Treatment of Cyanide Poisoning Associated with Fires

Abstract

Hydrogen cyanide is one of a number of nitrogen-containing substances produced in fires, although the extent to which hydrogen cyanide (HCN) contributes to morbidity and mortality is not completely clear. Much of the experimental and clinical data related to cyanide poisoning is based not on exposure to HCN, but upon oral poisoning with cyanide salts, from which extrapolation to HCN poisoning has to be undertaken with caution. The most important measure is to stop further exposure to hydrogen cyanide; thus the casualty needs to be removed from the source of HCN. There is evidence to suggest that oxygen is beneficial in cyanide poisoning. Very many antidotes have been studied experimentally in animals and a few of these have been used clinically. Those used clinically include sodium thiosulfate, which hastens the enzymatic detoxication of cyanide. Alternatively, hydrogen cyanide can be detoxified by complexation with heavy metals, either iron (Fe++) in the form of drug-induced methaemoglobin or cobalt. The only methaemoglobin formers that have been used clinically are amyl nitrite, sodium nitrite and 4-dimethylaminophenol. Sodium nitrite, together with sodium thiosulfate, forms the “classical therapy” for cyanide poisoning. Two cobalt compounds have been used clinically: dicobalt edetate (Kelocyanor) and hydroxocobalamin. Both appear effective, although the evidence base supporting their use is not vast.