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Rhinitis - Medicine Viva Guide

Definition

Rhinitis is inflammation of the nasal mucosa characterized by one or more of the following: nasal congestion, rhinorrhea (anterior or posterior), sneezing, and nasal itching. It is broadly divided into allergic and non-allergic subtypes.

Classification

Type	Key Features
Allergic Rhinitis (AR)	IgE-mediated, seasonal or perennial
Non-allergic (Vasomotor)	Profuse clear rhinorrhea, no allergen trigger
Non-allergic with Eosinophilia (NARES)	Eosinophils on nasal smear, negative allergy tests
Infectious	Viral (most common), bacterial, fungal
Drug-induced	OCP, reserpine, beta-blockers, rhinitis medicamentosa
Granulomatous	Sarcoidosis, Granulomatosis with Polyangiitis (Wegener's)
Hormonal	Pregnancy, hypothyroidism
Atrophic	Crusting, foul smell (ozena)
Mechanical/Obstructive	Septal deviation, adenoid hypertrophy, foreign body

Cummings Otolaryngology Head and Neck Surgery

Allergic Rhinitis (AR) - The Most Important Type

Epidemiology

AR ranks 5th among all chronic diseases in the US in terms of economic impact, with estimated annual direct costs of up to $5 billion. It accounts for ~3.5 million lost workdays per year. About 80% of patients with allergic asthma also suffer from AR, and AR is an independent risk factor for developing asthma.

Classification of AR

Seasonal (Hay Fever): Triggered by outdoor allergens - tree pollens (spring), grass pollens (summer/early fall)
Perennial: Year-round symptoms - triggered by indoor allergens: house dust mites, cat dander (most common animal allergen), cockroaches, indoor mold
Dust mites peak from August to December

Pathophysiology

Phase 1 - Sensitization

Allergen is deposited on nasal mucosa and taken up by antigen-presenting cells (APCs)
Mucosal epithelial cells secrete TSLP, which matures dendritic cells into TH2-promoting subtypes
TH2 cells drive B cells to produce allergen-specific IgE antibodies
IgE binds to high-affinity receptors (FcεRI) on mast cells and basophils

Key cytokines:

IL-4 and IL-13 → Enhanced IgE production
IL-5 → Enhanced eosinophil activity and prolonged eosinophil survival
IL-9 → Bronchial hyperreactivity

Phase 2 - Early Phase Reaction (within minutes)

On re-exposure, allergen cross-links IgE on mast cells → mast cell degranulation → release of:

Preformed mediators: Histamine, tryptase, kinins
Newly synthesized: Prostaglandins, leukotrienes, PAF

Results in: sneezing, watery rhinorrhea, nasal itching, congestion (within minutes)

Phase 2 - Late Phase Reaction (4-8 hours later)

Chemoattractants and adhesion molecules (ICAM-1, VCAM-1) recruit inflammatory cells:

Eosinophils, basophils, CD4+ lymphocytes, monocytes
These cells release a second wave of mediators
Nasal congestion dominates the late phase
Goldman-Cecil Medicine, p. 2355

Priming Phenomenon

A hallmark of AR - after repeated allergen exposure, the threshold dose to elicit symptoms decreases more than 5-fold by day 4 of consecutive challenges. This explains why patients worsen as the allergy season progresses even when pollen counts fall, and why they become hypersensitive to non-specific irritants (perfume, smoke, cold air).

Clinical Features

Classic Signs ("Allergic Stigmata")

Sign	Description
Allergic salute	Upward palm thrust against nose to relieve itching; causes a supratip crease at the junction of upper/lower lateral cartilages
Allergic shiners	Dark circles under eyes due to venous stasis
Dennie-Morgan lines	Extra wrinkle folds under the lower eyelid
Adenoid facies	Open mouth, high arched palate, long face, retracted jaw - from chronic mouth breathing

Symptoms

Paroxysmal sneezing
Watery (clear) rhinorrhea
Nasal congestion and pruritus
Conjunctival and pharyngeal itching
Postnasal drip
Loss of smell and taste
Nasal speech quality

Complications

Serous otitis media (1/3 to 1/2 of children with AR) - eustachian tube dysfunction
Rhinosinusitis - edematous mucosa obstructs sinus ostia
Nasal polyps (pearl-gray gelatinous masses - unusual in uncomplicated AR alone)
Sleep disturbance, snoring, sleep apnea-like symptoms
Asthma - 80% of asthmatic patients have AR
Epistaxis in children (from nose picking due to irritation)
Maxillomandibular alignment problems (overbite/underbite) from chronic mouth breathing

Nasal Examination Findings

Pale, bluish, edematous inferior turbinates (NOT pathognomonic)
Thin, clear secretions
No appearance is pathognomonic for AR

Diagnosis

1. History

Seasonal pattern, family history of atopy
Late-evening or early-morning symptoms suggest dust mite allergy
Improvement with change of environment

2. Nasal Smear (Hansel's Stain)

Eosinophils support allergic diagnosis but are not diagnostic alone
Elevated peripheral eosinophilia may support diagnosis (but can be absent)

3. Skin Prick Testing (SPT) - Gold Standard

Allergen applied epicutaneously with a lancet (1 mm depth)
Wheal ≥ 3 mm larger than negative control = positive
Sensitivity: 80-100%, Specificity: 70-90%
Stop antihistamines 2-7 days before testing
Contraindications: Severe asthma, history of anaphylaxis, beta-blocker use, pregnancy

4. Serum-Specific IgE (RAST/ImmunoCAP)

Less sensitive than SPT for inhalant allergens
Useful when SPT is contraindicated

5. Local Allergic Rhinitis (LAR) - Important Concept

A subset of patients have typical AR symptoms but negative skin testing and serum IgE. These patients have a localized nasal IgE response without systemic atopy. Diagnosis by nasal allergen challenge. Prevalence may be 47-62% of patients with perennial symptoms who test negative systemically.

Treatment

Step 1: Environmental Control (Allergen Avoidance)

Air conditioning with HEPA filters
Impermeable encasings for pillows and mattresses
Wash linens in hot water
Remove carpets, avoid fans and cool-mist vaporizers
Masks with microfoam filters for dust allergy

Step 2: Pharmacotherapy

Drug Class	Examples	Key Notes
Intranasal Corticosteroids (INCS)	Fluticasone, mometasone, budesonide	Most effective single agent for AR; reduces all nasal symptoms
Oral 2nd-gen Antihistamines	Loratadine, cetirizine, fexofenadine, levocetirizine, desloratadine	Less sedating than 1st gen; good for sneezing and rhinorrhea
Intranasal Antihistamines	Azelastine, olopatadine	Onset within minutes; may cause bitter taste or mild somnolence
Leukotriene Receptor Antagonists (LTRA)	Montelukast	Useful especially in AR with concurrent asthma
Topical Decongestants	Oxymetazoline, xylometazoline	Max 3 days use only - prolonged use causes rhinitis medicamentosa (rebound swelling)
Oral Decongestants	Pseudoephedrine, phenylephrine	No rebound, but less effective; side effects: insomnia, HTN, arrhythmias
Intranasal Ipratropium	Ipratropium bromide spray	Targets rhinorrhea; little effect on congestion
Saline irrigation	-	Thins secretions, mechanically clears allergens

Rhinitis Medicamentosa - Caused by prolonged use (>3 days) of topical decongestants; leads to rebound mucosal swelling and then chronic mucosal inflammation. Treatment = stop the topical decongestant.

Step 3: Allergen Immunotherapy (AIT) - Disease-Modifying

Two routes:

Subcutaneous Immunotherapy (SCIT): Injections started at dilute dose, escalated weekly over months to maintenance, then monthly. Introduced since 1911. Evidence from multiple systematic reviews.
Sublingual Immunotherapy (SLIT): Alternative route

Mechanism: Shifts immune response from TH2 to TH1/Treg dominance; IL-10 and Treg cells suppress total and allergen-specific IgE, increase IgG4 ("blocking antibody"), downregulate eosinophil function, decrease mast cell/basophil activation threshold.

Indications: Failed pharmacotherapy, desire for durable benefit, high risk for asthma or new sensitizations.

Contraindications to SCIT: Poorly controlled asthma, active autoimmune disease, malignancy, pregnancy (to initiate; maintenance can continue if pregnancy occurs during treatment).

Non-Allergic Rhinitis

Vasomotor (Idiopathic) Rhinitis

Perennial, profuse clear rhinorrhea and congestion
No allergen correlation, no eosinophilia
Triggers: temperature changes, strong odors, smoke, alcohol, exercise

NARES (Non-Allergic Rhinitis with Eosinophilia Syndrome)

Most common in adults
Eosinophilia on nasal smear
Negative allergy test results for specific allergens
Responds to intranasal steroids

Drug-Induced Rhinitis

Oral contraceptives, reserpine, hydralazine, beta-blockers (even eye drops), topical decongestants (rhinitis medicamentosa)

Key Viva Points to Remember

Rhinitis medicamentosa = rebound congestion from topical decongestants used >3 days
AR + asthma link: 80% of asthmatic patients have AR; AR is a risk factor for asthma - "one airway, one disease"
Pale, edematous turbinates are characteristic but NOT pathognomonic for AR
Nasal polyps are pearl-gray and gelatinous - unusual in uncomplicated AR alone; their presence should raise suspicion of complicating factors
Skin prick test threshold: wheal ≥3 mm above negative control = positive
Stop antihistamines before skin prick testing (2-7 days depending on half-life)
Pregnancy = contraindication to initiating SCIT, but maintenance can be continued
Local Allergic Rhinitis (LAR) = AR symptoms + negative systemic tests + positive nasal challenge
INCS are the most effective single pharmacological class for AR
1% to 2% of viral URIs (common colds) progress to bacterial sinusitis

Sources: Cummings Otolaryngology Head and Neck Surgery; Goldman-Cecil Medicine; Textbook of Family Medicine 9e

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