A patient with hypertensive emergency is started on intravenous sodium nitroprusside. During prolonged infusion at high doses, the patient develops metabolic acidosis and elevated lactate. Which mechanism explains this toxicity, and what is the specific antidote?
- A Methemoglobinemia from nitric oxide release; treat with methylene blue
- B Thiocyanate accumulation causing neurotoxicity; treat with hydroxocobalamin
- C Cyanide accumulation from nitroprusside metabolism; treat with sodium thiosulfate ✓
- D Peripheral vasodilation causing lactic acidosis; treat with norepinephrine
Correct answer: C. Cyanide accumulation from nitroprusside metabolism; treat with sodium thiosulfate
Explanation
Nitroprusside releases nitric oxide and cyanide. Cyanide inhibits cytochrome oxidase, causing histotoxic hypoxia and lactic acidosis. Sodium thiosulfate acts as a sulfur donor for rhodanese-mediated conversion of cyanide to renally excretable thiocyanate. Thiocyanate toxicity is neurological, not metabolic acidosis. Methylene blue treats methemoglobinemia, not cyanide poisoning.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
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