Anaphylaxis
A dramatic, acute atopic reaction, anaphylaxis is marked by the sudden onset of rapidly progressive urticaria and respiratory distress. A severe reaction may initiate vascular collapse, leading to systemic shock and possibly death.
Causes
Anaphylactic reactions result from systemic exposure to sensitizing drugs or other specific antigens. Such substances may be serums (usually horse serum), vaccines, allergen extracts (such as pollen), enzymes (L-asparaginase), hormones,
penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides (such as iron dextran), diagnostic chemicals (sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, and certain spiders) and, rarely, a ruptured hydatid cyst.
penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides (such as iron dextran), diagnostic chemicals (sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, and certain spiders) and, rarely, a ruptured hydatid cyst.
The most common anaphylaxis-causing antigen is penicillin. This drug induces a reaction 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.
After initial exposure to an antigen, the immune system responds by producing specific immunoglobulin antibodies in the lymph nodes. Helper T cells enhance the process. These antibodies (IgE) then bind to membrane receptors located on mast cells (found throughout connective tissue) and basophils.
When the body reencounters the antigen, the IgE antibodies, or cross-linked IgE receptors, recognize the antigen as foreign. This activates a series of cellular reactions that, if left unchecked, will lead to rapid vascular collapse and, ultimately, hemorrhage, disseminated intravascular coagulation, and cardiopulmonary arrest.
Complications
Untreated anaphylaxis causes respiratory obstruction, systemic vascular collapse, and death minutes to hours after the first signs and symptoms appear (although a delayed or persistent reaction may occur for as long as 24 hours).
Assessment
The patient, a relative, or another responsible person will report the patient’s exposure to an antigen. Immediately after exposure, the patient may complain of a feeling of impending doom or fright, weakness, sweating, sneezing, dyspnea, nasal pruritus, and urticaria. He may appear extremely anxious. Keep in mind that the earlier the signs and symptoms begin after exposure to the antigen, the more severe the anaphylaxis.
On inspection, the patient’s skin may display well-circumscribed, discrete cutaneous wheals with erythematous, raised, serpiginous borders and blanched centers. They may coalesce to form giant hives.
Angioedema may cause the patient to complain of a “lump” in his throat, or you may hear hoarseness or stridor. Wheezing, dyspnea, and complaints of chest tightness suggest bronchial obstruction. These are early signs of impending, potentially fatal respiratory failure.
Other effects may follow rapidly. The patient may report GI and genitourinary effects, including severe stomach cramps, nausea, diarrhea, and urinary urgency and incontinence. Neurologic effects include dizziness, drowsiness, headache, restlessness, and seizures. Cardiovascular effects include hypotension, shock, and cardiac arrhythmias, which may precipitate vascular collapse if untreated.
Diagnostic tests
No tests are required to identify anaphylaxis. The patient’s history and signs and symptoms establish the diagnosis. If signs and symptoms occur without a known allergic stimulus, other possible causes of shock, such as acute myocardial infarction, status asthmaticus, or heart failure, must be ruled out.