The following CBME core competencies are covered in this chapter. PE31.1: Describe the aetiopathogenesis, management and prevention of Allergic Rhinitis in Children.

Allergic Rhinitis: Symptoms, Treatment, Notes & MCQs

What is allergic rhinitis?

Allergic rhinitis (AR) is a common IgE-mediated hypersensitivity reaction of the nasal mucosa to airborne allergens. It commonly causes sneezing, nasal itching, watery rhinorrhoea, and nasal obstruction. Patients may also develop itchy or watery eyes, itching of the palate, and throat irritation. Allergic rhinitis commonly occurs with allergic conjunctivitis and asthma. Therefore, clinicians should assess patients for these associated conditions.

These are important topics for MBBS, ENT PG, INI-CET, FMGE and NEET PG preparation, especially ARIA classification, pathogenesis, diagnosis, treatment and clinical cases.

In this chapter, you will learn: allergic rhinitis symptoms and signs, seasonal versus perennial disease, ARIA classification, IgE-mediated pathogenesis, diagnosis and allergy testing, treatment with intranasal corticosteroids and antihistamines, allergen immunotherapy, clinical cases, viva points, and NEET PG-style MCQs.

Definition

What are the four classic symptoms of allergic rhinitis?

Rhinitis is diagnosed clinically when the patient has two or more of the following symptoms:

• Nasal discharge or rhinorrhoea
• Sneezing
• Nasal obstruction
• Nasal itching

The symptoms usually occur for at least 1 hour on most days for two or more consecutive days. Allergic rhinitis should be considered when these symptoms occur because of exposure to a relevant allergen and are supported by evidence of allergic sensitisation. Allergic rhinitis is part of the unified allergic airway, which involves the lungs (asthma) and eyes (conjunctivitis).

Epidemiology

Allergic rhinitis affects 0.8–39.7% of the population worldwide, with a prevalence of about 23% in Western Europe. Prevalence has increased in recent decades, possibly due to urbanisation, pollution, and reduced early-life microbial exposure.

The hygiene hypothesis suggests that reduced early-life microbial exposure may alter immune development and increase the risk of allergic disease. 

• Natural History of Allergic Rhinitis: A family history of atopy increases the risk of allergic diseases in children. The atopic march describes the typical progression of allergic diseases during childhood: atopic dermatitis → food allergy → allergic rhinitis → asthma.
• Allergic Rhinitis and Asthma: Allergic rhinitis and asthma commonly coexist because they share similar type 2 inflammatory mechanisms. Patients with allergic rhinitis have an increased risk of asthma and should be assessed for wheezing, cough, and breathlessness.
• Course with Age: The severity of allergic rhinitis varies between individuals and may change with age. Symptoms may improve with age in some patients.

ARIA Classification of Allergic Rhinitis

The ARIA classification is the preferred clinical classification because it considers both duration and severity.

Classification According to Duration

• Intermittent: Symptoms occur <4 days per week OR for <4 consecutive weeks
• Persistent: Symptoms occur >4 days per week AND for >4 consecutive weeks

Classification According to Severity

• Mild: No sleep disturbance, impairment of daily activities, impairment of school/work, or troublesome symptoms
• Moderate–severe: One or more of the above problems are present

Seasonal and Perennial Allergic Rhinitis

• Seasonal Allergic Rhinitis (SAR): Symptoms occur during specific seasons when particular pollens (e.g., from trees, grasses, weeds) are airborne.
• Perennial Allergic Rhinitis (PAR): Symptoms occur throughout the year because of exposure to indoor or persistent allergens (indoor moulds, house dust mites, cockroach allergens, and animal allergens).

Aetiology

Allergic rhinitis develops when a genetically susceptible individual becomes sensitised to an allergen and subsequently develops an IgE-mediated response after exposure.

1. Airborne Allergens

• Seasonal Allergens: Pollens (trees, grasses, weeds) that vary geographically and seasonally.
• Perennial Allergens: Include dust mites (thriving in bedding and carpets), molds, animal dander, and cockroaches.

2. Genetic Predisposition. A strong familial association exists. Children with one allergic parent have a 20% risk, rising to 47% if both parents are allergic.

Pathogenesis

AR develops in genetically predisposed individuals exposed to inhaled allergens. It progresses through three distinct phases.

1. Sensitisation phase: During the first relevant exposure, the allergen is taken up by antigen-presenting cells, particularly dendritic cells. These cells present allergen-derived antigens to T-helper cells and promote a type 2 immune response. Type 2 cytokines, particularly IL-4 and IL-13, promote B-cell switching to produce allergen-specific IgE. The IgE antibodies then bind to high-affinity FcεRI receptors on mast cells and basophils. The patient is now sensitised.
2. Acute Phase: Occurs within 5–30 minutes post-exposure due to preformed mediators like histamine. On subsequent exposure, the allergen cross-links IgE molecules on mast cells. This causes mast-cell activation and degranulation. Preformed and newly generated mediators, particularly histamine and lipid mediators, produce symptoms within minutes. The major symptoms include: Sneezing + itching + watery rhinorrhoea + nasal obstruction.
3. Late Phase: Develops 2–8 hours later; inflammatory cells migrate into the nasal mucosa. These include Eosinophils, T-helper cells, Basophils, and other inflammatory cells. The late phase produces persistent mucosal inflammation, oedema, and nasal obstruction.

Functions of mediators

Mast cell mediators play a crucial role in the body’s response to allergic stimuli. These mediators are responsible for various physiological effects that contribute to the inflammatory response. Below is an overview of the primary mediators and their functions:

• Histamine: It causes vasodilation and bronchospasm, leading to increased blood flow to the affected area and constriction of the airways. This contributes to symptoms such as redness, swelling, sneezing, itching, and difficulty breathing.
• Leukotrienes: These are vasoactive and bronchospastic mediators. They are involved in sustaining inflammatory responses and can lead to prolonged bronchoconstriction, particularly in asthma. Leukotrienes are important in causing nasal blockage.
• Prostaglandins: These are vasoactive substances that also contribute to bronchospasm. They play a role in regulating inflammation, pain, and fever, thus amplifying the body’s response to allergens.
• Cytokines (IL-4, IL-5, IL-13): These promote TH2 inflammatory responses and IgE production, driving the allergic cascade.
• Tumour Necrosis Factor-alpha (TNF-α): It facilitates the transmigration of neutrophils and eosinophils to sites of inflammation, enhancing the recruitment of these cells and amplifying the body’s response to allergens.

Clinical Features

Allergic rhinitis can occur at any age, although it commonly begins during childhood or adolescence. 

Symptoms

The four classic symptoms are sneezing, nasal itching, watery rhinorrhoea, and nasal obstruction. Patients may also report itchy eyes, postnasal drip, palate itching, reduced smell, headache, sleep disturbance, fatigue, and reduced concentration. Sneezing, itching, watery discharge, and nasal obstruction together strongly suggest allergic rhinitis.

Seasonal vs Perennial Symptom Patterns: Seasonal allergic rhinitis typically presents with paroxysmal sneezing (10–20 sneezes in a row), nasal obstruction, watery discharge, nasal itching, and sometimes bronchospasm. Perennial allergic rhinitis typically presents with persistent nasal congestion, postnasal drip, loss of smell, chronic cough, and hearing impairment.

Clinical Signs

• Nasal Signs: Examination may show pale or swollen nasal mucosa, watery or mucoid nasal discharge, inferior turbinate enlargement, and nasal obstruction.
• Allergic Salute: Children may repeatedly rub the nose upward with the palm because of nasal itching. This is called the allergic salute. Repeated rubbing may produce a transverse nasal crease.
• Ocular Signs: Patients may develop conjunctival redness, lacrimation, periorbital oedema, and allergic shiners. Allergic shiners are dark discolouration below the eyes caused partly by venous congestion associated with chronic nasal obstruction.
• Pharyngeal and Ear Findings: Chronic nasal obstruction may cause mouth breathing, throat irritation, and postnasal drip. Children with chronic nasal inflammation may also develop Eustachian tube dysfunction and otitis media with effusion, particularly when adenoidal hypertrophy coexists. A retracted tympanic membrane may be seen in such cases.

Note: Hoarseness and laryngeal oedema are not typical features of uncomplicated allergic rhinitis and should prompt consideration of another diagnosis.

Red Flags (Not Typical of Allergic Rhinitis)

Certain symptoms are not typical of allergic rhinitis and should prompt further investigation. These include unilateral symptoms, purulent discharge, epistaxis, pain, cartilage or mucosal loss, cosmetic changes, systemic illness, and refractory bleeding. These findings should prompt evaluation for conditions such as foreign body, chronic infection, nasal polyps, granulomatous disease, malignancy, or other structural pathology.

Diagnosis

The diagnosis of allergic rhinitis is primarily clinical.

History: Ask about

• Sneezing, itching, rhinorrhoea and obstruction
• Seasonal or occupational variation
• Exposure to pets, dust or pollens
• Symptoms at home, school or workplace
• Family history of atopy
• Asthma symptoms
• Allergic conjunctivitis
• Effect on sleep, school, work and daily activities
• Previous response to treatment

The history should identify a consistent relationship between symptoms and allergen exposure.

Examination: Examine the nose, eyes, ears, pharynx, and chest. Nasal examination may show pale oedematous mucosa and watery secretions.

Investigations:

• Allergy Testing: Allergy testing is not necessary in every patient. Skin-prick testing or serum allergen-specific IgE testing is useful when identifying a specific allergen will change management, particularly when considering allergen immunotherapy. A positive allergy test indicates sensitisation; correlate with clinical history to confirm relevance.
• Nasal Smear: Nasal eosinophilia can support an allergic inflammatory pattern, but it is not routinely required to diagnose allergic rhinitis.
• RAST: Measures allergen-specific IgE levels.
• Nasal Provocation Test: Observes reactions after direct allergen exposure.

Allergic Rhinitis in Children

Allergic rhinitis is common in children and can significantly affect sleep, school performance, daily activities, and quality of life. It may also worsen coexisting asthma. Recurrent infective rhinitis is common in young children and may mimic allergic rhinitis. Symptoms lasting more than 2 weeks, especially with nasal or ocular itching, suggest an allergic cause. In a child with persistent nasal obstruction and a relatively normal nasal mucosa, adenoidal hypertrophy should be considered. Skin-prick testing can be performed in children when identifying the responsible allergen will help management. In younger children, testing the back may be easier than testing the forearm.

Treatment is broadly similar to that in adults. 

• Intranasal corticosteroids are highly effective, but correct nasal-spray technique may be difficult for young children.
• Non-sedating antihistamines are useful, particularly for sneezing, itching, and rhinorrhoea.
• Use age-appropriate intranasal corticosteroids at the recommended dose and monitor growth in children receiving prolonged corticosteroid therapy.
• Depot corticosteroids are not recommended for allergic rhinitis.
• Allergen immunotherapy may be considered in selected children with confirmed allergen-specific disease that remains troublesome despite appropriate treatment. The suitability and minimum age depend on the specific immunotherapy product and route.

Complications

1. Recurrent sinusitis.
2. Nasal polyps.
3. Serous otitis media.
4. Prolonged mouth breathing leads to orthodontic problems.

Treatment

1. Avoidance of Allergens: The first step in management is to reduce exposure to known allergens. Patients should remove pets if possible, use allergen-proof bedding, and avoid specific food allergens when identified. Complete avoidance is often difficult, so pharmacological treatment remains important.

2. Pharmacotherapy

• Antihistamines: These control sneezing, itching, and nasal discharge. First-generation antihistamines cause drowsiness; second-generation antihistamines (e.g., loratadine, cetirizine) are non-sedating and preferred for long-term use. Intranasal antihistamines (e.g., azelastine) provide rapid local relief and may be combined with intranasal corticosteroids.
• Decongestants: These reduce nasal congestion. Topical decongestants (e.g., xylometazoline) should be used for no more than 3–5 days because prolonged use can cause rebound congestion and rhinitis medicamentosa. Oral decongestants (e.g., pseudoephedrine) may cause insomnia, tachycardia, and tremor.
• Corticosteroids: Intranasal corticosteroids are the most effective treatment for all symptoms, especially nasal blockage. They have a slow onset of action (several hours to days), and full benefit may take up to 2 weeks. Topical forms minimise systemic side effects; epistaxis may occur due to incorrect spray technique.
• Mast Cell Stabilisers (e.g., Sodium Cromoglicate): These prevent mast cell degranulation and have a modest effect on symptoms. They require four times daily dosing, which limits compliance, but are safe for use in young children.
• Leukotriene Receptor Antagonists (e.g., Montelukast): Effective for both asthma and allergic rhinitis.
• Anti-IgE Therapy (e.g., Omalizumab): This reduces IgE levels and is especially useful for coexisting asthma.

3. Immunotherapy: Immunotherapy is administered subcutaneously (SCIT) or sublingually (SLIT). It reduces IgE levels and raises IgG levels over time. It is recommended for refractory cases and can modify the disease course, offering long-lasting symptom reduction even after treatment has stopped. Treatment is usually continued for 3 years.

4. Biologics (Monoclonal Antibodies): Newer biologic agents are available for severe allergic disease, especially when associated with asthma.

• Omalizumab: Anti-IgE monoclonal antibody. Reduces all nasal symptoms and improves asthma control. Given monthly by injection. Reserved for severe allergic asthma with or without rhinitis.
• Dupilumab: Anti-IL-4 receptor antibody. Inhibits IL-4 and IL-13, key drivers of TH2 inflammation. Improves symptoms in patients with allergic rhinitis and asthma.
• Tezepelumab: Blocks thymic stromal lymphopoietin (TSLP), which is important in initiating airway inflammation.
• Tralokinumab: Anti-IL-13 antagonist.

Biologics are reserved for severe allergic disease, especially when associated with asthma.

5. ARIA Stepwise Treatment Approach: Treatment should depend on symptom severity, frequency, and response to previous treatment.

• For mild or intermittent symptoms, use an oral or intranasal antihistamine. Antihistamines are particularly effective for sneezing, nasal itching, and rhinorrhoea, but they provide less relief from nasal blockage.
• For persistent or moderate-to-severe symptoms, intranasal corticosteroids (INCS) are the most effective treatment. They improve nasal obstruction, sneezing, itching, and rhinorrhoea. An intranasal antihistamine can be added when symptoms remain troublesome. A fixed combination of INCS and intranasal antihistamine provides greater symptom control than either alone. 
• For inadequately controlled symptoms, reassess the diagnosis, treatment technique, adherence, and allergen exposure. Selected patients with persistent, allergen-specific disease may benefit from allergen immunotherapy.
• Systemic corticosteroids may be used as a short course in selected severe cases.
• Topical nasal decongestants may provide short-term relief but should generally be used for no more than 3–5 days because prolonged use can cause rhinitis medicamentosa.

6. Nasal Spray Technique (Viva Point): Aim the nozzle slightly outward, away from the nasal septum. Incorrect spray direction towards the septum increases the risk of epistaxis.

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NEET PG-Style MCQs

1. The most characteristic combination of symptoms in allergic rhinitis is: A. Fever, facial pain, purulent discharge and anosmia B. Sneezing, nasal itching, watery rhinorrhoea and nasal obstruction C. Epistaxis, crusting, anosmia and facial pain D. Unilateral obstruction, foul discharge and epistaxis
2. According to the ARIA classification, persistent allergic rhinitis is defined as symptoms: A. >4 days/week OR >4 consecutive weeks B. >4 days/week AND >4 consecutive weeks C. <4 days/week AND <4 consecutive weeks D. Daily for exactly 4 weeks
3. Which cytokine is most closely associated with eosinophil growth and survival? A. IL-2 B. IL-4 C. IL-5 D. IL-10
4. The antibody that binds to FcεRI receptors on mast cells during allergic sensitisation is: A. IgA B. IgE C. IgG D. IgM
5. The most effective single pharmacological treatment for nasal obstruction due to allergic rhinitis is: A. Oral antihistamine B. Intranasal corticosteroid C. Oral decongestant D. Sodium cromoglicate
6. A positive skin-prick test in a patient with rhinitis indicates: A. Definite clinical allergy B. Sensitisation that must correlate with the clinical history C. Bacterial infection D. Non-allergic rhinitis
7. Prolonged use of topical nasal decongestants may cause: A. Atrophic rhinitis B. Nasal polyposis C. Rhinitis medicamentosa D. Allergic fungal rhinosinusitis
8. Which finding is most suggestive of allergic rhinitis in a child? A. Unilateral foul-smelling nasal discharge B. Recurrent sneezing with nasal and ocular itching C. High fever with purulent nasal discharge D. Persistent unilateral epistaxis
9. Which drug should not routinely be used as first-line monotherapy for uncomplicated allergic rhinitis because of its neuropsychiatric safety concern? A. Mometasone B. Fexofenadine C. Montelukast D. Budesonide
10. Which treatment can provide disease-modifying benefit in selected patients with clinically relevant allergen sensitisation? A. Allergen immunotherapy B. Topical decongestant C. Oral decongestant D. Sodium cromoglicate

MCQ Answer Key: 1: B. 2: B. 3: C. 4: B. 5: B. 6: B. 7: C. 8: B. 9: C. 10: A.

Clinical Case-Based Questions

Case 1

A 12-year-old boy presents with recurrent bouts of sneezing, nasal itching, watery nasal discharge and nasal obstruction. Symptoms worsen when he cleans his bedroom. Examination shows pale oedematous inferior turbinates and watery secretions. Most likely diagnosis: Allergic rhinitis. Most appropriate initial treatment: Intranasal corticosteroid, with appropriate spray technique. Additional assessment: Ask about asthma and allergic conjunctivitis and identify clinically relevant allergen exposure.

Case 2

A 9-year-old child has persistent nasal obstruction, mouth breathing and snoring. There is no significant nasal itching or sneezing. Nasal mucosa appears relatively normal. Most likely diagnosis: Adenoidal hypertrophy rather than uncomplicated allergic rhinitis. Best next step: Examine the nasopharynx/adenoids using an appropriate clinical or endoscopic assessment. Management: Treat according to the severity of adenoidal disease and associated complications.

Case 3

A 25-year-old woman develops sneezing, nasal itching and watery rhinorrhoea every spring. Symptoms interfere with outdoor activities despite appropriate intranasal corticosteroid use. Testing demonstrates sensitisation to a pollen that matches her exposure history. Most likely diagnosis: Seasonal allergic rhinitis. Best next step: Optimise pharmacotherapy and discuss allergen immunotherapy if symptoms remain troublesome and the allergen is clinically relevant. Potential disease-modifying treatment: SCIT or SLIT, depending on allergen, product and suitability.

Case 4

A 35-year-old man uses xylometazoline nasal spray several times daily for several weeks because of persistent nasal obstruction. He now develops severe nasal blockage whenever he stops the spray. Most likely diagnosis: Rhinitis medicamentosa. Management: Stop the prolonged topical decongestant and institute appropriate anti-inflammatory treatment, commonly with an intranasal corticosteroid, while addressing the underlying rhinitis.

Frequently Asked Questions

1. What are the four classic symptoms of allergic rhinitis? The four classic symptoms are sneezing, nasal itching, watery rhinorrhoea, and nasal obstruction.
2. What is the ARIA classification of allergic rhinitis? ARIA classifies allergic rhinitis according to duration as intermittent or persistent and according to severity as mild or moderate–severe.
3. What is the best treatment for allergic rhinitis? Intranasal corticosteroids are a preferred and highly effective single-agent treatment, particularly when nasal obstruction is prominent.
4. What causes allergic rhinitis? Allergic rhinitis occurs when a sensitised person develops an IgE-mediated inflammatory response after exposure to a clinically relevant allergen.
5. What is the difference between seasonal and perennial allergic rhinitis? Seasonal allergic rhinitis is associated mainly with seasonal allergens such as pollens, whereas perennial disease is associated with persistent exposures such as house dust mites and animal allergens.
6. Is allergy testing necessary in allergic rhinitis? No. Allergy testing is not required for every patient. It is particularly useful when identifying a specific allergen will change management, such as when considering allergen immunotherapy.
7. Can allergic rhinitis cause asthma? Allergic rhinitis and asthma commonly coexist and share important type 2 inflammatory mechanisms. Patients with significant rhinitis should therefore be assessed for asthma symptoms.
8. What is the role of montelukast in allergic rhinitis? Montelukast is effective for both asthma and allergic rhinitis.
9. Can allergic rhinitis be permanently cured? Symptoms can usually be controlled effectively. Allergen immunotherapy can provide long-term disease-modifying benefit in appropriately selected patients.
10. How should an intranasal spray be used? The nozzle should generally be directed slightly away from the nasal septum to improve deposition and reduce the risk of epistaxis.

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Reference Textbooks.

• Scott-Brown, Textbook of Otorhinolaryngology-Head and Neck Surgery.
• Cummings, Otolaryngology-Head and Neck Surgery.
• Stell and Maran’s, Textbook of Head and Neck Surgery and Oncology.
• P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
• Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
• Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck Surgery.
• Hans Behrbohm, Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.

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Keywords: Allergic rhinitis, Allergy rhinitis treatment, Seasonal allergies, Hay fever, Allergic rhinitis symptoms, Rhinitis causes, Allergic rhinitis management, Treatment for allergic rhinitis, Chronic rhinitis, Allergy relief