DESCRIPTION

• Anaphylaxis is a serious, life-threatening, systemic allergic reaction that is rapid in onset, and is a result of mast cell and basophil activation and degranulation.
• Skin and mucosal symptoms such as flushing, itching, urticaria, or angioedema are present in 80–90% of patients with anaphylaxis. However, absence of skin findings does not exclude anaphylaxis.
• In fatal anaphylaxis, initial signs and symptoms may include respiratory distress without urticaria resulting in delayed diagnosis and treatment.

EPIDEMIOLOGY

• 1.6–5.1% lifetime prevalence
• Rate of occurrence appears to be increasing.
• Fatal in 0.5 to 0.7 cases per million people

ETIOLOGY

• IgE-mediated:
  • Foods (peanut, tree nuts, fish, shellfish, milk, egg, wheat, soy, sesame)
  • Medications (antibiotics especially β-lactams, NSAIDs, biologic products)
  • Venoms (usually from stinging insects, including fire ants)
  • Latex (direct exposure to natural rubber or ingestion of cross-reacting foods)
  • Other (vaccines, occupational allergens, and rarely inhaled allergens)
• Non–IgE-mediated:
  • Radiocontrast media (can also trigger IgE-mediated anaphylaxis)
  • Medications (opiates, NSAIDs, dextrans, vancomycin, polymyxin B)
  • Physical stimuli (exercise, cold, heat)
  • Ethanol
• If no identifiable trigger is found, anaphylaxis may be idiopathic in origin.

RISK FACTORS

Risk factors for severe anaphylaxis include the following:

• Asthma
• Older age
• Cardiovascular disease
• Mast cell disorder
• On β-blocker or angiotensin-converting enzyme (ACE) inhibitor therapy

PATHOPHYSIOLOGY

• In anaphylaxis, mast cells and basophils are activated via an IgE-mediated (most common) or non–IgE-mediated mechanism releasing preformed and newly generated mediators of inflammation.
  • Mediators include histamine, tryptase, proteoglycans, leukotrienes, prostaglandins, platelet-activating factor, and cytokines.
  • Local or systemic effects can include increased vascular permeability, vasodilation, smooth muscle contraction, complement activation, and coagulation.
• IgE-mediated anaphylaxis occurs when IgE is synthesized in response to allergen exposure (sensitization) and binds to high-affinity IgE receptors located on the surface of mast cells and basophils. Subsequent allergen exposure results in receptor-bound IgE aggregation and cell activation with mediator degranulation.
• Non–IgE-mediated anaphylaxis generally results from nonimmune stimulation of mast cells or basophils. Rarely, IgG and complement can be implicated.