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Int J Artif Organs. 1989 Jun;12(6):347-55.

Cyanide poisoning: pathophysiology and current approaches to therapy.

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Texas Tech University Health Sciences Center, Dep. of Internal Medicine, Lubbock.


Considering the difficulties following the administration of nitrites (or aminophenols) or cobalt-EDTA as well as the ineffectivenes of hydroxycobalamin and pyruvate, we feel that a more sensible treatment for acute cyanide intoxication is hemodialysis combined with the intravenous administration of sodium thiosulfate. The addition of hemodialysis to such a regimen is helpful in three ways. First, it removes the small extracellular reservoir of cyanide, particularly if the poison is still being absorbed from the gastrointestinal tract. Second, it corrects the severe lactic acidosis seen in virtually all cases of cyanide toxicity. As with most poisons death from metabolic acidosis alone is likely. Third, the removal of thiocyanate, the end product of cyanide metabolism, results in a maneuver which should decrease both tissue and plasma cyanide levels. The immediate treatment of acute cyanide intoxication is supportive, as it is with most all drugs and poisons. Gastric lavage using activated charcoal should be initiated immediately to remove any remaining cyanide in the gastrointestinal tract. Simultaneously, high flow oxygen should be administered either by nasal cannula or by endotracheal intubation. Correction of the metabolic acidosis should be instituted with bicarbonate. Immediate hemodialysis should be performed with the concomitant administration of thiosulfate. Animal studies suggest that continuous infusion of thiosulfate (12 mg/kg/hr) is more effective for treating cyanide intoxication than is bolus administration (41, 51). Bolus administration is the currently recommended form of thiosulfate therapy in humans. The Lilly kit contains a 50 ml ampule of thiosulfate having 12.5 gm, which in adults may be repeated once at one-half the dose.(ABSTRACT TRUNCATED AT 250 WORDS)

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