Anaphylaxis



Anaphylaxis


Helen M. Hollingsworth

Nereida A. Parada



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.









TABLE 140-1 Causes of IgE-mediated Anaphylaxis

























































Type


Agent


Example


Proteins


Allergen extracts


Pollen, dust mite, mold, animal dander



Enzymes


Chymopapain, streptokinase, L-asparaginase



Food


Egg white, legumes, milk, nuts, shellfish, wheat



Heterologous serum


Tetanus antitoxin, antithymocyte globulin, snake antivenom



Hormones


Insulin, ACTH, TSH, progesterone, salmon calcitonin



Vaccines


Influenza



Venoms


Hymenoptera



Others


Heparin, latex, thiobarbiturates, seminal fluid


Haptens


Antibiotics


β-Lactams, ethambutol, sulfonamides, vancomycin



Disinfectants


Ethylene oxide



Local anestheticsa


Benzocaine, tetracaine, xylocaine, mepivacaine



Others


Cisplatin, carboplatin


a Precise mechanism not established.
ACTH, adrenocorticotropic hormone; TSH, thyroid-stimulating hormone.









TABLE 140-2 Causes of Non-IgE-mediated Anaphylaxis




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Jun 11, 2016 | Posted by in CRITICAL CARE | Comments Off on Anaphylaxis

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Complement activation


Blood product transfusion in an IgA-deficient patient


Hemodialysisa


Direct release of chemical mediators of anaphylaxis


Protaminea


RCM


Ketamine


ACE inhibitorsa


Local anestheticsa


Codeine and other opiate narcotics


Highly charged antibiotics, including amphotericin B


Nonsteroidal anti-inflammatory medications (NSAIDs)b


Antineoplastic agents (e.g., paclitaxela, etoposidea)


Sulfiting agents


Exercisec


Idiopathic recurrent anaphylaxis