Allergic Rhinitis

36,697 views 56 slides Sep 11, 2014
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About This Presentation

allergic rhinitis


Slide Content

Ramesh Parajuli MS
Lecturer, Department of Otorhinolaryngology, Head & Neck Surgery
Chitwan Medical College Teaching Hospital
Bharatpur-10, Fax: 977-56-532937, Chitwan, Nepal
[email protected]
Allergic rhinitis

Definition
“IgE mediated hypersensitivity disease of mucous membranes of
nasal airways characterized by sneezing, watery nasal discharge ,
itching and nasal obstruction” (Durham, 1999)

Prevalence
•Global health problem
•Prevalence - 15% and 20% (Nathan et al.,1999)
•Higher in pediatric age group(Wright et al.,1994)
•Approx. 80% develop symptoms before age of 20
(Skoner et al., 2001)

•Not a severe disorder but significantly
alters patient’s social life
-school performance
-work productivity
•Substantial cost
Impact on quality of life

1. Genetic susceptibility:
2. Family history of atopy: e.g. asthma,eczema,hay
fever,urticaria
(Genes involved in atopy - loci on 5q,11q and 12q
chromosomes)
3. Environmental factors:
•Pollution-climate interaction
•Irritants
eg. fumes, tobacco smoke, diesel exhaust,
mosquito repellents, perfumes, scented sticks,
domestic sprays, bleaches
4. Exposure to allergens:
•Seasonal : Pollen, Fungus
•Perennial: Dust mite, domestic pets, cockroaches
Risk factors

5.Hygiene hypothesis
•Increased exposure to various allergensimmune maturationhelp decrease
the incidence of allergic diseases and asthma (Svanes C et al., 2003)
•Early environmental exposure to infectious agents, protects against
development of atopy (Tulic MK et al.,2003)
•Early nursery attendance also reduces subsequent atopy (Kramer et al.,2003)
•Lack of immune maturation (understimulated immune system) in
infancyallergic responses (Liu A,2007)

Pathogenesis
•Sensitization & Priming to specific antigen:
Inhaled allergen produces specific IgE antibody
which gets attached to mast cells
•Subsequent exposure to same antigen:
Allergen combines with specific IgE antibody ®
degranulation of mast cells ® chemical mediators
released

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

Symptoms
1. Running
2. Blocking
3. Sneezing
4. Itching

Signs
Nasal crease
Pale turbinate

Face:
• Bunny nose-frequent twitching of face
• Dennie-Morgan creases (in lower eyelid skin)
• Allergic shiners (dark discoloration below lower
eyelids)
Eye: Conjunctiva is congested, increased lacrimation
Ear: Aural fullness(ET dysfunction)
Throat: Chronic pharyngitis, laryngitis

Types of allergic rhinitis
•Seasonal allergic rhinitis:
Nasal discharge and conjunctivitis (more common)
•Perennial allergic rhinitis:
Nasal blockage (more common), Hyposmia
Less sneezing/nasal discharge /eye symptoms

ARIA classification= Allergic Rhinitis & its Impact on
Asthma
Rhinitis 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
Seasonal allergic rhinitis

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

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

History

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

Skin Prick test
Advantages:
1.Cheap
2.Immediate result
3.Sensitive
Contraindications:
1.Patients on antihistamines
2.Severe eczema
3.Previous anaphylaxis
4.Dermagraphism

(II) 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
Stabilized allergen is incubated with patient’s serumany specific IgE binds to
allergen identified by a second incubation with labelled anti-IgE.

Radio-allergosorbent test (RAST)
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

(III)Nasal allergen challenge (nasal provocation) test
Indication:
- +ve history & –ive SPT
•Subjective –symptom scores, VAS
•Objective –sneeze count, nasal
inspiratory peak flow ,
rhinomanometry , acoustic
rhinometry , spirometry,pulmonary
peak flow
Disadvantages
1.Time consuming
2.Difficult
3.Excessive lab facilities
4.Trained staff
5.Resuscitation equipment

CT scan-Nose and PNSNasal endoscopy

Complications (Co-morbidities)

•Nasal symptoms -noted 80% of
asthmatics
•Adults-Asthma present in 22.5% of
adults with AR, Vs 7.2% in general
population (Laynaert, 1999 )
•Children-Ratio of asthmatics with AR to
asthmatics without AR is even higher
(Wright et al.,1996)
•Effective treatment of allergic rhinitis
reduces development of subsequent
asthma (Ragab et al., 2006)

Differential diagnosis
1.Vasomotor rhinitis (Intrinsic rhinitis/NANIPER)
2.Sinonasal polyposis
3.Rhinitis medicamentosa
4.Hormonal rhinitis
(Pregnancy, Hypothyroidism, OCP use )
5.CSF leak
Take a moment to consider
differential diagnosis

Management of allergic rhinitis
1. Environmental control measures (Avoidance of allergens)
2. Patient education
3. Nasal douching
4.Medical therapy
5.Immunotherapy
6.Surgery

(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 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
General advice

Avoidance of indoor allergens

Avoidance of animal allergen
•Remove pet animals (cats, dogs)
from bedroom
•Wash the pet weekly

Measures to avoid house dust mite
•Mattress covers
•Covers for pillows & bedding
•Vacuuming
•Regulation of ventilation & humidity at home
•Liquid nitrogen
•Acaricides
•Protein denaturating agents- Tannic acid

•Avoid walking in open grassy spaces
during hot, dry days
•Keep windows closed
•Wear facemask & sunglasses when
moving out
Pollen avoidance measures

(II) Patient education
Educate patients on environmental control measures,
which involve both the avoidance of known allergens
(substances to which the patient has IgE-mediated
hypersensitivity) & the avoidance of nonspecific, or
irritant, triggers

(III) Nasal douching
Neti Pot: Home remedy to clean nasal passages
•Saline irrigation
•Improves quality of life

(IV) Medical therapy

1.Antihistamines:
Topical: Azelastine
Systemic: Cetirizine, Levocetirizine,Fexofenadine, Loratadine, Desloratadine
2.Nasal Decongestants:
Topical: Oxymetazoline, Xylometazoline
Systemic: Phenylephrine, Pseudoephedrine
3.Mast cell stabilizers: Sodium cromoglycate nasal drop
4.Anticholinergics: Ipratropium bromide nasal spray
5.Corticosteroids:
Topical :Beclomethasone,Budesonide,Mometasone,Fluticasone
Systemic: Prednisolone
6.Leukotriene receptor antagonists: Montelukast, Zafirlukast

Steroid
•Most effective treatment for Allergic rhinitis(AR)
-Topical: Nasal spray or nasal drop
-Systemic:Oral, extremely effective
•Reduces inflammation & consequent
hyperreacitvityreduce nasal symptoms, eye
symptoms, improve smell sense
•Topical steroid when combined with antihistamines
reduces risk of asthma exacerbation and hospitalization
by 50% or more (Adams et al., 2002, Crystal peters et
al., 2002)
•Fluticasone and mometasone have low systemic
bioavailabilitylower risk

Antihistamines
•Adverse effects of first generation antihistamines
“First-generation oral H1-antihistamines are not recommended when second-
generation ones are available, due to safety concerns”
(Allergy. 2008 Apr;63 Suppl 86:8-160)

GA
2
LEN- Global Allergy and Asthma European Network
Allergy. 2010 Apr;65(4):459-66

Significance of wide therapeutic window (fexofenadine)
Low H
1
-antihistamine dose High
Ineffective Therapeutic Window
Not tested for
adverse effects
Maximum
Studied dose
(Fexo 1380 mg)
Minimally
effective dose
(Fexo 60 mg)
Howarth PH. Advanced Studies in Medicine. 2004;4(7A):S508-512

Levocetirizine and desloratadine have some effects on nasal
obstruction (Wilson AM, 2002)

•Topical vasoconstrictor:
-imidazoline (eg, oxymetazoline)
• systemic (oral) vasocontrictor
-Phenylephrine
- Pseudoephedrine.
•Monotherapy with vasoconstrictors has limited role
•Oral decongestants + Antihistamineall cardinal
symptoms of allergic rhinitis targeted
Decongestants

Mast cell stabilizer
• Sodium cromoglycate inhibits degranulation of
sensitized mast cells
•2% Nasal drop: Use 3 to 4 times daily limits
compliance
•Poorly absorbed systemically excellent safety
record
•Used before the onset of symptoms
•Can be used in younger children < 2 years of age
Ipratropium Bromide
•Useful against nasal discharge
•Occasionally helpful in pts with AR who do not
respond to topical steroid(Dockhorn et al., 1999)

Zafirlukast performed no better than placebo - seasonal alllergic
rhinitis ( Pullerits T et al., 1999)
•Montelukast clinical efficacy seasonal Allergic rhinitis
(Chervinsky P et al., 2004)
•Montelukast + loratadine -superior reducing day time nasal
symptoms in seasonal Allergic rhinitis. (Meltzer EO et al., 2000)
•Montelukast + ebastine- better symptomatic control in allergic rhinitis.
•Montelukast -less effective than Intranasal steroid (Ratner PH et al.,
2003)
•Leukotriene antagonist (Montelukast) doesn’t appear more effective
than nonsedating antihistamines (Fexofenadine) (Wilson AM et al., 2004)
Antilukotrienes

(V) Immunotherapy
•Repeated administration of allergen extract
induce state of immunological tolerance
•Render an allergy patient less symptomatic
when exposed to the offending antigen
•Desensitization or Hyposensitization:
because complete elimination of the allergic
reaction is seldom achieved
•Subcutaneous injection or sublingual route

Contraindications
• Asthma(severe)
•Autoimmune diseases
•Beta-blockers or Anti-adrenergic medicines
•Children less than < 5 yrs
•Pregnancy (induction but not maintenance)
•Efficacy:
•Highly effective -selected patients (Grade A)
•Treatment for 3 to 4 yrs –improvement for 3 yrs following discontinuation
(Durham SR et al.,1999)
•Children –seasonal rhinitis-ITX for 3 yrs-2 to 3 fold reduction –developing
asthma (Moller et al.,2002)
•Offers long term disease modification & prophylaxis

Side effects of Immunotherapy
Local reactions - trivial
Systemic reactions-10%-up dosing phase
Occasionally – severe systemic reactions-
general urticaria , severe asthma or
anaphylaxis

(VI) Surgery
•Usually not indicated
•Not last resort but complementary
• Comorbid or complicating conditions eg
Marked DNS, Turbinate hypertrophy, CRS

(VII) Complementary and integrative medicine(CIM) therapies
•Honey – For seasonal AR caused by pollen
•Chinese herbal medicine
•Acupuncture

Recent advances
(VIII) Human monoclonal antibody(Anti-IgE)
•Omalizumab - recent developments in the treatment of atopic
diseases
first of several monoclonal antibodies (anti IgE antibody)
Modulation of allergic inflammation
expensive for routine treatment of AR primarily indicated -severe
asthma
•Multiple randomized, double-blind, placebo-controlled studies
-efficacy in seasonal and perennial AR (Vignola AM et al.,2004)
Continued research on the molecular mechanism of
allergic disease will inevitably generate new forms of
therapy.

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