The most common cause of cyanide poisoning is smoke inhalation. A source to the public is acetonitrile in the form of artificial fingernail remover. Cyanide poisoning produces cellular hypoxia by binding with the ferric iron of mitochondrial cytochrome oxidase, disrupting the electron transport chain and the ability of cells to use oxygen. Patients who inhale cyanide may rapidly develop coma, shock, seizures, lactic acidosis, and respiratory and cardiac arrest. Mild exposures following smoke inhalation are now being described. Diagnosis may be difficult in these patients, and emergency administration of an antidote may be lifesaving. Patients with smoke inhalation who show evidence of lactic acidosis should be suspected of cyanide poisoning. The body has a natural enzyme, called “rhodanese”, which can complex cyanide and sulphur to form mildly toxic thiocyanate. Intravenous administration of sodium thiosulphate provides the sulphur necessary to produce thiocyanate and is relatively safe. Sodium nitrite may also be administered, but its use is reserved for the most critical cases only, because it causes hypertension and methemoglobinemia.