Cyanide (CN−) salts and hydrogen cyanide (HCN) are highly toxic chemicals used in chemical synthesis, as rodenticides (eg, “gopher getter”), formerly as a method of execution, and as agents of suicide or homicide. Hydrogen cyanide is formed from the burning of plastics, wool, and many other synthetic and natural products. Cyanide is also released after ingestion of various plants (eg, cassava) and seeds (eg, apple, peach, and apricot).
Cyanide binds readily to cytochrome oxidase, inhibiting oxy-gen utilization within the cell and leading to cellular hypoxia and lactic acidosis. Symptoms of cyanide poisoning include shortness of breath, agitation, and tachycardia followed by seizures, coma, hypotension, and death. Severe metabolic acidosis is characteristic. The venous oxygen content may be elevated because oxygen is not being taken up by cells.
Treatment of cyanide poisoning includes rapid administration of activated charcoal (although charcoal binds cyanide poorly, it can reduce absorption) and general supportive care. The conven-tional antidote kit available in the USA includes two forms of nitrite (amyl nitrite and sodium nitrite) and sodium thiosulfate. The nitrites induce methemoglobinemia, which binds to free CN−creating the less toxic cyanomethemoglobin; thiosulfate is a cofac-tor in the enzymatic conversion of CN− to the much less toxic thiocyanate (SCN−).In 2006 the FDA approved a new cyanide antidote, a concen-trated form of hydroxocobalamin, which is now available as the Cyanokit (EMD Pharmaceuticals, Durham, North Carolina). Hydroxocobalamin (one form of vitamin B12) combines rapidly with CN− to form cyanocobalamin (another form of vitamin B12).