Anaphylaxis: recognition and emergency management — branching viva

Opening question

Examiner: Take me through this adolescent. What is the diagnosis, and what is your frame for managing her? [1]

Candidate: This is anaphylaxis. She has acute respiratory compromise — wheeze and dizziness — and a distributive-shock picture — pallor and presyncope — after a likely food allergen in a known peanut-allergic child. That meets the NIAID/FAAN criteria for anaphylaxis even though she has no rash. My frame is simple: give intramuscular adrenaline now, without waiting for a rash or a test, then support the airway, breathing and circulation, escalate if she does not respond, and keep her for observation because a biphasic reaction can recur. [1]

Examiner: She has no skin signs at all. Does that worry you, or reassure you? [1]

Candidate: It worries me. Up to a fifth of anaphylactic reactions have no skin or mucosal signs, and this girl is exactly the high-risk profile — the asthmatic adolescent with food anaphylaxis. The absence of a rash is the pitfall that delays adrenaline in fatal cases, so it is the reason to act faster, not to pause. [1]

Branch 1 — pathophysiology

Examiner: Explain the pathophysiology of anaphylaxis, and why adrenaline is the right drug. [3]

Candidate: On re-exposure, the allergen cross-links allergen-specific IgE bound to the Fc-epsilon-RI receptor on mast cells and basophils, and the cell degranulates. It releases preformed mediators — histamine, tryptase, heparin — and newly synthesised lipid mediators — leukotrienes, prostaglandins, platelet-activating factor. Those mediators increase vascular permeability and cause oedema, vasodilation with distributive shock, and bronchospasm. Adrenaline reverses all three limbs through its receptors: alpha-1 vasoconstricts and reduces the oedema and shock, beta-2 bronchodilates and stabilises the mast cell to cut off further mediator release, and beta-1 supports the heart. That is why no other drug can substitute for it. [3]

Examiner: She also has asthma. Why does that matter here? [3]

Candidate: Because the anaphylactic bronchospasm lands on an already reactive airway. Poorly controlled asthma is a recurring feature of fatal food anaphylaxis — it magnifies the respiratory failure and it is one reason this group dies. I would treat her asthma concurrently with the anaphylaxis, and at discharge I would make sure her asthma plan is optimised, because good asthma control is part of anaphylaxis prevention. [3]

Branch 2 — immediate management

Examiner: Walk me through the immediate steps and the adrenaline dose for this girl. [3]

Candidate: I would call for help and an ambulance, lie her flat with her legs raised to improve venous return — sitting her up could precipitate collapse — and give intramuscular adrenaline into the anterolateral thigh immediately. She is fifteen and over fifty kilograms, so the dose is 500 micrograms, which is 0.5 millilitres of the 1 milligram per millilitre concentration. I would repeat it every five minutes if there is no response. The anterolateral thigh is the site because absorption there is fastest and most reliable. [3]

Examiner: What adjuncts would you add, and what would you not use as a substitute? [4]

Candidate: I would give high-flow oxygen for hypoxia, an intravenous crystalloid bolus of 10 millilitres per kilogram for hypotension, and a nebulised bronchodilator for refractory wheeze. An H1 antihistamine relieves urticaria and pruritus if any appears, and a corticosteroid and an H2 blocker are traditional adjuncts. What I would not do is treat with an antihistamine or a steroid first, or instead of adrenaline — their onset is too slow and their effect too narrow to alter the acute course. Adrenaline is first-line and non-substitutable. [4]

Branch 3 — refractory escalation

Examiner: She has had two adrenaline doses and a fluid bolus and she is still shocked and wheezy. What now? [4]

Candidate: She is in refractory anaphylaxis, and I would escalate to an intravenous adrenaline infusion, starting at 0.1 to 1 microgram per kilogram per minute and titrating to her response, managed in the paediatric intensive care unit with senior support. Before I do, I would check two things: her medication list for a beta-blocker, and for any cofactor that is still driving the reaction. If she is on a beta-blocker and refractory to adrenaline, I would give glucagon, which bypasses the receptor blockade. I would reserve an intravenous bolus of about 1 microgram per kilogram for the peri-arrest or arrested patient under experienced hands, because concentrated IV adrenaline is dangerous outside that setting. [4]

Examiner: Why is glucagon the answer for the beta-blocked patient? [4]

Candidate: Because adrenaline works through the beta and alpha receptors, and a beta-blocker occupies the beta receptors that adrenaline needs to support the heart and relax the bronchial smooth muscle. Glucagon bypasses the receptor entirely — it acts directly on the cell to increase intracellular cyclic AMP through its own pathway — so it can support the circulation and reverse the refractory state even when adrenaline cannot. [4]

Branch 4 — investigation

Examiner: How would you use tryptase in this girl? [4]

Candidate: I would draw serum tryptase as soon as possible after onset, again at one to two hours, and at a baseline point at least twenty-four hours later. A rise that exceeds 1.2 times the baseline plus 2 micrograms per litre confirms mast-cell activation. Two cautions, though. First, the timing matters, because tryptase peaks and falls quickly, so a single late sample can be normal even in a genuine reaction. Second — and this is the point the examiner is testing — a normal tryptase never excludes anaphylaxis. Food-triggered reactions are often tryptase-normal, so I would never let the result delay or deny treatment. [4]

Branch 5 — observation and discharge

Examiner: She responds to the infusion and recovers. How long do you observe her, and what do you send her home with? [9]

Candidate: Because a biphasic reaction can recur one to seventy-two hours after the initial recovery, she cannot be discharged quickly — and she is high-risk because she needed multiple adrenaline doses and has asthma. I would admit her overnight for observation, supported by the paediatric repeat-epinephrine cohort evidence that maps when second doses fall and supports risk-stratified observation. A low-risk child — a single adrenaline dose, full recovery, no asthma — could be observed for around six hours, but not her. [9] [10]

Examiner: And the discharge package? [8]

Candidate: Before she leaves she must have the full prevention package: an adrenaline autoinjector, ideally two, with a device-matched trainer so she practises with what she carries; a written ASCIA action plan naming peanut as the trigger, the dose and the steps, copied to her school; a referral to the allergy clinic to confirm the trigger with skin-prick and specific-IgE testing; and explicit education — strict peanut avoidance, when and how to use the autoinjector, and to call an ambulance immediately and use a second device if there is no response. Because she is an adolescent, I would address the hesitation that leads young people to delay using their device, optimise her asthma control, and arrange a transition to adult allergy care. [8]

Wrap

Examiner: Summarise the anaphylaxis stance in one sentence. [3]

Candidate: Recognise anaphylaxis early — even without a rash — and give intramuscular adrenaline into the anterolateral thigh by weight or age, repeated every five minutes, because delayed adrenaline is the single reversible factor in fatal paediatric anaphylaxis; support the airway, breathing and circulation with oxygen and fluid; escalate to an adrenaline infusion and glucagon if refractory; draw timed tryptase but never let it delay treatment; observe for the biphasic reaction; and discharge every patient with an autoinjector, a written action plan and an allergy referral. [3] [8]