Anaphylactic reactions are type I, IgE-mediated reactions and result from many causes (Table 81-3). Cross-linking of the IgE molecule with the allergen leads to IgE receptor activation on the mast cell and basophil and release of mediators, including histamine, tryptase, tumor necrosis factor, platelet-activating factor, leukotrienes, prostaglandins, and cytokines. Other cell types involved in the reactions include monocytes, macrophages, eosinophils, neutrophils, and platelets. The mediator release results in the clinical picture of anaphylaxis.
From Young MC: General treatment of anaphylaxis. In Leung DYM, Sampson
HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 644. *In order of frequency.
Anaphylactoid reactions are due to nonimmunologic mechanisms. Mast cells and basophils can be activated by direct, nonspecific stimulation, although the exact underlying mechanism is unknown. Reactions to agents, such as opiates and radiocontrast material, are classic examples. Complement system activation also can result in mast cell and basophil activation. Anaphylatoxins, C3a and C5a, are named because of their ability to trigger mediator release and are generated in serum sickness. The most common cause of this type of reaction is transfusion with blood products. There are other causes of anaphylactoid reactions for which the mechanism has not been clarified.
Urticaria and angioedema are common skin conditions affecting 15% to 25% of individuals at some point in their lives. Most cases of urticaria are self-limited, but, for some patients, they are chronic. In approximately 50% of patients, urticaria and angioedema occur together. In the remaining 50%, 40% have urticaria alone and 10% have angioedema alone. The incidence of anaphylaxis in children is unknown.
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Raised, erythematous lesions with pale centers that are intenselypruritic characterize urticaria, commonly called hives (Fig. 81-1). The lesions vary in size and can occur anywhere on the body. Typically urticaria arises suddenly and may resolvewithin 1 to 2 hours or may persist for 24 hours. Angioedemais a similar process that involves the deeper dermis or subcutaneous tissue, with swelling as the principal symptom. Generally angioedema is not pruritic, may be mildly painful, andpersists for longer than 24 hours. In rare cases it may becomelife threatening if swelling affects the upper airway.
The clinical manifestations of anaphylaxis and anaphylactoid reactions are the same for children and adults. The signs and symptoms vary and can range from mild skin findings to a fatal reaction. Ninety percent of patients present with cutaneous symptoms, including urticaria, angioedema, flushing, and warmth; the absence of dermal symptoms does not exclude the diagnosis of anaphylaxis. Other affected organ systems include the respiratory tract (rhinorrhea, oropharyngeal edema, laryngeal edema, hoarseness, stridor, wheezing, dyspnea, and asphyxiation), cardiovascular system (tachycardia, hypotension, shock, syncope, and arrhythmias), gastrointestinal tract (nausea, abdominal pain, crampy diarrhea, and vomiting), and neurologic system (syncope, seizure, dizziness, and a sense of impending doom). The severity of an anaphylactic reaction is often proportionate to the speed of symptom onset.