Anaphylactic shock

Headshot of Chris Anderson, Vice Chair, Pediatrics
Chris Anderson
Vice Chair, Pediatrics
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Headshot of Hinah Parker, MD Ā· Assistant chair, Pediatrics
Hinah Parker
MD Ā· Assistant chair, Pediatrics
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Table of Contents

Anaphylactic shock is a severe, life-threatening allergic reaction that can occur rapidly and requires immediate medical intervention. This article provides an overview of the epidemiology, etiology, pathogenesis, pathophysiology, clinical features, diagnosis, and treatment of anaphylactic shock in children, tailored for pediatric residents.

Epidemiology

Anaphylaxis is a relatively rare but serious condition in children, with an estimated incidence of 0.1% to 0.5% per year. The prevalence of anaphylaxis appears to be increasing, particularly in developed countries, some of this may be access to healthcare and thus an ability to appropriately quantify cases. Common triggers include foods, insect stings, medications, and latex. Children with a history of atopy, such as asthma, eczema, or allergic rhinitis, are at higher risk of having an allergy severe enough to cause anaphylaxis.

Etiology

The causes of anaphylactic shock in children can be broadly categorized into:

Some of the top allergens are:

  • Peanuts and tree nuts.
  • Milk and eggs.
  • Shellfish and fish.
  • Wheat and soy.
  • Bees, wasps, hornets.
  • Fire ants.
  • Antibiotics (e.g., penicillin, cephalosporins, sulfa drugs).
  • Nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Latex.
  • Exercise-induced anaphylaxis.
  • Idiopathic anaphylaxis (no identifiable trigger).

Pathogenesis and pathophysiology

The pathogenesis of anaphylactic shock involves an IgE-mediated hypersensitivity reaction. Upon exposure to an allergen, sensitized mast cells, and basophils release a variety of mediators, including histamine, leukotrienes, and cytokines. These mediators cause:

Leads to hypotension and shock.

Results in fluid extravasation and edema.

Causes bronchoconstriction and respiratory distress.

Leads to airway obstruction.

Clinical features

The clinical presentation of anaphylactic shock can vary, but typically includes:

  • Urticaria (hives).
  • Flushing.
  • Conjunctivitis.
  • Angioedema (swelling of the face, lips, tongue).
  • Wheezing and bronchospasm.
  • Stridor.
  • Dyspnea (difficulty breathing).
  • Voice change.
  • Rhinorrhea.
  • Chest/throat tightness.
  • Hypotension.
  • Dizziness.
  • Tachycardia.
  • Syncope (fainting).
  • Nausea and vomiting.
  • Abdominal pain.
  • Diarrhea.
  • Dysphagia.
  • Altered mental status.
  • Tremor.
  • Vision changes.

Diagnosis

Diagnosis of anaphylactic shock is primarily clinical, based on the rapid onset of symptoms following exposure to a known or potential allergen. Key diagnostic criteria include:

Symptoms typically develop within minutes to hours of exposure.

  • Either two organ system involvement (skin/mucosal, respiratory, cardiovascular, gastrointestinal symptoms) in those with a likely allergen, or
  • Skin/mucosal involvement plus respiratory or cardiovascular compromise alone, or
  • Exposure to a known allergen with isolated low systolic blood pressure.

Rapid improvement with administration of epinephrine.

Not required and treatment should not be delayed to get lab work. However, tryptase levels in the acute setting can be helpful when the clinical picture is unclear and the diagnosis is in question.

Treatment

Treatment of anaphylactic shock involves immediate intervention to stabilize the patient and prevent further reactions:

  • Epinephrine:
    • Intramuscular injection (0.01mg/kg, max 0.5mg) is the first-line treatment.
    • Lateral thigh is the preferred location.
    • Can repeat every 5 minutes.
    • IV epi drips can be used for refractory cases.
  • Oxygen therapy: To maintain adequate oxygenation.
  • Positioning: Place the patient in a supine position with legs elevated.
  • Antihistamines: H1 and H2 blockers (e.g., diphenhydramine, ranitidine) for cutaneous symptoms.
  • Corticosteroids: Unclear benefit. Some recent data suggests use may increase the incidence of biphasic reaction.
  • Bronchodilators: For bronchospasm (e.g., albuterol).
  • Glucagon: For patients on beta blockers who may not respond well to epinephrine (as the beta agonist properties of the epi are being blocked), glucagon can increase cyclic AMP levels and thus bypass those effects.
  • Continuous monitoring of vital signs and oxygen saturation.
  • Intravenous fluids for hypotension.
  • Advanced airway management if needed (e.g., intubation).
  • Biphasic reactions: Recurrence of symptoms after initial reaction is resolved. Often occurs within the first 72 hours after initial event but highest risk is in the first 6–8 hours.
    • Those at highest risk are:
      • Patients with delayed epi administration (>90 min).
      • Patients who require >1 epi dose.
      • Severe asthma.
      • Required IV fluids due to hypotension.
      • Known drug trigger.
  • Identification and avoidance of triggers.
  • Prescription of an epinephrine auto-injector for emergency use, with teaching on use prior to discharge from healthcare facility.
  • Referral to an allergist for further evaluation and management.

Differential diagnosis

Hereditary angioedema should be considered in children who present with multiple episodes concerning for anaphylaxis or those presenting without a known trigger.

Conclusion

Anaphylactic shock in children is a medical emergency that requires prompt recognition and treatment. Understanding the epidemiology, etiology, pathogenesis, pathophysiology, clinical features, diagnosis, and treatment is essential for pediatric residents to provide optimal care. Early intervention with epinephrine and supportive measures can significantly improve outcomes and reduce the risk of complications.