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• W2079707981 abstract "The case report by O'Sullivan et al. (Anaesthesia 2001; 56: 768–71) describes a fatal adverse reaction during anaesthesia, with sudden loss of pulse and blood pressure. This was thought to be a kinin-mediated anaphylactoid reaction. The mechanism postulated was that a particular batch of Haemaccel® had abnormally high plasma activating ability, leading to activation of prekallekrein with the generation of kinin peptides including bradykinin. This is a potent vasodilator and widespread profound vasodilation was thought to have occurred. When investigating adverse reactions during anaesthesia, it is first essential to obtain a detailed record of events, including timing of the reaction in relation to drugs given and procedures, all drugs given and the clinical features and recorded data [1]. This reaction occurred 90 min after induction, ruling out induction agents as a cause; these cause reactions within minutes. Possible causes of a reaction at this time would be cementing the hip prosthesis, latex allergy or intravenous fluids or drugs given later during surgery. The hip prosthesis had been cemented at 78 min and this is known to cause reactions, but the clinical features are against this and there was no evidence of emboli at post-mortem. The clinical features were not those of histamine release where one would expect associated erythema, urticaria or angioedema, particularly of the face, as well as increased ventilation pressures. This is against latex allergy, an IgE-mediated reaction, which would be expected to have some of these features as well as hypotension. In addition, the time of onset is rather too late for latex allergy, which usually occurs by about 30 min from the start of surgery. A histamine release mechanism could have been confirmed by measuring the level of mast cell tryptase in the serum at post-mortem. This gives an index of mast cell activation. The clinical features, with sudden loss of pulse and blood pressure, continuing electrical activity and fall in end-expired carbon dioxide are compatible with severe widespread vasodilation and no cardiac output. The lack of features supporting histamine release suggests the reaction was not due to mast cell activation and not IgE-mediated. Kinin-mediated effects have been postulated to be the mechanism of adverse reactions to angiotensin converting enzyme (ACE) inhibitors, which can cause laryngeal or glottal oedema [2]. ACE inhibitors would prevent breakdown and clearance of bradykinin, prolonging its effect. Severe life-threatening angioedema can occur, and the airway is the usual site of this adverse reaction. The reasons for this localisation are not clear; however, angioedema, whatever the cause, shows a predilection for lips, eyelids, larynx or tongue. Hypotension has been described with ACE inhibitors, although rarely. It is assumed the severity of the reaction was related to massive generation of bradykinin and the fact that this was occurring throughout the vascular compartment. The continuing intravenous infusion would perpetuate generation of mediators. Skin prick tests are used to demonstrate specific IgE and are useful where this is the established mechanism of a reaction, e.g. following induction agents. Problems arise in interpretation of skin prick tests if the test substance has intrinsic histamine-releasing ability, as with some of the neuromuscular blocking drugs. There are anecdotal reports of colloids (Gelofusine) being the cause of adverse reactions during anaesthesia (L. J. F. Youlten, personal communication; my personal observation). Of six patients, most had negative skin prick tests but positive intradermal skin tests, suggestive of an IgE-mediated reaction. However, in some, the clinical features with sudden hypotension were more suggestive of a kinin-mediated reaction. The usual clinical course is for the reaction to begin some time (up to 20 min) after the start of the infusion of the colloid. This is in sharp contrast to reactions to induction agents which occur within a few minutes of the intravenous bolus. Although the case report identified particular batches of Haemaccel as having high kinin-generating ability, it may be that colloids have an intrinsic ability to generate kinins at a lower level in certain patients. If so, colloids may cause adverse reactions by more than one mechanism. This will be difficult to prove as there is no routine diagnostic test to demonstrate bradykinin production. It is important that anaesthetists are aware of these adverse reactions to colloid, and that in a patient with intra-operative cardiovascular collapse, where this is the cause, the appropriate action is, counter-intuitively, to stop the colloid infusion." @default.
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• W2079707981 date "2001-08-01" @default.
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• W2079707981 title "Adverse reactions to colloids" @default.
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• W2079707981 doi "https://doi.org/10.1046/j.1365-2044.2001.01916-3.x" @default.
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