Anaphylaxis

Abstract

Anaphylactic reactions are acute medical emergencies characterized by the abrupt onset of hemodynamic instability, respiratory distress from bronchoconstriction or laryngeal edema, urticaria, and angioedema. These clinical manifestations may occur singly or in any combination. Inciting stimuli are diverse, ranging from penicillin, Hymenoptera venom, and radiographic contrast media to exercise. The pathogenesis usually involves interaction of an antigen with specific immunoglobulin E (IgE) antibodies on the surface of mast cells or basophils, which then results in the release of chemical mediators from intracytoplasmic granules and the generation of arachidonic acid metabolites, including prostaglandin D2, and leukotrienes B4, C4, D4, and E4, at the cell membrane. Mediator release from mast cells and basophils may also be stimulated by non-IgE mechanisms, such as complement activation or direct mast cell/basophil activation. Mast cell and basophil—derived mediators have a panoply of effects, including vasodilatation, increased vascular permeability, smooth muscle contraction, airway mucous gland hypersecretion, and chemotaxis of neutrophils and eosinophils. These cellular events result in the observed clinical features. Effective treatment depends on prompt recognition of the clinical syndrome of anaphylaxis, interruption of antigen exposure and absorption when feasible, and administration of appropriate medication. Epinephrine is the drug of first choice for all of the manifestations of anaphylaxis. Adjunctive therapy with oxygen, fluid, H1 and H2 antihistamines, bronchodilators, corticosteroids, and other vasopressors is frequently necessary. Prevention of recurrence is vital. The roles of patient education, skin testing, pretreatment, and desensitization are reviewed.