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Anaphylactic Shock: Mechanisms and Treatment 12, 89-100 A.F.T Journal of REVIEW ARTICLE Accident and J Accid Emerg Med: first published as 10.1136/emj.12.2.89 on 1 June 1995. Downloaded from Emergency Medicine 1995 Anaphylactic shock: mechanisms and treatment 12, 89-100 A.F.T. BROWN Department of Emergency Medicine, Royal Brisbane Hospital, Brisbane, Queensland, Australia introduced the term 'allergy' although he assumed SUMMARY that the major allergic diseases, such as urticaria This paper reviews the mechanisms of and asthma, were due to the absence of anaphylactic shock in terms of the immunoglobulin antibodies.4 In 1921, Prausnitz and Kustner and non-immunoglobulin triggering events, and the demonstrated the ability to transfer a serum factor cellular events based on the rise in intracellular (termed reagin) in the serum of a sensitive patient cyclic AMP and calcium that release preformed to a non-sensitive recipient, although it was not granule-associated mediators and the rapidly until 1967 that Ishizaka and colleagues identified formed, newly synthesized mediators predo- this reagin as a new class of immunoglobulin minantly based on arachidonic acid metabolism. known as IgE. Finally, in 1975, Coombs and Gell These primary mediators recruit other cells with classified hypersensitivity reactions into three the release of secondary mediators that either immediate types and one delayed type, although potentiate or ultimately curtail the anaphylactic in practice these types need not necessarily occur reaction. The roles of these mediators in the various in isolation from each other.5 In immunological causes of cardiovascular collapse are examined. terms, anaphylaxis is an example of an immediate, The treatment of anaphylactic shock involves Type-1 hypersensitivity reaction. oxygen, adrenaline and fluids. The importance and safety of intravenous adrenaline are discussed. DEFINITION Combined Hi and H blocking antihistamines and Currently, the term anaphylaxis is best used to http://emj.bmj.com/ steroids have a limited role. Glucagon and other describe the rapid, generalized and often adrenergic drugs are occasionally used, and unanticipated, immunologically mediated events several new experimental drugs are being that occur after exposure to certain developed. foreign substances in sensitized Key words: adrenaline, anaphylactic shock, previously persons. Anaphylactoid reactions describe a clinically anaphylaxis, histamine H1 receptor blockaders, identical syndrome involving similar mediators but on September 24, 2021 by guest. Protected copyright. histamine H2 receptor blockaders not triggered by IgE antibody and not necessarily INTRODUCTION requiring previous exposure. Despite important aetiological distinctions, the term anaphylaxis is The first case of anaphylaxis was recorded on the commonly used to describe both of these clinical tomb of King Menes, an Egyptian Pharaoh who syndromes, even when the mechanisms are died suddenly in 2640 BC following a wasp sting.' unknown.3 The most common life-threatening The term anaphylaxis is derived from the Greek feature of acute anaphylaxis is cardiovascular and means literally 'against protection'.2 It was collapse or shock. Other life-threatening effects Correspondence: introduced in 1902 by Charles Richet and Paul include bronchospasm, angio-oedema and A.F.T. Brown, Portier following experiments with unexpected pulmonary oedema.6'7 This paper will focus on the Staff Specialist, fatal reactions on dogs sensitized to Portuguese mechanisms and both general and specific Department of man-of-war venom, observed the previous year treatment of anaphylactic shock. Emergency whilst on board Prince Albert of Monaco's yacht Medicine, Royal in the Brisbane Hospital, Mediterranean. Richet was subsequently awarded the Nobel Prize in Medicine and MECHANISMS OF Brisbane, ANAPHYLACTIC SHOCK Queensland 4029, Physiology in 1913.3 Australia At around the same time, in 1906, Von Pirquet Mechanisms of anaphylactic shock may be divided i 1994 Emergency Medicine A.F:T Brown into four main categories: the events that trigger the protein drugs acting as haptens such as antibiotics, anaphylactic reaction; the cellular events that then vitamins and steroids; vaccines; foods, including J Accid Emerg Med: first published as 10.1136/emj.12.2.89 on 1 June 1995. Downloaded from lead to mediator release; the clinical pharmacology milk, fish and nuts; venoms, particularly of of these mediators; and finally the cardiovascular Hymenoptera; and many other substances as responses of patients to these mediators. diverse as ethylene oxide, hydatid cysts and latex.8 Latex allergy was first reported in 1979, and has MECHANISMS: TRIGGERING caused intra-operative anaphylactic reactions.12 In EVENTS addition, allergy to the latex catheter-tip used in barium enemas has also been recorded, most The events that trigger anaphylaxis are either commonly in children with spina bifida or anaphylactic and IgE immunologically mediated, congenital urological abnormalities.13 or anaphylactoid and non-immunoglobulin mediated, although in many reactions there is ANAPHYLACTOID REACTIONS evidence of the involvement of multiple pathways (see Table 1). Anaphylactoid reactions are non-immunoglobulin mediated and are caused by mediator release that ANAPHYLACTIC IgE is triggered independently of reaginic antibodies. ANTIBODY REACTIONS These reactions do not require prior exposure, and patients may not react on every occasion. Most cases of anaphylaxis are IgE, or rarely IgG4, Anaphylactoid reactions may be due to mediated.8 Following previous exposure to an complement activation, coagulation/fibrinolysis antigen, IgE reaginic antibodies are released into system activation, or the direct pharmacological the circulation by plasma cells derived from B- release of mediators.8 lymphocytes, under the influence of helper T-cells. These antibodies bind to glycoprotein receptors COMPLEMENT ACTIVATION on tissue mast cells or blood-borne basophils, thereby sensitizing them. Subsequent re-exposure Complement activation via the classical pathway to the antigen cross-links the Fab portions of two or alternate pathway leads to the formation of surface-bound IgE molecules, activating the cell anaphylatoxins C3a, C4a and C5a. These and triggering the release of chemical mediators.9'10 anaphylatoxins stimulate mast cells and basophils In normal subjects there are up to 100 000 surface- to degranulate, releasing mediators that cause http://emj.bmj.com/ bound IgE molecules per mast cell, and in atopic local and systemic reactions. C3a and C5a also subjects up to half a million." directly induce increased vascular permeability, A vast range of substances induce IgE antibody smooth muscle contraction and neutrophil formation (see Table 2), including the following: chemotaxis.14,15 protein drugs such as insulin and ACTH; non- COAGU LATION/FI BRINOLYSIS on September 24, 2021 by guest. Protected copyright. Table 1. Causes of anaphylaxis/anaphylactoid SYSTEM ACTIVATION reactions Activation of the coagulation/fibrinolysis system Anaphylactic: IgE mediated via Hageman Factor XII leads either to plasmin See Table 2 production and activation of complement, or to the production of kinins such as bradykinin that cause Anaphylactoid: Non-IgE mediated (1) Complement activation vasodilatation and increased vascular (a) Classical pathway permeability.8"11 (b) Alternate pathway (2) Coagulation/fibrinolysis system activation DIRECT PHARMACOLOGICAL (3) Direct pharmacological release of mediators (a) Direct histamine release RELEASE OF MEDIATORS (b) Modulators of arachidonic acid metabolism The pharmacological release of mediators is seen (c) Sulphiting agents with opioids or radiocontrast media that release (4) Physical histamine directly.1'617 Alternatively, aspirin and (a) Exercise induced other non-steroidal anti-inflammatory drugs 90 (5) Idiopathic modulate arachidonic acid metabolism by 1994 Emergency Medicine Anaphylactic Table 2. Common causes of IgE (1) Protein drugs (hormones) shock: antibody formation J Accid Emerg Med: first published as 10.1136/emj.12.2.89 on 1 June 1995. Downloaded from Insulin, ACTH, vasopressin mechanisms and (2) Non-protein drugs (haptens) treatment (a) Antibiotics Penicillin, sulphonamides, cephalosporins (b) Vitamins Thiamine, folic acid (3) Vaccines (allergy probably to cultivating tissue) Pertussis, typhoid (4) Foods Eggs, fish, nuts, chocolate, fruits (5) Venoms Bee, wasp, fire ant, snake (6) Foreign protein agents Tetanus antitoxin, gamma globulin, venom antitoxin, semen (7) Enzymes Trypsin, chymotrypsin, penicillinase (8) Allergen extracts Pollen, mould, animal dander (9) Chemicals Ethylene oxide gas, formaldehyde (10) Parasites Hydatid cyst rupture (11) Latex Surgical gloves, catheter-tip interfering with the cyclo-oxygenase pathway, plasma histamine, suggesting that other equally leading to enhanced formation of lipoxygenase important mediators are involved. Mast cells and products such as the leukotrienes. Mast cell circulating basophils are the key cells in the allergic degranulation is not involved.'4 response, and produce two main groups of mediators following triggering.22 RARE, PHYSICAL AND http://emj.bmj.com/ IDIOPATHIC CAUSES PRIMARY, PREFORMED, Rare causes of anaphylactoid reactions include GRANULE-ASSOCIATED sulphiting agents used as food preservatives, and MEDIATORS exercise-induced anaphylaxis, first described in 1980, in which anaphylaxis is triggered by exertion, First, antigen cross links two surface-bound IgE on September 24, 2021 by guest. Protected copyright. or exertion following
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