Anaphylaxis

Anaphylaxis is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

Definition

Anaphylaxis is a rapidly developing, life-threatening systemic reaction mediated by the release of mast cell and basophil-derived mediators into the circulation. The peak severity is seen usually within 5–30 minutes.

Classification

Immunologic anaphylaxis

  • Allergic IgE-mediated anaphylaxis (type 1 hypersensitivity)
  • IgG-mediated anaphylaxis (rare)

Nonimmunologic anaphylaxis. Previously known as anaphylactoid reactions.

Epidemiology

Incidence of anaphylaxis is approximately 50–2000 episodes per 100,000 person-years. Fatality is estimated at 0.7%–2% per case of anaphylaxis. In the United States, the lifetime prevalence of anaphylaxis is reported to be 1.6%.1

Etiology

Immunologic causes

  • Foods, especially peanuts, tree nuts, shellfish, finned fish, milk, and eggs
  • Insect stings (bees, wasps, and fire ants)
  • Medications
  • Latex rubber
  • Blood products

Nonimmunologic causes

  • Radiocontrast media
  • Medications (i.e., NSAIDs, opiates, vancomycin, muscle relaxants, rarely ACE inhibitors, and sulfating agents)
  • Hemodialysis
  • Physical factors (cold temperature or exercise)
  • Idiopathic

Pathophysiology

Immunologic

  • Anaphylaxis is due to sensitization to an antigen and formation of specific IgE to that antigen. On re-exposure, the IgE on mast cells and basophils binds the antigen and cross-links the IgE receptor, which causes activation of the cells with subsequent systemic release of preformed mediators, such as histamine.
  • The release of mediators ultimately causes capillary leakage, cellular edema, and smooth muscle contractions resulting in the constellation of physical symptoms.

Nonimmunologic. Non–IgE-mediated anaphylaxis is also mediated by direct degranulation of mast cells and basophils in the absence of immunoglobulins.

Risk Factors

  • Persistent asthma: increased risk of fatal anaphylaxis if asthma is uncontrolled.
  • Cardiovascular disease: increased risk for death in older age.
  • Elevated baseline tryptase indicates possible mast cell disorder. Individuals with mastocytosis, a disease characterized by a proliferation of mast cells, are at higher risk for severe anaphylaxis from both IgE- and non–IgE-mediated causes.
  • Previous sensitization and formation of antigen-specific IgE with history of anaphylaxis.
  • Concomitant use drugs: beta-adrenergic blockers, ACE inhibitors, NSAIDs, alcohol, etc.
  • Cofactors such as exercise, fever, acute infection, premenstrual status, and emotional.
  • Sensitivity to seafood or iodine does not predispose to radiocontrast media reactions.

Prevention

  • For all types of anaphylaxis, recognition of potential triggers and avoidance are the best prevention.
  • Self-injectable epinephrine and patient education for all patients with a history of anaphylaxis.
  • Radiocontrast sensitivity reactions
    • Use of low-ionic contrast media is strongly suggested.
    • Premedication before procedure.
      • Prednisone 50 mg PO given 13, 7, and 1 hour before procedure.
      • Diphenhydramine 50 mg PO given 1 hour before procedure.
      • H2 blocker may also be given 1 hour before procedure.
  • Premedication is not 100% effective, and appropriate precautions for handling a reaction should be taken.
  • Anaphylaxis can be a presenting sign of underlying mastocytosis.
  • Red man syndrome from vancomycin. Symptoms can usually be prevented by slowing the rate of infusion and premedicating with diphenhydramine (50 mg PO) 30 minutes before start of the infusion.

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General Principles

Definition

Anaphylaxis is a rapidly developing, life-threatening systemic reaction mediated by the release of mast cell and basophil-derived mediators into the circulation. The peak severity is seen usually within 5–30 minutes.

Classification

Immunologic anaphylaxis

  • Allergic IgE-mediated anaphylaxis (type 1 hypersensitivity)
  • IgG-mediated anaphylaxis (rare)

Nonimmunologic anaphylaxis. Previously known as anaphylactoid reactions.

Epidemiology

Incidence of anaphylaxis is approximately 50–2000 episodes per 100,000 person-years. Fatality is estimated at 0.7%–2% per case of anaphylaxis. In the United States, the lifetime prevalence of anaphylaxis is reported to be 1.6%.1

Etiology

Immunologic causes

  • Foods, especially peanuts, tree nuts, shellfish, finned fish, milk, and eggs
  • Insect stings (bees, wasps, and fire ants)
  • Medications
  • Latex rubber
  • Blood products

Nonimmunologic causes

  • Radiocontrast media
  • Medications (i.e., NSAIDs, opiates, vancomycin, muscle relaxants, rarely ACE inhibitors, and sulfating agents)
  • Hemodialysis
  • Physical factors (cold temperature or exercise)
  • Idiopathic

Pathophysiology

Immunologic

  • Anaphylaxis is due to sensitization to an antigen and formation of specific IgE to that antigen. On re-exposure, the IgE on mast cells and basophils binds the antigen and cross-links the IgE receptor, which causes activation of the cells with subsequent systemic release of preformed mediators, such as histamine.
  • The release of mediators ultimately causes capillary leakage, cellular edema, and smooth muscle contractions resulting in the constellation of physical symptoms.

Nonimmunologic. Non–IgE-mediated anaphylaxis is also mediated by direct degranulation of mast cells and basophils in the absence of immunoglobulins.

Risk Factors

  • Persistent asthma: increased risk of fatal anaphylaxis if asthma is uncontrolled.
  • Cardiovascular disease: increased risk for death in older age.
  • Elevated baseline tryptase indicates possible mast cell disorder. Individuals with mastocytosis, a disease characterized by a proliferation of mast cells, are at higher risk for severe anaphylaxis from both IgE- and non–IgE-mediated causes.
  • Previous sensitization and formation of antigen-specific IgE with history of anaphylaxis.
  • Concomitant use drugs: beta-adrenergic blockers, ACE inhibitors, NSAIDs, alcohol, etc.
  • Cofactors such as exercise, fever, acute infection, premenstrual status, and emotional.
  • Sensitivity to seafood or iodine does not predispose to radiocontrast media reactions.

Prevention

  • For all types of anaphylaxis, recognition of potential triggers and avoidance are the best prevention.
  • Self-injectable epinephrine and patient education for all patients with a history of anaphylaxis.
  • Radiocontrast sensitivity reactions
    • Use of low-ionic contrast media is strongly suggested.
    • Premedication before procedure.
      • Prednisone 50 mg PO given 13, 7, and 1 hour before procedure.
      • Diphenhydramine 50 mg PO given 1 hour before procedure.
      • H2 blocker may also be given 1 hour before procedure.
  • Premedication is not 100% effective, and appropriate precautions for handling a reaction should be taken.
  • Anaphylaxis can be a presenting sign of underlying mastocytosis.
  • Red man syndrome from vancomycin. Symptoms can usually be prevented by slowing the rate of infusion and premedicating with diphenhydramine (50 mg PO) 30 minutes before start of the infusion.

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