Cyanide Poisoning: Pathophysiology and Current Approaches to Therapy

Abstract

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)

Hydroxocobalamin treatment of acute cyanide poisoning from apricot kernels

“…The literature suggests that the cyanide content of apricot kernels ranges from 0.122 to 4.09 mg/g 6. Very often, clinical signs of acute cyanide poisoning are non-specific and generalised, so an early diagnosis is very difficult 7. Initial symptoms can include: flushing, tachycardia, tachypnoea, headache, dizziness and agitation 3.…”

“…Hydroxocobalamin has a favourable tolerability profile11 and is also commonly used to treat vitamin B 12 deficiency, albeit in much smaller doses (1 mg rather than 5–10 g). Amyl nitrite sequesters cyanide, thus competing with cytochrome oxidase for cyanide ions1 7 to form cyanomethaemoglobin. Effective amyl nitrite treatment results in 10–30% methaemoglobinaemia,1 7 although this effect can also prove toxic as the ability of the blood to transport oxygen to the cells is reduced 12.…”

“…Amyl nitrite sequesters cyanide, thus competing with cytochrome oxidase for cyanide ions1 7 to form cyanomethaemoglobin. Effective amyl nitrite treatment results in 10–30% methaemoglobinaemia,1 7 although this effect can also prove toxic as the ability of the blood to transport oxygen to the cells is reduced 12. Sodium thiosulphate is a sulphur donor that reduces the toxicity of cyanide via the thiosulphate sulphurtransferase-mediated conversion of cyanide to thiocyanate, which can then be safely excreted in the urine 9…”

Treatment of cyanide poisoning in Australasia

“…Death from cyanide is one of the most rapid and dramatic seen in medicine 1 . Fortunately, serious acute cyanide poisoning is rare.…”

“…Death from cyanide is one of the most rapid and dramatic seen in medicine. 1 Fortunately, serious acute cyanide poisoning is rare. Of a total of 1 926 438 human poison exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System (TESS) during 1994, only 360 involved cyanide poisoning.…”