Rhinitis

 

• Pathophysiology

  Allergic rhinitis

  • IgE-mediated inflammation of nasal membranes.
  • Results from sensitisation to allergens such as dust mites, grass/tree/weed pollens ('hay fever', seasonal), animal dander, or occupational exposures.

  Non-allergic rhinitis

  Causes:

  • Vasomotor rhinitis.
  • Drugs: ACEi, β-blockers, aspirin, alcohol, cocaine.
  • Hormones: pregnancy, pill, hypothyroidism.
  • Physical irritants e.g. temperature or humidity changes.

• Presentation

  Chronic nasal congestion, rhinorrhea, and sneezing.

  Allergic rhinitis:

  • Nasal itch.
  • Associated allergic conjunctivitis (eye redness, watering, swelling, itching). Eczema and asthma are also linked.
  • Onset usually in childhood and improves with age.
  • May be seasonal.

  Non-allergic rhinitis:

  • Onset age later.
  • Often perennial (all year), though may have seasonal variation e.g. with cold weather.

• Investigations

  Skin prick testing is only indicated if there is uncertainty over whether the rhinitis is allergic or not.

• Management

  For allergic rhinitis, allergen avoidance is key.

  Medical

  Similar for allergic and non-allergic rhinitis, though oral therapies are usually only for allergic rhinitis.

  1st line options:

  • Intranasal antihistamines (azelastine): quick onset, PRN rescue treatment.
  • Intranasal corticosteroids (mometasone, fluticasone, beclometasone, betamethasone): regular preventive treatment, especially if nasal congestion predominates and/or polyps are present.
  • Oral non-sedating antihistamines (cetirizine, loratadine, fexofenadine): preventive or rescue treatment, useful for allergic rhinitis, especially with nasal discharge, sneezing, and conjunctivitis.

  Further options:

  • Intranasal: saline irrigation, decongestants (ephedrine, xylometazoline), sodium cromoglicate, ipratropium.
  • Oral (allergic rhinitis): montelukast, steroids (if severe).

• Complications

  • Sinusitis
  • Postnasal drip and chronic cough: treat with intranasal steroids or oral antihistamines.

• Antihistamines

  Mechanism

  • This section focuses on H1 receptor blockers, which is what is usually implied by 'antihistamines'.
  • H1 receptors have various locations (and effects), including airway smooth muscle (bronchoconstriction), vascular smooth muscle and capillary endothelium (inflammation), and CNS (wakefulness).
  • The sedating effects of older antihistamines comes from their ability to cross the blood-brain barrier and antagonise central H1 receptors. This also gives them anti-emetic effects via central anticholinergic activity and possibly via effects on the chemoreceptor trigger zone.

  Drugs and indications

  Sedating (first-generation):

  • Chlorphenamine, promethazine, cyclizine, diphenhydramine.
  • Used for nausea and insomnia, and pruritus when sedation is also desired. Chlorphenamine is used in anaphylaxis.

  Non-sedating (second-generation):

  • Cetirizine, loratadine, fexofenadine, azelastine (intranasal).
  • Used for allergic symptoms including rhinitis, urticaria, and pruritus.

  Side effects

  • Sedation. Although much less common, it can still occur with 'non-sedating' antihistamines, especially cetirizine.
  • Other effects: headache, psychomotor impairment, anticholinergic effects (urinary retention, dry mouth, blurred vision, GI upset). Again, these can occur with second-generation antihistamines, but are less common than with first-generation.
  • Azelastine can cause a bitter taste.