis and nasal
blockage. Surgery or radiotherapy alone is performed
for small tumours or else surgery (craniofacial resection)
followed by postoperative radiotherapy is done. A local
control of 50%–70% can be achieved.
Glomus tumours: They include paragangliomas,
chemodectomas or carotid body tumours. They arise
from the carotid body cells in the jugular bulb or middle ear (from tympanic nerve of Jacobson or auricular
nerve of Arnold). Treatment is surgical resection followed
by postoperative radiotherapy or alternatively SRS in a
single fraction or hypofractionated SRS. The local control
is very good, 90% or more.
Haemangioblastomas: They are benign vascular
tumours, most commonly seen as cerebellar tumours in
adults. They are associated with Von Hippel–Lindau disease. Treatment is with maximal safe resection or SRS.
Haemangiopericytomas: They are sarcomatous lesions from smooth muscle around the vessels and mostly seen in the base of skull, nose or orbit. They are highly
vascular and locally invasive tumours. The treatment is
preoperative embolization, followed by maximal safe
resection and postoperative radiotherapy. If the tumour is small, SRS is performed and a dose of 12–20 Gy
can be given in 1 or 2 fractions with a local control of
70%–90%.
Juvenile nasopharyngeal angiofibromas: They are usually seen in pubertal adolescent boys, present commonly
with nasal obstruction and epistaxis. They often contain
androgen receptors and may regress with oestrogen therapy. If present extracranially, embolization is followed
by surgery but for residual or intracranial tumours, radiotherapy is recommended with a dose of 30–50 Gy in
2–3 fractions. A local control of 80% can be achieved, as
tumours regress slowly over 2 years.
Nasal NK/T-cell lymphoma: Most commonly seen
in men in the age group of 50 years, with symptoms of
progressive ulceration and necrosis of nose and paranasal
sinuses. The treatment of choice is radiotherapy
(45–54 Gy) with adriamycin-based chemotherapy. The
overall survival rate is 50%–60%.
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TABLE 73.2 COMPLICATIONS OF RADIOTHERAPY
Early Late
1. Radiation sickness (loss of appetite and nausea)
2. Mucositis
3. Xerostomia
4. Skin reactions (erythema and dry or wet
5. Laryngeal oedema
6. Candida infections
7. Haematopoietic suppression
8. Acute transverse myelitis (rare)
TMJ, Temporomandibular joint.
SECTION VIII — Recent Advances
desquamation)
1. Permanent xerostomia
2. Skin changes (atrophy of skin and subcutaneous fibrosis)
3. Decaying of teeth (secondary to xerostomia)
4. Osteoradionecrosis (mandible more than maxilla)
5. Cartilage necrosis
6. Trismus (fibrosis of TMJ and muscles)
7. Transverse myelitis (Lhermitte syndrome)
8. Radiation retinopathy and cataract
9. Endocrinal deficit (thyroid and pituitary)
10. Serous otitis media and sensorineural hearing loss and vestibular symptoms
11. Radiation-induced malignancy (thyroid cancer and osteosarcoma of orbit)
12. Brain injury (somnolence syndrome and brain necrosis)
SIDE EFFECTS OF RADIATION
Acute toxicity is due to effect of radiation on rapidly dividing tissues such as skin, mucosa and bone marrow. It
depends on the dose and schedule of radiotherapy and
accompanying chemotherapy. Late toxicity is due to lateresponding tissues such as spinal cord, brain cells and
connective tissues. It correlates with total dose and dose
per fraction.
Table 73.2 lists acute and delayed toxicities of radio-
therapy.
CARE OF PATIENT DURING
RADIOTHERAPY
CARE OF SKIN
Side effects can be minimized by proper care such as
avoidance of exposure to sun, chemical irritants, and
application of lotions and ointments (except those
prescribed by the radiotherapist). Do not rub or scrub
the skin.
CARE OF ORAL CAVITY AND DENTITION
Xerostomia and mucositis are the main problems. Dental
caries follow xerostomia. Mucositis is painful and interferes with food intake and nutrition.
Oral hygiene can be maintained by rinsing the
mouth and gargling several times a day. Use only nonalcoholbased gargles. Salt and sodium bicarbonate gargles
help to clean the thick saliva and mucus. Mild antiseptic lotion can be used. Mucositis is managed by dietary
modification and topical anaesthetics.
Use of a soft brush and application of a fluoride gel
prevents tooth decay. Pre-irradiation extraction of loose
and carious teeth is recommended to prevent osteoradionecrosis.
CARE OF HAEMOPOETIC SYSTEM
Patients undergo weekly haemograms to check for white
cells, haemoglobin level and platelet counts. Corrective
measures are taken if counts fall. A good level of haemoglobin is useful to carry oxygen to the target area for a
better effect of radiation.
CARE OF INFECTIONS
Patients undergoing radiotherapy are immunosuppressed
and may require treatment for concurrent infections. Antibiotic, antifungal or antiviral drugs may be needed.
CARE OF NUTRITION
Patients are advised to consume a high-protein diet with
vitamins and minerals. Good hydration with plenty of
fluids and electrolytes should be maintained.
Blended liquid or semisolid diet can be used in patients
with odynophagia or dysphagia. Sometimes Ryles tube
feeding or percutaneous endoscopic gastrostomy may be
needed to maintain nutrition. Diet should incorporate
iron, calcium and vitamin supplements.
PSYCHOLOGICAL AND EMOTIONAL
COUNSELING
Psychological counselling may be required from time to
time during or after radiotherapy to counter depression
due to prolonged illness and complications.
HOSPITAL ADMISSION
Hospital admission may be required in cases of severe
infection, nutritional deprivation, supportive treatment
and for respiratory, vascular or neurological complications following acute or delayed effects of radiation.
Chapter 74
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Chemotherapy for Head
and Neck Cancer
Chemotherapy may be used alone or in combination with
other modalities of treatment. Most of the head and neck
malignancies are squamous cell cancers and the drugs
found effective are methotrexate, cisplatin, bleomycin
and 5-fluorouracil. Adriamycin has been used for certain
nonsquamous carcinomas (e.g. adenoid cystic carcinoma)
and dacarbazine for melanomas. Lymphomas of the head
and neck, both Hodgkin and non-Hodgkin types, are also
treated by chemotherapy because of their multifocal origin and widespread involvement.
TYPES OF CHEMOTHERAPY
palliatiVe chemotherapy. Cytotoxic drugs, singly or
in combination, are used to treat advanced, recurrent or
metastatic disease with an aim to relieve the symptoms
and to prolong life in some of them.
• When used before surgery or radiation, it is called
induction or anterior chemotherapy. It helps to reduce tumour burden and micrometastases that can occur at
the time of surgery or in the period before radiation.
• When used simultaneously with radiotherapy, it acts as a
radiosensitizer to cells which are otherwise radioresistant.
• When used after surgery or radiation, it is called posterior
chemotherapy and is aimed to cure micrometastases.
PRETREATMENT WORK-UP
OF THE PATIENT
Patient who is a candidate for cancer chemotherapy
should be worked up in the following manner:
1. History and clinical examination (exclude kidney,
heart and lung disease)
2. Haematological tests
• Haemoglobin
• Total and differential
count
• Platelet count
3. Urine exam
4. Biochemistry
• Blood urea nitrogen
• Creatinine
• Liver function tests
5. Radiology
• X-ray chest (Bleomycin causes interstitial pulmo-
nary fibrosis)
6. Pulmonary function tests (for Bleomycin)
7. ECG (for Adriamycin)
8. Audiogram (Cisplatin causes high frequency hearing
loss)
9. Nutritional status
As a baseline, as many
of the drugs are
myelosuppressive
Methotrexate and
cisplatin are nephrotoxic
SINGLE AGENT VS MULTIDRUG
COMBINATION THERAPY
Methotrexate, cisplatin, bleomycin and 5-fluorouracil
have been used as single agents in various dosage forms.
drugs with the object to improve overall response rate
and duration of response. A trend is emerging that combination of two or more drugs improves the response rate
and definitely improves the quality of patient’s life but it
has failed to improve the duration of response.
DRUGS USED IN CANCER THERAPY
Commonly used anticancer drugs and their side effects
are listed in Table 74.1.
TOXICITY OF ANTICANCER DRUGS
Most of the drugs act on rapidly dividing cells and therefore include also normal cells as those of hair follicles,
gastrointestinal mucosa and bone marrow causing alopecia, stomatitis, nausea, vomiting, diarrhoea, anaemia,
leukopenia and thrombocytopenia. Some drugs have selective action on kidney (methotrexate, cisplatin), nerves
(vincristine and cisplatin), heart (adriamycin) and bladder
(cyclophosphamide).
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SECTION VIII — Recent Advances
TABLE 74.1 COMMONLY USED ANTICANCER DRUGS AND THEIR SIDE EFFECTS
Drugs Type of neoplasm Conventional doseaSide effects Remarks
1. Methotrexate Squamous cell
cancer. Acute
leukaemia
lymphomas
2. 5-Fluorouracil
(5-Fu)
3. Cyclophosphamide • Squamouscancer
4. Dacarbazine • Melanoma
5. Bleomycin Squamous cell
6. Adriamycin
(Doxorubicin)
7. Actinomycin-D Rhabdomyosarcoma
8. Vincristine
(Oncovin)
9. Cisplatin Squamous cell
10. Paclitaxel Squamous cell
a
Follow instructions given with drug literature. Most of the drugs are given according to surface area of the body, which is calculated according to weight
and height of a person.
Squamous
cell cancers.
Nonsquamous
tumours of breast
and GI tract
• Lymphomas
• Leukaemia
• Neuroblastoma
• Multiplemyeloma
• Sarcomas
cancer,Lymphoma
• Lymphoma
• Sarcomas
• Esthesioneuro-
blastomas.
• Salivarygland
cancer Paediatric
malignancy
• Lymphoma
• Squamouscell
cancer Rhabdomyosarcoma
cancer
cancer of head
and neck
40 mg/m2 i.v.
weekly, high dose
can be given with
leucovorin rescue
• 10–15mg/kgi.v.
daily. Not more
than 1 g in single
bolus for 4–5
days.
• Repeatedat
weekly intervals
60–120 mg/m2 i.v.
daily × 5 days for
3 weeks
250 mg/m2 × 5
days every 3
weeks
10–20 mg/m2 once
or twice weekly,
i.m. or i.v.
60–90 mg/m2 i.v.
every 3 weeks.
Cardiomyopathy if
total dose exceeds
(500 mg/m2)
0.5 mg/m2 i.v. × 5
days
1.5 mg/m2 i.v. once
or twice monthly.
Single dose should
not exceed 2 mg
80–120 mg/m2 i.v.
infusion every 3
weeks
135–350 mg/m2
as 3 h infusion
every 3 weeks
• Bonemarrowsuppression
mucositis of oral and GI
mucosa.
• Maculopapularrash.
• Renalandhepatictoxicity
Myelosuppression (Neutropenia
thrombocytopenia at 1–2
weeks). Mucositis (nausea
and vomiting, stomatitis and
diarrhoea). Skin (alopecia,
hyperpig- mentation,
maculopapular rash, handfoot syndrome)
• Haemorrhagiccystitis
• Nauseaandvomiting
Alopecia
• Neutropeniaat1–2weeks
with recovery at 2–3 weeks.
• Cessationofmenses.
• Permanentinfertility
Severe nausea and vomiting
Myelosuppression Flu-like
symptoms (fever, malaise,
myalgia) for several weeks
Alopecia
• Pneumonitis(drycoughand
rales) and pulmonary fibrosis.
• Feverandchillsinrst
24 h. (give antipyretics)
Anaphylactic reaction
• Alopecia
• Erythema,
hyperpigmentation
Stomatitis
• Cardiotoxic
• Alopecia
• Stomatitis,nausea,vomiting
and diarrhoea
• Neutropenia,
thrombocytopenia which
recovers by 3 weeks
• Myelosuppression
• Nauseaandvomiting
• Mucositisanddiarrhoea
• Alopecia
• Maculopapularrash
• Neurotoxic(sensoryand
motor neuropathy)
• Constipation(givestool
softeners) Alopecia
• GIT(nausea,vomiting)
• Renaltoxicity
• Haematologic
(anaemia, neutropenia,
thrombocytopenia)
• Neurologic(peripheral
neuropathy)
• Ototoxicity(4–8kHz)
Neutropenia and infection.
Peripheral neuritis
• Excretedviaurine.
Hydration and alkalinization
of and urine before and after
drug administration reduces
the risk of complications.
• Liverfunctiontestsbefore
use
Not given in poorly nourished
patients
• Hydratethepatientwell
before and after drug
administration.
• Avoidbarbituratesduring
therapy
• WeeklyX-raychest.
• Usewithcareinpatients
of pulmonary and renal
disease. Do not exceed
total dose of 400 units, as it
causes. Pulmonary fibrosis.
(1 unit =1 mg)
• CardiotoxicityisseeninECG
• Urinemayberedfor1–2
days
Avoid extravasation into
soft tissue at the time of
injection
Avoid extravasation into tissues
• Adequateprehydration
• Mannitoldiuresis.
• Donotusedrugif
creatinine clearance is
below 40 mL/min
Colony stimulating agents to
counteract neutropenia
Chapter 75
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HIV Infection/AIDS and ENT
Manifestations
ACQUIRED IMMUNODEFICIENCY
SYNDROME
Acquired immunodeficiency syndrome is caused by retroviruses. Those infecting the human beings are of two
types: (i) HIV type I—which is the most common and
very pathogenic and (ii) HIV type II—which is less common and less pathogenic. Once virus enters the body, it
attacks T-lymphocytes and other cells which have CD4
surface marker. CD4 T-lymphocytes are normally associated with helper-inducer function of the immune system.
With the fall in CD4 lymphocytes below 500 cells/mm3,
(normal 600–1500 cells/mm3), the immune system starts
breaking down with the appearance of opportunistic
infections and unusual malignancies, when it is called
AIDS. When CD4-cell count falls below 200 cells/mm3,
death occurs within 2–3 years.
MODES OF TRANSMISSION
HIV infection is transmitted through:
1. Sexual contact—homosexual or heterosexual.
2. Use of nonsterile needles, syringes or other skin-piercing instruments.
3. Blood and blood products.
4. Infected mother to infant—During pregnancy, during
birth, and via breast milk.
High-risk groups include (i) heterosexually promiscu-
ous individuals (ii) homosexuals (iii) prostitutes and truck
drivers (iv) IV drug users (v) recipients of blood and blood
products (haemophilics, thalassaemia patients and those
undergoing dialysis and (vi) children born to HIV infected mothers.
Major hazard to healthcare workers is from blood and
body fluids like amniotic, pleural, peritoneal or pericardial fluid.
Risk of acquiring infection from the specimens of
urine, stool, saliva, sputum, tears, sweat and vomitus is
negligible unless they are visibly bloody.
HISTORY AND EPIDEMIOLOGY OF HIV
INFECTION IN INDIA
AIDS virus was isolated in 1983 and was called HTLV III/
LAV (human T-cell lymphotropic virus type III or lymphoadenopathy associated virus). Later its name was
changed to HIV (Human Immunodeficiency Virus).
In India, HIV disease was first documented in 1986 in
sex workers in Chennai (erstwhile Madras) and Ministry
of Health and Family welfare launched AIDS Control Programme in 1987. In 1992, NACO (National AIDS control
organization) established state level societies (SACS-State
AIDS control societies) in various states, union territories
and three cities. With the concerted effort, NACO has
brought 57% reduction in new HIV cases in the last decade with 2.74 lakh cases in 2000 to 1.6 lakh cases in 2011.
HIV prevalence has steadily declined from 0.41% in 2001
to 0.35% in 2006 and 0.25% in 2011.
Prevalence of HIV/AIDS, according to NACO, in the
year 2007 and 2011 is shown in Table 75.1.
As on 2011, 86% of patients were in the age group of
15–49 years and 7% were children, below 15 years. Of all
infections, 61% are in males and 39% in females. About
1.48 lakh people have died due to AIDS related causes in
2011. Four states where disease is highly prevalent are
Andhra Pradesh, Maharashtra, Karnataka and Tamil Nadu.
STRUCTURE OF HIV-I VIRION (FIGURE 75.1)
1. Lipid membrane has two layers.
2. Envelope glycoproteins
(a) Glycoprotein 120 (helps virus to bind to host cell).
(b) Glycoprotein 41 (helps in fusion of viral and cel-
lular membranes).
3. Viral core proteins
(a) Matrix protein p17
(b) Capsid protein p24
(c) Nucleocapsid protein p6, p7
(d) Single-stranded RNA: Two copies
(e) Viral enzymes
(i) Reverse transcriptase
(ii) Integrase
(iii) Protease
LIFE CYCLE OF HIV
1. Virus enters the body of an individual through various
modes of transmission. It binds to CD 4+ receptors sit-
uated on the surface of helper T-cells and macrophag-
es. Such receptors are also present on monocytes, mac-
rophages and CNS dendritic cells.
2. Fusion of virus to cell membrane allows the viral core
to be injected into the host cell.
3. Reverse transcriptase, an enzyme present in viral core,
changes viral RNA to DNA and the latter migrates to
host genome.
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SECTION VIII — Recent Advances
TABLE 75.1 HIV PREVALENCE IN INDIA
Indicator Year 2007 Year 2011
Prevalence 0.33% 0.27%
Total number of persons living
with HIV
Number of adult new HIV
infection
Number of annual AIDS related
deaths
Figure 75.1. Structure of HIV-I virion.
22,52,253 20,88,642
1,23,890 1,16,456
2,06,671 147,729
4. Viral integrase helps viral DNA to integrate into host’s
genome and the latter is then called a provirus.
5. Provirus directs synthesis of new HIV particles.
6. During RNA transcription, there is also formation of
protein precursors or polyproteins which are cleaved
by proteases to form functional viral proteins. The latter increase the infectivity of the new virus particles.
The new viruses originating from the host cells bind to
new cells and the cycle goes on.
Immunodeficiency arises from loss of helper T-lym-
phocytes, which play an important role in cell-mediated
immunity. Monocytes harbour the virus and disseminate
disease but their number does not change.
COURSE OF DISEASE
After exposure, the disease runs through the following
stages:
1. Initial viraemia. Primary infection with HIV, first
causes viraemia which produces mild clinical disease
like fever, headache, body aches and pains, macular
skin rash and lymph nodes enlargement. This picture
resembles infections like mononucleosis and subsides
in 1–2 weeks. The virus is then taken up by lymphoid
organs like lymph nodes, tonsils, adenoids and spleen.
Initial plasma viraemia lasts for a few weeks and then
no virus can be detected in plasma.
2. Latent period. This is the asymptomatic period and
may last for a variable period, on an average 10 years.
In up to 5–10% of cases latent period may be 15 years
or more. They are called long-term survivors or long-term
nonprogressors. In some cases, about 10%, latent period is short, nearly 3 years. They are called rapid progres-
sors. During this period no virus is detectable in plasma
though it is replicating in the lymphoid tissue and the
CD4 T-helper cell number and function is deteriorating. Antibody test becomes positive in 2–4 months of
infection.
3. Advanced disease. It starts after several years. The
CD4 T-cell count falls below 200 cells/mm3 and patient
becomes susceptible to opportunistic infections. There
are clinical signs and symptoms of AIDS and death
may occur within 2 years.
ENT MANIFESTATIONS OF HIV INFECTION
HIV infection causes loss of helper T-cell population,
which is important in cell-mediated immunity. As the
T-cell count gradually diminishes, morbidity and mortality
due to HIV increase.
Three types of lesions are seen:
1. Opportunistic infections. All types of infection can
occur: viral, bacterial, protozoal, mycobacterial or fungal. They can involve any area of ear, nose and throat,
head and neck, and central nervous system.
2. Unusual malignancies. Kaposi sarcoma (KS) and lymphomas are common. KS can involve skin, mucous
membranes or viscera. KS may be seen in the skin of
face (nose, ear or external ear canal), neck or extremities. It can also occur in oral, nasal, nasopharyngeal,
oropharyngeal or laryngeal mucosa. KS causes obstructive symptoms.
Non-Hodgkin lymphoma can involve nodal and ex-
tranodal sites (see infra). Hodgkin lymphoma is less
common.
3. Neurological disorders. They can be due to primary
HIV infection or opportunistic organisms. Primary
HIV infection of CNS can cause encephalopathy (AIDS
dementia complex), myelopathy, peripheral neuropathy and cranial nerve involvement, most often VIIth
but occasionally Vth and VIIIth.
HIV manifestations in different areas in ENT and Head
& Neck are given below.
1. Ear. Viral, bacterial or fungal infections which can in-
volve external, middle or internal ear are:
• Kaposi sarcoma
• Seborrhoeic dermatitis of external canal
• Malignant otitis externa
• Serous otitis media
• Acute otitis media
• Pseudomonas and candida infection of the external
and middle ear
• Mycobacterial infections
• Sensorineural hearing loss—due to viral infection
of auditory nerve or cochlea and demyelination of
CNS
• Herpes zoster (Ramsay–Hunt syndrome)
• Facial paralysis
2. Nose and paranasal sinuses
• Herpetic lesions of nose
• Recurrent sinusitis
Chapter 75 — HIV Infection/AIDS and ENT Manifestations
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423
• Chronic sinus infection
• Fungal sinusitis
• Kaposi sarcoma
• Lymphomas–B cell type
• Burkitt lymphoma
3. Oral cavity and oropharynx
• Candidal infection of oral cavity can be thrush-like,
atrophic or hypertrophic forms of candidiasis. Candida infection also involves oropharynx, hypopharynx or oesophagus. They cause difficulty and painful swallowing.
• Herpetic lesions of palate, buccal mucosa, lips or
gums. Such lesion may form large ulcers
• Giant aphthous ulcers
• Adenotonsillar hypertrophy.
• Generalized lymphadenopathy
• Kaposi sarcoma of palate
• Non-Hodgkin lymphoma of tonsil or tongue
• Hairy leukoplakia (see infra)
• Gingivitis
4. Larynx
• Laryngitis—fungal, viral (herpes simplex, cytomeg-
alovirus) or tubercular
• Kaposi sarcoma
• Non-Hodgkin lymphoma
5. Salivary Glands
• Parotitis
• Xerostomia
• Diffuse parotid enlargement
• Lymphoepithelial cysts of parotid. They arise from
parotid nodes, often on both sides.
• Kaposi sarcoma
• Non-Hodgkin lymphoma
6. Neck
Lymphadenopathy. It could be only a follicular hyper-
plasia or due to a disease such as tuberculosis, histoplasmosis, toxoplasmosis or non-Hodgkin or Hodgkin
lymphoma.
KAPOSI SARCOMA
It is a multicentric neoplasm which may involve any part
of the skin, mucosa or the viscera. There is excessive proliferation of spindle cells of vascular origin. It is noninvasive and respects the fascial planes. In the oral cavity, Kaposi sarcoma is mostly seen in the palate, but may occur
on the tongue or gingiva or on the posterior wall of the
pharynx. It appears purplish in colour and may need to
be differentiated from angioma or pyogenic granuloma.
It can occur at any stage of HIV infection, even in those
with normal CD4 counts. Size of the tumour may vary
from a few mm to several centimetres. Diagnosis is based
on biopsy which may show proliferation of spindle cells,
endothelial cells, extravasation of red blood cells and
haemosiderin-laden macrophages. Treatment includes
localized radiation, intralesional vinblastine or cryotherapy. Systemic chemotherapy may be given in those with
multiple lesions.
NON-HODGKIN LYMPHOMA
HIV patients have high incidence of lymphomas. B-cell
lymphomas are more common (90%) and many are due
to Epstein–Barr virus. Risk of lymphomas increases as
disease progresses generally in patient with CD4+ count
less than 200/mm3. CNS lymphomas occur in late stages
of the disease while systemic ones can occur early. Both
nodal and extranodal sites can be involved; the latter include nose and paranasal sinuses, tonsils, nasopharynx,
tongue, orbit and larynx. They also involve gastrointestinal tract, lung and bone marrow. Cervical lymphadenopathy can occur.
Hodgkin lymphoma is less common.
HAIRY LEUKOPLAKIA
It is a white, vertically corrugated lesions on the anterior
part of the lateral border of tongue. It is probably caused
by Epstein–Barr virus. It develops early and gives clue to
HIV infection. AIDS develops in 50% of such patients in
16 months or 80% in 30 months. Differential diagnosis
includes leukoplakia, carcinoma in situ, hypertrophic
candidiasis or lichen planus. Biopsy should be done to
confirm.
DIAGNOSTIC TESTS
Diagnostic tests are based on identification of antibodies
or viral antigens. Antibodies are formed within 3 months
(2 weeks–12 weeks) of infection.
1. ELISA test (enzyme-linked immunosorbent assay).
It is a very sensitive test (sensitivity more than 95.5%).
2. Western blot. It is a confirmatory test and specific for
HIV antibodies.
3. CD4 count. Normal count is 600–1500/mm3. Decreasing counts indicate immune compromise and
the corresponding risk for development of opportunistic infections and malignancies. Disease has been
classified according to CD4 counts such as (i) less than
500 cells/mm3; (ii) 200–499 cells/mm3 or (iii) less than
200 cells/mm3; AIDS-defining illnesses appear when
CD4 count fall below 200/mm3.
4. p24 antigen assay. It detects p24 core protein of HIV.
The test is positive even prior to seroconversion. High
levels of p24 antigen are present before development
of antibodies and are useful in those suspected of acute
HIV syndrome.
5. PCR tests. They determine HIV-RNA. Two important
tests are reverse transcriptase PCR and branched DNA
assay. They determine number of copies of RNA per
millilitre of plasma and indicate viral load.
HIV INFECTION AND HEALTHCARE
WORKERS
Doctors, particularly the surgeons, nurses and laboratory
staff handling the blood, blood-stained body fluids and
other secretions may contract the disease as occupational hazard. They should follow the universal precautions
(vide infra) considering that every sample they handle is
potentially infected. The risk is due to:
1. Needle-stick injury. Hollow needle (e.g. injection needle) is more dangerous than solid needle (e.g. suture
needle). The risk is. 0.3%, i.e. (1:300).
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SECTION VIII — Recent Advances
2. Cuts with contaminated knife or other sharp instruments.
3. Exposure of open wound to infected blood or body
fluid of the patient. Entry of virus can also occur
through an area of dermatitis.
4. Large mucous membrane exposure, e.g. by splatter
of blood, amniotic fluid, etc. Risk is 0.09%.
5. Exposure of skin to infected blood and body fluids.
Use of gloves and gown/coat is protective.
MANAGEMENT
Several factors need to be taken into account before management and the initiation of a prophylactic treatment.
1. Hollow needle vs solid needle. Hollow needles (injection needle) have more chance to introduce infected
blood.
2. Superficial vs deep cut. Deeper cuts are more dangerous.
3. Source patient having or not having HIV and if yes,
how serious is his condition due to advanced HIV disease and the antiretroviral drugs being used by him
(Ist or IInd line) for the possibility of exposure to drug
resistant virus.
4. Condition of healthcare worker, e.g. pregnancy and
other diseases he/she suffers from and the medication
he/she is using for such ailments.
First step after exposure is to wash the area thoroughly
with water and apply an antiseptic. ELISA test should be
done as soon as possible to establish negative base line
and to repeat the test at 6 weeks, 3 months and 6 months
for any seroconversion.
If decision is made to start drug prophylaxis, it is
recommended to start two drugs of nucleoside analogue
reverse transcriptase inhibitor group for 4 weeks for routine
exposures (zidovudine and lamivudine or lamivudine and
stavudine) and three drug regimen for high-risk exposure.
Treatment should be started immediately certainly not
later than 24 h. Seroconversion has been noted in spite of
this prophylaxis, therefore avoidance of exposure by universal precaution is the best.
UNIVERSAL PRECAUTIONS
• Wash hands before and after patient or specimen
contact.
• Handle the blood of all patients as potentially
infectious.
• Wear gloves for potential contact with blood and body
fluids. All sharps like blades, needles, etc. to be put in
impermeable container and destroyed.
• During operation, knife to be passed to the surgeon in
a tray.
• Place used syringes immediately in a nearby imperme-
able container; DO NOT recap, bend or manipulate
needle in anyway!
• Use double gloves where they are likely to be pierced
as in fracture surgery. Quality of gloves is important
as many of them may have holes. Impermeable gloves
are also available.
• Wear protective eyewear and mask if splatter with
blood or body fluids is anticipated (e.g. bronchoscopy,
oral surgery).
• Wear gowns when splash with blood or body fluids is
anticipated.
• Handle all linen soiled with blood and/or body secre-
tions as potentially infectious.
• Refrain from patient care if you suffer from exudative
or weeping skin lesion or dermatitis.
• Process all laboratory specimens as potentially infectious.
• Wear mask to protect against TB and other respiratory
organisms (HIV is not airborne).
ANTIRETROVIRAL DRUGS
There are four major classes of antiretroviral drugs:
1. Nucleoside reverse transcriptase inhibitors (prevent
conversion of RNA to DNA.).
• Zidovudine (AZT)
• Didanosine (ddI)
• Zalcitabine (ddC)
• Stavudine (d4T)
• Lamivudine (3TC)
2. Non-nucleoside reverse transcriptase inhibitors (prevent conversion of RNA to DNA). They bind to reverse
transcriptase.
• Delavirdine
• Nevirapine
• Efavirenz
• Tenofovir (nucleotide analogue)
3. Protease inhibitors (prevent cleavage of viral proteins
into their functional forms by binding to viral protease
enzyme.
• Saquinavir
• Ritonavir
• Indinavir
4. Fusion inhibitors (interfere with entry of virus into target cells). They bind to HIV–gp 41
• Enfuvirtide
Antiretroviral drugs can prevent progression of HIV
to AIDS. Drug resistance can occur. Second line drugs are
more expensive. Toxicity of drugs should be kept in mind.
Drug interactions are common and should be avoided.
Combination drug therapy is more effective and prevents
drug resistance; it is the standard of treatment today to
combine two or more drugs.
SECTION IX
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Clinical Methods in ENT
and Neck Masses
S e c t i o n o u t l i n e
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77 Neck Masses, 445
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