SUMMARYCyanide is a potent and rapidly-acting asphyxiant which prevents tissue utilization of oxygen by inhibition of the cellular respiratory enzyme, cytochrome oxidase. Inhalation or ingestion of cyanide produces reactions within a few seconds and death within minutes. Cyanide toxicity of dietary origin has been implicated in acute animal deaths and as major etiologic factors in toxic ataxic neuropathy in man and as a cause of vision failure in humans suffering from tobacco amblyopia and leber's hereditary optic atrophy. Diagnosis of cyanide toxicity may be confirmed by a variety of laboratory procedures, but accurate assay is essential for proper conclusions from analysis of animal tissues several hours after death or from human samples in instances of chronic dietary exposure. Biological detoxification of cyanide is available through several routes, and the application of sodium nitrite with sodium thiosulfate or administration of methylene blue are effective treatment procedure. The environmental availability of cyanide in its various forms necessitates an understanding of its pathophysiology and responsible management of hazardous situations.
OCCURRENCECyanide is present in many industrial and municipal waste waters. The most important source of this cyanide pollution is the effluents of electroplating processes, metal finishing, metallurgy, steel processing, and petroleum industries. Hydrocyanic acid (HCN) and its alkali salts like sodium cyanide and potassium cyanide are found in vermicidal fumigants, insectides, rodenticides, metal polishes (especially silver polish), electroplating solutions and photographic processes. Hydrogen cyanide is also generated by action of mineral acids on cyanide salts for use as a fumigant. Several reported deaths following the use of sodium nitroprusside for the elective induction of hypotension during general ansthesia have been attributed to the accumulation of cyanide in the blood (1,2,3 (pH 9.0-12.0), and the permeability constant for HCN (pka = 9.2) was calculated to be 25 times greater than that of the cyanide ion (CN-).Since the initial build up of absorption rate was shown to depend on the diffusion constant, HCN was absorbed with very little lag whereas CN absorption rate increased for about 90 minutes. The results obtained by the authors permitted estimations of the early time courses of absorption (by combination of CN -and HCN contributions) for different exposures, and the resulting absorption patterns were compared with the detoxification rates of cyanide and the body burden producing toxic effects. Their calculations showed, for example, that a large area contact with 10% NaCN at pH 11.4 leads to clinical signs of toxicity within 25 minutes and death in about 1 hour. Observations in the small number of industrial accidents available for comparison were in agreement with the calculations. Therefore, cyanide absorbed by the skin from clothing wetted with NaCN solution may lead to toxic effects in certain cases.A greater part of the absorbed cyanide is rapidly...