ALLERGIC RHINITIS

&
VASOMOTOR RHINITIS

Dr. Ritesh Mahajan

ENT Consultant
GMC, Kathua
•It is an IgE-mediated immunologic response of nasal
mucosa to airborne allergens.

•Characterized by watery nasal discharge, nasal

obstruction,

•Sneezing and itching in the nose.

Facts about Nasal Allergies
• An extremely common disease worldwide, affecting 10 to 25% of the

population

• Commonest allergy encountered in clinical practice and constitutes more

than 50% of all allergies seen in India

• Top 10 reasons for visit to primary care clinics

• The condition impacts heavily on health-related quality of life

TYPES OF AR
• Seasonal
▫ Usually pollens, and outdoor molds

• Perennial
▫ Caused by indoor allergens i.e. cockroach, dust
mite, pets, and certain molds

• Episodic

• Occupational
Causes of AR
Globally important allergens
• House dust mites

• Grass, tree and weed

pollen

• Pets

• Cockroaches

• Molds
Mediators and symptoms in Allergic rhinitis
Histamine Immediate rhinitis
symptoms
Leukotrienes
• Itch, sneezing
Prostaglandins
Mast cell • Watery discharge
Bradykinin,
• Nasal congestion
PAF
IgE
Allergen B cell

IL-4
Chronic rhinitis
VCAM-1 symptoms
T cell IL-3, -5
Eosinophil • Nasal blockage
(mast cell)
GM-CSF • Loss of smell
• Nasal
hyperreactivity
AETIOLOGY
• Inhalant allergens. They may be seasonal or
perennial.

• Seasonal allergens include pollens from trees, grasses and

weeds.

• Perennial allergens are present throughout the year.

• They include molds, dust mites, cockroaches and dander from

animals.

• Dust includes dust mite, insect parts, fibres and animal

danders.

• Dust mites live on skin scales and other debris and are found
in the beddings, mattresses, pillows, and carpets.
Genetic predisposition

• Plays an important part.

• Chances of children developing allergy are 20

and 47%, respectively,

• if one or both parents suffer from allergic

diathesis.
PATHOGENESIS

• Inhaled allergens produce specific IgE antibody in

the genetically predisposed individuals.

• This antibody becomes fixed to the blood basophils

or tissue mast cells by its Fc end.

• On subsequent exposure, antigen combines with

IgE antibody at its Fab end.

• This reaction produces degranulation of the mast

cells with release of several chemical mediators.
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY

• Vasodilation, mucosal oedema, infiltration with

eosinophils, excessive secretion from nasal glands
or smooth muscle contraction.

• A “priming affect” has also been described, i.e.

mucosa earlier sensitized to an allergen will react
to smaller doses of subsequent specific allergen.

• It also gets “primed” to other nonspecific antigens

to which patient was not exposed
Pathophysiology
• Early response –

• IgE coated mast cells recognize allergens in the mucosal lining, and
undergo degranulation.

• Preformed histamine, heparin, tryptase, kininogenase, and chymase

cause the initial damage.

• Newly formed mediators include leukotrienes and prostaglandins.

They are produced by breakdown of phospholipid cell membrane.
These cause vessels to leak leading to watery rhinorrhea, nasal
edema/congestion, and sneezing/pruritis
Pathophysiology
• Late response –

• Mast cells also secrete chemokines that promote

VCAM, and E-selectin expression on endothelial cells.

• These allow other leukocytes to attach, and migrate into

tissues. IL-5 is a potent chemoattractant of
eosinophils, T lymphocytes, and macrophages.

• Over the course of 4 to 8 hours, these cells release there

contents, causing further inflammation.
Symptoms
• Rhinorrhea

• Cough/sneezing

• Nasal congestion

• Post nasal drip

• Nasal pruritis

• Watery eyes

• General fatigue

• Diminished quality of life

 Clinical Manifestations

Classical Symptoms Others

Repetitive sneezing Eye symptoms

Watery rhinorrhea Ear symptoms

Nasal itching Postnasal drainage

Nasal congestion
History
• Onset, timing, duration, seasonality, severity,
associated symptoms, aggravating/alleviating
factors

• Thorough environmental history

• Family history of atopy

• Suspected allergens

• Nasal trauma
Physical
• General appearance
▫ Allergic shiners, allergic salute, malaise

• Nose
▫ Septal deviation, polyps, drainage, turbinate hypertrophy, hyponasality

• Mouth
▫ Cobblestoning of oropharynx

• Ear
▫ Middle ear pathology

• Neck
▫ Lymphadenopathy, thyroid enlargement

• Chest
▫ Wheezing

• Skin
▫ Eczema, dermatitis
• Nasal signs

• Include transverse nasal crease due to constant

upward rubbing of nose simulating a salute (allergic
salute).

• Pale and oedematous nasal mucosa which may

appear bluish. Turbinates are swollen. Thin, watery
or mucoid discharge is usually present.

• Ocular signs

• Include oedema of lids, congestion and cobblestone

appearance of the conjunctiva, and dark circles
under the eyes (allergic shiners).
• Otologic signs

• Include retracted tympanic membrane or serous

otitis media as a result of eustachian tube blockage.

• Pharyngeal signs

• Include granular pharyngitis due to hyperplasia of

submucosal lymphoid tissue.
• Prolonged mouth breathing as seen in adenoid
hyperplasia.

• Laryngeal signs

• Include hoarseness and oedema of the vocal cords.

Differential Diagnosis
• Non-allergic rhinitis
▫ Infectious, NARES, vasomotor rhinitis, atrophic rhinitis,
drug induced, hormonally induced, exercise, reflex

• Structural/mechanical factors
▫ Septal deviation, turbinate hypertrophy, adenoid
hypertrophy, foreign body, tumor

• Inflammatory/immunologic
▫ Wegener’s, sarcoidosis, midline granuloma, SLE, Sjogren’s

• CSF rhinorrhea
Diagnosis of allergic rhinitis: Essential

• Detailed personal and family allergic history.

• Intranasal examination – anterior rhinoscopy

• History of eye symptoms

• Haematology – AEC / Total IgE

• Allergy skin tests performed by allergist, eg, skin tests

and/or

• Measurement of allergen specific IgE antibody in serum

(Radioallergosorbent tests) - RAST
Diagnosis of allergic rhinitis
Additional tests

• Nasal endoscopy

• Nasal secretions/scrapings for cytology (done rarely)

• Nasal challenge test with allergen, including

rhinomanometry

• CT scan
INVESTIGATIONS
• 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 non allergic

rhinitis,

• e.g. NARES (non allergic rhinitis with eosinophilia

syndrome).
INVESTIGATIONS
• 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
 Allergy skin prick testing

• Skin prick test / positive result

INVESTIGATIONS

• Specific IgE measurements.

• It is an in vitro test to find the specific allergen.

• There is a good correlation between the skin tests and

specific IgE measurements.

• However both false positive and false negative

• results can occur.

• It is therefore recommended to correlate the two tests

with clinical symptoms.
In vitro testing

• RAST (radioallergosorbent assay) measures antigen

specific IgE

• Safe and highly sensitive

• Better for patients taking beta-blockers (may be

impossible to treat anaphylaxis)

• Patients on antihistamines (skin testing is unreliable)

• Patients with dermatographism, and children that

cannot tolerate skin testing
RAST
• RAST is a radioimmunoassay test developed in
the late 60's for the detection of specific serum
IgE antibodies. Initial studies demonstrated a
96% efficiency, sensitivity and specificity.

• The modified RAST is the form now used,

introduced by Fadal and Nalebuff in 1977 with
the advantages of increased test sensitivity
without a loss in specificity.
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.

• More sophisticated techniques are available now.

CO MORBIDITIES
THE ALLERGIC INFLAMATION DOES NOT LIMIT ITSELF TO
THE NASAL AIRWAY . MULTIPLE CO MORBIDITIES HAVE
BEEN ASSOCIATED WITH RHINITIS…

OTITIS
MEDIA
WITH
EFUSION
UPPER
RESPIRATORY NASAL
INFECTION
POLYPOSIS
ALLERGIC
RHINITIS

ASTHMA SINUSITIS
 ARIA – Allergic Rhinitis & Its Impact on Asthma
CLASSIFICATION
Intermittent Persistent
. < 4 days per week . ≥ 4 days per week
. or < 4 weeks and ≥ 4 weeks

Moderate-severe
Mild
one or more items
• Normal sleep and
No impairment of daily . abnormal sleep
activities, sport, leisure . impairment of daily activities,
Normal work and sport, leisure
school
. abnormal work and school
• No troublesome
symptoms . troublesome symptoms
Step-wise management of allergic Rhinitis

Immunotherapy
Step 3

Pharmacotherapy
Step 2

Allergen Avoidance and

Step 1
Environmental Control
Allergen avoidance and environmental control

House dust mites:

▫ Provide adequate ventilation to

decrease humidity
▫ Wash bedding regularly at 60°C
▫ Use vacuum cleaner, Dispose of feather bedding
▫ Replace carpets with linoleum or wooden floors
▫ Remove curtains, pets and stuffed toys from bedroom
Pollen:

▫ Very difficult to avoid!

▫ Remain indoors with windows closed at peak
pollen times
▫ Wear sunglasses
▫ Use air-conditioning, where possible
• Pet Allergens Cockroach Allergens

▫ Exclude pets from ▫ Eradicate cockroaches with

bedrooms and, where appropriate insecticide
possible, from home
▫ Eliminate dampness, cracks
▫ Vacuum carpets, in floors, ceilings, cover
mattresses and upholstery food; wash surfaces,
regularly floors, fabrics to
remove
▫ Wash pets regularly allergen

Molds

▫ Ensure dry housing

▫ Use ammonia to remove mold from bathrooms and other wet
spaces
 Medical Management of Allergic Rhinitis as per new
ARIA guidelines

Intermittent Symptoms Persistent Symptoms

Mild Moderate-severe Mild Moderate-severe

Oral H1 blocker Intranasal Cs

and/or LTRA If nose very blocked
Oral H1 blocker Oral H1 blocker Intranasal H1 blocker and/or add oral CS or decongestant
Intranasal H1 and/or LTRA decongestant Intranasal CS or LTRA
decongestant Intranasal H1 Review patient
No Improvement : blocker and/or after 2-4 weeks
switch or add decongestant Improved
No improvement Not improved
LTRA Intranasal CS step up
Improved: continue for Step-down and Review
1 month continue diagnosis,
If intranasal CS treatment for > compliance, or
reduced by1/2 3 month other causes

Itch/sneeze/Rhinorrhoea Rhinorrhoea: Blockage: add LTRA or decongestant or

add H1 blocker add ipratropium oral CS (short term) or increase CS
 Pharmacotherapy

Medications used to treat allergic rhinitis:

Antihistamines
Decongestants
Antihistamine-decongestant combinations
Intra Nasal Corticosteroids
INCS + Antihistamine combinations
Mast Cell stabilizers
Anticholinergics
Antileukotrienes
Pharmacotherapy of allergic rhinitis

First generation oral antihistamines

• Chlorpheniramine, diphenydramine, promethazine.

• Use limited by sedative and anticholinergic effects

New generation oral antihistamines

• Azelastine, cetirizine, desloratadine, ebastine, fexofenadine,
levocetirizine, loratadine, mizolastine

• First line treatment for intermittent or mild persistent

allergic rhinitis
Mast cell Stabilisers

Disodium cromoglycate (DSCG) and nedocromil

• Prophylactic – Start before Exposure, Seasonal

• Require frequent administration:

DSCG four times/day,
Nedocromil two times/day

• Excellent safety profile for use in children and pregnancy

• Orally not active ; Only topical

Ketotefen
• Effective orally
Anti-cholinergic compounds

Ipratropium bromide

▫ Effective in controlling watery nasal discharge but not

sneezing or obstruction.

▫ Unwanted effects may include nasal dryness, irritation

and burning.

▫ Only topical action

▫ Mainly indicated in VMR (Chr. Rhinorrhoea Syndrome)

Decongestants

Oral Tablets (Pseudoephedrine)

▫ Less effective than sprays: no rhinitis medicamentosa

▫ Effective when combined with an oral antihistamine

▫ Usually avoided in:

Children <1 year, pregnancy, hypertension,

cardiopathy, prostatism, glaucoma
Decongestants

Topical Sprays

(Phenylephrine, Oxy/Xylo-metazoline)

▫ Very effective in treating nasal obstruction

▫ Limit treatment to 3-10 days depending on physician

recommendations

▫ Application for >10 days may lead to unwanted side

effects - Rhinitis medicamentosa
Antileukotrienes

Montelukast
• Less effective than inhaled corticosteroids and antihistamines

• May have additive effect with antihistamines

• Efficacy in aspirin-induced rhinitis and asthma

• Expensive

• Both Early and Late phase action

• Very effective in AR + Asthma

Topical corticosteroids

• Beclomethasone

• Budesonide

• Flunisolide

• Fluticasone

• Mometasone
Topical corticosteroids

• Most potent anti-inflammatory agents

• Effective in treatment of all nasal symptoms

including obstruction

• Once or twice daily administration

• Superior to antihistamines for all nasal symptoms

• First line pharmacotherapy for moderate-severe

persistent allergic rhinitis
Systemic corticosteroids

• Short courses (< 5 days) can be prescribed for severe

refractory symptoms (Oral)

• Use with caution in children and in pregnancy if no

alternative is available

• Concern regarding osteoporosis should limit use

• Intramuscular injections should be avoided

Immunotherapy
• Immunotherapy has been shown to be efficacious in treating
allergic rhinitis, asthma, and allergy.

• Successful immunotherapy is associated with:

▫ Shift from TH2 to TH1 lymphocyte immune response to allergen

▫ Immunologic tolerance – decline in allergen specific

responsiveness

▫ Increases in allergen specific IgG blocking antibody

▫ Relationship between efficacy and specific IgE titers are variable

Immunotherapy

• In patients with allergic rhinitis, must have symptoms of AR after

natural exposure to aeroallergen, demonstrable evidence of
clinically relevant specific IgE antibodies and one of the following:

▫ Poor response to pharmacotherapy or allergen avoidance

▫ Unacceptable adverse side effects to medications

▫ Coexisting AR and asthma

▫ Possible prevention of asthma in children

▫ Desire to avoid long-term pharmacotherapy

Immunotherapy

• In order to mix the immunotherapy vaccine, specific

allergens must be known

• Vaccine should use standardized extracts

• Immunotherapy requires a compliant patient, due to its long

duration

• Providers need to be prepared to handle patient with

anaphylaxis.
Types of immunotherapy

• Injectable vaccine – mainstay of therapy in the US

• Sublingual - used widely in Europe

• Intranasal - currently under investigation for children and

adults with allergic rhinitis.
Future directions

• >75% of allergic asthmatics have rhinitis

• >40% of allergic rhinitis patients have allergic conjunctivitis

• Humanized monoclonal antibodies against IgE, e.g. omalizumab are

effective for treatment of moderate to severe allergic asthma. Such
therapy:

▫ Decreases free IgE levels and down-regulates IgE receptors on mast

cells

▫ Preliminary study indicates omalizumab is effective for nasal and

ophthalmic symptoms of intermittent and persistent allergic
rhinitis
 VASOMOTOR RHINITIS

&

OTHER FORMS OF RHINITIS

Vasomotor rhinitis

• Inflammation of the nasal mucosa consequent to

imbalance in the autonomic nerve supply to the
nasal cavity

• Parasympathetic over activity—vasodilatation and

engorgement of the turbinates and increased
mucous secretion

• Sympathetic—opposite response
Nasal cycle

• Physiological cyclical events of congestion and

decongestion taking place alternating between the
two nasal cavities

• During quiet respiration we breath through one

side for some time and later through the other
‘Shift system’

• Controlled by autonomic nervous system

Nasal cycle is normally influenced
by-
• Climate • Exaggerated response
• to these trigger factors
Respiration
is vasomotor rhinitis
• Exercise
• Emotions
• Posture
• ‘Manifest form of nasal
• Endocrine
cycle’
• Drugs
Clinical features- symptoms
• Nasal symptoms triggered by the factors that affect
the nasal cycle

• Alternating nasal obstruction

• Early morning rhinorrhoea

• Watery-mucoid rhinorrhoea

• May be associated with allergic rhinitis

Signs & Diagnosis
• Enlarged reddish turbinates especially the
inferior turbinate

• No generalized mucosal congestion or odema

• Based on clinical presentation

• After ruling out other forms of rhinitis by

detailed history/ clinical examination and
investigations (diagnosis by exclusion)
Treatment

• Avoid triggering factors if possible

• Nasal decongestants: Topical/ systemic whenever

indicated

• Avoid long term use of decongestants

• Vidian neurectomy

• Turbinate reducing procedures

Rhinitis medicamentosa
• Chronic inflammation of the nasal mucosa due to
prolonged use of topical nasal decongestants

• After the effect of nasal decongestant wears off– rebound

congestion

• Tendency to use the more drug and more often—

tachyphylaxis (loss of responsiveness)—addiction

• Organic changes in the nasal mucosa

Pathology

• Prolonged use of nasal decongestants

• Edema and hypertrophy of the nasal mucosa

• ‘Crowded nose’

• Persistent nasal obstruction

Symptoms

• Nasal obstruction- bilateral

• Initially responds minimally to nasal decongestants and

later no response to it

• Persistent and total block—mouth breathing, snoring,

sleep apnoea syndrome, insomnia, irritability, day-time
somnolence, etc.

• Dry throat- recurrent pharyngitis/ laryngitis

• ET dysfunction—retracted drum--deafness
Signs

• Grossly edematous and congested nasal mucosa-

generalized

• Septal thickening

• Nasal airway reduced— ‘Crowded nose’

• Dry throat

• TM may be retracted
Treatment

• STOP NASAL DECONGESTANTS- Topical or systemic

• Systemic or topical steroids to reduce nasal edema

• SMD/ partial turbinectomy

Rhinitis of pregnancy

• Pregnant woman may develop rhinitis due to hormonal

changes. nasal mucosa becomes edematous and blocks
the airway.

• Generally ,local measures such as limited use of nasal

drops, topical steroids and limited surgery to turbinate's
are sufficient to relieve the symptoms.
Emotional rhinitis

• Psychological states like anxiety, tension, hostility,

humiliation, resentment and grief are all known to cause
rhinitis.

• Treatment is proper counseling, imipramine which has

both antidepressant and anticholinergic effects is useful.
Rhinitis due to hypothyroidism

• Hypothyroidism leads to hypo activity of the sympathetic

system with predominance of parasympathetic activity
causing nasal stuffiness and colds.

• Replacement of thyroid hormone relieves the condition.

Gustatory rhinitis
• Spicy and pungent food may in some people produce
rhinorrhea, nasal stuffiness,lacrimation,sweating and even
flushing of face.

• This is a cholinergic response to stimulation sensory receptors

on the palate.

• It can be relieved by ipratropium bromide nasal spray , a few

min before meals.
THANK YOU