I. GENERAL PRINCIPLES
A. Anaphylaxis is a severe and potentially fatal form of immediate hypersensitivity (immunoglobulin E [IgE]-mediated antigen recognition). An anaphylactoid reaction is caused by a mechanism other than IgE recognition of antigen.
B. In this chapter, IgE-mediated and non-IgE-mediated reactions are referred to as anaphylactic reactions.
II. PATHOPHYSIOLOGY
A. Binding of allergenic antigen (
Table 140-1) to adjacent IgE molecules on sensitized mast cells/basophils activates synthesis and secretion of mediators of anaphylaxis, such as histamine, leukotrienes (LTC4, LTD4, and LTE4), and cytokines.
B. Mast cell and basophil activation also occur through a variety of non-IgE-mediated mechanisms (
Table 140-2).
III. CLINICAL FEATURES
A. The major clinical features of anaphylaxis are urticaria, angioedema, respiratory obstruction (stridor, wheezing, breathlessness), and vascular collapse (dizziness, hypotension, loss of consciousness), with urticaria being the most common.
B. Additional clinical manifestations include a sense of impending doom, rhinorrhea, generalized pruritus and swelling, dysphagia, vomiting, and abdominal pain.
C. Physical examination of a patient with anaphylactic shock often reveals a rapid, weak, irregular, or unobtainable pulse; tachypnea, respiratory distress, cyanosis, hoarseness, or stridor, diminished breath sounds, wheezing, and hyperinflated lungs; urticaria, angioedema, or conjunctival edema. Only a subset of these may occur in any given patient.
D. Laboratory findings include elevation of blood histamine and mature β-tryptase, and total tryptase levels, low complement levels, and disseminated intravascular coagulation (DIC). Documentation of an elevated serum or plasma total tryptase at the time of the reaction compared with baseline levels provides support for diagnosis of anaphylaxis. A normal tryptase level does not exclude anaphylaxis.
E. Arrhythmias may occur.