A patient receiving sodium nitroprusside infusion for hypertensive emergency over several days develops metabolic acidosis, confusion, and a rise in mixed venous oxygen saturation. The toxicity responsible, and the agent given to prevent or treat it, are:
- A Thiocyanate accumulation, managed with forced alkaline diuresis
- B Methemoglobinemia, managed with methylene blue
- C Cyanide intoxication from impaired hepatic metabolism, managed with thiosulfate ✓
- D Rebound hypertension from renin surge, managed with captopril
Correct answer: C. Cyanide intoxication from impaired hepatic metabolism, managed with thiosulfate
Explanation
Nitroprusside releases five cyanide moieties per molecule, which normally combine with thiosulfate in liver and kidney to form thiocyanate, excreted renally. With prolonged infusions, high doses, or hepatic impairment, free cyanide accumulates, blocking cytochrome oxidase. Tissues then cannot extract oxygen, so mixed venous oxygen saturation rises alongside lactic acidosis. Sodium thiosulfate provides substrate for detoxification and is the standard prophylactic co-infusion in high-risk settings.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
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