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HIGH-YIELD FACTS

  • Epinephrine is the first-line medication for the treatment of anaphylaxis, regardless of the severity.

  • In children, food is the most common trigger for anaphylaxis.

  • Airway compromise can occur rapidly.

  • If there is hypotension in anaphylaxis, give two to three fluid boluses (20 cc/kg) in addition to epinephrine; if hypotension persists, an epinephrine continuous infusion should be considered.

Anaphylaxis is a severe, potentially life-threatening syndrome due to a hypersensitivity reaction involving two or more organ systems. It often occurs within minutes after exposure to an offending allergen; however, it can present up to many hours after. Manifestations can include a pruritic rash, urticaria, or angioedema; nausea, vomiting, or abdominal pain; respiratory compromise associated with airway edema and bronchospasm; and cardiovascular compromise that can result in distributive shock.

The estimated rate of anaphylaxis in the pediatric population in the United States ranges from 0.18% to 0.54%; however, this likely is an underestimate of the true severity of the problem due to underdiagnosis, underreporting, and miscoding.1,2 Food allergy is the most common cause of anaphylaxis (up to 85% of pediatric cases), and is increasing in frequency with over 170 known food allergens.3–5 Anaphylaxis from food allergy leads to approximately 150 fatalities in the United States each year, and the more rapid the onset of symptoms, the more likely the reaction will be life-threatening.6,7 In up to 50% of all anaphylaxis cases, adults and children, no precipitating cause is initially identified; therefore the emergency physician must have a high level of suspicion for the disorder to recognize the symptoms and initiate proper treatment.8 Asthma and atopy are known to have a strong association with anaphylaxis, which may aid in a more rapid diagnosis.5,9,10

PATHOPHYSIOLOGY

Anaphylaxis is a syndrome that can be caused by multiple immunologic pathways.3 Anaphylactic reactions are primarily mediated by IgE. An initial exposure to an allergen results in the development of a specific IgE antibody to the antigen which resides on the cell membrane of basophils and mast cells. When a subsequent exposure to the allergen occurs, the allergen binds to the IgE on the basophil and mast cells, and stimulates the release of multiple mediators, including histamine, tryptase, leukotrienes, and prostaglandins.3 These mediators lead to increased production and release of respiratory secretions, increased bronchial smooth muscle tone, decreased vascular smooth muscle tone, and increased capillary permeability.

Non-IgE–mediated pathways for anaphylaxis include direct release of immunomodulators from both mast cells and basophils. Inciting substances for the non-IgE–mediated pathway include latex and antibiotics and do not need prior exposure to trigger the response.3

Anaphylactoid reactions can also result in anaphylaxis; however, this is due to direct activation of the complement pathway or the bradykinin cascade.3 Intravenous (IV) contrast allergy is an example of an anaphylactoid reaction.

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