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  Epinephrine is the first-line medication for the treatment of anaphylaxis. Second-line treatment consists of antihistamines and corticosteroids.

  
  
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  Urticaria may be the first sign of what might progress to angioedema or anaphylaxis.

  
  
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  For patients with respiratory symptoms or throat swelling, perform a rapid assessment of the airway and intubate early.

  
  
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  Attempt to determine and then discontinue the inciting agent.

An allergic reaction is the body’s way of responding to foreign substances that come in contact with the skin, nose, eyes, respiratory tract or gastrointestinal tract. Examples of allergens are dust, pollen, plants, medications, foods, latex, and insect bites. Anything can be an allergen. Allergic reactions can range from mild local urticarial eruptions to severe and life-threatening airway obstruction, respiratory failure, and circulatory collapse. Urticaria, or “hives,” is an immunoglobulin E (IgE)-mediated hypersensitivity reaction to an allergen resulting in red, raised wheals that itch and sting. Circulating antibodies bind the allergen and IgE receptors on mast cells. In response, mast cells release inflammatory substances (histamine, bradykinin), which results in increased vascular permeability. Urticaria is one of the most common skin lesions seen in the emergency department (ED) in both young and older patients. About 20% of the population experiences at least 1 attack of urticaria in their lifetime.

Angioedema is nonpitting edema of the deeper layers of the skin owing to a loss of vascular integrity caused by inflammatory mediators. It is not pruritic but can cause burning, numbness, or pain, generally in the face or neck. Approximately 94% of the cases of angioedema presenting to the ED are drug-induced. Most drug-induced angioedema occurs in patients taking angiotensin-converting enzyme (ACE) inhibitors. About 0.1–0.2% of the patients treated with ACE inhibitors will develop angioedema. There are 2 main types of angioedema based on the underlying mechanism. Mast cell angioedema is mediated by IgE, similar to urticaria. Bradykinin, an inflammatory mediator, is causal in both hereditary and ACE inhibitor–induced angioedema, although the mechanism for the bradykinin increase differs.

Anaphylaxis is a severe systemic allergic reaction that can present rapidly with hypotension, bronchospasm, and laryngeal edema. About 500–1,000 persons in the United States die every year as a result of anaphylaxis. Beta-lactam antibiotics and Hymenoptera stings constitute the most common causes of anaphylaxis. Anaphylaxis is IgE-mediated and results from release of histamine, leukotrienes, and prostaglandins from inflammatory cells. The result is a systemic increase in vascular permeability, vasodilation, and smooth muscle contraction.

History

Patients with urticaria present with transient, pruritic, well-circumscribed lesions that are erythematous, nonpitting plaques (wheals) surrounded by an erythematous ring (flare) (Figure 97-1). Patients with angioedema present with swelling of the face, lips, tongue, eyelids, distal extremities, or genitalia. The swelling is nonpitting and may occur with urticaria. ACE inhibitor–induced angioedema has a predilection for the face (Figure 97-2). Patients with anaphylaxis present with a sensation of impending doom or “lump in the throat” followed by shortness of breath, chest pain, hypotension, nausea, vomiting, or diarrhea. More than 90% of patients have urticaria or angioedema. Most patients present with signs and symptoms within seconds of exposure to an allergen; however, symptoms may be delayed up to a few hours after exposure.