Allergic Rhinitis

& Vasomotor
Rhinitis

Dr.Kaminee Kumar Tripura

MBBS, DLO (BSMMU)
Assistant Professor,
President Abdul Hamid Medical College & Hospital, Kishoreganj.
 Rhinitis

Infective Non-infective

Seasonal Perennial

Allergic Non-allergic

Eosinophilic Non-eosinophilic
Allergic rhinitis

A very common ailment

10-20% annual prevalence

Male predominance

More common in young adult

About 10% of all visits to physicians
Allergic rhinitis
 Etiology
 Genetic predisposition (Atopy)
 Provoking allergens
 Role of pollution
Atopy
 Tendency to develop an exaggerated IgE
antibody response
 Allergy is the clinical expression of atopic
disease (rhinitis, asthma or dermatitis)
 Inheritance:
 Autosomal dominant
 Autosomal recessive
 Multifactorial
Allergens

Allergens

Seasonal Perennial

dust mites, molds, animal

Pollen (grass,tree,weeds)
dander, fibers,
Fungal spores
cockroaches
Allergens
 Pollen:
 Grass: early spring (most potent)
 Trees: late spring (weakest)
 Weeds: late summer
 (moderately potent)
 Fungal spores: summer and
autumn
 Cladosporium, Alternaria, Aspergillus,
Basidiospores, Didymella
Dust mites (dermatophagoids pteronyssinus et
farinie)
Occupational
allergens

Latex: health professionals and patients

Drugs: pharmaceutical workers

Flour: bakers and grain workers

Animal dander: lab workers

Wood dust: carpenters & saw mill workers

Colophony: electronic workers

Washing powders: soap powder manufacturers

Platinum salt: refiners
Food allergens

Preservatives: sulphites, benzoates, tartrazine

Histamine rich food: cheese, fish

Cross reacting

Birch pollen: apple, tomato, potato, almond, walnut, cashew nut,
cherry, carrot

Grass pollen: bean, pea, wheat, rye

Mugwort pollen: banana, melon

Cow’s milk: goat and sheep milk

Hen’s egg: meat

Peanut: pea, bean
Drug allergens
 Aspirin and other NSAIDs
 β-blockers and other adrenergic blockers
 ACE inhibitors
Pollution
 Environmental pollutants exacerbate symptoms
 Perfumes, tobacco smokes, traffic fumes,
domestic sprays, bleach etc
Pathophysiology
 Type I hypersensitivity
 Mediated by a number of inflammatory cells and
chemical mediators
 Characterized by an acute and late phase
Cellular components

Mast cells

Basophils

Eosinophils

Macrophages

Lymphocytes
Chemical mediators

Immediate  Late
 
Histamine Interleukins: 2,3,4,5
 
Bradykinins GM-CSF

Leukotrienes  VCAM

Prostaglandins

PAF
Acute phase: Late phase:
 Within minutes of Ag-  4-6 hrs after allergen
Ab reaction provocation
 Due to release of
 Due to recruited cells and
newly formed protein
chemical mediators mediators
 Vasodialation, increase  ILs, GM-CSF, VCAM, etc
vascular permeability
 Congestion is main
 Itching, sneezing, symptom
rhinorrhoea
Clinical
presentation
 Rhinitis by definition:
 Either two symptoms of rhinorrhoea, sneezing,
congestion
 For more than one hour
 On most days either seasonally or throughout
year
Symptoms

Watery nasal discharge

Sneezing
 Nasal congestion
 Post-nasal drip
 Itching of nose,
 eyes, palate
 Raw sensation of throat
 Redness of eyes
 Periorbital swelling
 Chest tightness
Skin lesions
Signs
 Watery nasal discharge
 Mucosa pale or bluish
 Turbinates may be boggy and wet
 Decreased air patency
 Allergic salute
 Congestion of eyes
 Periorbital edema
 Polyps
 Adenoid facies
 Wheeze
Clinical
presentation

Seasonal 
Perennial
 
Particular season Throughout year
 
Acute inflammation Long standing
 
Clear rhinorrhoea Viscous and purulent
 
Sneezing & conjuctivitis Less common
common
 PND, loss of smell &  More common due long
taste, ET dysfunction standing inflammation
less common
Complications

Serous otitis media

Sinusitis

Associated systemic allergy

Nasal polyposis
Investigations
 For confirmation of allergy
 Skin testing
 Antigen specific IgE level
 Total IgE level
 Nasal smear for
 eosinophils DLC
 Radiology
 Plain radiograph
 CT scan
Skin testing

Gold standard Reaction between Ag and
 sensitized mast cells in
Principle skin

Classic wheal
and flare
response

Acute phase in 2-
Late phase in 4-6hrs
5min Max at 15mins
Wheal and
Erythema and wheal
induration
Skin testing: classification

Skin tests

Epicutaneous Intracutaneous

Scratch test Single dilution

Prick-puncture Multiple
test dilution
Treatment

Allergen avoidance

Pharmacotherapy

Oral and topical steroids

Oral and topical antihistamines

Mast cell stabilizers

Vasoconstrictors and anti-
 cholinergics
 Immunotherapy
Surgery
Allergen avoidance
 Prevention is best
 Dust mites can be avoided by using pillow &
matress covers / vaccum cleaning / proper
ventilation
 Animals: removing furred animals / separate
room / frequent cleaning
 Pollen: shutting windows of cars & houses /
using masks/ avoiding grassy fields
Steroids

Oral steroids best for severe acute allergy

Reserved for refractory cases

Topical steroids are first line treatment

Act in late phase

Available as freon propellant inhalers and aqueous
sprays

Later are well tolerated, pleasant and well distributed in
NC

Intra-turbinate repository preparations act for 4-6wks
Corticosteroids : sprays
 Preparations
 Dexamethasone
 Beclomethasone

Flunisolide

Triamcinolone

Budesonide
 Fluticasone
 Mometasone
Corticosteroid : sprays
 Complications:
 Nasal irritation

Dryness

Crusting

Nasal bleeding

perforation
 Local infection

Systemic side effects with very high doses

Failure due to non-compliance
Antihistamines
 Most effective when taken prophylactically
 Most effective at reducing symptoms of sneezing,
nasal itching, and rhinorrhea.
 First generation are more potent / lipid soluble /
cross BBB

More sedation / bladder obstruction / dryness

Second generation are less sedative
Leukotriene inhibitors
 Act similar to antihistamines by competitive
inhibition of the leukotriene receptor.
 Very successful in Asthma
 The data available to date do not clearly support a
unique role of leukotriene inhibitors in the
treatment of allergic rhinitis.
 Eg: Zileuton (LOX inhibitor)
Zafirlucast, Montelucast (receptor
antagonist)
Mast cell
stabilizers
 Prophylactic
 Relieve both acute and late symptoms
 Safe
 Preparations:
 Sod. Chromoglycate (topical spray)
 Ketotifen (oral)

Nedochromil
Decogestants
 Alpha adrenergic blockers
 Symptomatic improvement in nasal blockage
 Topical preparations should not be used for more
than 2wks at a time
 Rhinitis medicamentosa
 hypertension
 Eg:
 Systemic: pseudoephidrine, phenylpropanolamine
 Topical: oxy and xylo-metazoline
Anti-cholinergics
 Only symptomatic improvement of rhinorrhoea
 Side effects: dryness, crusting, thickened
secretion, raised IOP, blurring of vision, bladder
obstruction,
 Eg: topical Ipratropium bromide
Comparison

Drug Itch/ sneezing Discharge Blockage Hyposmia

Chromolyn + + ± -

Antihistamines +++ ++ ± -

Ipratropium - +++ - -

Topical - - +++ -
decongestants
Topical steroids +++ +++ ++ +

Oral steroids +++ +++ +++ ++

Immunotherapy
 Initial intradermal test (SET)
 After the initial doses have been administered and
tolerated, the injections are increased until the
dose reaches maximum level
 Watch for unacceptable effects (wheal of 3cm or
more or worsening of systemic symptoms
 Twice a wk until response achieved
 Once a wk for one year
 Maintenance: once in 2-3 wks for
3-5yrs
Mechanismof
immunotherapy
 Gradual increase of allergen-specific IgG antibodies --
especially IgG4 subclasses (blocking antibody)
 intercept and neutralize allergen before it bound to cell-surface
IgE
 form IgG-antigen-IgE complex and bind to the IgG receptor
resulting co-aggregation with the IgE receptor and inhibition of
IgE receptor triggering
 decreased allergen-specific IgE antibodies
 increase IgA and IgM antigen-specific B lymphocytes
 May limit antigen penetration into the body from
mucosa
Surgery
 Should not be considered “a last resort” but rather
complementary to medical trt, when needed
 May be:
 Septal correction
 Turbinate surgery
 Polyp removal
Vasomotor
rhinitis
Vasomotor Rhinitis
 Non-allergic, non-infective, non-structural, non-
autoimmune rhinitis
 Intrinsic rhinitis / Intrinsic rhinopathy / Perennial
rhinitis
 rhinorrhoea syndrome
Physiology
 Venous sinusoids are located between capillaries and venules in
submucosa of turbinates
 These surrounded by smooth muscle fibrils capable of
constriction and dilatation
 When filled with blood, the turbinates engorge (as erectile tissue)
 Innervated by ANS
 Parasymp.: vasodilatation and mucus production
 Symp.: vasoconstriction
 Normally symp. tone dominates
 In vasomotor rhinitis: parasymp. tone dominates
Etiology
 Emotional disturbances
 Drugs (reserpine / hydralazine / OCP, etc)
 High temperature
 Humidity
 Pregnancy / premenstrual
 period Honeymoon rhinitis
 Hypothyroidism
 Dusts, chemicals, perfumes, smoke,
 etc Gustatory rhinitis
 Recumbency rhinitis
 Nasal cycle
 NARES
Epidemiology

Prevalence of IR 7-21%

1/3rd eosinophilic

Out of those defined as having perennial rhinitis
only 30-60% are positive to allergy tests. Rest
belong to IR.

With advancing age number of cases with non-
eosinophilic variety increase
Clinical picture:
symptoms

Eosinophilic  Non-eosinophilic
 
Obstruction: Mild
 
severe Rhinorrhoea: Severe
 
Hyposmia: usual
mild Rare
 
Sneezing: minimal Minimal
 
Itching: minimal minimal
Clinical picture:
signs
 Eosinophilic  Non-eosinophilic
 Mucosal swelling: Marked  Mild
 ITH: marked  Mild
 Polyps: frequent (30%)  Never
 Sinus mucosal  Rare
thickening: frequent
 Good response to  Respond to anti-
steroids cholinergics
Clinical
picture
 Allergic rhinitis  Vasomotor rhinitis
 Sneezing and nasal itching  Hyposmia and nasal
highly suggestive congestion predominant
 Rhinitis in childhood  Rhinitis developing
in adults
Clinical
picture
 Aspirin sensitivity:
 IR: 1%
 IR with polyposis: 8%
 IR with polyposis with Asthma: 70%
 Association with bronchial asthma:
 Non-eosinophilic IR: 13%

Eosinophilic IR: 14%

AR: 58%

Nasal polyposis: 71%
Diagnosis
 Diagnosis of exclusion

No h/o allergy / seasonal variation / itching or sneezing

No structural abnormality / infection
 ITH / nasal polypi
 Tests for allergy negative
Treatment

Supportive

Medical

Surgical
Supportive treatment

Head end up by 300

Regular vigorous exercise

Avoid known irritating factors

Avoid emotional breakdowns
Medical treatment
 Eosinophilic:  Non-eosinophilic
 Topical steroid  Anticholinergics
 Topical and oral  Anticholinergic/
decongestants sympathomimetics
 Mast cell stabilizers
Surgical treatment
 Obstructive:  Rhinorrhoea:
 Inf turbinate surgery  Vidian neurectomy
 Middle turbinate
surgery
 Nasal polyp
surgery
Thank You