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Reasonable suspicion of cyanide toxicity is adequate grounds for initiation of treatment. Treatment of cyanide toxicity consists of. discontinuing the administration of sodium nitroprusside; providing a buffer for cyanide by using sodium nitrite to convert as much hemoglobin into methemoglobin as the patient can safely tolerate; and then Treatment of cyanide toxicity requires the cessation of nitroprusside and, for severe toxicity, use of the cyanide antidote kit. Cyanide toxicity from nitroprusside may be prevented by concomitant administration of sodium thiosulfate infusions. EM@3AM: Cyanide Toxicity Amyl nitratesodium thiosulfatesodium nitrite (Cyanide Antidote Kit). Amyl nitritecrush pearls and place near nares 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 volnea generic name Avoidance of cyanide toxicity: As described in the package insert – CLINICAL PHARMACOLOGY section, when more than 500 mcg/kg of sodium nitroprusside is

Pharmacokinetic calculation of the rise in cyanide level showed that mono-infusion of SNP together with thiosulphate is a procedure free of danger and Cyanide toxicity is generally considered to be a rare form of poisoning. Patients receiving sodium nitroprusside at high doses or for more than 5 days should have 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.

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