Urticaria and angioedema — branching viva

Viva format

The examiner takes the candidate through four escalating branches, each anchored to a patient. At each stage the candidate must state the reasoning before the action, name the active guideline, and respect the bradykinin versus histamine split. The examiner probes the why and the corners. [1]

Branch 1 — Acute urticaria in the young child

Examiner: A four-year-old boy presents with itchy pink lumps over his trunk. Each one moves and fades within hours, replaced by new ones elsewhere. He had a viral cold three days ago. He is afebrile, well, with no swelling and no breathing difficulty. How do you manage this? [1]

The model answer confirms that the individual wheals resolve within twenty-four hours leaving normal skin, which is the hallmark of ordinary acute urticaria. Viral upper respiratory tract infection is the commonest identifiable trigger in this age group. The child is assessed for airway and circulation involvement to exclude anaphylaxis, examined for angioedema, and asked about drug triggers (especially NSAIDs and antibiotics). Treatment is a standard-dose non-sedating second-generation antihistamine, with a short course of oral corticosteroid only if distress is severe. The family is reassured, given a safety-net for airway and anaphylaxis signs, and told that most acute urticaria resolves within days. Routine allergy testing is not indicated for a single self-limiting episode. [1]

Examiner probe: "Why do you not send a specific IgE panel, and what would change your mind?" [1]

The candidate explains that a single episode of acute viral-triggered urticaria does not warrant allergy testing, because the trigger is apparent and the condition is self-limiting. A specific IgE panel or skin prick testing is reserved for a history of reproducible symptoms after a specific food or drug exposure, because false-positive results lead to unnecessary elimination diets and anxiety. [1]

Branch 2 — Chronic spontaneous urticaria and the stepwise ladder

Examiner: Now a seven-year-old with daily itchy wheals for eight weeks. She is otherwise well. Walk me through your assessment and management. [3]

The model answer confirms the diagnosis of chronic spontaneous urticaria — daily wheals for six weeks or more, with individual lesions under twenty-four hours and normal skin after — and screens for alarm features: lesions lasting over twenty-four hours, bruising, pain, fever, weight loss and arthralgia. Their absence supports a clinical diagnosis without extensive testing. The candidate states that routine allergy panels are not indicated and begins the four-step ladder: a standard-dose second-generation antihistamine daily, up-titration to four times the standard dose if uncontrolled within two weeks, then omalizumab, then specialist immunomodulation such as cyclosporine or dupilumab. Quality of life is assessed, because treatment intensity should track impact. [1] [3]

Examiner probe: "What did the omalizumab trials show, and where does dupilumab fit?" [7]

The candidate states that the pivotal phase III trials (ASTERIA I, ASTERIA II, GLACIAL) demonstrated that omalizumab significantly reduced itch and wheal activity in chronic spontaneous urticaria refractory to antihistamine, making it the licensed third-line biologic. Dupilumab, supported by the LIBERTY-CSU CUPID phase III trials, adds a second biologic option for refractory disease, expanding the specialist toolkit. Both are specialist-led, with age-cut-offs that vary by jurisdiction. [7] [8]

Branch 3 — Recurrent angioedema without wheals

Examiner: Now a ten-year-old with recurrent facial swelling for a year. The swelling is not itchy, lasts days, and his father was intubated once for throat swelling. What is going on, and what is the single most important test? [9]

The model answer recognises the bradykinin pathway immediately. Angioedema without wheals, a family history of similar swelling, and a relative's airway event make hereditary angioedema the leading diagnosis. The single most important initial investigation is a serum C4 level: low both during and between attacks in hereditary angioedema types I and II, and a normal C4 effectively excludes these forms. If low, the candidate proceeds to C1-inhibitor antigenic and functional assays to confirm and type the disease. [9] [10]

Examiner probe: "Why will antihistamines, adrenaline and steroids not help this child?" [9]

The candidate explains that hereditary angioedema is bradykinin-mediated: C1-inhibitor deficiency allows unopposed kallikrein activity, generating bradykinin, which produces deep-tissue angioedema without itch or wheals. Antihistamines block H1 receptors, adrenaline and steroids suppress mast-cell activation — none of these touch a bradykinin-driven attack. Acute attacks need C1-inhibitor concentrate or icatibant, and prophylaxis may use lanadelumab or C1-inhibitor concentrate. The child needs an on-demand plan, a medical-alert device and family screening from childhood. [9] [10]

Branch 4 — Anaphylaxis presenting as urticaria

Examiner: A child arrives with acute widespread urticaria, wheeze, hypotension and abdominal pain after a food exposure. How do you sequence your response? [13]

The model answer recognises anaphylaxis, not urticaria. The urticaria is the visible sign of a systemic event. The candidate gives intramuscular adrenaline into the anterolateral thigh immediately, followed by oxygen, supine positioning and intravenous fluid for hypotension. The airway and breathing are supported as needed. The trigger is identified, the child is observed for a biphasic reaction, and an adrenaline autoinjector and a written action plan are provided before discharge, with allergy referral. Antihistamines and corticosteroids are adjuncts, not the definitive treatment — adrenaline is. [13]

Examiner probe: "The family asks why you did not just give an antihistamine for the rash. What do you say?" [13]

The candidate explains that the rash was the visible sign of anaphylaxis — a life-threatening systemic allergic reaction — and that adrenaline is the definitive treatment because it reverses vasodilation, bronchospasm and airway oedema. An antihistamine would relieve itch but would not treat the hypotension or the airway, and delaying adrenaline for symptomatic rash treatment is the classic error in anaphylaxis. [13]

Closing synthesis

A passing candidate keeps four ideas in tension throughout: urticaria is transient itchy wheals from mast-cell histamine, confirmed by the twenty-four-hour rule; the six-week clock separates acute from chronic and triggers the stepwise ladder; the single most important split is histamine- versus bradykinin-mediated angioedema, because it determines whether antihistamines and adrenaline will work or fail; and acute urticaria with airway or circulation involvement is anaphylaxis until proven otherwise and gets adrenaline first. [1] [9] [13]