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Anaphylaxis is a potentially fatal acute allergic response that causes a sudden release of mast cell and basophil mediators, which often then results in multiple organ system abnormalities.


IgE-mediated anaphylaxis occurs after allergen-specific IgE antibodies bind to high-affinity mast cell and basophil receptors, causing mast cell and basophil degranulation. Non–IgE-mediated anaphylaxis involves the direct release of mast cell and basophil mediators independent of receptor binding. Typical IgE-mediated triggers include foods, insect stings, latex, and antibiotics, while non-IgE mediated triggers include opiates, contrast dyes, and blood transfusions.

H1 receptor stimulation can cause vasodilation, tachycardia, and bronchospasm.

H1 and H2 receptor stimulation are involved in headache, vascular permeability, flushing, hypotension, pruritis, and nasal congestion.1


The yearly incidence of anaphylaxis is still less than 1% despite increases in the incidence and prevalence of allergic disease. Death is rare, with prior studies showing case fatality rates of 0.6%2 and an incidence of anaphylaxis of 10.5 per 100,000 person years in pediatric cases reviewed.3 Patients with atopy are at increased risk for anaphylaxis, women have a higher incidence than men, and in many cases the cause of anaphylaxis goes undetermined.4 In patients with multiple allergic reactions and in those with insect venom hypersensitivity, a baseline tryptase is advised to screen for mastocytosis.

In the inpatient setting, antibiotics, blood products, contrast materials, latex, and muscle relaxants are common triggers.5 Food anaphylaxis is now the most common cause of anaphylaxis in the emergency rooms in the United States, and peanuts, tree nuts, fish, and shellfish account for the most severe food reactions.6

Other common allergenic foods include milk, egg, wheat, soy, and sesame. Bee stings, medication allergies, exercise, and vaccines, including allergen immunotherapy, are other common triggers.


The majority of anaphylactic reactions occur within 1 hour of exposure, and a more rapid symptom onset usually yields a more severe reaction. Intravenous exposures generally cause more immediate and severe reactions, while oral exposure usually results in a more delayed presentation and more gastrointestinal symptoms. Table 47-1 lists the clinical criteria for diagnosing anaphylaxis. Fatalities tend to occur within 30 minutes after allergen exposure due to cardiovascular collapse and/or respiratory failure. Cardiovascular collapse can occur in anaphylaxis without cutaneous or respiratory symptoms. In biphasic anaphylactic reactions, symptoms, often more severe, recur after resolution of the initial symptoms. Most biphasic reactions will occur within half an hour to 4 hours after the initial symptoms. There are reports of biphasic symptoms up to 12 hours later. Delayed epinephrine administration and more severe initial symptoms have been noted to be associated with biphasic reactions.

TABLE 47-1Clinical Criteria for Diagnosing Anaphylaxis

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