Symptoms include headache, confusion, dizziness, weakness, lethargy, coma, hypotension and cardiac arrest. Classic symptoms include cherry-red flushing of the skin and bitter-almond smell of the breath, but these are rarely seen, or identified post-mortem.

Occupational exposures, combustion of industrial materials in house and vehicular fires and some pharmaceuticals (sodium nitroprusside) can also cause CN poisoning, CN is absorbed via inhalation as well as via skin, gastrointestinal system and mucous membranes. The most common exposure site for cyanide is fires in enclosed space as products containing nitrogen (plastic, vinyl, wool, silk, cotton, paper) produce cyanide from incomplete combustion. Therefore, cyanide poisoning must be recognized quickly and treated as soon as possible. Cyanide is metabolized rapidly so concentrations are undetectable a few hours after exposure. Secondarily, cyanide inhibits free radicles, stimulates NDMA receptors causing apoptosis, and inhibits glutamic acid decarboxylase which decreases GABA and increases risk of seizures. Inability to utilize oxygen causes histotoxic hypoxia. Cells shift to anaerobic metabolism, with rapid accumulation of lactic acid and subsequent metabolic acidosis-the hallmark of cyanide poisoning.

Molecules bind to the ferric ion of cytochrome-c oxidase blocking this final step in the oxidative phosphorylation pathway and inhibiting the production of ATP.

Cyanide is a potent mitochondrial toxin which can cause death within a matter of minutes.

Cure for cyanide