allergic rhinitis and nasal polyps

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ALLERGIC RHINITIS 

Dr Ravikumar MS(ENT)

 Assoc Prof 

Raichur Institute Of Medical Sciences

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Objectives

• Understanding what allergic rhinitis is

• How to recognize allergic rhinitis

• Treatment

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Definition

Allergic rhinitis (AR) = IgE mediated immunologicresponse of nasal mucosa to air borneallergens,characterised by

• Nasal congestion

• Nasal pruritis

• Rhinorrhea

• Sneezing

Nasal sx lasting > 1 hr on most days.

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Ages affected

• Not seen until after age 4 or 5.

 – (Takes approx 3 pollen season exposures).

• 10-15% in adolescents (adolescents and

young adults).

• Peak age 30 (decades 2, 3 and 4).

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Predisposition

• Genetic:

 – Positive FHx (polygenic inheritance)

 – Negative FHx does not rule out dx of AR

• Atopic dermatitis:

 – Early sign of predisposition to allergy.

• Previous exposure/environmental factors

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Comorbidities ass’d with AR 

• Asthma

• Sinusitis

• Otitis Media (with effusion)

(AR occurs frequently in pts with asthma and

atopic dermatitis.)

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Types of Allergic Rhinitis

• Seasonal (intermittent sx)

• Perennial (chronic & persistent sx)

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Seasonal Rhinitis

• Pollen:  – Spring = Trees 

 – Summer = Grass 

 – Fall = Weeds 

• Mold:

 – Spores in outdoors have seasonal variation(reduced #’s in winter, increased in

summer/fall due to humidity).• House dust mites: 

 – Generally a “perennial” allergen, but may beincreased in damp autumn months.

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Perennial Rhinitis• Fungi/mold: 

 – Exposure peaks accompany activities such asharvesting, cutting grass and leaf raking.

• Pet Dander (cats, dogs):

 – Can linger up to 4 months after pet removal.

• House dust mites: 

• Cockroaches: – Respiratory allergy

food allergens-

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Pathophysiology of Allergic Rhinitis

Source: Cumming’s Otolaryngology: Head & Neck Surgery 

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Symptoms

Direct:• Nasal congestion

• Rhinorrhea

• Pruritis• Sneezing

• Eye tearing & pruritis

• Ear & palate pruritis

• Post nasal drip

• Anosmia

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Symptoms

Non-nasal:

• Sore throat

• Chronic cough

• Mouth breathing

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Symptoms

Psychosocial/Cognitive:• Fatigue

• Depression

• Irritability• Anxiety

• Sleep disturbance

• Poor concentration• Impaired learning, decision making and

psychomotor speed

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Diagnosis

• History

• Physical exam

• Skin prick testing, Nasal smear,

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History• General medical hx

• Rhinological sx – (environmental and/or occupational factors)

• Family Hx

• Frequency of sx – (daily, episodic, seasonal, perennial)

• Duration

• Severity (increased, decreased or same)

• Qualitate nasal discharge: – AR: clear and watery

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Physical exam

Nose 

• Nasal mucosa classically pale blue, but not

diagnostic (60%).

• Thick yellowish secretions suggest

infection.

• Structural deformities that may impede air

flow (deviated nasal septum, nasal polypys,hypertrophied turbinates).

• “Allergic Salute” 

• “Dennie-Morgan” line 

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Eyes

• “Allergic Shiners” 

• Conjunctivitis

• Tearing

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drtbalu's otolaryngology online 18

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Ears• Fluid

• Infection

Lungs

•Wheezing

• Persistent coughing

Other areas 

• Stigmata of atopic diseases in conjunctionwith nasal sx:

 – atopic eczema, asthma

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Skin Prick Testing

• IgE-mediated rxn (Type I).

• Small, but significant potentail for

anaphylactic rxn.• Wheal & flare response (15-20 minutes)

• Includes a “positive” and “control” soln. 

• Positive rxn = over 3cm wheal with ass’d flare

and pruritis (no rxn to neg control).

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In vitro serum test (RAST)

• Radioallergosorbent test

• Serum levels of specific IgE antibodies.

• No longer performed• IMMUNOCAP  – newer technology widely

performed

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Nasal smears

• Eosinophils may help differentiate “allergic”

from “infectious” rhinitis (neutrophils).

• Peripheral blood eosinophil counts 

 – does not assist in allergy diagnosis.

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Allergic Rhinitis

• Therapeutic options – Avoidance

 – Intranasal steroids

 – Antihistamines

 – Decongestants

 – Anticholinergics

 – Cromolyn

 – Leukotriene modifiers

 – Systemic steroids

 – Immunotherapy

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Antihistamines

First Generation

• diphenhydramine• Mechanism: inhibition of histamine (H1)

receptors.

• Effect: reduce sneezing, nasal pruritis andrhinorrhea, but not congestion.

• Side Effects: anticholinergic activity -->

adverse CNS effects.

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Antihistamines

Second Generation

• cetirizine, loratadine, fexofenadine• Mechanism: inhibit histamine (H1)

receptors.

• Effect: same as First generation.• Note:

 – Nonsedating

• Topical preparation available

 –Azelastine

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Decongestants (oral/topical)• i.e.: Oral

 – Pseudoephedrine

 – Phenylephrine• Topical

 – More effective than systemic

 – Oxymetazoline (0.05%)

 – Phenylephrine (1%)

• Mechanism: alpha-adrenergic agonist.

• Effect: vasoconstriction

•Side effects: – Oral: HA, nervousness, irritability, tachycardia,

palpitations, insomnia.

 – Topical(nasal): prolonged use (>5-7 days) leads torhinitis medicamentosa

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Corticosteroids (intranasal)

• i.e: Fluticasone, mometasone

• Mechanism:

• Effect: reduce nasal blockage, pruritis,

sneezing and rhinorrhea

C ti t id ( ti d)

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Corticosteroids (continued)Note: Fluticasone,mometasone

• most potent single medication for tx of AR.

• intanasal: acts locally.

• goal: control sx with lowest possible dose.

• >90% achieve symptomatic relief.

Side effects: nasal irritation, bleeding (nasal

septal perforation).

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Cromolyn Sodium (intranasal)

• Mechanism: mast cell stabilizing agent -->reduces release of histamine and othermediators.

• Effects: reduces nasal pruritis, sneezing,

rhinorrhea and congestion.

• Note:

 – prophylactic use: start before pollinosis sx or

unavoidable/predictable exposures.• Side effects: locally, <10% of pts (sneezing,

nasal stinging, burning, irritation).

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Ipratropium (intranasal)• i.e.: Atrovent (intransal)

• Mechanism: inhibits muscarinic cholinergicreceptors.

• Effect: reduces watery rhinorrhea (no effect

on nasal itching, sneezing or nasalcongestion).

• Side effects: irritation, crusting, epistaxis.

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Leukotrine inhibitors

• Monteleukast – new medication

Equal in effectiveness to antihistamines

» Combination of monteleukast and an

antihistamine superior to each agent alone

All i Rhi iti

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Allergic Rhinitis• Therapeutic options

 – Immunotherapy• Reserved for unavoidable allergens and inadequate response

to standard therapies

• Effects- Rise in serum-specific IgG

 – Suppression of IgE

 – Shift from TH2 to TH1 profile

 – Reduction of inflammatory cells in the nasal mucosa and secretions

• Onset of action 12 weeks after starting therapy, increases slowly over 1-2 years

• Subcutaneous (SCIT)

 – Antigen extract is injected into the skin

• Sublingual (SLIT) – Antigen is applied under the tongue

 – Widely used in Europe

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NASAL POLYPI 

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Definition

• The term polyp derived from Latin word

“Polypous” Many footed 

• Defined as simple oedematous hypertrophic

nasal mucosa

• Can be unilateral / bilateral

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• Simple nasal polyp1

• Fungal polyp2

• Malignant polyp3

Classification

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Simple nasal polypi

• Also known as

inflammatory polyp

• Ethmoidal polyp

• Antrochoanal polyp

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Aetiology

• Chronic rhinosinusitis

• Asthma

• Autonomic nervous system dysfunction• Genetic predisposition

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Aetiology

• aspirin intolerance

• Cystic fibrosis• Allergic fungal sinusitis

• kartagener’s syndrome

• Young’s syndrome • Nasal mastocytosis

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Site of origin

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Examination

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Examination

• Smooth glossy multiple

mass seen in anterior

rhinoscopy• Insensitive on probing.

Probe can be passed

around the polyp

• Soft and mobile

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Malignant polypi

• Also known as sentinel polyp

• Caused due to mucosal oedema resulting

from the malignant tumor

• All nasal polypoidal mass removed from

elderly patients should be subjected to HPE

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45

/ l h f

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A/C polyp theories of 

etiopathogenesis

• Proetz theory

• Bernoulli’s phenomenon 

• Mucopolysaccharide changes

• Infections

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Bernoulli’s phenomenon 

Pressure drop occurs next to the constriction.

This causes a suction effect pulling the sinus

mucosa into the nasal cavity.

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Mucopolysaccharide theory

• Proposed by Jakson

• Changes in the mucopolysaccharide present

in the ground substance causes nasal

polyposis

• These changes causes excessive water

retention causing swelling of nasal mucosa

which appears polypoidal

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Infection / inflammation

• Acinous mucous glands inside the antrum

gets blocked

• This forms a cystic lesion within the sinus

cavity

• This cyst gradually enlarges to completely fill

the antrum

• It exits via the accessory ostium to reach the

nasal cavity

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R f t i i ti f AC

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Reasons for posterior migration of AC

polyp

• The accessory ostium is present posteriorly

• Inspiratory air current is more powerful than

expiratory current there by pushing the polyp

posteriorly

• The natural slope of nasal cavity is directed

posteriorly

• Cilia beats towards the choana

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P i

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Posterior

rhinoscopy

• Polyp can be seen atthe level of choana

• Antrochoanal polyp

can be seen exitingout of accessory

ostium

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Parts of antrochoanal polyp

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Differential diagnosis

• Meningocele

• Angiofibroma

• Sq cell carcinoma

• Enlarged turbinates

• Inverted papilloma

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Radiology

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Medical Management

• Antihistamines ?

• Nasal decongestant

• Steroids

• Antibiotics ?

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Treatment

• Traditional polypectomy

• Caldwel Luc procedure 

• Microdebrider• Endoscopic sinus surgery

• Recurrence

 – Multiple small polyps common – Large and antro-coanal less so

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AC polyp / Ethmoidal polypi

Ethmoidal polypi Antrochoanal polyp

Seen in adults Seen in children and adolescents

Allergy is the common cause Infection is the common cause

Multiple (bunch of grapes) Unilateral

Arises from ethmoidal labyrinth Arises from maxillary antrum

Seen easily on anterior rhinoscopy Seen commonly in post nasal exam

X ray PNS may show hazy ethmoids and

normal maxillary sinuses

X ray PNS shows hazy maxillary antrum

Mostly bilateral Usually unilateral

Recurrence is common Recurrence is uncommon

Polypectomy Caldwel luc surgery in recurrent cases

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