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ANAPHYLAXIS

Anaphylaxis is an acute, potentially life-threatening systemic allergic reaction. It is most commonly triggered by interaction of an allergen with specific IgE antibody bound to mast cells and basophils, leading to cell activation and mediator release. Non–IgE-mediated direct mast-cell degranulation can also result in mediator release.

Epidemiology

  • Lifetime prevalence for all triggers is 0.05–2%.

  • Incidence is thought to be increasing.

  • Food is the most common cause of anaphylaxis, affecting up to 8% of young children and 3–4% of adults.

  • Drugs are the second most common cause of anaphylaxis.

  • Approximately 1% of all cases of anaphylaxis (all causes) have a fatal outcome in the United States (including ~200 from food).

Etiology

  • Major causes are food (milk, egg, soy, wheat, peanut, tree nut, fish, and shellfish), medications (antibiotics, aspirin, NSAIDs, biologics, chemotherapeutics, muscle relaxants, blood products, radiocontrast media), latex, insect stings (especially bee venom), and allergy immunotherapy

  • Rare causes include

    • ✓ Exercise-induced anaphylaxis—reaction triggered by exertion, cardiovascular exercise, or fast-paced walking. Reaction may be food-dependent (anaphylaxis occurs with exercise only after eating a specific food) or independent of food exposure.

    • ✓ Alpha-1,3-galactose (alpha-gal syndrome)—tick-related immune response following a bite by a Lone Star tick. Patients experience characteristic a delayed mild-to-severe systemic allergic reaction after ingestion of red meat.

    • ✓ Idiopathic anaphylaxis—may be related to hormone cycle, rare hidden food additives or underlying mast-cell instability.

Differential Diagnosis

  • Other causes of shock: Hypovolemic, cardiogenic, and septic

  • Cardiopulmonary instability: Myocardial infarction, pulmonary embolism, pneumothorax, vasovagal reaction

  • Allergic/immunologic: Status asthmaticus, scombroid poisoning, hereditary angioedema, non–IgE-mediated reactions (serum sickness, DRESS, leukotriene-mediated reactions)

  • Oncologic/hematologic: Carcinoid syndrome, pheochromocytoma, systemic mastocytosis (which increases risk of anaphylaxis)

Pathophysiology

  • Previous exposure to an allergen (antigen) leads to allergen-specific IgE antibody production.

    • ✓ IgE binds to the surface of mast cells and basophils.

    • ✓ Upon subsequent exposure, the antigen binds cell-bound IgE, triggering cell activation and degranulation.

    • ✓ Sometimes, there is no known prior allergen exposure and reaction occurs on the first known exposure.

  • Mediators involved include histamine, arachidonic acid derivatives (prostaglandins and leukotrienes), tryptase, bradykinin, and platelet-activating factor.

    • ✓ These mediators cause smooth-muscle spasm (bronchi, coronary arteries, and gastrointestinal tract), increased vascular permeability, vasodilation, and complement activation.

    • ✓ Conditions that may develop include urticaria, angioedema, wheezing, emesis, diarrhea, hypotension, and occasionally altered mental status.

  • Nonimmunologic (previously known as anaphylactoid) reactions result from non–IgE-mediated degranulation of mast cells and basophils. This can occur with radiocontrast media, NSAIDs, opiates, and other agents

Clinical Manifestations

  • Exposure to a known allergen and/or prior history of anaphylaxis is a helpful sign, but it is not always present.

  • Onset is typically within 30 minutes after exposure to allergens. Symptoms typically progress very rapidly. At times, reactions may occur up to 2 hours after exposure

  • When treated, symptoms usually resolve ...

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