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Cyanide poisoning is commonly viewed as a rare but dramatic event, occurring in industrial or laboratory settings as the result of accidental releases of hydrogen cyanide (HCN) gas (e.g. in the case of fire) or salts in the case of suicide attempts.
In fact, cyanide poisoning is considerably more common than is generally appreciated. Multiple clinical and post-mortal studies have demonstrated that HCN contributes to the toxicity of fire smoke.
Cyanide acts primarily through its strong affinity for the iron-containing heme moiety, binding to numerous critical enzyme systems in the body and rendering them inactive. Of late, increasing attention has been paid to the relationship of cyanide and nitric oxide. The interactions appear to be complex, with cyanide inducing nitric oxide production by binding to N-methyl-D-aspartate (NMDA) receptors, as well as binding to nitric oxide synthase. The latter may be overcome by the presence of nitric oxide synthase inhibitors.
Probably, the majority of the cyanide poisoning cases are due to smoke inhalation in closed-space fires.
So far, there are no clear data available on the prevalence of cyanide poisoning in smoke inhalation.
This information would be of great interest for all emergency physicians since a proven or supposed cyanide poisoning does not only requires an intensive supportive care, including the administration of supplemental oxygen and artificial ventilation, blood pressure support, and anticonvulsants, but also a rapid administration of a cyanide antidote.
Therefore, it is the goal of this survey to assess the prevalence of cyanide poisoning in smoke inhalation victims. Only the data of patients with a cyanide measurement before specific antidote treatment will be included
Full description
Cyanide poisoning is commonly viewed as a rare but dramatic event, occurring in industrial or laboratory settings as the result of accidental releases of hydrogen cyanide (HCN) gas (e.g. in the case of fire) or salts in the case of suicide attempts.
In fact, cyanide poisoning is considerably more common than is generally appreciated. Multiple clinical [1-4] and post-mortal studies [5-10] have demonstrated that HCN contributes to the toxicity of fire smoke.
Cyanide acts primarily through its strong affinity for the iron-containing heme moiety, binding to numerous critical enzyme systems in the body and rendering them inactive [11]. Of late, increasing attention has been paid to the relationship of cyanide and nitric oxide. The interactions appear to be complex, with cyanide inducing nitric oxide production by binding to N-methyl-D-aspartate (NMDA) receptors [12], as well as binding to nitric oxide synthase. The latter may be overcome by the presence of nitric oxide synthase inhibitors.
Probably, the majority of the cyanide poisoning cases are due to smoke inhalation in closed-space fires.
So far, there are no clear data available on the prevalence of cyanide poisoning in smoke inhalation.
This information would be of great interest for all emergency physicians since a proven or supposed cyanide poisoning does not only requires an intensive supportive care, including the administration of supplemental oxygen and artificial ventilation, blood pressure support, and anticonvulsants, but also a rapid administration of a cyanide antidote.
Therefore, it is the goal of this survey to assess the prevalence of cyanide poisoning in smoke inhalation victims. Only the data of patients with a cyanide measurement before specific antidote treatment will be included.
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