Journal: Anesth Analg 107(2):620-624, 2008
Reprint: Dept of Anesthesiology and Intensive Care Medicine, SRH Zentralklinikum Suhl, Albert-Schweitzer str. 2, 98527 Suhl, Germany (W Schummer MD, DEAA, EDIC) JJ.01 JA0916/016 ©2009
Faculty Disclosure: Abstracted by J. Joyce, who has nothing to disclose.
Most episodes of anaphylaxis respond to treatment with a single dose of epinephrine. However, severe anaphylaxis can be associated with cardiovascular collapse that is difficult to manage. Because anaphylaxis is uncommon, unpredictable, and may be fatal, a prospective, randomized, controlled trial in humans on the best management is difficult and guidelines are based on theory and anecdotes only. In 2004, these authors reported the management of anaphylactic shock due to succinylated gelatin solution in a 59-year-old patient with coronary artery disease. The clinical response while following the Advanced Cardiac Life Support resuscitation guidelines was disappointing. After the administration of vasopressin, hemodynamic function was restored almost immediately.
This report presents six more cases in which the authors used vasopressin during treatment of anaphylactic shock. Pharaoh Menes’ death in 2600 BC after a wasp sting is renowned as the first report of anaphylaxis. Even today, data about the incidence and severity of anaphylaxis are limited. The estimated incidence during anesthesia ranges from 1:10,000 to 1:20,000 anesthesia cases. Anaphylactic shock occurring during anesthesia is lethal in about 3%-10% of cases, with neuromuscular blocking drugs being responsible for more than half of these events. Anaphylactic shock is associated with systemic vasodilation and increased vascular permeability, causing a mixed distributive-hypovolemic shock pattern. Circulating blood volume may decrease by as much as 35% within 10 minutes because of extravasation, resulting in poor venous return, hypotension, tissue hypoperfusion, and cellular anoxia.
Epinephrine has been considered useful in the treatment of anaphylaxis since 1925. Retrospective analyses have indicated that epinephrine and fluid resuscitation are effective treatments for anaphylaxis occurring during anesthesia. When little or no evidence is available, recommendations based on clinical experience and physiological rationale should be considered. The cases reported here demonstrate clearly that vasopressin may help if circulatory function deteriorates quickly despite adequate standard treatment. Sympathetic excess frequently results in hemodynamically significant tachycardia. This itself can result in myocardial or cerebrovascular ischemia, decreased cardiac output, or degeneration into ventricular dysrhythmias, even in the absence of coronary artery disease.
The precise mechanism of the vasopressor action induced by vasopressin remains unclear. In vasoplegic shock states, vasopressin restores vascular tone by at least 4 mechanisms: 1) activation of V1 receptors that mediate vasoconstriction via Gq protein activation of phospholipase C; 2) the ability to close adenosine triphosphate-sensitive K channels while activation of adenosine triphosphate-sensitive K channels produces cellular hyperpolarization resulting in vasodilation; 3) modulation of nitric oxide; and 4) enhancement of adrenergic and other vasoconstrictor drugs. In addition, vasopressin could act during anaphylaxis as an "anti-inflammatory drug" by antagonizing the effects of nitric oxide.
During anaphylactic shock, distribution in vasoactive action of vasopressin seems to be optimal: vasoconstriction in skin, skeletal muscle, intestine and fat, with relatively less constriction of coronary and renal vasculature, and cerebral vasodilation. |
