[Acute poisoning with carbon monoxide (CO) and cyanide (CN)]

Frédéric J Baud
Therapeutische Umschau. Revue Thérapeutique 2009, 66 (5): 387-97
A critical analysis of acute CO and CN poisonings evidences that the lone toxicological similarity between CO and CN is their ability to avidly bind iron ions in the different hemoproteins. Otherwise, CO is a stable not-metabolized molecule while CN is a highly reactive molecule with extensive metabolism. CO impairs the ability of erythrocytes to transfer oxygen while CN has no effect. Both toxicants act in the mitochondria with CN resulting in the complete and sustained blockade of cellular respiration inducing severe lactic acidosis while CO does not. Acute CO poisoning mostly alters neurological cognitive function and even consciousness without significant alteration of vital functions while CN primarily alters consciousness with early onset of severe alteration of vital functions. Severe CO poisonings requires hours of exposure while severe CN poisoning occurs within seconds or minutes of exposure. Both gases may result in brain damage and sequelae. Brain imaging clearly shows significant differences in the locations and types of CO- and CN-induced brain damages, further supporting different mechanisms of action. Oxygen is the lone treatment of CO poisoning while in CN poisonings antidotes associated to oxygen are more efficient than oxygen alone. Unfortunately, there are several conditions where the easily detected and potentially toxic CO still continues to mask other potent toxicants. The lack of awareness of emergency physicians, clinical toxicologists, and neuroradiologists regarding the role of other toxic gases whose important role is recognized in combustion toxicology or environmental medicine precludes any progress in the understanding of the mechanisms of toxicity and in the treatment of these poisonings resulting in a particularly high rate of morbi-mortality.

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