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Anaphylaxis is a serious allergic reaction, with a rapid onset; it may cause death and requires emergent diagnosis and treatment. Consensus clinical criteria have been developed to provide consistency for diagnosis (Table 14-1).1,2,3
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The terms anaphylactic and anaphylactoid were previously applied to immunoglobulin E (IgE)-dependent and IgE-independent events, respectively. Because the final pathway in both events is identical, anaphylaxis is the term now used to refer to both.4 Hypersensitivity is an inappropriate immune response to generally harmless antigens, manifesting a continuum from minor to severe manifestations. Anaphylaxis represents the most dramatic and severe form of immediate hypersensitivity.
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Foods, medications, insect stings, and allergen immunotherapy injections are the most common provoking factors for anaphylaxis, but any agent capable of producing a sudden degranulation of mast cells or basophils can induce anaphylaxis (Table 14-2).5,6 Latex hypersensitivity is increasing in prevalence in the general population, with a resultant risk for anaphylaxis. In addition, a significant number of anaphylaxis cases have no identified cause, termed idiopathic anaphylaxis.7 The lifetime individual risk of anaphylaxis is estimated to be 1% to 3%, but the prevalence of anaphylaxis may be increasing.8 Although allergic reactions are a common cause for ED visits,9 anaphylaxis is likely underdiagnosed.10,11
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Anaphylaxis, for the most part, arises from the activation of mast cells and basophils through a mechanism involving crosslinking of IgE and aggregation of the high-affinity receptors for IgE.6 Upon activation, mast cells and/or basophils quickly release preformed mediators from secretory granules that include histamine, tryptase, carboxypeptidase A, and proteoglycans. Downstream activation of phospholipase A2, followed by cyclooxygenases and lipoxygenases, produces arachidonic acid metabolites, including prostaglandins, leukotrienes, and ...