Allergic Rhinitis

1. ALLERGIC RHINITIS
Dr Harjitpal Singh
Assistant Professor(ENT),
Dr RKGMC, Hamirpur

2. WHAT IS ALLERGY
• It is an altered state of reactivity to an organic
substance, i.e. allergen.
• It is an immunoglobulin E (IgE)-mediated
immunological response of nasal mucosa
• Atopy means a tendency to develop allergic
diseases.

3. ALLERGIC RHINITIS
DEFINITION: It is a symptomatic disorder of nose
induced by an IgE mediated inflammation after
allergen exposure.
Allergic Rhinitis is characterized by
• Watery Nasal discharge,
• Nasal obstruction,
• Excessive sneezing and
• Itching in the nose.

4. ALLERGIC RHINITIS
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.

5. AETIOLOGY
• Inhalent Allergens: They may be seasonal or perennial
Seasonal allergens include pollens from trees,
grasses and weeds. They vary geographically.
Perennial allergens are present throughout the year
regardless of the season. They include moulds,
dust mites, cockroaches and animal dander.
• Molds: The common fungal spores in India are:
Cladosporium, Fusarium, Alternaria,
Curvularia, Aspergillus, Mucor, Phoma,
Penicillium and Trichoderma.
• Insects: Indoor allergens from cockroach antigens play an
important role in aggravating asthma in
sensitive subjects.

6. AETIOLOGY
• Indoor allergies: to bedbugs, house flies,
mosquitoes and fleas have also been reported.
• Animals: Among the animal allergens (dander,
saliva, hair and feathers), most common are
cats and dogs. Other mammals causing
sensitization among humans are horses, rabbits,
guinea pigs, monkeys and mice.
• House dust: Dust of household origin is a complex
mixture of animals, fungi, algae, insect debris,
human epithelial scales, plants and food
remnants.

7. AETIOLOGY
• Dust mite: It has been proved that mites in
mattresses can sensitize people. In India,
Dermatophagoides farinae is the more
dominant species.
• Ingestants: Foods are especially important in
children. There may be one obvious substance,
such as eggs, strawberries, nuts or fish; but in
nasal allergy.
• Drugs: Aspirin and iodides, hypotensive and other
cholinergic drugs, and insulin injections are
known to cause allergy reactions.

8. PREDISPOSING FACTORS
• Hereditary: Genes on chromosomes 5, 6, 11, 12 and
14 seem to control inflammatory process in
atopy. Genetic predisposition plays an important
part.
• Endocrine: Pubertal, marital, natal and menopausal
conditions have the potential to influence the
nose significantly.
• Psychological: It is one of the main etiological
factors in cases of vasomotor rhinitis.
• Physical: Changes in the humidity, temperature and
pollution of air can contribute to the
development of allergic rhinitis.

9. PREDISPOSING FACTORS
• Infection: Viral and bacterial infection may
increase the permeability of the tissue to
allergens.
• Irritants: Fumes (e.g. diesel oil), pepper, tobacco
smoke and pollution are also predisposing
factors.
• Contacts: Contacts to skin or nasal mucosa are
not common causes of nasal allergy, but
coexistent dermatitis should be excluded.

10. PATHOGENESIS
• Inhaled allergens produce specific IgE antibody in the
genetically predisposed individuals.
• This antibody becomes fixed to the blood basophils or
tissue mast cells .
• This reaction produces degranulation of the mast cells
with release of several chemical mediators.
• These mediators are responsible for symptomatology of
allergic disease.

11. PATHOGENESIS
• Depending on the tissues involved, there may be:
Vasodilation,
Mucosal oedema,
Infiltration with eosinophils,
Excessive secretion from nasal glands or
Smooth muscle contraction.
• A mucosa earlier sensitized to an allergen will react to
smaller doses of it subsequently, this is called “priming
affect”.
• It also gets “primed” to other nonspecific antigens to
which patient was not exposed.

12. PATHOGENESIS
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.
• It consists of sneezing, rhinorrhoea nasal
blockage or bronchospasm.
• It is due to release of vasoactive amines like
histamine.

13. PATHOGENESIS
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.

14. MEDIATORS RELEASED BY SENSITIZED MAST CELLS
Name of mediator Effects
Preformed
Histamine Vasodilatation and bronchospasm
Neutrophil chemotactic factor Attracts neutrophils
Heparin Enhances phagocytosis
Eosinophilic chemotactic factor for anaphylaxis Attracts eosinophils
Newly formed
Prostaglandins Vasoactive and bronchospastic
Leukotriene Vasoactive and bronchospastic
Platelets aggregating factor Platelets release histamine & serotonin
Thromboxane A Spasmogenic
Tumor necrosis factor Attracts neutrophils and eosinophils

15. CLINICAL FEATURES
• No age or sex predilection. Usually the onset is at 12–16
years of age.
• Cardinal symptoms of seasonal nasal allergy include
Paroxysmal sneezing, 10–20 sneezes/episode,
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.

16. CLINICAL FEATURES
• Symptoms of perennial allergy are not so severe.
They include: frequent colds,
persistently stuffy nose,
loss of sense of smell,
postnasal drip,
chronic cough and
hearing impairment.

17. CLINICAL FEATURES
Signs of allergy may be seen in the nose, eyes, ears,
pharynx or larynx.
• Nasal signs include:
Transverse nasal crease (allergic salute),
Pale and oedematous nasal mucosa.
Turbinates are swollen.
Thin, watery or mucoid discharge.
• Ocular signs include:
Oedema of lids,
Congestion and cobblestone appearance of the
conjunctiva, and
Dark circles under the eyes (allergic shiners).

18. CLINICAL FEATURES
Congestion and Edema of Nasal Mucous Membrane

19. CLINICAL FEATURES
Allergic Conjunctivitis

20. CLINICAL FEATURES
• Otologic signs include:
Retracted tympanic membrane or
S.O.M as a result of eustachian tube blockage.
• Pharyngeal signs include:
Granular pharyngitis due to hyperplasia of
submucosal lymphoid tissue.
• Laryngeal signs include:
Hoarseness and
Oedema of the vocal cords.
A child with perennial allergic rhinitis may
show all the features of adenoid hyperplasia.

21. DIAGNOSIS
• It is based on duration 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

22. DIAGNOSIS
INVESTIGATIONS
1.Total and differential count.
Peripheral eosinophilia may be seen but this is an
inconsistent finding. The eosinophil count of the blood
is raised, especially in the morning, and always in the
presence of an extrinsic allergen.
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 challenge
test. Nasal eosinophilia is also seen in certain
nonallergic rhinitis ,e.g. NARES (nonallergic rhinitis with
eosinophilia syndrome).

23. DIAGNOSIS
3.Skin tests. These tests help to identify specific allergen. They are
prick, scratch and intradermal tests.
(a) Skin prick test. 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 histamine and the diluent used in allergen
solution.
(b) Specific IgE measurements. It is an in vitro test. There is a good
correlation between the skin tests and specific IgE
measurements.

24. DIAGNOSIS
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.
6. Elimination tests It can occasionally be helpful,
especially in suspected food allergies.

25. DIAGNOSIS
7. Special tests for allergy
– Diagnostic nasal endoscopy
– Saccharin test to test nasociliary function of
nasal mucosa (normal duration is 30 minute).
8. Paper Radioimmunosorbent Test (PRIST) : It is
based on incubating IgE containing serum
with radioactive labeled anti IgE and total
concentration of IgE will be proportional to
measured radIoactivity.

26. DIFFERENTIAL DIAGNOSIS

27. COMPLICATIONS/ASSOCIATED CONDITIONS
1. Recurrent sinusitis because of obstruction to the
sinus ostia. It occurs as AR progresses. The common
manifestations are generalized thickening of the
lining mucosa, fluid effusion into the sinuses.
2. Formation of nasal polypi in about 2%.
3. Orthodontic problems and other ill-effects of
prolonged mouth breathing especially in children.
4. 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.

28. COMPLICATIONS/ASSOCIATED CONDITIONS
5. Eyes: Ocular features include edema of lids, congestion,
cobblestone conjunctiva, and allergic shiners (dark
circles under the eyes).
6. Pharynx: Hyperplasia of submucosal lymphoid tissue
manifests as granular pharyngitis. Persistent AR in
children can result in “adenoid faces” and orthodontic
problems.
7. Larynx: Edema of vocal cords present with hoarseness
of voice

29. TREATMENT
Treatment can be divided into:
1. Avoidance of allergen.
2. Treatment with drugs.
3. Immunotherapy.
4. Local surgical interventions.

30. TREATMENT
1. Avoidance of allergen. This is most successful if the
antigen involved is single.
• Animal dander-Removal of a pet from the house,
• House dust mites- Encasing the pillow or mattress
with plastic sheet, avoid carpets
• Change of place of work/JOB.
• Pollens-Pollens release occurs in the early morning, so
window should be shut/ air condioned rooms
•A particular food article to which the patient is
found allergic can be eliminated from the diet.

31. TREATMENT
2. Treatment with drugs
(a) Antihistaminics:
• Antihistamines effectively block histamine released from mast cells by
reaction of allergen with IgE antibody.
• They are competitive inhibitors of the histamine receptors.
• They control rhinorrhoea, sneezing and and nasal itch.
First-generation: Chlorpheniramine, Brompheniramine,
Diphenhydramine,, Hydroxyzine etc.
Second-generation: Non-sedating H1 receptor-blocking
Loratidine, Cetrizine (derived from hydroxyzine).
They do not readily cross blood-brain barrier.
Third-generation: They are metabolites and congeners of existing drugs,
include Fexofenadine (active metabolite of terfenadine),
Desloratadine (derived from loratadine),
Levocetrizine (from cetrizine)

32. TREATMENT
(b) Sympathomimetic drugs (nasal decongestants):
• Alpha-adrenergic drugs constrict blood vessels and
reduce nasal congestion and oedema.
• They also cause central nervous system stimulation.
• Oral (pseudoephedrine and phenylephrine): The
common side effects of oral decongestants are
insomnia, tremor and tachycardia.
• Topical (Oxymetazoline and Xylometazoline):
Indiscriminate use can lead to rhinitis
medicamentosa.

33. TREATMENT
(c) Corticosteroids:
• Have anti-inflammatory action and not
immunosuppressive effects.
• Corticosteroid drugs are available in oral,
intramuscular, intravenous and intranasal forms.
Oral corticosteroids:
Are very effective in controlling the symptoms of
allergic rhinitis but their use should be limited to
acute episodes.
They have several systemic side effects.

34. TREATMENT
Topical (steroid nasal spray):
 Long-term topical corticosteroid (flunisolide,
beclomethasone, mometasone, budesonide, fluticasone
and triamcinolone) nasal therapy is an effective,
comparatively safe.
 Inhibit recruitment of inflammatory cells into the nasal
mucosa and suppress late-phase allergic reaction
 Their potential side effects are epistaxis, nasal irritation,
crusting and nasal septal perforation and potential risk
of growth inhibition in children.
 They have also been used in rhinitis medicamentosa
while withdrawing topical use of decongestant nasal
drops.

35. TREATMENT
(d) Mast cell stabilizers (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.

36. TREATMENT
(e)Anticholinergics.
Inhibits mucous membrane glandular secretion of
nose.
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.
First-generation antihistamines also have systemic
anticholinergic activity.
Does not cause rhinitis medicamentosa

37. TREATMENT
(f) Leukotriene receptor antagonists.
Act by inhibiting formation of leukotrienes or
blocking their effect
They include montelukast,pranlukast and zafirlukast
etc.
Montelukast specifically targets the cysteinyl
leukotriene receptor.
They are well-tolerated and have few side effects.
Combination therapy (montelukast 10 mg and
levocetrizine 5 mg) is reported to be a more effective
strategy than monotherapy.

38. TREATMENT
(g) Anti-IgE.
It reduces the IgE level and has an anti
inflammatory effect.
Omalizumab is such a drug, it is a recombinant
monoclonal antibody to IgE,
It is indicated in children above 12 years who
have moderate to severe asthma.
Use is limited due to its high cost and parenteral
administration.

39. TREATMENT
3. Immunotherapy
 Immunotherapy or hyposensitization 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.
 It is discontinued if uninterrupted treatment for 3 years
shows no clinical improvement.

40. TREATMENT
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.
Allergen immunotherapy, although highly effective is
highly restricted to patients with severe disease, a
minimum spectrum of allergies and in patients who fail
to respond to usual treatment. In view of systemic side
effects,the treatment is confined to specialist centres.

41. TREATMENT
• Contraindications to immunotherapy
1.Coexistent asthma
2.Patients on beta blockers
3.Other medical or immunologic diseases
4.Children less than 5 yrs
5.Pregnancy.

42. TREATMENT
4.Surgery
 Surgery can be an adjuvant management in some
refractory cases of AR when conservative treatment fails.
 The adjuvant surgical procedures employed for the
management of AR include the following:
• Antral wash out: It is done when AR is complicated by
chronic maxillary sinusitis. Sinus openings are obstructed
due to edema around the osteomeatal complex (OMC).
• Currently, functional endoscopic sinus surgery (FESS) has
been replacing antral wash. Endoscopic sinus surgery may
also be needed to relieve symptoms of rhinosinusitis or if
polyps are obstructive, they are removed.

43. TREATMENT
4.Surgery
• Cauterization: The cauterization produces fibrosis by
coagulation (chemical/thermal), which subsequently
destroys the nerve endings, blood vessels and mucous
glands.
 Chemocautery by silver nitrate.
Electrocautery by red hot galvanocautery probes.
Submucous diathermy of inferior turbinate. It unlike
chemocautery or electrocautery, does not destroy
mucosal surface epithelium which performs
mucociliary clearance of the mucus

44. TREATMENT
4.Surgery
• Septal correction
• Total inferior turbinectomy: An effective operation for
establishing the nasal airway, some adverse effects in
long-term follow up, such as oozing, hyposmia and
atrophic rhinitis.
• Laser and cryosurgery: Laser and cryosurgery are found to be
useful surgical treatments for AR and vasomotor rhinitis
• Vidian neurectomy: Vidian neurectomy, which is now no
more popular, destroys the preganglionic
parasympathetic secretomotor nerve fibers that supply
to the nasal mucosa.

45. QUALITY OF LIFE
Although not a severe disease, allergic rhinitis
significantly alters patient’s social life, affects
learning performance at school and work
productivity in an individual.

46. SPECIAL CIRCUMSTANCES
• PAEDIATRIC ALLERGIC RHINITIS
Diagnosis of allergic Rhinitis is
Difficult in small children who have between 6
and 8 colds per year and whose skin prick tests
tend to lag behind their local nasal allergy.
Treatments are also few and oral antihistamines
are used.
Sedative ones are avoided as they impair
cognitive function.
The only intranasal formulation licensed for
younger children is sodium cromoglycate.

47. TREATMENT
Saline drops may be used too in children under
two.
Fluticasone propionate is licensed for above
four yrs children and for other steroids, like
triamcinolone and beclomethasone ,the age
limit is five or six yrs.
Budesonide is not allowed in kids.

48. TREATMENT
• PREGNANCY
Preexisting allergic rhinitis may be exacerbated by
pregnancy or it can occur de novo in pregnancy,
probably due to high circulating oestrogen levels. These
symptoms disappear at delivery.
There are no medications considered safe for allergic
rhinitis in pregnancy. However the least absorbed
topical nasal corticosteroid would seem a sensible
option for the treatment of existing rhinitis. Use of
topical decongestants is also known to have associated
with congenital malformation.

49. TREATMENT
• ASTHMA
Since most asthamatics have concomitant
rhinitis, a treatment that relieves both would be
optimal.
Oral corticosteroids are extremely effective but have
severe side effects and so are reserved for most
difficult end of patient spectrum, being used for hay
fever or aggressive polyposis and asthma.

50. THANKS