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ANAPHYLAXIS

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Anaphylaxis is an acute, potentially life-threatening systemic allergic reaction. It is most commonly triggered by interaction of an allergen with specific IgE antibody bound to mast cells and basophils leading to cell activation and mediator release. Non-IgE-mediated direct mast cell degranulation results in mediator release.

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EPIDEMIOLOGY

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  • Lifetime prevalence for all triggers is 0.05–2%

  • Food is the most common cause of anaphylaxis, affecting up to 8% of young children and 3–4% of adults

  • Drugs are the second most common cause of anaphylaxis

  • Anaphylaxis leads to 500–1000 deaths per year in the United States

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ETIOLOGY

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  • Major causes are food (milk, egg, soy, wheat, peanut, tree nut, fish, and shellfish); medications (antibiotics, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), biologics, chemotherapeutics, muscle relaxants, blood products, radiocontrast media); latex; insect stings (especially bees and wasps); and allergy immunotherapy

  • Rare causes include exercise-induced and idiopathic forms

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DIFFERENTIAL DIAGNOSIS

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  • Other causes of shock (hypovolemic, cardiogenic, and septic), myocardial infarction, pulmonary embolism, status asthmaticus, pneumothorax, vasovagal reaction, serum sickness, hereditary angioedema, scombroid poisoning, carcinoid syndrome, pheochromocytoma, and underlying systemic mastocytosis (which increases risk of anaphylaxis)

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PATHOPHYSIOLOGY

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  • Previous exposure to an allergen (antigen) leads to allergen-specific IgE antibody production. IgE binds to the surface of mast cells and basophils. Upon subsequent exposure, the antigen binds cell-bound IgE, triggering cell activation and degranulation. At times, there is no known prior allergen exposure and reaction occurs on first known exposure

  • Mediators involved include histamine, arachidonic acid derivatives (prostaglandins and leukotrienes), tryptase, bradykinin, and platelet-activating factor. These mediators cause smooth muscle spasm (bronchi, coronary arteries, and GI tract), increased vascular permeability, vasodilation, and complement activation. Patients therefore develop urticaria, angioedema, wheezing, emesis, diarrhea, and hypotension

  • Nonimmunologic (previously known as anaphylactoid) reactions result from non-IgE-mediated degranulation of mast cells and basophils. This can occur with radiocontrast media, NSAIDs, opiates, and other agents

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HISTORY

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  • Exposure to a known allergen and/or prior history of anaphylaxis is helpful but not always present

  • Onset is typically within 30 minutes from exposure to allergens. Symptoms typically progress very rapidly. At times, reactions may occur up to 2 hours post exposure

  • When treated, symptoms usually resolve within a few hours. However, biphasic responses can occur in up to 20% of cases with recurrence of symptoms 8–10 hours later

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CLINICAL MANIFESTATIONS

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  • Cutaneous (80–90% of patients): Urticaria, pruritus, flushing, and angioedema. Patients with severe manifestation of anaphylaxis do not always present with skin findings

  • Respiratory (60% of patients): Lower airway symptoms include wheezing, cough, stridor, chest tightness, and dyspnea. Upper airway symptoms include: sneezing, congestion/rhinorrhea, dysphonia, laryngeal edema (drooling), and hoarseness

  • Gastrointestinal (45% of patients): Nausea, vomiting, abdominal pain, diarrhea

  • Cardiovascular (45% of patients): Chest pain, palpitations, tachycardia or bradycardia, dysrhythmia, hypotension, shock, cardiac arrest

  • CNS (15% of patients): Feeling of ...

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