CHAPTER 128: Anaphylactic and Anaphylactoid Reactions

KEY POINTS

• Anaphylaxis is an acute life-threatening systemic reaction that results from sudden systemic release of mediators from mast cells and basophils.

• Degranulation of mast cell and basophils are commonly mediated by IgE antibody. Other nonimmunologic mechanisms including direct activation of these cells have been described.

• The incidence of anaphylaxis appears to be rising, especially among young people.

• Foods followed by medications (eg, antibiotics and NSAIDs) are the most common cause of anaphylaxis in the outpatient setting.

• Medications, for example, antibiotics, muscle relaxants, blood products, and radiocontrast media, are common causes of anaphylaxis in the hospital.

• Onset of symptoms of anaphylaxis is usually immediate but can be delayed by 2 to 10 hours.

• Cutaneous symptoms are common but hemodynamic collapse and shock can occur in the absence of skin manifestations.

• The hemodynamic symptoms of anaphylaxis are secondary to the widespread vasodilation and profound intravascular fluid loss.

• Careful history and physical examination are most important in the diagnosis of anaphylaxis. Measurement of serum tryptase and histamine can be helpful.

• Prompt recognition, administration of epinephrine, and intravascular volume replacement are key factors in the successful outcome of this potentially fatal event.

INTRODUCTION/DEFINITION

The traditional definition of anaphylaxis is “a systemic, immediate hypersensitivity reaction caused by immunoglobulin E (IgE)–mediated immunologic release of mediators from mast cells and basophils.” The term “anaphylactoid” reaction has been traditionally defined as a clinically similar event not mediated by IgE.^1,2 More recently, the World Allergy Organization (WAO) has referred to anaphylaxis as a “severe, life-threatening, generalized or systemic hypersensitivity reaction.” It suggested that the term ‘‘anaphylactoid reaction’’ be eliminated, and that all episodes clinically similar to IgE-mediated reactions be called anaphylaxis.³

The difficulty in determining the clinical manifestations that define an anaphylactic event was highlighted in a symposium sponsored by the National Institute of Health and the Food Allergy and Asthma Network.^4,5 This symposium was convened to define the clinical manifestations of anaphylaxis required to establish a diagnosis. No true definition, in the classic sense of the term, resulted from the deliberations of this group, but they did define a clear-cut constellation of signs and symptoms requiring the necessity for treatment with epinephrine. They formulated three clinical scenarios during which anaphylaxis was highly likely as a cause of the event and thus epinephrine therapy mandated. These scenarios can be summarized briefly as follows:

1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both and at least one of the following:

   1. Respiratory compromise

   2. Reduced BP or associated symptoms of end-organ dysfunction

2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours):

   1. Involvement of the skin-mucosal tissue

   2. Respiratory compromise

   3. Reduced BP or associated symptoms

   4. Persistent gastrointestinal symptoms

3. Reduced BP after exposure to known allergens for that patient (minutes to several hours).

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