The concern of a terrorist attack using cyanide, as well as the gradual awareness of cyanide poisoning in fire victims, has resulted in a renewed interest in the diagnosis and treatment of cyanide poisoning. The formerly academic presentation of cyanide poisoning must be replaced by more useful knowledge, which will allow emergency physicians and rescue workers to strongly suspect cyanide poisoning at the scene. Human cyanide poisonings may result from exposure to cyanide, its salts, or cyanogenic compounds, while residential fires are the most common condition of exposure. In fire victims, recognition of the cyanide toxidrome has been hampered by the short half-life in blood and poor stability of cyanide. In contrast, carboxyhemoglobin, as a marker of carbon monoxide poisoning, is easily measured and long-lasting. No evidence supports the assumption of the arbitrary fixed lethal thresholds of 50% for carboxyhemoglobin, and 3 mg/L for cyanide, in fire victims. Preliminary data, drawn when comparing pure carbon monoxide and pure cyanide poisonings, suggest that a cyanide toxidrome can be defined considering signs and symptoms induced by cyanide and carbon monoxide, respectively. Prospective studies in fire victims may provide value in clarifying signs and symptoms related to both toxicants. Cyanide can induce a lifethreatening poisoning from which a full recovery is possible. A number of experimentally efficient antidotes to cyanide exist, whose clinical use has been hampered due to serious side effects. The availability of potentially safer antidotes unveils the possibility of their value as first-line treatment, even in a complex clinical situation, where diagnosis is rapid and presumptive.
Acute carbon monoxide poisoning with low saturation of carboxyhaemoglobin: a forensic retrospective study in Shanghai, China