Anaphylactic Shock

Pathophysiology

Sensitization:

Upon initial exposure to an allergen, the body produces IgE antibodies specific to that allergen. These antibodies bind to the surface of mast cells and basophils.

Re-exposure:

When re-exposed to the same allergen, it binds to the IgE on mast cells and basophils, causing degranulation.

Release of Mediators:

Degranulation releases various mediators, including histamine, leukotrienes, prostaglandins, and cytokines.

Effects of Mediators

• Histamine causes vasodilation, increased vascular permeability, and bronchoconstriction.
• Leukotrienes and prostaglandins further contribute to bronchoconstriction and vascular effects.
• Cytokines amplify inflammation, leading to tissue damage.

Clinical Features

Respiratory Symptoms:

Shortness of breath, wheezing, bronchospasm, stridor due to airway narrowing.

Cardiovascular Symptoms:

Hypotension, tachycardia, and in severe cases, shock.

Gastrointestinal Symptoms:

Nausea, vomiting, abdominal cramps.

Cutaneous Symptoms:

Urticaria (hives), flushing, angioedema.

Common Drugs That May Cause Anaphylactic Shock

• Antibiotics: Particularly beta-lactams, such as penicillins and cephalosporins.
• Vaccines: Certain vaccines, especially those with egg protein components.
• Radiocontrast Media: Used in imaging, such as CT scans.

Diagnosis

Primarily clinical, based on symptoms and rapid onset after exposure to a known allergen. Laboratory tests (if available): Serum tryptase levels may be elevated.

Management

Immediate Action:

• Remove the allergen if possible.
• Place the patient in a supine position with legs elevated to improve venous return.

Pharmacological Treatment:

• Epinephrine (1:1000 solution): The drug of choice. Administer intramuscularly in the anterolateral thigh (0.3–0.5 mg in adults, 0.01 mg/kg in children). Repeat every 5–15 minutes as needed.
• Antihistamines: H1 blockers (e.g., diphenhydramine) and H2 blockers (e.g., ranitidine) to alleviate urticaria and itching.
• Corticosteroids: IV hydrocortisone or methylprednisolone can help prevent late-phase reactions, though they are not effective in the acute phase.
• Bronchodilators: Nebulized beta-agonists (e.g., salbutamol) for persistent bronchospasm.
• IV Fluids: Normal saline to manage hypotension.
• Vasopressors (if needed): In cases of refractory shock, additional vasopressors (e.g., norepinephrine) may be administered.

Observation and Follow-Up

Observe patients for at least 4–6 hours after stabilization for biphasic reactions. Educate at-risk patients on allergen avoidance and provide an epinephrine auto-injector.

Prevention

Avoid known allergens. Consider desensitization therapy if indicated for severe allergies.