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The word anaphylaxis (ana: backward; phylaxis: guard, or “against protection”) was coined by Paul Portier and Charles Richet, two scientists who unexpectedly induced acute anaphylaxis in their experimental dogs during an attempt to produce vaccines for prophylaxis against a toxin (actinotoxin) from a sea anemone, Actinia sulcata.1 Anaphylaxis is a severe, life-threatening, systemic event caused by immediate hypersensitivity reaction. Although it is relatively infrequent during pregnancy, the potentially fatal effects on the mother and the unborn baby warrant prompt recognition and immediate management. Severe anaphylaxis, in general, affects 1 to 3 per 10,000 population,2 but the incidence during anesthesia is reported to range from as high as 1 in 4000 to 1 in 25,000.3 The prevalence of anaphylaxis in pregnant patients is approximately 3 per 100,000 deliveries.4


Anaphylaxis is a systemic form of immediate hypersensitivity reaction caused by immunoglobulin E (IgE)–mediated release of mediators from mast cells and basophils. Exposure to allergen in a susceptible individual initiates a cascade of events, including activation of helper T-2 cells (TH2 cells) and stimulation of IgE-secreting B cells. IgE then binds to FceRI receptors on mast cells and basophils. After several episodes of exposure to the inciting allergen, a cross-linkage develops between the receptors by the allergen that triggers the mast cells to release mediators, including histamine, tryptase, tumor necrosis factor, and so on. These mediators then produce the serious manifestations of anaphylactic reaction in various organ systems such as the respiratory system (stridor, bronchospasm, hypoxia), cardiovascular system (hypotension, tachycardia, dysrhythmia), cutaneous system (erythema, pruritus, urticaria, angioedema), and gastrointestinal system (nausea, vomiting, diarrhea).5

Pregnant patients are thought to be predisposed to anaphylaxis as a result of alteration in cellular immunity, possibly due to increased level of progesterone.6 Also, increased production of TH2-type cytokine (which initiates the immediate hypersensitivity reaction) by maternal T cells at the fetomaternal interface and simultaneous inhibition of cytokine production from TH1 cells (which normally play a role in allograft rejection) during pregnancy help to maintain the pregnancy and to prevent fetal loss.7,8


During anesthesia, neuromuscular blocking agents (succinylcholine, rocuronium), latex (gloves, tourniquet), and antibiotics (penicillins and other cephalosporins) are implicated as the most common agents in the etiology of anaphylactic reactions. Other less frequently involved agents include colloids, propofol, chlorhexidine, iodinated contrast media, local anesthetics, and so on.9,10

In one of the earliest reports, succinylcholine was implicated to be a causative agent for anaphylaxis in pregnant women.11 Several other agents have since been implicated in obstetric patients, including muscle relaxants,12 anesthetic induction agents,13 bee stings,14 latex,15, 16, 17, and 18 latex and chlorhexidine,19 synthetic colloid solutions,20,21 ranitidine,22,23 iron,24 antivenin after ...

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