Introduction
This topic covers acute poisoning with cyanide compounds: where the poison comes from, how it stops cellular respiration, how to recognise it, how to confirm and treat it, and what outcome to expect. Cyanide is a fast-acting poison, so the emphasis in an exam answer is on early recognition and immediate antidote treatment.
Sources and classification of cyanide compounds
Cyanide toxicity arises from free cyanide ion (CN) or from hydrogen cyanide (HCN), which is a gas at body temperature. Compounds that release cyanide are grouped by their source:
Mechanism of toxicity
- Cytochrome c oxidase block: cyanide binds the ferric iron of cytochrome a3 (complex IV) in the mitochondrial respiratory chain, so cells cannot use oxygen.
- Histotoxic hypoxia: oxygen delivery is normal, but tissues cannot extract or use it. Aerobic ATP production falls and anaerobic glycolysis produces lactate.
- Most affected organs: tissues with the highest oxygen demand, namely the brain, heart and conduction system, are damaged first.
- Absorption: HCN gas is absorbed within seconds through the lungs; liquid and salts are absorbed quickly from the gut, and liquid can also be absorbed through the skin.
- Detoxification: the liver enzyme rhodanese (thiosulfate sulfurtransferase) converts cyanide to thiocyanate, which is excreted by the kidneys. This step needs sulfur donors such as thiosulfate. Cyanide itself is cleared quickly, but thiocyanate persists longer.