Etiology

The most common causes of anaphylaxis in children are different for hospital and community settings. Anaphylaxis occurring in the hospital results primarily from allergic reactions to medications and latex. Food allergy is the most common cause of anaphylaxis occurring outside the hospital, accounting for about one half of the anaphylactic reactions reported in pediatric surveys from the USA, Italy, and South Australia (Table 143-1). Peanut allergy is an important cause of food-induced anaphylaxis, accounting for the majority of fatal and near-fatal reactions. In the hospital, latex is a particular problem for children undergoing multiple operations, such as patients with spina bifida and urologic disorders, and has prompted many hospitals to switch to latex-free products. Patients with latex allergy may also experience food-allergic reactions from homologous proteins in foods such as bananas, kiwi, avocado, chestnut, and passion fruit.

Epidemiology

The overall annual incidence of anaphylaxis in the United States is estimated at 50 cases/100,000 persons/yr, totaling >150,000 cases/yr. An Australian parental survey found that 0.59% of children 3-17 yr of age had experienced at least 1 anaphylactic event.

Pathogenesis

Principal pathologic features in fatal anaphylaxis include acute pulmonary hyperinflation, pulmonary edema, intra-alveolar hemorrhaging, visceral congestion, laryngeal edema, and urticaria and angioedema. Acute hypotension is attributed to vasomotor dilation and/or cardiac dysrhythmias.

Most cases of anaphylaxis are the result of activation of mast cells and basophils via cell-bound allergen-specific IgE molecules. Patients initially must be exposed to the responsible allergen to generate allergen-specific antibodies. In many cases, the child and the parent are unaware of the initial exposure, which may be due to passage of food proteins in maternal breast milk. When the child is reexposed to the sensitizing allergen, mast cells and basophils and possibly other cells such as macrophages release a variety of mediators (histamine, tryptase) and cytokines that can produce allergic symptoms in any or all target organs. Clinical anaphylaxis may also be caused by mechanisms other than IgE-mediated reactions, sometimes termed anaphylactoid reactions, including direct release of mediators from mast cells by medications and physical factors (morphine, exercise, cold), disturbances of leukotriene metabolism (aspirin and nonsteroidal anti-inflammatory drugs), immune aggregates and complement activation (blood products), and probable complement activation (radiocontrast dyes, dialysis membranes).

Clinical Manifestations and Diagnosis

The onset of symptoms may vary somewhat depending on the cause of the reaction. Reactions from ingested allergens (foods, medications) are delayed in onset (minutes to 2 hr) compared with those from injected allergens (insect sting, medications) and tend to have more gastrointestinal symptoms. Initial symptoms vary with the etiology and may include any of the following constellation of symptoms: pruritus about the mouth and face; a sensation of warmth, weakness, and apprehension (sense of doom); flushing, urticaria and angioedema, oral or cutaneous pruritus, tightness in the throat, dry staccato cough and hoarseness, periocular pruritus, nasal congestion, sneezing, dyspnea, deep cough and wheezing; nausea, abdominal cramping, and vomiting, especially with ingested allergens; uterine contractions (manifesting as lower back pain; not uncommon); and faintness and loss of consciousness in severe cases. Some degree of obstructive laryngeal edema is typically encountered with severe reactions. Cutaneous symptoms may be absent in up to 20% of cases, and the acute onset of severe bronchospasm in a previously well asthmatic person should suggest the diagnosis of anaphylaxis. Sudden collapse in the absence of cutaneous symptoms should also raise suspicion of vasovagal collapse, myocardial infarction, aspiration, pulmonary embolism, or seizure disorder. Laryngeal edema, especially with abdominal pain, suggests hereditary angioedema (Chapter 142).

Laboratory Findings

Laboratory studies may indicate the presence of IgE antibodies to a suspected causative agent, but this result is not definitive. Plasma histamine is elevated for a brief period but is unstable and difficult to measure in a clinical setting. Plasma β-tryptase is more stable and remains elevated for several hours but often is not elevated, especially in food-induced anaphylactic reactions.

Diagnosis

A National Institutes of Health (NIH)–sponsored expert panel has recommended an approach to the diagnosis of anaphylaxis (Table 143-2). The differential diagnosis includes other forms of shock (hemorrhagic, cardiogenic, septic), vasopressor reactions including flush syndromes such as carcinoid syndrome, excess histamine syndromes (systemic mastocytosis), and ingestion of monosodium glutamate (MSG), scombroidosis, and heriditary angioedema. In addition, panic attack, vocal cord dysfunction, pheochromocytoma, and red man syndrome (due to vancomycin) should be considered.

Table 143-2 DIAGNOSIS OF ANAPHYLAXIS

Anaphylaxis is highly likely when any one of the following three criteria is fulfilled:

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