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SECTION IV — Diseases of Pharynx
TABLE 53.1 SUBSITES IN THE OROPHARYNX
• Baseoftongue
• Tonsilandtonsillarfossa
• Faucialarch
• Pharyngealwall
TABLE 53.2 TNM CLASSIFICATION AND STAGING
OF OROPHARYNGEAL CANCER (AJCC, 2002)
Primary tumour (T)
T
1
T
2
T
3
T4a Tumour invades the larynx, deep/extrinsic
T4b Tumour invades lateral pterygoid muscle,
Regional lymph nodes (N)
N
X
N
0
N
1
N
2
N
2a
N
2b
N
2c
N
3
Distant metastasis (M)
M
X
M
0
M
1
Stage grouping
0 Tis N
I T
II T
III T
IVA T4a N
IVB T4b Any N M
IVC Any T Any N M
Tumour 2 cm or less in greatest dimension
Tumour more than 2 cm but not more than
4 cm in greatest dimension
Tumour more than 4 cm in greatest
dimension
muscle of tongue, medial pterygoid, hard
palate or mandible
pterygoid plates, lateral nasopharynx, or
base of skull or encases carotid artery
Regional lymph nodes cannot be assessed
No regional lymph node metastasis
Metastasis in a single ipsilateral lymph
node, 3 cm or less in greatest dimension
Metastasis in a single ipsilateral lymph
node, more than 3 cm but not more
than 6 cm in greatest dimension, or in
multiple ipsilateral lymph nodes, none
more than 6 cm in greatest dimension,
or in bilateral or contralateral lymph
nodes, none more than 6 cm in greatest
dimension
Metastasis in a single ipsilateral lymph node
more than 3 cm but not more than 6 cm
in greatest dimension
Metastasis in multiple ipsilateral lymph
nodes, none more than 6 cm in greatest
dimension
Metastasis in bilateral or contralateral
lymph nodes, none more than 6 cm in
greatest dimension
Metastasis in a lymph node more than 6 cm
in greatest dimension
Distant metastasis cannot be assessed
No distant metastasis
Distant metastasis
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
M
0
0
M
0
1
1
2
3
T
1
T
2
T
3
T4a N
T
1
T
2
T
3
T4a N
Any T N
0
N
0
N
0
N
0
N
1
N
1
N
1
0
1
N
2
N
2
N
2
2
3
Figure 53.1. An exophytic growth at the base of the tongue.
Spread
1. local. Lesions are deeply infiltrative and spread to
the rest of tongue musculature, epiglottis and pre-epiglottic space, tonsil and its pillars, and hypopharynx.
2. lymphatic. Seventy per cent of the cases show cervical metastases either unilateral or bilateral at the time
of initial consultation. Jugulodigastric nodes are the first
to be involved. Most often level II, III and IV nodes are
involved.
3. distant metastases. Bones, liver and lungs may be
involved.
Diagnosis
Lesions can be seen on indirect laryngoscopy but palpation of the tumour should never be omitted. Palpation under anaesthesia when tissues are relaxed gives better idea
of the degree of infiltration of tissues. Lesion is usually
far more extensive than it appears on mirror examination. Computed tomography scan is recommended for
tumour and nodal staging. Biopsy is essential to know its
histology.
Treatment
Treatment may vary from centre to centre, some favouring radiotherapy, others surgery and still others radiotherapy followed by salvage surgery.
Tumours which are radiosensitive such as anaplastic
carcinoma, lymphoepithelioma or lymphoma are treated
by radiotherapy to the primary and neck nodes.
For T1 and T2 squamous cell carcinoma with N0 or N1
neck, surgical excision with block dissection is preferred
and if neck dissection specimen reveals a stage more than
N1, postoperative radiation is added.
T3 and T4 lesions require surgical excision with mandibular resection, neck dissection and postoperative
radiation.
T4 lesions, which also extend into anterior two-thirds
of tongue or vallecula, require extensive surgery with total glossectomy and laryngectomy in addition to the radial neck dissection.
Chemotherapy may be combined with radiotherapy
and surgery in such cases.
For advanced cancers, in patients with poor health,
only palliation with radio- or chemotherapy may be
Figure 53.2. Carcinoma right base of the tongue. (A) Endoscopic view. (B) Secondaries in jugulodigastric nodes.
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required. They often end up into tracheostomy and gastrostomy in the terminal phase to restore their air and
food passages and strong analgesics for relief of pain.
Chapter 53 — Tumours of Oropharynx
307
B. CARCINOMA TONSIL AND TONSILLAR
FOSSA
Squamous cell carcinoma is the most common and
presents as an ulcerated lesion with necrotic base
( Figure 53.3). Lymphomas may present as unilateral tonsillar enlargement with or without ulceration and may
simulate indolent peritonsillar abscess (Figure 53.4).
Spread
1. local. Tumour may spread locally to soft palate and
pillars, base of tongue, pharyngeal wall and hypopharynx. It may invade pterygoid muscles and mandible resulting in pain and trismus. Parapharyngeal space may
also get invaded.
2. lymphatic. Fifty per cent of the patients have initial
cervical node involvement at the time of presentation.
Jugulodigastric nodes are the first to be involved.
3. distant metastases. They are seen in late cases.
Clinical Features
Persistent sore throat, difficulty in swallowing, pain in
the ear or lump in the neck are the presenting symptoms.
Later on, bleeding from the mouth, fetor oris and trismus
may occur.
Diagnosis
Palpation of tonsillar area should never be omitted to find
the extent of tumour. Biopsy is essential for histological
typing.
Figure 53.3. A squamous cell carcinoma involving the tonsil, pillars
and soft palate.
Treatment
1. radiotherapy. Early and radiosensitive tumours are
treated by radiotherapy along with irradiation of cervical
nodes.
Figure 53.4. Lymphoma right tonsil presenting as unilateral tonsillar
enlargement.
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Figure 53.5. An ulcerative lesion of the palatine arch. It was a
well-differentiated squamous cell carcinoma.
SECTION IV — Diseases of Pharynx
D. CARCINOMA OF POSTERIOR AND
LATERAL PHARYNGEAL WALL
Lesions remain asymptomatic for a long time. They may
spread submucosally to the adjoining areas such as tonsil, soft palate, tongue, nasopharynx or hypopharynx.
They may also invade parapharyngeal space or anterior
spinal ligaments. Sixty per cent of patients may have
lymph node metastases. Bilateral nodal involvement is
common.
Treatment is irradiation or surgical excision of growth
with skin grafting. This is often combined with block
dissection when nodes are palpable. Access to posterior
pharyngeal wall is through lateral pharyngotomy with or
without mandibular osteotomy.
2. surgery. Excision of the tonsil can be done for early
superficial lesions. Larger lesions and those which invade bone require wide surgical excision with hemimandibulectomy and neck dissection (commando operation).
3. combination therapy. Surgery may be combined
with pre- or postoperative radiation. Chemotherapy may
be given as an adjunct to surgery or radiation.
C. CARCINOMA OF FAUCIAL (PALATINE)
ARCH
Soft palate, uvula and anterior tonsillar pillar comprise
the faucial arch. Carcinoma in these sites is often of squamous cell variety. Lesions are superficially spreading and
well-differentiated with late tendency for nodal metastases (Figure 53.5). Thus they behave more like carcinomas
of the oral cavity.
Spread may occur locally to the contiguous structures
or lymph nodes. Upper deep cervical and submandibular
nodes may be involved.
Patients with palatine arch cancer usually present with
persistent sore throat, local pain or earache. Growth may
have been noticed by the patient while using the mirror,
or by his physician while examining his throat or by the
dentist.
Treatment is irradiation or surgical excision.
PARAPHARYNGEAL TUMOURS
Parapharyngeal space is described on p. 299 (refer
Figure 52.6). It lies lateral to the pharynx. Both benign
and malignant tumours are seen. They cause a bulge in
lateral pharyngeal wall of oropharynx and distort the
pillars and soft palate, and thus mimic neoplasms of the
oropharynx. Commonly seen tumours are those from the
deep lobe of parotid, neurogenic (e.g. neurilemmoma),
chemodectoma (from carotid body), lipoma or aneurysm
of internal carotid artery.
STYALGIA (EAGLE SYNDROME)
It is due to elongated styloid process or calcification of
stylohyoid ligament. A normal styloid process is 25 mm;
if greater than 30 mm, it is considered to be elongated.
Patient complains of pain in tonsillar fossa and upper
neck which radiates to the ipsilateral ear. It gets aggravated on swallowing. Diagnosis can be made by transoral
palpation of the styloid process in the tonsillar fossa, by
a radiograph (such as anteroposterior view with open
mouth or lateral view of skull) or by a CT scan with 3D
reconstruction. Many persons may have elongated styloid process but remain asymptomatic and do not need
treatment. Symptomatic styloid process can be excised by
transoral or cervical approach.
Chapter 54
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Tumours of the Hypopharynx
and Pharyngeal Pouch
TUMOURS OF HYPOPHARYNX
Benign tuMourS. They are exceptionally uncommon
and include papilloma, adenoma, lipoma, fibroma and
leiomyoma. They present as smooth well-defined masses
which are sometimes pedunculated and mobile.
MaLignant tuMourS. Carcinoma of the hypopharynx
is very common in India. Practically, most of the tumours
are squamous cell type with various grades of differentiation. The various subsites involved are: (i) pyriform sinus,
(ii) postcricoid region and (iii) posterior pharyngeal wall,
in that order of frequency.
A. CARCINOMA PYRIFORM SINUS
It constitutes 60% of all hypopharyngeal cancers, mostly
affecting males above 40 years of age. Growth is either
exophytic or ulcerative and deeply infiltrative. Because of
the large size of the pyriform sinus, growths of this region
remain asymptomatic for a long time. Metastatic neck
nodes may be the first to attract attention.
Spread
1. Locally, the growth may spread upwards to the val-
lecula and base of tongue; downwards to postcricoid region; medially to aryepiglottic folds and ventricles. It may
infiltrate into the thyroid cartilage, thyroid gland or may
present as a soft tissue mass in the neck.
2. Lymphatic spread occurs early. Pyriform fossa has
a rich lymphatic network. Seventy-five per cent of the
patients have cervical nodal metastases when first seen,
with half of them having bilateral involvement. Upper
and middle group of jugular cervical nodes are often involved. Sometimes, nodes make their appearance long
after the primary has been eradicated.
3. Distant metastases often occur late and may be
seen in lung, liver and bones.
Clinical Features
Early symptoms are few. Something sticking in the throat
and “pricking sensation” on swallowing may be the earliest symptoms. Referred otalgia, pain on swallowing and
increasing dysphagia may follow. A mass of lymph nodes
high up in the neck may be the first sign. Hoarseness
and laryngeal obstruction indicate laryngeal oedema or
spread of disease to the larynx.
Diagnosis
Growth and its extent can often be seen on mirror examination. Sometimes, pooling of secretions obstructs the
view. Barium swallow and CT scan are helpful to evaluate
the extent of growth and status of lymph nodes.
Endoscopic examination is necessary for biopsy and
accurate assessment of the extent of growth and also to
find out any synchronous primary at any other site.
Treatment
Early growth without nodes can be cured by radiotherapy with the advantage of preserving the laryngeal
function.
If growth is limited to pyriform fossa and does not extend to postcricoid region, total laryngectomy and partial pharyngectomy is done. Remaining pharynx can be
primarily closed. This is often combined with elective or
prophylactic block dissection of lymph nodes.
If growth extends to postcricoid region, total laryngectomy and pharyngectomy is done along with block dissection. Pharyngo-oesophageal segment is reconstructed
with myocutaneous flaps or stomach pull-up.
Planned postoperative radiotherapy can be given routinely to all cases. Patients with no palpable nodes (N0
neck) can also be given radiotherapy avoiding block
dissection.
B. CARCINOMA POSTCRICOID REGION
This constitutes 30% of laryngopharyngeal malignancies. Paterson–Brown–Kelly (Plummer–Vinson) syndrome
characterized by hypochromic microcytic anaemia is an
important aetiological factor as one-third of patients of
postcricoid carcinoma may be suffering from it.
Spread
Usually an ulcerative type of lesion arises from postcricoid region. Local spread often occurs in an annular fashion causing marked dysphagia. Growths may invade cervical oesophagus, arytenoids or recurrent laryngeal nerve
at cricoarytenoid joint.
Lymphatic spread involves paratracheal lymph nodes
and may be bilateral due to the midline nature of lesions.
They may not be clinically palpable.
Clinical Features
Females are usually affected, sometimes in the early age
group of twenties and thirties. Progressive dysphagia is
the predominant presenting symptom. This may cause
progressive malnutrition and weight loss. Sometimes,
voice change and aphonia may be produced due to infiltration of recurrent laryngeal nerve or posterior cricoarytenoid muscles affecting vocal cord mobility.
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SECTION IV — Diseases of Pharynx
Diagnosis
Postcricoid growths may not be visible on indirect laryngoscopy. Oedema and erythema of the postcricoid region
and pooling of secretions in the hypopharynx are suggestive of growth. Laryngeal crepitus, felt normally while
moving larynx over the cervical spine, may be lost.
Lateral soft tissue radiograph of the neck may show
an increased prevertebral shadow. Barium swallow is essential to find the lower extent of the disease. Endoscopy
is always done to take biopsy and assess the extent of
lesion.
Treatment
Prognosis is poor both with irradiation and surgical treatment. Some prefer to give radiotherapy initially. It has the
advantage of preserving laryngeal function. Failed cases
are subjected to laryngo-pharyngo-oesophagectomy with
stomach pull-up or colon transposition to reconstruct
pharyngo-oesophageal segment. Many feel that initial
surgery, if feasible, gives better results.
C. CARCINOMA POSTERIOR
PHARYNGEAL WALL
This is the least common of laryngopharyngeal malignancy constituting only 10% of them. They are mostly
seen in males above 50 years of age.
Figure 54.1. Hypopharyngeal (Zenker’s) diverticulum. Hypopharyngeal mucosa herniates through the Killian’s dehiscence—a weak area
between two parts of inferior constrictor muscle.
Spread
Growth is usually exophytic but may be ulcerative. It remains localized until late and then spreads to the prevertebral fascia, muscles and vertebrae.
Lymphatic spread is usually bilateral due to midline
nature of the lesion. Fifty per cent of the patients with
cancer of posterior pharyngeal wall have nodal metastasis on their initial examination. Retropharyngeal nodes,
though not clinically palpable, may also be involved.
Clinical Features
Dysphagia or spitting of blood may be the presenting
symptom. Some may present with a palpable mass of
nodes in the neck without any symptoms pointing to the
primary tumour.
Diagnosis
Indirect mirror examination often reveals the tumour.
Lateral soft tissue radiography may show vertical extent
and thickness of the tumour and any involvement of cervical vertebrae. Endoscopy is essential for biopsy and accurate assessment of the tumour and to find any synchronous primary at any other site.
Treatment
Early lesions, particularly exophytic, can be treated by
radiotherapy with preservation of laryngeal function.
Early small lesions can also be excised surgically via lateral pharyngotomy and primary repair with equally good
results. Advanced lesions may require laryngopharyngectomy and block dissection of neck with repair of the food
channel. Gross 5-year cure rate is only 19%.
Figure 54.2. Potential sites for hypopharyngeal diverticulum.
PHARYNGEAL POUCH
Also called hypopharyngeal diverticulum or Zenker’s
diverticulum, it is a pulsion diverticulum where pharyn-
geal mucosa herniates through the Killian’s dehiscence—
a weak area between two parts of the inferior constrictor
(Figures 54.1 and 54.2).
AETIOLOGY
Exact cause is not known. It is probably due to spasm of
cricopharyngeal sphincter or its incoordinated contractions during the act of deglutition. It is usually seen after
60 years of age.
PATHOLOGY
Herniation of pouch starts in the midline. It is at first behind the oesophagus and then comes to lie on its left.
Mouth of the sac is wider than the opening of oesophagus
and food preferentially enters the sac.
CLINICAL FEATURES
Dysphagia is the prominent feature. It appears after a
few swallows when the pouch gets filled with food, and
presses on the oesophagus. Gurgling sound is produced
on swallowing. Undigested food may regurgitate at night,
Chapter 54 — Tumours of the Hypopharynx and Pharyngeal Pouch
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when patient is recumbent, causing cough and aspiration pneumonia. Patient is often malnourished due to
dysphagia. Patients with pharyngeal pouch may have associated hiatus hernia. Rarely carcinoma can develop in
long-standing cases of pharyngeal pouch.
DIAGNOSIS
Barium swallow will show the sac and its size.
TREATMENT
1. Excision of pouch and cricopharyngeal myotomy.
This is done through cervical approach.
2. Dohlman’s procedure. The partition wall between
the oesophagus and the pouch is divided by diathermy
through an endoscope. This is done in poor risk debilitated patients.
3. Endoscopic laser treatment. It is similar to Dohlman’s procedure. Partition between the pouch and
oesophagus is divided by CO2 laser using operating
microscope.
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Chapter 55
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Snoring and Sleep Apnoea
SNORING
It is an undesirable disturbing sound that occurs during
sleep. It is estimated that 25% of adult males and 15% of
adult females snore. Its prevalence increases with age.
DEFINITION OF TERMS
• Sleep apnoea. It is cessation of breathing that lasts for
10 s or more during sleep. Less than five such episodes
is normal.
• Apnoea index. It is number of episodes of apnoea
in 1 h.
• Hypopnoea. It is reduction of airflow. Some define it
as drop of 50% of airflow from the base line associated
with an EEG defined arousal or 4% drop in oxygen
saturation.
• Respiratory disturbance index (RDI). Also called
apnoea–hypopnoea index. It is the number of apnoea
and hypopnoea events per hour. Normally RDI is less
than five. Based on RDI, severity of apnoea has been
classified as mild, 5–14; moderate, 15–29; and severe
≥ 30.
• Arousal. Transient awakening from sleep as a result of
apnoea or respiratory efforts.
• Arousal index. It is number of arousal events in 1 h.
Less than four is normal.
• Sleep efficiency. Minutes of sleep divided by minutes
in bed after lights are turned off.
• Multiple sleep latency test or nap study. Patient is
given four or five scheduled naps usually in the daytime. Latency period from wakefulness to the onset of
sleep and rolling eye movement (REM) sleep are measured. It is performed when narcolepsy is suspected or
daytime sleepiness is evaluated objectively.
nasopharynx such as septal deviation, turbinate hypertrophy, nasal valve collapse, nasal polypi or tumours; in oral
cavity and oropharynx such as elongated soft palate and
uvula, tonsillar enlargement, macroglossia, retrognathia,
large base of tongue; or its tumour; in the larynx and lar-
yngopharynx such as laryngeal stenosis or omega-shaped
epiglottis.
Other causes include obesity and thick neck with collar size exceeding 42 cm. Use of alcohol, sedatives and
hypnotics aggravates snoring due to muscle relaxation.
SITES OF SNORING
Sites of snoring may be soft palate, tonsillar pillars or hypopharynx. It may vary from patient to patient and even
in the same patient thus making surgical correction a difficult decision. Sometimes sites of snoring are multiple
even in the same patient.
SYMPTOMATOLOGY
Excessive loud snoring is socially disruptive and forms
snoring-spouse syndrome and is the cause of marital discord sometimes leading to divorce. In addition, a snorer
with obstructive sleep apnoea may manifest with:
• Excessive daytime sleepiness
• Morning headaches
• General fatigue
• Memory loss
• Irritability and depression
• Decreased libido
• Increased risk of road accidents
Table 55.1 shows an Epworth sleepiness scale.
MECHANISM OF SNORING
Muscles of pharynx are relaxed during sleep and cause
partial obstruction. Breathing against obstruction causes vibrations of soft palate, tonsillar pillars and base of
tongue producing sound. Sound as loud as 90 dB has
been recorded during snoring.
Snoring may be primary, i.e. without association with
obstructive sleep apnoea (OSA) or complicated, i.e. associated with OSA. Primary snoring is not associated with
excessive daytime sleepiness and has apnoea–hypnoea
index of less than five.
AETIOLOGY
In children most common cause is adenotonsillar hypertrophy. In adults cause of snoring could be in the nose or
TREATMENT
1. Avoidance of alcohol, sedatives and hypnotics.
2. Reduction of weight.
3. Sleeping on the side rather than on the back.
4. Removal of obstructing lesion in nose, nasopharynx,
oral cavity, hypopharynx and larynx. Radiofrequency
has been used for volumetric reduction of tissues of
turbinates, soft palate and base of tongue.
5. Performing uvulopalatoplasty (UPP) surgically with
cold knife or assisted with radiofrequency (RAUP) or
laser (LAUP).
SLEEP APNOEA
Apnoea means no breathing at all. There is no movement
of air at the level of nose and mouth. It is of three types.
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SECTION IV — Diseases of Pharynx
TABLE 55.1 EPWORTH SLEEPINESS SCALE
Situation Score (0–3)
• Sittingandreading
• WatchingTV
• Sittinginactiveinapublicplace(e.g.theatre
or in a meeting)
• Beingapassengerinacarfor1hwithout
break
• Lyingdowntorestintheafternoonwhen
circumstances permit
• Sittingandtalkingtosomeone
• Sittingquietlyafteralunchwithoutalcohol
• Sittinginacarwhilestoppedintrafcfora
few minutes
0 = never dozing off; 1 = slight chance of dozing off; 2 = moderate
chance of dozing off; 3 = high chance of dozing off.
1. Obstructive. There is collapse of the upper airway resulting in cessation of airflow. Other factors may be
obstructive conditions of nose, nasopharynx, oral cavity and oropharynx, base of tongue or larynx.
2. Central. Airways are patent but brain fails to signal the
muscles to breathe.
3. Mixed. It is combination of both types.
PATHOPHYSIOLOGY OF OSA
Apnoea during sleep causes hypoxia and retention of carbon dioxide which leads to pulmonary constriction leading to congestive heart failure, bradycardia and cardiac
hypoxia leading to left heart failure, and cardiac arrhythmias sometimes leading to sudden death. During sleep
apnoea, there are frequent arousals which cause sleep
fragmentation, daytime sleepiness and other manifestations. Table 55.2 lists the consequences of obstructive
sleep apnoea.
TABLE 55.2 CONSEQUENCES OF OBSTRUCTIVE
SLEEP APNOEA
• Congestiveheartfailure/corpulmonale
• Polycythaemiaandhypertension
• Atrialandventriculararrhythmiasandleftheartfailure
• Attacksofangina
• Snoringspousesyndrome
• Lossofmemory
• Decreasedlibido
• Trafcaccidents
PHYSIOLOGY OF SLEEP
A normal healthy adult sleeps for 7–8 h. Sleep occurs in
two phases: non-REM and REM. The two phases occur
in semiregular cycles, each cycle lasting for 90–120 min.
There are thus three or four cycles of sleep.
Non-REM Sleep
It forms 75–80% of sleep and occurs in four stages:
1. Stage I. Transition from wakefulness to sleep. It constitutes 2–5% of sleep. EEG shows decrease of alpha and
increase of theta waves. Muscle tone is less. Person can
be easily aroused from this stage.
2. Stage II. Characterized by sleep spindles or ‘K’ complexes and decrease in muscle tone. It constitutes 45–
55% of sleep.
3. Stage III. Forms 3–8% of sleep, characterized by delta
waves. It is deep sleep.
4. Stage IV. Forms 10–15% of sleep, characterized by del-
ta waves. It is deep, most restful sleep.
REM Sleep
Forms 20–25% of total sleep, characterized by rapid eye
movements, increased autonomic activity with erratic
cardiac and respiratory movements. Dreaming occurs
in this stage but muscular activity is decreased so that
dreams are not enacted.
See Table 55.3 for differences between non-REM and
REM sleep.
CLINICAL EVALUATION OF A CASE
OF SLEEP APNOEA
History
Patient’s bed partner gives more reliable information than
the patient himself because latter does not know what
happened during sleep. History should include snoring
during sleep, restless disturbed sleep, gasping, choking or
apnoeic events and sweating. In the daytime, there is history of excessive daytime sleepiness (Epworth sleepiness
scale is more often used, see Table 55.1) and fatigue, irrita-
bility, morning headaches, memory loss and impotence.
Also one should elicit history of body position during
sleep, use of alcohol, sedatives and caffeine intake, mouth
breathing and history of menopause or having hormonal
replacement therapy.
TABLE 55.3 DIFFERENCES BETWEEN NON-REM AND REM SLEEP
Duration 75–80% of sleep 20–25% of sleep
Eye movements No eye rolling Rapid conjugate eye movements
Autonomic activity Less autonomic activity gives slow heart rate, low BP,
Brain activity Minimal Brain is active (REM sleep is also called activated brain
Muscular activity Functional but less Decreased. Since muscles are relaxed, snoring and OSA
EEG Passes from alpha to delta waves from stage I to IV Mixed frequency, low-voltage waves with occasional
Dreaming No Yes
Non-REM REM
Increased autonomic activity with fluctuations in BP,
slow and steady respiration
heart rate and respiration
in a paralyzed person)
occurs in this stage
bursts of saw-tooth waves
Chapter 55 — Snoring and Sleep Apnoea
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315
Physical Examination
Risk factors include male gender, obesity and age above
40 years.
1. Body mass index. It is calculated by dividing body
weight in kilograms by height in metres squared. Normal BMI, 18.5–24.9; overweight, 25–29%; and obesity,
30–34.9. Obese patients need to reduce weight.
2. Collar size. Neck circumference at the level of cricothyroid membrane is measured. Collar size should not
exceed 42 cm in males and 37.5 cm in females.
3. Complete head and neck examination. Look for tonsillar hypertrophy, retrognathia, macroglossia, elongated
soft palate and uvula, base of tongue tumours, septal deviation, nasal polyps, turbinate hypertrophy and nasal
valve collapse. Also examine nasopharynx and larynx.
4. Muller’s manoeuvre. A flexible endoscope is passed
through the nose and the patient asked to inspire vigorously with nose and mouth completely closed. Look
for collapse of the soft tissues at the level of base of
tongue and just above the soft palate. Level of pharyngeal obstruction can be found.
Systemic examination is done to look for hyperten-
sion, congestive heart failure, pedal oedema, truncal obesity and any sign of hypothyroidism.
Cephalometric radiographs are taken for craniofacial
anomalies and tongue base obstruction.
Polysomnography. It is the “gold standard” for di-
agnosis of sleep apnoea and records various parameters
which include:
• EEG (electroencephalography)—to look for non-REM
or REM sleep and stages of non-REM sleep.
• ECG (electrocardiography)—for heart rate and rhythm.
• EOM (electroculogram)—for rolling eye movements.
• EMG (electromyography)—recorded from submental
and tibialis anterior muscle.
• Pulse oximetry—to assess oxygen saturation of blood
to know lowest SaO2 during sleep.
• Nasal and oral airflow—for episodes of apnoea and hy-
popnoea.
• Sleep position—helps to know whether apnoea/hypo-
pnoea episodes occur in supine or lateral recumbent
position.
• Blood pressure.
• Oesophageal pressure. Not done in all laboratories.
Negative oesophageal pressure helps to know degree of
breathing efforts made by the patient.
Split-night polysomnography. In this study, the first
part of night is used in usual polysomnography while the
second part of night is used in titration of pressures for
continuous positive airway pressure (CPAP). It is not recommended because episodes of sleep apnoea occur more
often in the second half of night and are thus missed.
Titration of pressures for CPAP should ideally be done on
a second night.
Polysomnography can differentiate between primary
snoring, pure OSA and central sleep apnoea.
Treatment (Nonsurgical)
1. Change in lifestyle. Those with mild disease and minimal symptoms can be treated with weight loss and
dietary changes but those with cor pulmonale as a result of severe OSA may require surgery.
(a) Use of alcohol in the evening aggravates OSA. Sed-
atives/hypnotics taken at night also have the same
effect.
(b) Smoking should be avoided.
(c) Reduction of weight is helpful.
2. Positional therapy. Patient should sleep on the side,
as supine position may cause obstructive apnoea. A
rubber ball can be fixed to the back of shirt to prevent
adopting supine position.
3. Intraoral devices. They alter the position of mandible or tongue to open the retropalatal airway and
relieve snoring and sleep apnoea. Mandible advancement device (MAD) keeps the mandible forward while
tongue-retaining device (TRD) keeps tongue in anterior position during sleep. They help improve or abolish
snoring. MAD is also useful in retrognathic patients.
4. Continuous positive airway pressure (CPAP). It pro-
vides pneumatic splint to airway and increases its calibre. Optimum airway pressure for device to open the
airway is determined during sleep study and is usually
kept at 5–20 cm H2O. About 40% of patients find the
use of CPAP device cumbersome and difficult to carry
with them when travelling and thus stop using it.
When CPAP is not tolerated, a BiPAP (bilevel positive
airway pressure) device is used. It delivers positive pressure at two fixed levels—a higher inspiratory and a lower
expiratory pressure. Now an autotitrating PAP (APAP) is
also available which continuously adjusts the pressure.
Their disadvantages are same as those of CPAP.
surgery. It is indicated for failed or noncompliant medical therapy.
Permanent tracheostomy is the “gold standard” of
treatment but it is not accepted socially and has complications of its own. It is usually not a preferred option by
patients.
1. Nasal surgery. Nasal obstruction may be the pri-
mary or the aggravating factor for OSA. Septoplasty to
correct deviated nasal septum, removal of nasal polyps
and reduction of turbinate size help to relieve nasal obstruction. Sometimes nasal surgery is also indicated for
efficient use of CPAP.
2. Oropharyngeal surgery. Uvulopalatoplasty (UPP) is
the most common procedure performed for snoring and
OSA. It is 80% effective in snoring but OSA is relieved
only in 50%. Some patients of OSA are known to relapse
in long-term studies because of another site becoming active in the cause of obstruction (e.g. base of tongue). UPP
can be laser or radiofrequency assisted.
3. Tonsillectomy and/or adenoidectomy. Surgical
treatment is tailored to the level of obstruction:
(a) Nose and nasopharynx (level I).
(b) Soft palate and tonsils (level II).
(c) Tongue base and pharynx (level III).
Sometimes more than one level is involved.
4. Advancement genioplasty with hyoid suspen-
sion. It is done in patients where base of tongue also
contributes to OSA. Patients with retrognathia and
micrognathia are also the candidates.
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