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The toxicity of cyanide or hydrocyanic acid is well know since decades. Typically such intoxications will have an apoplectic course, sometimes reported as “all or nothing” – immediate death or survival [e.g.163], while other publications challenge this [198].
A variety of antidotes has been introduced for the treatment of such poisonings, starting with methylene blue, to nitrites and 4-dimethylaminophenol as methemoglobin forming agents, to cobalt-containing drugs like Co-EDTA or hydroxocobalamin. A consistently recommended antidote still is sodium thiosulfate.
It is less know that cyanide poisoning can occur as sequelae to intoxications with cyanogenic agents like organic nitriles, aliphatic as well as olefinic ones. In the emergency room of the occupational medical department of a large chemical plant we have been surprised in the last years by several very severe poisonings with cyanide levels in the potentially dangerous range. Such a degree of cyanide formation so far had not been seen. Thus it is important to report our observations.
Whereas nitriles mainly are handled in chemicals plants by chemical workers, they may – rarely- also play a role in acute exposures of the general public, as shown by a railroad accident with liberation of acrylonitrile in Germany in February 2002 (unpublisheb), and in reports on oral ingestions of nail-removers containing acetonitrile. In the industry acetonitrile is a very common, propionitrile a rare solvent, whereas acrylonitile is used in latices production and especially in the productions of ABS (acrylonitrile-butadiene-styrene)-plastics. Nevertheless, reports in literature on such poisoning are scarce, and they do not deal primarily with aspects of metabolism, cyanide levels, and treatment options. Clearly there is a lack of data and guidelines concerning such poisonings, even in occupational medicine, but also in clinical toxicology.
In contrast, another indirect source of cyanide exposures is discussed widely in the last years, mainly because of possible exposures of the general public, but also of firefighters and rescue personnel. This source is smoke inhalation. Many substances from natural ones like wool to plastics like ABS-plastics and polyurethanes can yield a substantial amount of HCN gas when burning or smouldering. Together with the enormous amount of other toxins released in fires, from chlorine, phosgene, hydrochloric acid gases, nitrous oxides, carbon monoxide and dioxide, to organics like acrolein and benzene, HCN may well play an important part in the toxicity of smoke. However, there is an intense discussion in literature about the importance of cyanide in smoke inhalations, of its occurrence, its amount, its sequelae, but also about practical measures to be taken in the treatment of smoke inhalation patients that is the necessity and choice of cyanide antidotes.
The aims of the study are first to report on poisonings with different nitriles seen in the last decade in a large chemical plant, including biomonitoring data. From these casuistics the clinical symptoms of such poisonings, an eventual influence of different routes of exposure, results of repeated biomonitoring, and especially the treatment options will be shown.
In addition, a study has been performed in smoke inhalation victims from residential fires. The concentrations of carbon monoxide and cyanide were measured, and eventual correlations between these parameters and clinical data reported in the literature were examined. The choice of antidotes in smoke inhalations in hampered by the fact, that the patients may present with a CO-hemoglobinemia, which means the part of the hemoglobin is unable to bind and transport oxygen. Thus the choice of cyanide antidotes, if required, would be problematic, as some will induce a further hypoxemia. So it is of interest to assess, what role cyanides really do play in smoke inhalations, whether and what antidotes are needed, and what room is left for which antidotes.
The existing literature has to be discussed under different aspects. First the reports and recommendations for nitrile poisonings and smoke inhalations have to be assessed, but in addition questions like evidence for occurrence of HCN in smoke, lethal cyanide levels in blood, and their possible correlations to COHb and clinical signs must be addressed.
From the data of the nitrile casuistics and the smoke inhalation study and from the literature discussion treatment recommendations for both situations can be derived.

Poisoning --- Smoke Inhalation Injury --- Cyanides