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Chapter 30
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Allergic Rhinitis
It is an IgE-mediated immunologic response of nasal mucosa to airborne allergens and is characterized by watery
nasal discharge, nasal obstruction, sneezing and itching
in the nose. This may also be associated with symptoms
of itching in the eyes, palate and pharynx. Two clinical
types have been recognized:
1. Seasonal. Symptoms appear in or around a particular
season when the pollens of a particular plant, to which
the patient is sensitive, are present in the air.
2. Perennial. Symptoms are present throughout the year.
AETIOLOGY
inhalant allergens. They may be seasonal or perennial. Seasonal allergens include pollens from trees, grasses
and weeds. They vary geographically. The knowledge
of pollen appearing in a particular area and the season in which they occur is important. Their knowledge
also helps in skin tests. Perennial allergens are present
throughout the year regardless of the season. They include molds, dust mites, cockroaches and dander from
animals. Dust includes dust mite, insect parts, fibres and
animal danders. Dust mites live on skin scales and other
debris and are found in the beddings, mattresses, pillows,
carpets and upholstery.
genetic predisposition. plays an important part. Chanc-
es of children developing allergy are 20 and 47%, respectively, if one or both parents suffer from allergic diathesis.
PATHOGENESIS
Inhaled allergens produce specific IgE antibody in the genetically predisposed individuals. This antibody becomes
fixed to the blood basophils or tissue mast cells by its Fc
end (Figure 30.1 ). On subsequent exposure, antigen
combines with IgE antibody at its Fab end. This reaction
produces degranulation of the mast cells with release of
several chemical mediators, some of which already exist
in the preformed state while others are synthesized afresh.
These mediators (Figure 30.2) are responsible for symptomatology of allergic disease. Depending on the tissues
involved, there may be vasodilation, mucosal oedema, infiltration with eosinophils, excessive secretion from nasal
glands or smooth muscle contraction. A “priming affect”
has also been described, i.e. mucosa earlier sensitized to
an allergen will react to smaller doses of subsequent specific allergen. It also gets “primed” to other nonspecific
antigens to which patient was not exposed (Figure 30.3).
Nonspecific nasal hyper-reactivity is seen in patients of
allergic rhinitis. There is increased nasal response to normal stimuli resulting in sneezing, rhinorrhoea and nasal
congestion. Clinically, allergic response occurs in two
phases:
1. Acute or early phase. It occurs immediately within
5–30 min, after exposure to the specific allergen and
consists of sneezing, rhinorrhoea nasal blockage and/
or bronchospasm. It is due to release of vasoactive
amines like histamine.
2. Late or delayed phase. It occurs 2–8 h after exposure
to allergen without additional exposure. It is due to
infiltration of inflammatory cells—eosinophils, neutrophils, basophil, monocytes and CD4 + T cells at the
site of antigen deposition causing swelling, congestion
and thick secretion. In the event of repeated or continuous exposure to allergen, acute phase symptomatology overlaps the late phase.
CLINICAL FEATURES
There is no age or sex predilection. It may start in infants
as young as 6 months or older people. Usually the onset
is at 12–16 years of age.
The cardinal symptoms of seasonal nasal allergy include
paroxysmal sneezing, 10–20 sneezes at a time, nasal obstruction, watery nasal discharge and itching in the nose.
Itching may also involve eyes, palate or pharynx. Some
may get bronchospasm. The duration and severity of
symptoms may vary with the season.
Symptoms of perennial allergy are not so severe as that
of the seasonal type. They include frequent colds, persistently stuffy nose, loss of sense of smell due to mucosal
oedema, postnasal drip, chronic cough and hearing impairment due to eustachian tube blockage or fluid in the
middle ear.
Signs of allergy may be seen in the nose, eyes, ears,
pharynx or larynx.
• Nasal signs include transverse nasal crease—a black
line across the middle of dorsum of nose due to constant upward rubbing of nose simulating a salute (al-
lergic salute), pale and oedematous nasal mucosa which
may appear bluish. Turbinates are swollen. Thin, watery or mucoid discharge is usually present.
• Ocular signs include oedema of lids, congestion and
cobble-stone appearance of the conjunctiva, and dark
circles under the eyes (allergic shiners).
• Otologic signs include retracted tympanic membrane
or serous otitis media as a result of eustachian tube
blockage.
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Figure 30.1. (A) Structure of IgE antibody. Fc end is attached to the mast cell or blood basophil while Fab end is the antigen binding site. (B) Release
of mediator substances from mast cell producing symptoms of nasal allergy. One antigen bridges two adjacent molecules of IgE antibody.
SECTION II — Diseases of Nose and Paranasal Sinuses
Scan to play Allergic Rhinitis.
• Pharyngeal signs include granular pharyngitis due to
hyperplasia of submucosal lymphoid tissue. A child
with perennial allergic rhinitis may show all the features of prolonged mouth breathing as seen in adenoid
hyperplasia.
• Laryngeal signs include hoarseness and oedema of
the vocal cords.
DIAGNOSIS
new allergic rhinitis and its impact on asthma
(aria) classiFication (table 30.1). It is based on du-
ration and symptoms of disease. Duration of symptoms is
subdivided into intermittent or persistent and severity of
disease into mild, moderate or severe.
This new system of classification helps in treatment
guidelines.
A detailed history and physical examination is helpful,
and also gives clues to the possible allergen. Other causes
of nasal stuffiness should be excluded.
INVESTIGATIONS
1. Total and differential count. Peripheral eosinophilia
may be seen but this is an inconsistent finding.
2. Nasal smear. It shows large number of eosinophils in
allergic rhinitis. Nasal smear should be taken at the
time of clinically active disease or after nasal chal-
lenge test. Nasal eosinophilia is also seen in certain
Figure 30.2. Release of mediators from mast cell when challenged
by allergic or nonspecific stimuli.
Figure 30.3. Both allergic and nonspecific stimuli act on mast cells or
blood basophils releasing several mediator substances responsible for
symptomatology of allergy.
Chapter 30 — Allergic Rhinitis
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189
TABLE 30.1 CLASSIFICATION OF ALLERGIC
RHINITIS (ARIA)
• Duration of disease
• Intermittent: Symptoms are present
– Less than 4 days a week or
– For less than 4 weeks
• Persistent: Symptoms are present
– More than 4 days a week or
– For more than 4 weeks
• Severity of disease
• Mild: None of the following symptoms are present
– Sleep disturbance
– Impairment of daily activities, leisure and sport
– Impairment of school or work
– Troublesome symptoms
• Moderate to severe: One or more of the above symptoms are
present
nonallergic rhinitis, e.g. NARES (nonallergic rhinitis
with eosinophilia syndrome).
3. Skin tests. These tests help to identify specific allergen.
They are prick, scratch and intradermal tests.
a. Skin prick test. This is an excellent method to dem-
onstrate the allergen. A drop of concentrated allergen solution is placed on the volar surface of the
forearm or back and a sharp needle pricked into the
dermis through the drop. It introduces the allergen
into the dermis. A positive reaction is manifested
by the formation of a central wheal and a surrounding zone of erythema (flare) within 10–15 min.
Simultaneously a control test is performed with his-
tamine and the diluent used in allergen solution.
b. Specific IgE measurements. It is an in vitro test to find
the specific allergen. There is a good correlation
between the skin tests and specific IgE measurements. However both false positive and false negative results can occur. It is therefore recommended
to correlate the two tests with clinical symptoms.
4. Radioallergosorbent test (RAST). It is an in vitro test
and measures specific IgE antibody concentration in
the patient’s serum.
5. Nasal provocation test. A crude method is to challenge the nasal mucosa with a small amount of allergen placed at the end of a toothpick and asking the
patient to sniff into each nostril and to observe if allergic symptoms are reproduced. More sophisticated
techniques are available now.
COMPLICATIONS
Nasal allergy may cause:
1. Recurrent sinusitis because of obstruction to the sinus
ostia.
2. Formation of nasal polypi in about 2%.
3. Serous otitis media.
4. Orthodontic problems and other ill-effects of prolonged mouth breathing especially in children.
5. Bronchial asthma. Patients of nasal allergy have
four times more risk of developing bronchial asthma.
Twenty to thirty per cent of patients with rhinitis have
asthma.
TREATMENT
Treatment can be divided into:
1. Avoidance of allergen.
2. Treatment with drugs.
3. Immunotherapy.
1. aVoidance oF allergen. This is most successful if
the antigen involved is single. Removal of a pet from
the house, encasing the pillow or mattress with plastic
sheet, change of place of work or sometimes change of
job may be required. A particular food article to which
the patient is found allergic can be eliminated from the
diet.
2. treatment with drugs
1. Antihistaminics. They control rhinorrhoea, sneezing
and nasal itch. All antihistaminics have the side effect
of drowsiness; some more than the other. The dose
and type of the antihistaminic has to be individualized. If one antihistaminic is not effective, another
may be tried from a different class.
2. Sympathomimetic drugs (oral or topical). Alpha-adren-
ergic drugs constrict blood vessels and reduce nasal
congestion and oedema. They also cause central
nervous system stimulation and are often given in
combination with antihistaminics to counteract
drowsiness. Pseudoephedrine and phenylephrine are
often combined with antihistaminics for oral admin-
3. Corticosteroids. Oral corticosteroids are very effective
in controlling the symptoms of allergic rhinitis but
their use should be limited to acute episodes which
have not been controlled by other measures. They
have several systemic side effects.
4. Sodium cromoglycate. It stabilizes the mast cells and
prevents them from degranulation despite the formation of IgE-antigen complex. It is used as 2% solution
for nasal drops or spray or as an aerosol powder. It is
useful both in seasonal and perennial allergic rhinitis.
5. Anticholinergics. They block rhinorrhoea both of the
allergic and nonallergic rhinitis. Ipratropium bromide
has been used as nasal spray to control rhinorrhoea.
There are no systemic side effects.
6. Leukotriene receptor antagonists. They include montelukast, pranlukast and zafirlukast. They block cysteinyl
leukotriene type receptors. They are well-tolerated
and have few side effects.
7. Anti-IgE. It reduces the IgE level and has an antiinflammatory effect. Omalizumab is such a drug.
It is indicated in children above 12 years who have
moderate to severe asthma. It is not yet approved for
allergic rhinitis.
3. immunotherapy. Immunotherapy or hyposensitiza-
tion is used when drug treatment fails to control symptoms or produces intolerable side effects. Allergen is
given in gradually increasing doses till the maintenance
dose is reached. Immunotherapy suppresses the formation of IgE. It also raises the titre of specific IgG antibody.
Immunotherapy has to be given for a year or so before
significant improvement of symptoms can be noticed.
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SECTION II — Diseases of Nose and Paranasal Sinuses
It is discontinued if uninterrupted treatment for 3 years
shows no clinical improvement.
Subcutaneous immunotherapy is often used but now
sublingual and nasal routes are also being employed. The
latter can be used with doses 20–100 times greater than
used by the subcutaneous route.
A step-care approach is recommended by ARIA for
allergic rhinitis treatment.
• Oral antihistamines or intranasal cromolyn sodium is
recommended for mild intermittent disease.
• For allergic symptoms of moderate severity or for per-
sistent disease intranasal corticosteroids can be used as
monotherapy.
• For severe symptoms, combination therapy with oral
nonsedating antihistamines and intranasal steroids is
used.
• For severe and persistent symptoms in spite of the
above treatment a short course of oral steroids and immunotherapy is recommended.
• If nasal obstruction persists a short course of intranasal
decongestant can be used. Oral decongestant can be
combined with antihistamines.
• Avoid allergen and irritants in all forms of disease.
Nonallergic rhinitis can coexist with allergic rhinitis.
Nonspecific stimuli produce allergic rhinitis-like symptoms due to hyper-reactivity of nasal mucosa.
Chapter 31
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Vasomotor and Other Forms
of Nonallergic Rhinitis
VASOMOTOR RHINITIS (VMR)
It is nonallergic rhinitis but clinically simulating nasal allergy with symptoms of nasal obstruction, rhinorrhoea
and sneezing. One or the other of these symptoms may
predominate. The condition usually persists throughout
the year and all the tests of nasal allergy are negative.
PATHOGENESIS
Nasal mucosa has rich blood supply. Its vasculature is
similar to the erectile tissue in having venous sinusoids
or “lakes” which are surrounded by fibres of smooth
muscle which act as sphincters and control the filling or
emptying of these sinusoids. Sympathetic stimulation
causes vasoconstriction and shrinkage of mucosa, while
parasympathetic stimulation causes vasodilation and engorgement. Overactivity of parasympathetic system also
causes excessive secretion from the nasal glands.
Autonomic nervous system is under the control of hypothalamus and therefore emotions play a great role in
vasomotor rhinitis. Autonomic system is unstable in cases
of vasomotor rhinitis. Nasal mucosa is also hyper-reactive
and responds to several nonspecific stimuli, e.g. change
in temperature, humidity, blasts of air, small amounts of
dust or smoke.
SYMPTOMS
1. Paroxysmal sneezing. Bouts of sneezing start just af-
ter getting out of the bed in the morning.
2. Excessive rhinorrhoea. This accompanies sneezing
or this may be the only predominant symptom. It is
profuse and watery and may even wet several hand-
kerchiefs. The nose may drip when the patient leans
forward and this may need to be differentiated from
CSF rhinorrhoea (see p. 183).
3. Nasal obstruction. This alternates from side to side.
Usually more marked at night. It is the dependent side
of nose which is often blocked when lying on one side.
4. Postnasal drip.
SIGNS
Nasal mucosa over the turbinates is generally congested
and hypertrophic. In some, it may be normal.
COMPLICATIONS
Long-standing cases or VMR develop nasal polypi, hypertrophic rhinitis and sinusitis.
TREATMENT
Medical
1. Avoidance of physical factors which provoke symptoms, e.g. sudden change in temperature, humidity,
blasts of air or dust.
2. Antihistaminics and oral nasal decongestants are helpful in relieving nasal obstruction, sneezing and rhinorrhoea.
3. Topical steroids (e.g. beclomethasone dipropionate,
budesonide or fluticasone), used as spray or aerosol,
are useful to control symptoms.
4. Systemic steroids can be given for a short time in very
severe cases.
5. Psychological factors should be removed. Tranquillizers may be needed in some patients.
Surgical
1. Nasal obstruction can be relieved by measures which
reduce the size of nasal turbinates (see hypertrophic
rhinitis). Other associated causes of nasal obstruction,
e.g. polyp, deviated nasal septum, should also be corrected.
2. Excessive rhinorrhoea, not corrected by medical therapy and bothersome to the patient, can be relieved by
sectioning the parasympathetic secretomotor fibres to
nose (vidian neurectomy).
OTHER FORMS OF NONALLERGIC RHINITIS
Nasal mucosa responds to several different stimuli producing symptoms of rhinitis. Some of these conditions
have acquired specific eponyms. Some authorities categorize them under the catch-all term of vasomotor
rhinitis.
1. Drug-inDuceD rhinitiS. Several antihypertensive
drugs such as reserpine, guanethidine, methyl dopa and
propranolol are sympathetic blocking agents and cause
nasal stuffiness. Some anticholinesterase drugs, e.g. neostigmine, used in the treatment of myasthenia gravis,
have acetylcholine like action and cause nasal obstruction. Contraceptive pills also cause nasal obstruction
because of oestrogens.
2. rhinitiS MeDicaMentoSa. Topical decongestant na-
sal drops are notorious to cause rebound phenomenon.
Their excessive use causes rhinitis. It is treated by withdrawal of nasal drops, short course of systemic steroid
therapy and in some cases, surgical reduction of turbinates, if they have become hypertrophied.
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SECTION II — Diseases of Nose and Paranasal Sinuses
3. rhinitiS oF Pregnancy. Pregnant women may develop persistent rhinitis due to hormonal changes. Nasal
mucosa becomes oedematous and blocks the airway.
Some may develop secondary infection and even sinusitis. In such cases, care should be taken while prescribing
drugs. Generally, local measures such as limited use of
nasal drops, topical steroids and limited surgery (cryosurgery) to turbinates are sufficient to relieve the symptoms.
Safety of the developing fetus is not established for newer
antihistaminics and they should be avoided.
4. honeyMoon rhinitiS. This usually follows sexual
excitement leading to nasal stuffiness.
5. eMotionaL rhinitiS. Nose may react to several
emotional stimuli. Psychological states like anxiety, tension, hostility, humiliation, resentment and grief are all
known to cause rhinitis. Treatment is proper counselling
for psychological adjustment. Imipramine, which has
both antidepressant and anticholinergic effects, has been
found useful.
6. rhinitiS Due to hyPothyroiDiSM. Hypothyroidism leads to hypoactivity of the sympathetic system with
predominance of parasympathetic activity causing nasal
stuffiness and “colds.” Replacement of thyroid hormone
relieves the condition.
7. guStatory rhinitiS. Spicy and pungent food may
in some people produce rhinorrhoea, nasal stuffiness,
lacrimation, sweating and even flushing of face. This
is a cholinergic response to stimulation of sensory receptors on the palate. Spicy food, particularly the red
pepper, contains capsaicin which is known to stimulate sensory nerves. It can be relieved by ipratropium
bromide nasal spray (an anticholinergic), a few minutes
before meals.
8. nonairFLow rhinitiS. It is seen in patients of laryngectomy and tracheostomy. Nose is not used for airflow and the turbinates become swollen due to loss of
vasomotor control. Similar changes are also seen in nasopharyngeal obstruction due to choanal atresia or adenoidal hyperplasia, the latter having the additional factor
of infection due to stagnation of discharge in the nasal
cavity which should otherwise drain freely into the nasopharynx.
Chapter 32
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Nasal Polypi
Nasal polypi are non-neoplastic masses of oedematous
nasal or sinus mucosa. They are divided into two main
varieties:
1. Antrochoanal polyp.
2. Bilateral ethmoidal polypi.
ANTROCHOANAL POLYP
(SYN. KILLIAN’S POLYP)
This polyp arises from the mucosa of maxillary antrum
near its accessory ostium, comes out of it and grows in
the choana and nasal cavity. Thus it has three parts.
1. Antral, which is a thin stalk.
2. Choanal, which is round and globular.
3. Nasal, which is flat from side to side.
AETIOLOGY
Exact cause is unknown. Nasal allergy coupled with sinus
infection is incriminated. Antrochoanal polypi are seen
in children and young adults. Usually they are single and
unilateral.
SYMPTOMS
Unilateral nasal obstruction is the presenting symptom.
Obstruction may become bilateral when polyp grows into
the nasopharynx and starts obstructing the opposite choana (Tables 32.1 and 32.2). Voice may become thick and
dull due to hyponasality. Nasal discharge, mostly mucoid,
may be seen on one or both sides.
SIGNS
As the antrochoanal polyp grows posteriorly, it may be
missed on anterior rhinoscopy. When large, a smooth
greyish mass covered with nasal discharge may be seen.
It is soft and can be moved up and down with a probe.
A large polyp may protrude from the nostril and show a
pink congested look on its exposed part (Figure 32.1).
Posterior rhinoscopy may reveal a globular mass filling
the choana or the nasopharynx. A large polyp may hang
down behind the soft palate and present in the oropharynx (Figure 32.2A–B ).
Examination of the nose with an endoscope may reveal a choanal or antrochoanal polyp hidden posteriorly
in the nasal cavity (Figure 32.3).
See Table 32.3 for differences between antrochoanal
and ethmoidal polypi.
DIFFERENTIAL DIAGNOSIS
1. A blob of mucus often looks like a polypus but it would
disappear on blowing the nose.
2. Hypertrophied middle turbinate is differentiated by its
pink appearance and hard feel of bone on probe testing.
3. Angiofibroma has history of profuse recurrent epistaxis. It is firm in consistency and easily bleeds on probing.
4. Other neoplasms may be differentiated by their fleshy
pink appearance, friable nature and their tendency to
bleed.
X-rays of paranasal sinuses may show opacity of the involved antrum. X-ray (lateral view), soft tissue nasopharynx, reveals a globular swelling in the postnasal space. It
is differentiated from angiofibroma by the presence of a
column of air behind the polyp. Non-contrast CT scans
and paranasal sinuses show the extent of the polyp.
TREATMENT
The treatment of choice for antrochonal polyp is endoscopic sinus surgery. It has superseded earlier operations
of simple polypectomy and Caldwell–Luc operation performed for recurring cases.
An antrochoanal polyp is easily removed by avulsion
either through the nasal or oral route. Recurrence is uncommon after complete removal. In cases which do recur,
Caldwell–Luc operation may be required to remove the
polyp completely from the site of its origin and to deal
with coexistent maxillary sinusitis. These days, endoscopic sinus surgery has superceded other modes of polyp
removal. Caldwell–Luc operation is avoided.
BILATERAL ETHMOIDAL POLYPI
AETIOLOGY
Aetiology of nasal polypi is very complex and not wellunderstood. They may arise in inflammatory conditions
of nasal mucosa (rhinosinusitis), disorders of ciliary motility or abnormal composition of nasal mucus (cystic fibrosis). Various diseases associated with the formation of
nasal polypi are:
1. Chronic rhinosinusitis. Polypi are seen in chronic rhinosinusitis of both allergic and nonallergic origin. Nonallergic rhinitis with eosinophilia syndrome (NARES) is
a form of chronic rhinitis associated with polypi.
2. Asthma. Seven per cent of the patients with asthma of
atopic or nonatopic origin show nasal polypi.
3. Aspirin intolerance. Thirty-six per cent of the patients
with aspirin intolerance may show polypi. Samter’s
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SECTION II — Diseases of Nose and Paranasal Sinuses
TABLE 32.1 COMMON CAUSES OF UNILATERAL
NASAL OBSTRUCTION
• Vestibule
• Furuncle
• Vestibulitis
• Stenosis of nares
• Atresia
• Nasoalveolar cyst
• Papilloma
• Squamous cell carcinoma
• Nasal cavity
• Foreign body
• Deviated nasal septum (DNS)
• Hypertrophic turbinates
• Concha bullosa
• Antrochoanal polyp
• Synechia
• Rhinolith
• Bleeding polypus of septum
• Benign and malignant tumours of nose and paranasal sinuses
• Sinusitis, unilateral
• Nasopharynx
• Unilateral choanal atresia
triad consists of nasal polypi, asthma and aspirin
intolerance.
4. Cystic fibrosis. Twenty per cent of patients with cystic
fibrosis form polypi. It is due to abnormal mucus.
5. Allergic fungal sinusitis. Almost all cases of allergic
fungal sinusitis form nasal polypi.
6. Kartagener syndrome. This consists of bronchiectasis
sinusitis, situs inversus and ciliary dyskinesis.
7. Young syndrome. It consists of sinopulmonary dis-
ease and azoospermia.
8. Churg–Strauss syndrome. Consists of asthma, fever,
eosinophilia, vasculitis and granuloma.
Figure 32.1. An antrochoanal polyp projecting through the left
nostril in a 14-year-old patient.
9. Nasal mastocytosis. It is a form of chronic rhinitis in
which nasal mucosa is infiltrated with mast cells but
few eosinophils. Skin tests for allergy and IgE levels are
normal.
PATHOGENESIS
Nasal mucosa, particularly in the region of middle meatus and turbinate, becomes oedematous due to collection
of extracellular fluid causing polypoidal change. Polypi
which are sessile in the beginning become pedunculated
due to gravity and excessive sneezing.
PATHOLOGY
In early stages, surface of nasal polypi is covered by ciliated columnar epithelium like that of normal nasal mucosa
but later it undergoes a metaplastic change to transitional
and squamous type on exposure to atmospheric irritation. Submucosa shows large intercellular spaces filled
with serous fluid. There is also infiltration with eosinophils and round cells.
TABLE 32.2 COMMON CAUSES OF BILATERAL
NASAL OBSTRUCTION
• Vestibule
• Bilateral vestibulitis
• Collapsing nasal alae
• Stenosis of nares
• Congenital atresia of nares
• Nasal cavity
• Acute rhinitis (viral and bacterial)
• Chronic rhinitis and sinusitis
• Rhinitis medicamentosa
• Allergic rhinitis
• Hypertrophic turbinates
• DNS
• Nasal polypi
• Atrophic rhinitis
• Rhinitis sicca
• Septal haematoma
• Septal abscess
• Bilateral choanal atresia
• Nasopharynx
• Adenoid hyperplasia
• Large choanal polyp
• Thornwaldt’s cyst
• Adhesions between soft palate and posterior pharyngeal wall
• Large benign and malignant tumours
SITE OF ORIGIN
Multiple nasal polypi always arise from the lateral wall of
nose, usually from the middle meatus. Common sites are
uncinate process, bulla ethmoidalis, ostia of sinuses, medial surface and edge of middle turbinate. Allergic nasal
polypi almost never arise from the septum or the floor of
nose.
SYMPTOMS
1. Multiple polypi can occur at any age but are mostly
seen in adults.
2. Nasal stuffiness leading to total nasal obstruction may
be the presenting symptom.
3. Partial or total loss of sense of smell.
4. Headache due to associated sinusitis.
5. Sneezing and watery nasal discharge due to associated
allergy.
6. Mass protruding from the nostril.
SIGNS
On anterior rhinoscopy, or endoscopic examination,
polypi appear as smooth, glistening, grape-like masses
Chapter 32 — Nasal Polypi
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Figure 32.2. (A) An antrochoanal polyp seen hanging in the oropharynx from behind the soft palate on the right side of uvula. (B) Polyp after
removal.
Scan to play Posterior Rhinoscopy.
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often pale in colour (Figure 32.4). They may be sessile or
pedunculated, insensitive to probing and do not bleed
on touch. Often they are multiple and bilateral. Longstanding cases present with broadening of nose and increased intercanthal distance. A polyp may protrude from
the nostril and appear pink and vascular simulating neoplasm (Figure 32.5 ). Nasal cavity may show purulent
discharge due to associated sinusitis.
Probing of a solitary ethmoidal polyp may be necessary to differentiate it from hypertrophy of the turbinate
or cystic middle turbinate.
DIAGNOSIS
Diagnosis can be easily made on clinical examination.
Computed tomography (CT) scan of paranasal sinuses is
essential to exclude the bony erosion and expansion suggestive of neoplasia. Simple nasal polypi may sometimes
be associated with malignancy underneath, especially in
people above 40 years and this must be excluded by histo-
Figure 32.3. An endoscopic view of a choanal polyp on the right
side.
TABLE 32.3 DIFFERENCES BETWEEN ANTROCHOANAL AND ETHMOIDAL POLYPI
Antrochoanal polypi Ethmoidal polypi
Age Common in children, can occur in adults Common in adults
Aetiology Infection Allergy or multifactorial
Number Solitary Multiple
Laterality Unilateral Bilateral
Origin Maxillary sinus near the ostium Ethmoidal sinuses, uncinate process, middle
Growth Grows backwards to the choana; may hang down behind the
soft palate
Size and shape Trilobed with antral, nasal and choanal parts. Choanal part
may protrude through the choana and fill the nasopharynx
obstructing both sides
Recurrence Uncommon, if removed completely Common
Treatment Endoscopic sinus surgery Endoscopic sinus surgery
logical examination of the suspected tissue. CT scan also
helps to plan surgery.
turbinate and middle meatus
Mostly grow anteriorly and may present at
the nares
Usually small and grape-like masses
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