For cyanide poisoning, which antidote is appropriate treatment?

• A. Atropine
• B. Pyridoxine
• C. Deferoxamine
• D. Sodium nitrite

Answer: (D)

In cyanide poisoning, the immediate problem is that cyanide blocks cellular respiration by inhibiting cytochrome c oxidase. The antidote strategy often used is to create a form that cyanide will preferentially bind, pulling it away from the crucial enzyme system and allowing detoxification to proceed.

Sodium nitrite works by inducing methemoglobinemia. Methemoglobin contains ferric iron (Fe3+) that has a high affinity for cyanide. When nitrite converts some hemoglobin to methemoglobin, cyanide preferentially binds to this methemoglobin to form cyanomethemoglobin. This sequesters cyanide away from cytochrome oxidase, allowing oxidative phosphorylation to resume. The cyanide-bound methemoglobin is then detoxified downstream, typically with thiosulfate, which converts cyanide to the less toxic thiocyanate that is excreted in urine.

The other agents listed do not address cyanide’s mechanism: atropine counters cholinergic effects (not involved in CN poisoning); deferoxamine chelates iron (not cyanide); pyridoxine is used for other toxicities (not CN). While hydroxocobalamin is another modern CN antidote, sodium nitrite is the one that directly leverages methemoglobin formation to neutralize cyanide.