Refractory anaphylaxis in the beta-blocked patient

This is refractory anaphylaxis — a severe reaction with airway, breathing and circulatory compromise that has responded poorly to two doses of intramuscular adrenaline. The diagnosis is clinical and is not in doubt: the rapid multi-system onset after contrast meets the criteria. The reason for the poor response is almost certainly the beta-blocker, which occupies the beta-adrenergic receptors that adrenaline needs in order to produce its bronchodilator, vasoconstrictor and cardiac effects; the ACE-inhibitor may additionally worsen the angioedema.^[1]

The escalation is twofold. First, the specific antidote for the beta-blocked patient is glucagon, which bypasses the beta-receptor and raises intracellular cyclic-AMP directly: a 1 to 2 milligram intravenous bolus, repeated or followed by an infusion, with attention to its emetic effect (the patient is protected from aspiration). Second, an intravenous adrenaline infusion is commenced, carefully titrated to the blood pressure, by a clinician experienced in its use, because the intravenous bolus is arrhythmogenic. The airway is managed proactively — the early involvement of anaesthesia for a definitive airway before the stridor progresses to complete obstruction — high-flow oxygen is given, a rapid crystalloid bolus is run for the capillary leak, and nebulised adrenaline and bronchodilators are added. The team prepares for the possibility of cardiac arrest and the need for advanced life support.^[2]

The lesson the candidate takes is that a poor response to adrenaline is not a reason to abandon adrenaline but to escalate it, to look for the beta-blocker, and to give glucagon — and to secure the threatened airway before it is lost.^[1]