A patient in hypertensive emergency receives a sodium nitroprusside infusion for over 48 hours. She develops tachycardia, air hunger, metabolic acidosis with elevated lactate, and a fruity breath odor. The most likely explanation and appropriate step are:

• A Cyanide toxicity from excessive infusion, stop the drug and give thiosulfate or hydroxocobalamin ✓
• B Thiocyanate accumulation causing hypothyroidism, stop the infusion and monitor TSH
• C Reflex sympathetic activation causing myocardial ischemia, add a beta-blocker and continue nitroprusside
• D Hypertensive encephalopathy, increase the infusion rate to control blood pressure faster

Explanation

Nitroprusside metabolizes to free cyanide, which is normally converted to thiocyanate by rhodanese using thiosulfate. Infusions above roughly 2 mcg/kg/min for prolonged periods overwhelm this pathway, producing cyanide toxicity with anaerobic metabolism, lactic acidosis, and almond-like breath odor. Treatment is stopping the infusion plus thiosulfate, hydroxocobalamin, or nitrites. Thiocyanate toxicity occurs later, mainly in renal failure, causing CNS effects rather than severe acidosis.

Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.