Allergic anaphylaxis occurs when a patient’s immune system responds inappropriately to a food, drug, or other protein and is mediated by IgE (antibodies); like all allergic reactions, it requires pre-exposure. Common allergens are penicillin or other beta-lactam antibiotics, tree nuts, Hymenoptera venom, and shellfish. But…non-IgE mediated reactions can also occur: Originally known as an anaphylactoid reaction or idiopathic anaphylaxis, triggers act directly on both mast cells and basophils; they are not IgE mediated and do not require pre-exposure. Triggers for non-IgE mediated anaphylaxis include: vancomycin, opiates, aspirin, NSAIDs, temperature, and exercise. Signs, symptoms, and treatment for both IgE mediated and non-IgE mediated anaphylactic reactions is the same. Patient history while useful to avoid triggers, remains somewhat unreliable for predicting future events, especially initial reactions. And, anaphylaxis is on the rise. While epinephrine remains the mainstay of treatment, it is not always successful and fatalities are possible even with treatment. In most cases, anaphylaxis is a mono-phasic reaction: What you see is what you get. That said, roughly 20-30 percent of all anaphylactic reactions are biphasic with the original signs and symptoms returning 3-10+ hours later (rebound). H1 and H2 blockers (antihistamines) and corticosteroids are used to help prevent biphasic reactions, but are not always successful; the available data is inconclusive. Some outdoor programs with long evacuation times carry oral prednisone to be administered under direct physician control—via cell or satellite phone—or by written standing orders
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