Page 4 of 12
DR14.1-2 | Urticaria Angioedema Classification and Management — Summary & Reflection
KEY TAKEAWAYS
Urticaria is recurrent, intensely itchy wheals of superficial dermal oedema, each individual lesion lasting less than 24 hours; angioedema is the same process in the deeper dermis and subcutis, producing diffuse, less itchy, longer-lasting swelling with a predilection for lips, eyelids, tongue, and larynx. Urticaria is classified by duration (acute <6 weeks vs chronic ≥6 weeks) and, in chronic disease, by trigger (spontaneous, often autoimmune, vs inducible — dermographism, cold, cholinergic, pressure, solar). The pathogenesis is mast-cell degranulation releasing histamine, which explains both the clinical features and why H1-antihistamines work; precipitants include NSAIDs/aspirin, opioids, foods, infections, physical stimuli, and autoimmunity. Crucially, angioedema may instead be bradykinin-mediated (ACE-inhibitor-induced or hereditary C1-inhibitor deficiency), presents without wheals, and does not respond to antihistamines. The key mimic is urticarial vasculitis (lesions >24 hours, painful, resolving with bruising → biopsy). Management is a ladder: second-generation non-sedating H1-antihistamine first-line, up-dosed to 4× if needed, with omalizumab added for refractory chronic spontaneous urticaria; sedating first-generation agents are avoided long-term. Angioedema with airway compromise or anaphylaxis is an emergency treated with intramuscular adrenaline, and bradykinin-mediated angioedema requires drug withdrawal and specific therapy.
REFLECT
Think back to a patient you have seen — in casualty, the ward, or the OPD — who presented with an itchy rash or a swelling, or imagine the patient in our opening scenario. With the framework from this module, how would you now classify the eruption (acute or chronic, spontaneous or inducible), and what single question in the history would most change your management? Consider, too, the prescribing dimension: how many of your future patients will be on an NSAID or an ACE-inhibitor, and how will you recognise when one of those drugs is the cause of the swelling in front of you? Finally, rehearse the emergency in your mind — if the next patient's tongue begins to swell and their voice changes, can you say, without hesitation, what your first action will be? Building these reflexes now, before the emergency arrives, is what turns knowledge into safe practice.