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Anaphylaxis

Kristin Barkley, DNP, CRNA

Anaphylaxis

  • Estimated frequency: ~1 in 3,500–20,000 anesthetized patients.
  • ~60–70% are IgE-mediated Type I reactions.
  • Neuromuscular blocking drugs are the most common drug class implicated.
  • Succinylcholine and rocuronium are the most frequently involved NMBAs.

 

Types of Hypersensitivity Reactions

Type I — Anaphylactic/Immediate

  • Mediator: IgE
  • Examples: drug allergy, hay fever, asthma, hives

Type II — Cytotoxic

  • Mediators: IgG, IgM, complement
  • Examples: blood transfusion reactions, acute transplant rejection

Type III — Immune Complex

  • Mediators: IgG, IgM, neutrophils, complement
  • Examples: systemic lupus erythematosus, rheumatoid arthritis

Type IV — Delayed (Cell-mediated)

  • Mediators: T cells, monocytes/macrophages, cytokines
  • Examples: poison ivy, transplant rejection

Type V — Stimulatory

  • Mediator: humoral antibodies
  • Example: Graves’ disease

 

SCOPe Guide

Strategies

Recognition (Grading)

  • Grade I: cutaneous signs — generalized erythema, urticaria, angioedema.
  • Grade II: Grade I + hypotension, tachycardia, cough, difficult ventilation.
  • Grade III: hypotension, tachycardia/bradycardia, arrhythmias, bronchospasm.
  • Grade IV: cardiac and/or respiratory arrest, pulseless electrical activity.

Treatment

  • Stop suspected trigger.
  • Position: Trendelenburg to improve venous return.
  • Ventilation: ensure 100% O2.
  • Manage hypotension — Epinephrine is first-line:
    • Grade II: 10–20 mcg SC/IM.
    • Grade III: 100–200 mcg SC/IM/IV every 1–2 minutes as needed.
    • Grade IV: 1 mg IV; repeat per ACLS.
  • Secondary vasopressor: Vasopressin 2–10 units IV if needed.
  • Refractory vasoplegia: Methylene blue (inhibits guanylate cyclase → ↓cGMP) may be considered.
  • Fluids: Crystalloid 10–30 mL/kg or colloid 10 mL/kg.
  • Bronchospasm: Albuterol or ipratropium inhalers; Terbutaline 0.25 mg SC.
  • Antihistamines:
    • H1: Diphenhydramine or Hydroxyzine 0.5–1.0 mg/kg IV.
    • H2: Ranitidine 50 mg IV or Famotidine 20 mg IV.
  • Airway edema / inflammation: Steroids are adjuncts (not immediate effect).
    • Hydrocortisone 250 mg IV.

Clinical Optimization

  • Presentation under anesthesia: cutaneous signs may be obscured by drapes; watch for hypotension, tachycardia, bronchospasm → hypovolemia, shock, hypoxemia → arrest.
  • Pathophysiology: re-exposure → IgE cross-linking on mast cells/basophils → degranulation → mediator release:
    • Histamine: vasodilation, ↑permeability (edema/urticaria), pulmonary edema.
    • Leukotrienes: bronchoconstriction, ↑permeability.
    • Prostaglandin D2: bronchoconstriction.
    • Platelet-activating factor: bronchoconstriction, ↑permeability.
  • Epinephrine is primary:
    • Stabilizes mast cells/basophils (↓degranulation).
    • α11: ↑BP and inotropy; β2: bronchodilation.

Pearls

  • Rapid recognition and treatment prevent progression and refractory shock.
  • Epinephrine first, then fluids and adjuncts.
  • Consider timing: immediate after IV drug vs delayed after oral/topical exposure.

 

Media

  • Elisha S, Heiner JS, Nagelhout JJ. Nurse Anesthesia. 7th ed. Elsevier; 2023.

 

References

  • Elisha S, Heiner JS, Nagelhout JJ. Nurse Anesthesia. 7th ed. Elsevier; 2023.

Media Attributions

  • sequence-of-events

License

Icon for the Creative Commons Attribution-NonCommercial 4.0 International License

The Scope Copyright © by Bailey Freeman, DNP, CRNA; Angela Mordecai, DNP, CRNA; Brian Cornelius, DNP, CRNA; and Kristin Barkley, DNP, CRNA is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.