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Toxicity. The toxicity of nitroprusside is related to its potent antihypertensive effects and the accumulation of toxic metabolites (cyanide, thiocyanate, and methemoglobin). 1. Cyanide toxicity: Nitroprusside combines with hemoglobin and is subsequently metabolized to 5 cyanide ions and cyanmethemoglobin. Cyanide then converts to thiocyanate ...
Cyanide poisoning may result from a variety of exposures, including structural fires, industrial exposures, medical exposures such as sodium nitroprusside, and certain foods. In domestic countries, the most common cause of cyanide poisoning is domestic fires.
Risk factors may include hypoalbuminemia, cardiopulmonary bypass procedures, or the administration of moderate to high doses of nitroprusside. Treatment of cyanide toxicity requires the cessation of nitroprusside and, for severe toxicity, use of the cyanide antidote kit.
Cyanide toxicity, manifested by altered mental status and metabolic (lactic) acidosis, may occur with rapid high-dose infusion (10–15 mcg/kg/min) for periods of 1 hour or longer. Patients with depleted thiosulfate stores (eg, malnourished) may have elevated cyanide levels at lower infusion rates.
The cyanide anion release concurrent with nitroprusside administration is associated with potential cyanide accumulation and severe toxicity. Agents to ameliorate the untoward effects of cyanide are limited by various problems in their practicality and effectiveness.
It is this form of CN poisoning that results in metabolic (lactic) acidosis 12 and a narrow arteriovenous O 2 difference. Cyanide also inhibits a number of non-electron-chain enzymes, 11 accounting for many of its toxic effects.
Cyanide toxicity is a rare complication of sodium nitroprusside that can be difficult to diagnose in critically ill patients. We describe a case of cyanide toxicity after cardiac surgery that presented as lactic acidosis after discontinuation of nitroprusside.
Sodium thiosulfate and hydroxocobalamin have both been empirically used for cyanide toxicity and have specifically been evaluated for cyanide toxicity associated with sodium nitroprusside. Cobinamide is an investigational agent currently being evaluated for efficacy and safety in the treatment of cyanide toxicity.
cyanide poisoning. A low systemic vascular resistance, anion gap metabolic acidosis, ele-vated arterial lactate concentrations, and depressed oxygen consumption are typical of SNP-induced cyanide poisoning, as are sepsis, hepatic failure, toxic shock syndrome, and sys-temic inflammatory response syndrome. Sodium Nitroprusside 3
Nitroprusside is cyanogenic and on a molar basis contains 44 percent cyanide by weight. Nitroprusside acts directly and rapidly to dilate vascular smooth muscle. Upon withdrawal ofNP, vasodilation is rapidly reversed.