Anaphylaxis: New Clues to Clinical Patterns and Optimum Treatment

Mark T. O'Hollaren, MD

August 09, 2002

In This Article


Anaphylaxis may be described as an overwhelming allergic reaction, typically involving multiple systems in the body, and representing a true medical emergency. It may be caused by a number of factors, but typically occurs in response to a foreign protein, which could be a food, drug, or other external allergen. Histamine, which is contained in mast cells throughout the body, may be released in massive amounts to create or to produce the symptoms and signs found with acute anaphylaxis. The largest concentration of mast cells exists in the skin, the lungs, and the gastrointestinal tract; but mast cells also exist in smaller amounts in other areas of the body. In response to contact with what could be extremely small amounts of this allergenic protein, an escalating cascade of mast cell mediator release may ensue.

The release of histamine granules from mast cells throughout these various body systems produces a number of clinical findings. First, histamine may cause vasodilation, resulting in hypotension and, in some cases, shock. Second, it may affect the heart directly, and it appears that both H1 and H2 histamine receptors may play a role in the cardiovascular manifestations of acute anaphylaxis. These cardiac manifestations, in addition to hypotension, may include tachycardia or more serious ventricular arrhythmias as well. The tachycardia experienced in anaphylaxis may occur by direct stimulation of histamine on the heart, or may be a reflex tachycardia as a result of hypotension. In addition, cardiac ischemia may take place, and those with pre-existing coronary artery disease are obviously at increased risk of an adverse ischemic event should they experience hypoperfusion due to shock.

Gastrointestinal symptoms may occur, including abdominal cramping, nausea, vomiting, and diarrhea, which may be explosive. Respiratory symptoms of anaphylaxis may include nasal congestion, rhinorrhea, sneezing, throat tightness, laryngeal edema, and acute bronchospasm. Central nervous system symptoms have been reported, and may include seizures, altered mentation due to hypoxemia, and cerebral hypoperfusion due to profound hypotension. Finally, the most common clinical manifestation of acute anaphylaxis includes cutaneous symptoms and signs such as flushing, urticaria, and angioedema.

Anaphylaxis typically involves multiple body symptoms and may initially present with upper respiratory symptoms or cutaneous symptoms, which may rapidly progress to life-threatening anaphylaxis. Death from anaphylaxis most commonly occurs from asphyxiation, and less commonly from complications of hypotension.

Those who treat patients who experience anaphylaxis are also struck by the fact that prior to the onset of any of the above symptoms, patients may often experience a "feeling of impending doom."

It is important that patients are warned to pay attention to that feeling, and to ready their self-treatment kits such as injectable epinephrine, antihistamines, and corticosteroids. As will be discussed later, the foundational corner stone of management of acute anaphylaxis is intramuscular injection of epinephrine and treatment with H1 and H2 blocking antihistamines. Corticosteroids are also helpful in the management of acute anaphylaxis. In addition, the tremendous fluid requirement for volume replacement and cardiovascular fluid resuscitation in patients with acute anaphylaxis will also be discussed.


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