Anaphylaxis is a dramatic and widespread acute atopic reaction marked by the sudden onset of rapidly progressive urticaria and respiratory distress. A severe anaphylactic reaction may precipitate vascular collapse, leading to systemic shock and, sometimes, death.
The causes of anaphylactic reaction are ingestion of or other systemic exposure to a sensitizing drug or other substance.
Sensitizing substances include serums (usually horse serum), vaccines, allergen extracts, enzymes (such as l-asparaginase), hormones, penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides, diagnostic chemicals (sulfobromophthalein, sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, and insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, mosquitoes, and certain spiders).
A common cause of anaphylaxis is penicillin, which induces anaphylaxis in 1 to 4 of every 10,000 patients treated with it. Penicillin is most likely to induce anaphylaxis after parenteral administration or prolonged therapy and in atopic patients who are allergic to other drugs or foods.
An anaphylactic reaction requires previous sensitization or exposure to the specific antigen, resulting in the production of specific immunoglobulin (Ig) E antibodies by plasma cells. This antibody production takes place in the lymph nodes and is enhanced by helper T cells. IgE antibodies then bind to membrane receptors on mast cells (found throughout connective tissue, often near small blood vessels) and basophils.
On reexposure, the antigen binds to adjacent IgE antibodies or cross-linked IgE receptors, activating a series of cellular reactions that trigger degranulation — the release of powerful preformed chemical mediators (such as histamine, prostaglandins, and platelet activating factor) from mast cell stores. IgG or IgM enters into the reaction and activates the release of complement fractions.
This acute phase of the response occurs within minutes of exposure. Because of the systemic nature of the exposure, activation of mast cells is widespread, and the massive release of these powerful mediators near blood vessels leads to vascular collapse by stimulating contraction of certain groups of smooth muscles and by increasing vascular permeability. In turn, increased vascular permeability leads to decreased peripheral resistance and plasma leakage from the circulation to extravascular tissues (which lowers blood volume, causing hypotension, hypovolemic shock, and cardiac dysfunction).
In the later phase of this response (8 to 12 hours later), other mediators are synthesized and released, including chemokines, leukotrienes, and cytokines. These agents mediate the inflammatory response by recruiting eosinophils and lymphocytes. This delayed response may be less dramatic than the acute phase of anaphylaxis, but with a diffuse inflammatory response, further smooth-muscle contraction and edema can occur and progress to grave systemic symptoms.
An anaphylactic reaction produces sudden physical distress within seconds or minutes after exposure to an allergen. A delayed or persistent reaction may occur up to 24 hours later. The severity of the reaction is inversely related to the interval between exposure to the allergen and the onset of symptoms. Usually, the first signs and symptoms include a feeling of impending doom or fright, weakness, sweating, sneezing, shortness of breath, nasal pruritus, urticaria, and angioedema, followed rapidly by symptoms in one or more target organs.
Cardiovascular signs include hypotension, shock, and sometimes cardiac arrhythmias, which, if untreated, may precipitate circulatory collapse.
Respiratory signs and symptoms can occur at any level in the respiratory tract and commonly include nasal mucosal edema, profuse watery rhinorrhea, itching, nasal congestion, and sudden sneezing attacks. Edema of the upper respiratory tract, resulting in hypopharyngeal and laryngeal obstruction (hoarseness, stridor, and dyspnea), is an early sign of acute respiratory failure, which can be fatal.
GI and genitourinary signs and symptoms include severe stomach cramps, nausea, diarrhea, and urinary urgency and incontinence.
Anaphylaxis can be diagnosed by the rapid onset of severe respiratory or cardiovascular symptoms after ingestion or injection of a drug, vaccine, diagnostic agent, food, or food additive or after an insect sting. If these symptoms occur without a known allergic stimulus, rule out other possible causes of shock (such as acute myocardial infarction, status asthmaticus, and heart failure).
Caution: Rapid infusion of aminophylline may cause or aggravate severe hypotension.
CLINICAL TIP: Even after the acute anaphylactic event has been controlled, patients must be counseled about the risks of delayed signs and symptoms. Any recurrence of shortness of breath, chest tightness, sweating, angioedema, or other signs and symptoms must be reported immediately.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
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