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Anaphylaxis and allergic emergencies

Anaphylaxis and allergic emergencies

Anaphylaxis and allergic emergencies

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Pathophysiology & Triggers - The Reaction Ignition

  • Type I (Immediate) Hypersensitivity: Initial exposure to an allergen prompts IgE antibody production. Subsequent exposure leads to allergen cross-linking of IgE on mast cells and basophils.
  • Massive Mediator Release: This triggers degranulation, releasing pre-formed mediators like histamine and tryptase, causing vasodilation, increased vascular permeability, and smooth muscle spasm.

IgE-mediated mast cell activation vs. cytokine activation

  • Common Triggers:
    • Foods: Peanuts, tree nuts, shellfish, milk
    • Medications: Penicillin, NSAIDs, anesthetics
    • Insect Stings: Bees, wasps, fire ants
    • Other: Latex, exercise

⭐ Serum tryptase is a specific marker for mast cell activation and helps confirm an anaphylaxis diagnosis, peaking 1-2 hours post-reaction.

Clinical Presentation - Signs of System Shock

Symptoms manifest rapidly, often within 5-30 minutes of allergen exposure across multiple systems.

  • Cutaneous (~90%):
    • Urticaria (hives), diffuse pruritus
    • Angioedema (swelling of lips, tongue, face)
  • Respiratory:
    • Dyspnea, wheezing (bronchospasm)
    • Stridor, hoarseness (laryngeal edema)
  • Cardiovascular:
    • Hypotension (SBP < 90 mmHg or >30% drop)
    • Tachycardia, dizziness, or syncope
  • Gastrointestinal:
    • Nausea, vomiting, abdominal cramps

⭐ Be aware: Cutaneous findings may be absent in up to 20% of cases, especially in rapid-onset, profound shock.

Diagnostic Criteria - Nailing the Diagnosis

  • Diagnosis is clinical. Any 1 of the following 3 criteria confirms anaphylaxis.
  • Confirmatory Test: Serum tryptase can confirm the diagnosis retrospectively; levels peak 1-2 hours after reaction onset.

⭐ Hypotension is not required for diagnosis. The most common presentations involve skin and respiratory symptoms without a drop in blood pressure.

Acute Management - The Epi‑sode Response

Immediate Action: ABCs & Epinephrine

  • FIRST-LINE: Intramuscular (IM) Epinephrine is critical.

    • Adult Dose: 0.3-0.5 mg (1:1000 solution) into anterolateral thigh.
    • Pediatric Dose: 0.01 mg/kg (max 0.3 mg).
    • May repeat every 5-15 minutes.
  • ADJUNCTIVE THERAPY:

    • Antihistamines: H1 blockers (Diphenhydramine) + H2 blockers (Ranitidine/Famotidine).
    • Glucocorticoids: (Methylprednisolone) to prevent biphasic reactions.
    • Supportive: IV fluids for refractory hypotension; nebulized albuterol for bronchospasm.

⭐ A biphasic reaction (symptom recurrence 1-72 hours after initial resolution without re-exposure) can occur in up to 20% of patients. Observation is key.

Epinephrine auto-injector administration steps

Biphasic & Refractory - The Second Wave

  • Biphasic Anaphylaxis: Symptom recurrence 1-72 hours post-resolution without re-exposure to the allergen.
  • Refractory Anaphylaxis: Persistent symptoms despite receiving ≥2 doses of epinephrine.
    • Management: IV epinephrine drip. Consider glucagon for patients on beta-blockers.
  • Disposition: Observe patients for 4-8 hours after complete symptom resolution to monitor for a potential second wave.

⭐ Corticosteroids are administered with the aim of preventing biphasic reactions, though evidence for efficacy is varied.

High‑Yield Points - ⚡ Biggest Takeaways

  • Anaphylaxis is a Type I (IgE-mediated) hypersensitivity reaction; requires prior sensitization.
  • Intramuscular epinephrine is the first-line, life-saving treatment and should never be delayed.
  • Airway compromise (stridor, hoarseness) is a primary cause of death; secure the airway early.
  • Biphasic reactions can occur 1-72 hours after apparent resolution; always observe patients.
  • Aggressive IV fluids are critical to counter distributive shock from massive vasodilation.
  • Adjunctive therapies (antihistamines, corticosteroids) treat symptoms but do not replace epinephrine.

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