Recognise chronic spontaneous and inducible urticaria, separate mast-cell angioedema from bradykinin disease and vasculitis, investigate selectively and escalate non-sedating antihistamine treatment without unnecessary food restriction.
Confirm that lesions are true wheals: raised, itchy, blanching and evanescent, with individual marks disappearing within 24 hours. Ask families to outline one lesion and photograph it over time. Establish frequency beyond six weeks, angioedema duration, cold, pressure, heat, exercise, water, scratching, medicines, infection and exact food timing.
Chronic spontaneous urticaria is a mast-cell disorder even when no trigger is found. The term idiopathic does not mean psychological. Food allergy produces discrete reproducible episodes after exposure rather than near-daily random wheals. NSAIDs can lower mast-cell threshold and exacerbate disease without being the original cause.
Examination between flares may be normal. During a flare, check lesion morphology, dermatographism, swelling and airway, breathing or circulation features. Fixed painful purpura, joint signs, fever, lymphadenopathy or organ enlargement redirects to vasculitis or systemic disease. Recurrent abdominal pain and swelling without itch or wheals redirects to bradykinin angioedema.
Mast cells activate without a consistent external trigger, often through autoimmune IgG or IgE pathways that remain clinically unconfirmed.
Cold, heat, pressure, vibration, exercise, water or scratching reproducibly activates mast cells at a physical threshold.
Intercurrent viral illness and NSAIDs can exacerbate established urticaria, although routine infection screening rarely identifies a persistent cause.
Hereditary or acquired C1-inhibitor dysfunction increases bradykinin, causing non-pruritic swelling without mast-cell wheals or antihistamine response.
Histamine and other mediators dilate superficial vessels and increase permeability, creating raised itchy transient dermal wheals.
The same mast-cell process in subcutaneous or submucosal tissue produces angioedema lasting longer than superficial wheals.
Functional antibodies can stimulate IgE receptors or related pathways, explaining spontaneous recurrence without a discoverable environmental allergen.
Excess bradykinin opens deeper vascular barriers without histamine, so wheals, itch and response to antihistamine are absent.
An itchy raised blanching lesion changes shape and site and disappears completely from that location within 24 hours.
Itchy deeper swelling accompanies wheals and generally improves with antihistamine, although resolution may take up to 72 hours.
Cold, pressure, heat, sweat or scratching reproducibly creates local wheals after a definable physical stimulus.
Painful or burning lesions remain fixed beyond 24 hours and leave bruising, pigmentation or systemic inflammatory symptoms.
Non-pruritic swelling without wheals, recurrent abdominal pain and poor antihistamine response suggests hereditary or acquired angioedema.
Reproducible symptoms within minutes to two hours of one food, often with vomiting or respiratory change, differ from daily spontaneous wheals.
Painful fixed lesions lasting over 24 hours with residual bruising, fever, joint or renal features reflect small-vessel inflammation.
Non-itchy swelling without wheals, recurrent severe abdominal pain and family history supports C1-inhibitor or bradykinin-pathway disease.
Fixed target lesions persist for days and may involve acral sites or mucosa rather than migrating within hours.
Persistent pigmented lesions, flushing, systemic mediator episodes or fever with inflammatory features requires specialist mast-cell or autoinflammatory assessment.
Laryngeal or tongue swelling can obstruct airflow and requires immediate emergency management rather than routine urticaria treatment.
Severe itch, visible swelling and sedating medication disrupt sleep, concentration, school attendance, sport participation and social confidence.
Misattributing chronic spontaneous disease to food can produce nutritional deficiency, anxiety, social restriction and unnecessary adrenaline auto-injector dependence.
Repeated or prolonged systemic steroid courses cause weight, mood, blood-pressure, glucose, bone and infection harm without durable control.
A wheal that vanishes within hours fits mast-cell urticaria; a fixed bruising lesion points toward vascular inflammation.
A food eaten regularly cannot plausibly explain random daily wheals unless each exposure reproduces the same immediate event.
Wheals and itch suggest histamine, while isolated abdominal and submucosal swelling suggests bradykinin and different treatment.
Consistent second-generation antihistamine up-dosing is more evidence based than combining several sedating and non-sedating products haphazardly.
CSU treatment uses a fixed specialist dose rather than calculation from body weight and total IgE as in allergic asthma.
Calling fixed bruising lesions ordinary urticaria.
Blaming chronic spontaneous wheals on foods without timing evidence.
Ordering broad allergy panels for classic CSU.
Using sedating antihistamines throughout the school day.
Maintaining repeated systemic corticosteroid courses.
Missing hereditary angioedema when wheals are absent.
Treating airway compromise with antihistamine instead of adrenaline.
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A child has recurrent painful raised lesions that remain in the same place for 36 hours and leave bruising. What is the most appropriate interpretation?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Treat with a second-generation H1 antihistamine every day, not only after wheals erupt. Use an age-licensed dose, then specialist-supported up-dosing to as much as fourfold when control remains inadequate. Avoid sedating antihistamines for routine care because cognition, sleep architecture and school safety matter. Identify and minimise aggravating NSAIDs when clinically relevant.
Severe refractory CSU from age 12 may receive omalizumab 300 mg subcutaneously every four weeks through specialist care. Response is assessed using activity and control scores, not serum IgE. Selected refractory cases may use ciclosporin with renal and blood-pressure monitoring. Provide an emergency plan only for genuine airway or anaphylaxis risk, not for every wheal.
Renal impairment requires dose review and some children still become drowsy; avoid stacking multiple antihistamines or unplanned up-dosing without documenting age, response and safety.
Administer with anaphylaxis capability, record batch and monitor injection reactions; reassess benefit before prolonged treatment and do not use it to treat acute anaphylaxis.