Allergic Rhinitis

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. Ca rdinal 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 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: A re 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 i f 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