The phenomenon of anaphylaxis was discovered by Portier and Richet in 1903.[1,2] They injected dogs with toxins from sea anemone with the intent of generating protective antibodies. Unexpectedly, they found that certain dogs became ill with a rapid heartbeat and collapse. Because this syndrome was the precise opposite of protection or prophylaxis, they termed it anaphylaxis.
Subsequent investigations have shown that anaphylaxis is an immunologically mediated event, most commonly associated with production of IgE antibodies in humans.[3] Animal models have shown that both IgE and IgG antibody classes can trigger anaphylaxis. Mast cells and basophils possess the high affinity IgE receptor, FcεR1, and release mediators of anaphylaxis, including histamine, tryptase, carboxypeptidase A, prostaglandin D2, leukotrienes, and platelet-activating factor (PAF) following activation.[4]
Anaphylaxis is a serious and impressive immunologic reaction with an abrupt, and often unexpected, onset and potentially rapid, fatal outcome if untreated.
Characteristics of Anaphylaxis
Diagnosis of Anaphylaxis
Criteria for Grading the Severity of Anaphylaxis
Recently, criteria for grading the severity of anaphylaxis have also been utilized.[7,8] These criteria specify three categories:
• Grade 1: acute allergic reaction
• Grade 2: mild to moderate anaphylaxis
• Grade 3: severe anaphylaxis
Patients with an acute allergic reaction (grade 1 anaphylaxis) only have cutaneous and upper respiratory tract findings, such as generalized skin lesions, pruritus, rhinitis/conjunctivitis, urticaria, local edema, and angioedema, without any systemic symptoms or signs or evidence of other organ involvement.
Patients with mild to moderate anaphylaxis (grade 2) have evidence of grade 1 anaphylaxis and respiratory, cardiovascular, gastrointestinal, or neurologic features. The additional features include shortness of breath or dyspnea, wheeze, hoarseness, and nausea or vomiting with associated physical findings, such as bronchospasm, but with systolic blood pressure greater than 90 mm Hg, respiratory rate less than 25/min, and a normal Glasgow Coma Scale score.
Patients with severe anaphylaxis (grade 3) present with the findings listed for grade 2 and potentially life-threatening symptoms or signs. These include one or more of the following:
•Loss of consciousness, syncope, dizziness, or lightheadedness at any time
• Systolic blood pressure less than 90 mm Hg, Glasgow Coma Scale score less than 15 (related to cardiovascular system collapse and/or neurologic dysfunction from hypoperfusion, hypoxia)
•Dyspnea, wheeze, hoarseness, or bronchospasm
•Stridor, cyanosis, laryngeal edema, or a respiratory rate ≥ 25/min
Manifestations of anaphylaxis involving the cutaneous, gastrointestinal, and respiratory organs tend to worsen with each grade and have implications for treatment and life support. Thus, grade 1 anaphylaxis is characterized by involvement of only the skin, mucous membranes, and/or upper airway, whereas grade 2 or mild to moderate anaphylaxis is characterized by the same findings as grade 1 plus involvement of another organ system. Grade 3 or severe anaphylaxis is defined as the same features for grade 2 plus severe life-threatening respiratory or cardiovascular signs.
Classification and Causes of Anaphylaxis
Previously, anaphylaxis had been separated into categories such as true anaphylaxis and anaphylactoid reactions.[ 6] Anaphylactoid reactions were defined as similar to those of anaphylaxis, but triggered by non-IgE mechanisms, such as reactions to nonsteroidal anti-infl ammatory drugs, including aspirin(Drug information on aspirin) and ibuprofen(Drug information on ibuprofen), reactions to radiocontrast dye exposure, and exercise. More recently, anaphylaxis has been classified as immunologically mediated with subcategories of those reactions that are IgE-mediated and those that are not.[6]
Various agents stimulate IgE antibodies and cause IgE-mediated anaphylaxis. These include exposures primarily through ingestion, injection, or sting. Foods are common anaphylaxis-inducing agents, including peanuts, tree nuts, shellfish, milk, eggs, fish, soy, sesame seeds, and wheat in children, and shellfish in adults.[3] Approximately 3% of young children are allergic to milk[9] and approximately 2% of adults are sensitive to shellfish.[10]
Virtually any oral or injection medication may provoke an anaphylactic reaction, including injections of allergen employed in immunotherapy for the treatment of allergic respiratory disease.[11] An example of anaphylaxis mediated by IgG antibodies are transfusion reactions in patients deficient in IgA who have IgG antibodies to IgA.[12] Although the mechanism of anaphylaxis in IgA-deficient patients has not been thoroughly studied, it seems most likely that formation of immune complexes with fixation of complement and generation of anaphylatoxin are important.[13]
