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Allergic rhinitis

SNOMED: 61582004874 words•Updated 03/03/2026
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Exam Tips

  • Classify severity using impact: mild (no sleep/activity impairment) vs moderate-severe (sleep, school/work, leisure affected).
  • Intermittent means <4 days/week or <4 weeks; persistent means >=4 days/week and >=4 weeks.
  • Unilateral symptoms, epistaxis, facial pain, anosmia, foul/discoloured discharge, or onset <2 years should trigger search for alternative diagnoses.
  • In OSCEs, ask about trigger timing (tree spring, grass early summer, weeds longer season, mite worse on waking, occupational improvement on days off).
  • For prescribing stations: intranasal steroid is usually first-line; always counsel spray technique, adherence, and epistaxis risk.
  • Image cue for viva revision: inspect an ENT atlas image showing pale boggy inferior turbinates and conjunctival injection in allergic rhinoconjunctivitis (see figure in your core ENT chapter on rhinitis).

Definition

Allergic rhinitis is a chronic, IgE-mediated inflammatory disorder of the nasal mucosa triggered by exposure to aeroallergens such as pollens, house dust mite, moulds, or animal dander. It typically causes sneezing, watery rhinorrhoea, nasal itch, and congestion, and is classified clinically by duration (intermittent vs persistent) and impact on function (mild vs moderate-severe).

Pathophysiology

Disease begins with sensitisation: inhaled allergen is presented to T-helper-2 lymphocytes, driving IL-4/IL-13 mediated class switching to allergen-specific IgE. IgE binds mast cells in nasal mucosa; on re-exposure, mast-cell degranulation (histamine, leukotrienes, prostaglandins) causes the early phase (itch, sneeze, rhinorrhoea). A late inflammatory phase follows (eosinophils, basophils, T cells; IL-5 dominant), producing persistent mucosal oedema and nasal blockage. This upper-airway inflammation is linked to lower-airway disease ("united airway" concept), explaining strong comorbidity with asthma.

Risk Factors

  • Family history of atopy, especially parental allergic rhinitis
  • Personal atopic history (eczema, asthma) and childhood food allergy
  • Repeated exposure to aeroallergens (house dust mite, pollens, moulds, animal dander)
  • Occupational exposure (e. g, flour, wood dust, latex, laboratory animals, chlorine-containing environments)

Clinical Features

Symptoms

  • Paroxysmal sneezing
  • Nasal itching
  • Watery rhinorrhoea
  • Nasal obstruction/congestion (often bilateral)
  • Postnasal drip and cough
  • Itchy, red, watery eyes (allergic rhinoconjunctivitis)
  • Snoring, mouth breathing, sleep disturbance
  • Symptoms linked to trigger pattern (seasonal pollen, perennial indoor allergens, work-related variation)

Signs

  • Pale or bluish, oedematous nasal mucosa with clear secretions
  • Conjunctival injection/lacrimation
  • Allergic shiners and Dennie-Morgan lines
  • Transverse nasal crease from repeated 'allergic salute'
  • Mouth breathing in chronic nasal obstruction

Investigations

Clinical diagnosis from focused allergy history:Typical bilateral itch/sneeze/rhinorrhoea/congestion pattern with identifiable triggers and exclusion of red flags
Skin-prick testing (specialist/allergy service or trained setting):Immediate wheal-and-flare response to relevant allergen
Serum allergen-specific IgE:Positive specific IgE to suspected allergen when skin testing is unavailable/unsuitable
Assessment for comorbid asthma (history, peak flow/spirometry as indicated):Variable airflow obstruction or suggestive symptoms supporting united airway disease
ENT assessment or nasal endoscopy (if atypical/unilateral/red-flag features):Helps identify alternative diagnoses such as polyps, foreign body, structural lesions, tumour, or CSF leak

Management

Lifestyle Modifications

  • Educate on trigger avoidance tailored to sensitisation profile (e. g, high-pollen day strategies, pet allergen reduction, dust-mite control)
  • Nasal saline irrigation for symptom relief and mucus clearance
  • Occupational history and workplace exposure reduction; consider occupational health referral if work-related pattern
  • Address sleep and school/work impact; optimise adherence and spray technique

Pharmacological Treatment

Intranasal corticosteroids (first-line for persistent or moderate-severe disease)

  • Fluticasone propionate nasal spray 50 micrograms/spray: adults and >=12 years initially 2 sprays each nostril once daily (200 micrograms/day), then 1 spray each nostril once daily maintenance
  • Mometasone furoate nasal spray 50 micrograms/spray: adults and >=12 years 2 sprays each nostril once daily; children 3-11 years 1 spray each nostril once daily
  • Beclometasone dipropionate aqueous nasal spray 50 micrograms/spray: 1-2 sprays each nostril twice daily (max as per product/BNF age band)

Most effective class for nasal blockage and global control. Check technique and adherence before stepping up. Safety: epistaxis, nasal irritation; rare septal perforation (avoid spraying toward septum). Use lowest effective dose; monitor growth in children on prolonged corticosteroid therapy.

Non-sedating oral H1-antihistamines (intermittent/mild disease or add-on)

  • Cetirizine 10 mg once daily (adults and children >=12 years)
  • Loratadine 10 mg once daily (adults and children >=6 years)
  • Fexofenadine 120 mg once daily for seasonal allergic rhinitis (>=12 years)

Good for itch/sneeze/rhinorrhoea; less effective than intranasal steroids for obstruction. Prefer non-sedating options. Safety: avoid first-generation sedating antihistamines when alertness is required (driving/exams); caution with alcohol/CNS depressants.

Intranasal antihistamine

  • Azelastine nasal spray 1 spray each nostril twice daily (age-dependent licensing)

Rapid onset; useful PRN or as add-on to intranasal steroid when control is incomplete.

Short-course nasal decongestant (rescue only)

  • Xylometazoline 0.1% nasal spray: 1 spray each nostril up to 2-3 times daily for a maximum of 7 days (adult strength)

Use only briefly for severe blockage. Safety: prolonged use causes rhinitis medicamentosa (rebound congestion).

Leukotriene receptor antagonist (selected patients, especially with concomitant asthma)

  • Montelukast 10 mg at night (adults; paediatric doses by age)

Not first-line for isolated rhinitis; consider when asthma coexists. Safety warning: neuropsychiatric reactions (sleep disturbance, mood/behaviour change); counsel patients and review promptly if symptoms occur.

Allergen immunotherapy (specialist care)

  • Grass pollen sublingual tablet immunotherapy (e. g, Grazax) started pre-season and continued long-term in selected patients
  • Subcutaneous allergen immunotherapy where indicated and supervised

Consider for severe, confirmed IgE-mediated disease refractory to optimized pharmacotherapy. Contraindications/cautions include uncontrolled asthma and inability to manage anaphylaxis risk; requires specialist assessment and monitoring.

Surgical / Interventional

  • Not routine for allergic inflammation itself
  • Consider inferior turbinate reduction (e. g, radiofrequency) only for persistent obstructive symptoms with turbinate hypertrophy despite maximal medical therapy
  • Correct coexisting structural pathology when present (e. g, septal deviation) after careful phenotype assessment

Complications

  • Impaired quality of life and daytime function
  • Sleep disturbance and possible contribution to obstructive sleep apnoea symptoms
  • Reduced school/work performance and concentration
  • Comorbid asthma and poorer asthma control
  • Allergic conjunctivitis
  • Rhinosinusitis and possible nasal polyp disease
  • Oral allergy syndrome (pollen-food syndrome)

Prognosis

Allergic rhinitis often follows a long-term or lifelong relapsing course rather than complete remission, although severity fluctuates with exposure and age. Prognosis is generally good with correct diagnosis, trigger management, and stepwise pharmacotherapy, with substantial improvement in symptoms and quality of life in most patients.

Sources & References

💊BNF Drug References(8)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 578)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 632)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 570)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 578)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 570)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 579)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 577, 578)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 134)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 579)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 615)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 633)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 633)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 112)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 133, 134)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 134)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 579, 580)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 111, 112)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1361)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 578)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 97)[context]

Sources

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