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Cyanide

المؤلف:  Sue Jickells , Adam Negrusz (Editors)

المصدر:  Clarkes Analytical Forensic Toxicology

الجزء والصفحة:  p111-112

2026-09-24

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Cyanide

Severe or fatal cyanide poisoning is relatively rare and mostly involves suicidal ingestion. Hydrogen cyanide (HCN; prussic acid) is a highly toxic volatile liquid. Fumes of hydrogen cyanide are given off when cyanide salts are mixed with acids or produced in the stomach following oral ingestion. Although HCN has a characteristic almond-like odour, about 50% of the population are unable to smell it. Soluble salts of cyanide include potassium and sodium cyanide, which are used industrially in electroplating and metal processing and as laboratory reagents. Less soluble salts of cyanide include silver and gold cyanide, and mercuric cyanide, which also release HCN on contact with strong acids. HCN may also be formed as a combustion product in fires from nitrogen-containing materials such as wool and silk or synthetic polymers such as polyurethanes, polyamides and polyamides (Baud et al. 1991; Barillo et al. 1994, Chaturvedi et al. 2001). Less common sources of cyanide include the accidental or intentional ingestion of cyanogenic plants or their seeds. The signs and symptoms of cyanide toxicity appear rapidly after inhalation of HCN or inges tion of cyanide salts; the estimated fatal doses are approximately 100 mg HCN or 300 mg potassium cyanide (Ellenhorn et al. 1997). Early neurological signs include headache, dizziness, anxiety and confusion. In severe cases there may be a rapid loss of consciousness, respiratory failure and convulsions that lead to cardiorespir atory arrest and death. Cyanide is metabolised rapidly in the liver by an enzyme (rhodanase) to thiocyanate (SCN), which is largely nontoxic. As a consequence, blood cyanide concentrations decline rapidly after exposure or ingestion, with an estimated elimination half-life of 1–2 h. A number of antidotes are useful in the treatment of cyanide poisoning (e.g. cobalt EDTA and hydroxocobalamin). In postmortem cases after suicidal ingestion of cyanide salts, elevated levels of cyanide may occur in blood samples taken from the heart or other central sites owing to postmortem diffusion of unadsorbed cyanide from the stomach. Hence blood samples should be taken from peripheral sites such as the femoral vein. It should also be noted that bacteria and fungi can break down or generate cyanide in the body or in specimens. Precautions should, therefore, be taken to collect blood into anticoagulated tubes that contain sodium fluor ide to prevent/minimise microbial growth in the sample. Where there is evidence of putrefaction in the body before sampling, this should be taken into account when interpreting data on cyanide levels. Quantitative analysis of cyanide in stomach contents can be helpful when the route of ingestion is uncertain. In cases of fire, inhalation of smoke and fumes can result in concentrations of cyanide of up to 1 mg/L in blood, both in antemortem and in postmortem specimens. Reference values for cyanide in blood are <0.05 mg/L. Minor signs and symptoms of toxicity are associated with blood concentrations up to 1 mg/L, and severe symptoms with higher concentrations, up to 20 mg/L, on admission to hospital after suicidal ingestion or industrial exposure (Singh et al. 1989)