Allergic rhinitis

Allergic rhinitis by Dr Marjan

1. ALLERGIC RHINITIS DR.MARJAN.M

2. First description of Hay fever

3. Definition and classification Epidemiology Pathophysiology and mechanisms Risk factors Evaluation and diagnosis Associated conditions MANAGEMENT

4. Rhinitis is defined clinically as having two or more symp t oms of #anterior or posterior rhinorrhoea , #sneezing # nasal blockage and/or itching of the nose during two or more Consecutive days for more than one hour on most days . Noninfectious rhinitis has been classified as either Allergic or non-allergic. Allergic rhinitis is characterized by inflammatory changes in the nasal mucosa caused by exposure to inhaled allergen in a sensatised individual resulting in the above symptoms. It is an IgE mediated reaction. The diagnosis of an allergic rhinitis alle rgic s ymptoms + history with diagnostic tests (skin prick testing or by measuring specific IgE levels in the blood (RAST)

5. Allergic rhinitis I ntermittent (IAR) Persistent (PER) disease Acc to severity as Mild or moderate/severe

6. Aetiology Genetic factors (parents if atopic - 3 – 6 times )( genes involved are 5q, 11q &12q) Exposure to an allergen ( Seasonal : pollen, fungus //// Perennial: dust mite, domestic pets, cockroaches) Environmental factors: pollution climate interaction: Irritants ( Fumes, tobacco smoke, diesel exhaust, mosquito repellents, perfumes, scented sticks, domestic sprays, bleaches ) Hygiene hypothesis Children who live on farms, contact with livestock, larger family size, more frequent infections and unhygienic contact  less likely to develop Possible protective effect of microbial exposure. Reduced exposure to infective agents  reduces the Th1 Response  an overdrive of the Th2 immune response  excessive production of IgE . Worms is also protective, possibly because of the production of blocking antibodies (IgG4).Eradication increases skin allergy to aeroallergen Urbanized, western lifestyle promotes AR.

7. The ‘ atopic march ’ in children refers to the sequential development of allergic diseases, often starting in infants with Atopic eczema  A llergic rhinitis  A llergic asthma

8. PREVALENCE Prevalence : 0.8% -- 39.7% Higher in pediatric age group App 80% develop before 20yrs.

9. Pathophysiology Sensitization: development of specific IgE  allergens reach antigen-presenting cells ( apcs )  APCs promote Th2 polarization  T h2 promotes production of allergen-specific IgE inhaled allergen produces specific I gE antibody which gets attached to mast cells

10. Subsequent response: development of symptoms Subsequent exposure to same antigen  allergen combines with specific IgE antibody → degranulation of mast cells → chemical mediators released

11. Acute or early phase response Occurs 5–30 min after antigen exposure • release of inflammatory mediators • increased nasal gland secretion → runny nose • mucosal edema & vasodilation → nose block • nerve irritation → sneezing & itching LATE OR DELAYED PHASE RESPONSE • occurs 2-8 hours after antigen exposure • infiltration by inflammatory cells (eosinophils, neutrophils, basophils, monocytes & cd4+ t lymphocytes) • edema, congestion & thick nasal secretion • sneezing & itching decreases

12.  In atopies, allergen molecules are inhaled and presumably not completely cleared by the mucociliary system.  They reach antigen presenting cells in the nose, the most important of which are dendritic cells / Langerhans cells.  They capture antigen, process it and present it to naive T cells in the local lymph nodes.  If no additional signal is present then a T-cell response will not ensue.  In atopic individuals, Th2 cells predominate at the sites of allergic response.

13. SYMPTOMS Seasonal allergic rhinitis: nasal discharge and conjunctivitis (more common) Perennial allergic rhinitis: nasal blockage (more common) less sneezing/nasal discharge /eye symptoms hyposmia • Rhinorrhea - clear /mucoid Sneezing( in allergic disease often marked is by explosive paroxysms of 5 to 10 sneezes or more ) NASAL BLOCK • Itchy nose, ears, eyes and palate • Post nasal drip • Congestion • Anosmia • Headache • Earache • Tearing of eyes • Red eyes • Swollen eyes • Fatigue • Drowsiness • Malaise

14. Seasonal allergic rhinitis  pollen: Spring (march- june ) = tree pollen Summer (may-august) = grass Fall (august- october ) = weeds  mold: Spores in outdoors have seasonal Variation (reduced in winter, increased in Summer/fall due to humidity)  house dust mites: Generally “perennial” allergen, But increased in damp autumn months

15. Perennial allergic rhinitis  fungi/mold: Exposure peaks accompany activities Such as harvesting & cutting grass  pet dander (cats, dogs): Up to 4 months after pet removal  house dust mites: Live in bedding & carpets  cockroaches: Respiratory allergy Important allergen

16. SIGNS Crease on tip of nose with crusting – D arrier’s line Allergic salute- child pushes tip of nose up with base of palm as an attempt to control itching Allergic gape- mouth breathing from nasal obstruction

17. Face: Bunny nose- frequent twitching of face Periorbital puffiness Dark circles around eye- ALLERGIC SHINERS (pooling of blood under eyes due to swelling of tissues in nasal cavity) Creases in lower eyelids due to spasm of superior tarsal muscle and skin edema to hypoxia DENNIS MORGAN LINES Eye : Conjuctival congestion , Epiphora Ear: Aural fullness(ET dysfunction) Throat: Chronic pharyngitis, laryngitis

18. O/E Anterior rhinoscopy Asymptomatic - normal mucosa Active stage – PALE , boggy, edematous nasal mucosa with watery discharge Bulky inferior & middle turbinates , mulberry shaped Posterior rhinoscopy  Halitosis  High arched palate (chronic mouth breathing)  Malocclusion (common)  Tonsillar hypertrophy  Cobblestoning of the oropharyngeal wall  Pharyngeal postnasal dischargePost nasal drip

19. Inferior Turbinate Classification System (A) Grade 1 (0%–25% of total airway space) (B) Grade 2 (26%–50% of total airway space) (C) Grade 3 (51%–75% of total airway space) (D) Grade 4 (76%–100% of total airway space)

20. dd of chronis rhinitis

21. Diagnosis 1.History 2.Physical exam 3.Allergy diagnosis (I) Skin prick test (SPT) (II) Blood tests for allergy: Total IgE , Specific IgE (III) Nasal allergen challenge test

22. HISTORY

23. Skin tests – Introduce allergen into skin & check the site after 10-15 min for an immediate local allergic reaction – wheal and flare >2mm) Method: small lancet to introduce an allergen into the skin. If the patient is sensitized to the allergen then IgE sensitized mast cells will degranulate and cause a wheal and flare reaction in the skin. Negative (saline) and positive (histamine) controls are also used Positive skin tests only give a guide to degree of atopy & not implies nasal allergy to same allergen High sensitivity and specificity (around 80%)

24. Skin prick test (SPT) Rapid, efficient & cost effective Contain multiple antigens (pollen, mold, dust mite, animal dander)

25. Blood tests for allergy 1.Total IgE : Rarely helpful as 50% pts have IgE levels within normal range 2.Specific IgE : ( i ) Radio- allergosorbent test (RAST) (ii)Modified RAST The safety profile of serum serum IgE testing is the bests Not influenced by drugs or skin disease levels of sIgE may correlate with severity of AR symptoms

26. RAST( Radio allergo sorbent test Procedure  Specific allergen bound to paper disc  test serum added to it & incubated  specific IgE ab , if present in serum will bind to allergens & form complexes.  Radioisotope labeled anti- I gE Ab then introduced to Medium which binds to pre-existing complexes on paper disc  Resultant “ allergen- IgE –anti- IgE ” then measured in a γ counter & the amount of Ab calculated.

27. Indications: 1. When there is C/I to SPT 2. Where SPT unavailable 3. When SPT difficult to interpret Disadvantages : More expensive Delayed(takes longer) No more sensitive or specific to SPT Test may give false positive of false negative results.

28. Scale The RAST test is scored on a scale from 0 to 6 : RAST rating IgE level (KU/L) comment < 0.35 ABSENT OR UNDETECTABLE ALLERGEN SPECIFIC IgE  0.35 - 0.69 LOW OF ALLERGEN SPECIFIC IgE  0.70 - 3.49 MODERATE LEVEL OF ALLERGEN SPECIFIC IgE  3.50 - 17.49 HIGH LEVEL OF ALLERGEN SPECIFIC IgE  17.50 - 49.99 VERY HIGH LEVEL OF ALLERGEN SPECIFIC IgE  55.00 - 100.00 VERY HIGH LEVEL OF ALLERGEN SPECIFIC IgE  > 100.00 EXTREMELY HIGH LEVEL OF ALLERGEN SPECIFIC

29. PRIST Paper Radio Immunosorbent Test Principle Incubating the IgE containing serum with Radioactively labeled anti- IgE Total conc of IgE is then proportional to measured Radioactivity

30. Nasal challenge tests Also known as nasal provocative test Sniff suspected allergen and the no. & Severity of s ymptoms noted. Subjective –symptom scores, VAS Objective –sneeze count, nasal inspiratory peak flow , rhinomanometry , acoustic rhinometry , spirometry , pulmonary peak flow Indication: - + ve history & – ve SPT Disadvantages 1.Time consuming 2.Difficult 3.Excessive lab facilities 4.Trained staff 5.Resuscitation equipment

31. Routine radiographic imaging is not recommended for the diagnosis of allergic rhinitis but to may be needed to rule out othe diseases Xray Low density haziness seen in PNS Occasionally polyps

32. Nasal endoscopy

33. CT scan-Nose and PNS

34. COMPLICATIONS: • Allergic asthma • Chronic otitis media • Hearing loss • Chronic nasal obstruction • Sinusitis • Orthodontic malocclusion in children

35. Nasal symptoms -noted 80% of asthmatics Adults-asthma present in 22.5% of adults with AR, vs 7.2% in general population Children-ratio of asthmatics with AR to asthmatics without AR is even higher Effective treatment of allergic rhinitis reduces development of subsequent asthma

36. Management of allergic rhinitis The prevention of allergic rhinitis • Methods of reducing allergen exposure • Pharmacological treatment of allergic rhinitis • Immunotherapy for allergic rhinitis • Surgical treatment • Complementary therapies

37. (I) Avoidance of allergens Best treatment method Not always practical Indoor allergens: Removing allergen from the indoor environment should be a primary strategy for the management and treatment of allergic disease Outdoor allergens :avoid contact

38. General advice -- reduce allergen exposure • chidren should breastfeed for at least the first three months after birth parents should not smoke in pregnancy or near children Avoid irritants : smoke, dust, vehicular & other atmospheric pollutants, • Physical factors – extreme changes in temperature can produce symptoms like allergic rhinitis but are non- IgE mediated responses • Avoid foods & drugs to which you are allergic • Avoid occupational irritants or change profession

39. Avoidance of indoor allergens

40. Pharmacological treatment of allergic rhinitis The most widely used and effective medications - oral or topical antihistamines and topical nasal steroids. It should be stressed that these medications aim to achieve improved symptom control and are not a cure for allergy. They generally need to be taken for as long as there is allergen exposure causing symptoms. Symptom control is better for patients with intermittent allergic rhinitis if they start treatment prior to exposure to the allergen to which they are sensitized.

41. ANTIHISTAMINES first-line treatment -- symptoms of running, sneezing and nasal and eye itching and have no problem with nasal obstruction. Second generation- loratadine and cetirizine are non-sedating, safe for long-term use-- can be used for children. They have a rapid onset of action (usually less than an hour) and will give symptom reduction on a once daily dosing. Topical antihistamines (for example azelastine)

42. INTRANASAL GLUCOCORTICOSTEROIDS INTRANASAL Glucocorticosteroids-- most effective treatment for allergic rhinoconjunctivitis. Topical use in the form of a spray or drops is preferred to oral use to reduce side effects, first_x0002_line treatment of choice in patients who complain of nasal block. several hours or days and it can take two weeks for full benefit to be noticed Side effects of intra-nasal steroids are few--EPISTAxis.( incorrect use) Minor growth retardation has been noted in children--INTRANASAL beclometasone fluticasone(FROM 4 YEARS) or mometasoneAND TRIAMCINOLONE( FROM 6 YEARS)

43. ORAL STEROIDS: Prednisolone 20–40mg/day LEUKOTRIENE RECEPTOR ANTAGONISTS (LTRAS) Cysteinyl leukotrienes are a family of eicosanoid inflaMmatory mediators (LTC4, LTD4 and LTE4) produced in leukocytes, mast cells, eosinophils, basophils and macrHphages by the oxidation of arachidonic acid by the enzyme arachidonate 5–lipoxygenase. Their effects are to cause bronchoconstriction, increase vascular permeability and attract inflammatory cells and as such are involved in the processes underlying asthma and allergic rhinitis Sodium cromoglicate nasal spray has modest effects on rhinitis symptoms but must be used four times daily, which limits compliance.67 It has no side effects and can be used on young children Cromoglicate eye drops can be effective against ocular itching.

44. DECONGESTANTS Topical (e.g. xylometazoline) and systemic decongestants (e.g. pseudoepedrine) more effective, More rapid onset of action. They reduce nasal obstruction , ALlow access of topical steroid into an otherwise obstructed nose. The disadvantage is of rebound vasodilation when their use is stopped( RHInitis medicamentosa) A maximum length of treatment of 7–10 days therefore is advised. Systemic decongestants may also have side effects such as insomnia, tachycardia and tremor

45. IPRATROPIUM Topical ipratropium bromide spray is effective - watery rhinorrhoea, useful addition to a topical steroid if rhinorrhoea is not being well controlled. Side effects are infrequent but include prostatic symptoms and worsening of glaucoma. NASAL DOUCHING Saline nasal douches may help with symptom control and can physically remove an allergen from the nasal mucosa. If pollen levels are high regular douching may be of benefit.

46. IMMUNOTHERAPY(DEENSENSITATION) is a method of inducing tolerance to an allergen and therefore reducing unwanted symptoms. If allergic rhinitis is refractory to pharmacotherapy or severe Helps in reducing the specific serum IgE level decreases the basophil sensitivity increases IgG blocking antibody level , thus preventing allergen from reaching mast cells and subsequent mast cell degranulation . It can be given subcutaneously by injection (SCIT) or sublingually in drops or tablets (SLIT) Patients considered are those who have severe symptoms but whose response to standard medical treatment has been unsatisfactory, or those patients who have unacceptable side effects from their medication.

47. PROCEDURE SCIT there is usually an updosing phase of between 2 and 4 months when the dose of allergen is gradually increased to the maintenance dose. This maintenance dose is then injected every 4–6 weeks for a 3-year period. SLIT may be updosed or, in some treatment protocols, the patient starts with the maximum dose and continues with this daily for 3 years transient redness and itching around an injection site, or oral itching, and can be reduced by pre-treatment with an oral antihistamine. SIDE EFFECTS: urticaria, bronchoconstriction or anaphylaxis and resuscitation facilities with adrenaline must be avaiLable Almost all reactions will occur within 30 minutes of treatment therefore patients should be observed for an hour after injection

48. Recent exposure of the nose to allergen may lead to asymptomatic eosinophil infiltration and a pro_x0002_inflammatory mucosal environment – a concept known as priming .

49. ANTI IGE AB- OMALIZUMAB risk of causing anaphylaxis and is expensive. It is administered by monthly injection. Currently it is recommended only for patients with severe allergic asthma with or without rhinitis symptoms.

50. SURGICAL THERAPY Limited Submucosal turbinectomy - reduces size of boggy turbinates Septoplasty – correction of deviation of septum Sinus surgery – clearance of sinuses if sinusitis is present

51. THANK YOU