Anaphylaxis

Basics

Systemic, generalized response to an allergen, typically soon after exposure

Description

  • Immunologically mediated (IgE, IgG, and immune complex complement related) acute systemic reaction following antigen exposure in a sensitized person
  • Nonimmunologically mediated acute systemic reactions are called “nonallergic anaphylaxis,” the term anaphylactoid reaction has been eliminated.
  • System(s) affected: cardiovascular, endocrine/metabolic, gastrointestinal (GI), hematologic/lymphatic/immunologic, pulmonary, and skin/exocrine

Epidemiology

  • Predominant age: all ages
  • Predominant sex: male = female

Incidence

  • Up to 47,000 cases of idiopathic anaphylaxis with no identifiable cause occur each year.
  • Drug-induced anaphylaxis occurs in 1/2,700 hospitalized patients (most common = antibiotics).
  • Anaphylaxis deaths: 0.3 to 0.7/100,000 per year
  • Food allergic reactions constitute 1/3 to 1/2 of all anaphylactic reactions worldwide.
  • Asthmatics are at a higher risk of severe anaphylaxis than nonasthmatics. Female asthmatics are at greater risk of anaphylaxis than males.
  • Common triggers
    • Antibiotics, NSAIDs, latex, perioperative anaphylaxis (muscle relaxants), radiocontrast media, hymenoptera stings, food, antisera, reactions associated with dialysis (hollow-fiber dialyzers), biologic agents, idiopathic

Etiology and Pathophysiology

  • IgE-mediated mast cell degranulation with release of biochemical mediators and chemotactic substances
  • Chemical mediators: Histamine and products of arachidonic acid metabolism (leukotrienes, thromboxane, prostaglandins, and platelet-activating factor) cause smooth muscle spasm, mucus secretion, increased vascular permeability, activation of nociceptive neurons, platelet adherence, eosinophil activation, and chemotaxis.
  • Mast cell and basophils recruit other inflammatory pathways including kallikrein-kinin, complement, and coagulation pathways.
  • Anaphylactic shock (distributive plus hypovolemic): fluid extravasation causing hemoconcentration and reduced venous return to the heart equals low-filling pressure and reduced cardiac output

Genetics
Genetic predisposition for sensitization to antigens

Risk Factors

  • Previous anaphylaxis
  • History of atopy or asthma

General Prevention

  • Strictly avoid inducing drugs and foods.
  • For those with history of anaphylaxis, carry epinephrine autoinjector at work/school and in vehicle. Protect autoinjectors from temperature extremes.
  • If allergic to bee stings, avoid areas where insect exposure is likely. Avoid wearing insect attractants (e.g., perfumes, colored clothing); avoid bare feet outdoors.
  • Carry or wear a medical alert ID about the anaphylaxis-causing substance or event.
  • Caution with use of β-blockers, ACE inhibitors, ARBs, MAOIs, and some TCAs if other agents will suffice (will decrease effectiveness of epinephrine)
  • When radiologic contrast is unavoidable, use of low-osmolar contrast agents (e.g., iothalamate) reduces the risk of contrast reactions to 3%.
    • Only 0.2% were considered severe.
    • Stop β-blockers before using contrast materials.
    • Pretreat with diphenhydramine (50 mg IV) and steroid (e.g., methylprednisolone 60 mg IV q6h) until procedure. Start methylprednisolone the day before the procedure is scheduled.
ALERT
  • Have a latex-free kit (gloves, etc.) available for the treatment of latex-allergic patients. Some latex-allergic patients react to tropical fruits, such as kiwi, bananas, avocados, and chestnuts.
  • Avoid β-blockers.

Commonly Associated Conditions

  • Asthma
  • Atopy

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