Editorial II

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Abstract
In 1969, Hurwitz1 commented that the more drugs a patient receives, the greater the risk of an untoward reaction. Multiple drugs need to be used in surgery, since no single drug supplies all pharmacological needs, and this encourages unexpected drug interaction and pharmacological response. Problems are compounded by the necessity to use the intravenous route for drug administration, thus bypassing the body’s primary immune filters and presenting high concentrations of noxious chemicals directly to sensitive cells, notably mast cells and basophils.2 The substances liberated include histamine, eicosanoids and cytokines. The clinical outcome is not infrequently an immediate exaggerated systemic inflammatory response presenting hypotension and bronchospasm with varying degree of severity and which may, or may not, be immune (antibody) mediated. All such clinical presentations are usually referred to as anaphylactoid until laboratory and in vivo analysis can establish a genuine immediate immune‐mediated hypersensitivity response (type I, IgE‐mediated anaphylaxis) or otherwise, and the causative agent responsible. There are other types of drug hypersensitivity response, notably IgG (type III)‐mediated response to certain clinically used dextrans and a multiplicity of responses to penicillins (potentially types I, II and III). In the majority, cause and effect is somewhat transparent and the immediate hypersensitivity response, with its requirement for immediate clinical intervention, is the greatest threat to the patient. Identification of the reaction mechanism is important both for the patient’s surgical future and as defence for the anaesthetist in the increasing tide of litigation. The predominant cause of such a reaction is a neuromuscular blocking agent (NMBA) or, rarely, a hypnotic agent.3