Cyanide poisoning by fire smoke inhalation

Abstract

Smoke inhalation is a common cause of cyanide poisoning during fires, resulting in injury and even death. In many cases of smoke inhalation, cyanide has increasingly been recognized as a significant toxicant. The diagnosis of cyanide poisoning remains very difficult, and failure to recognize it may result in inadequate or inappropriate treatment. Findings suggesting cyanide toxicity include the following: (a) a history of enclosed-space fire; (b) any alteration in the level of consciousness; (c) any cardiovascular changes (particularly inexplicable hypotension); and (d) elevated plasma lactate. The feasibility and safety of empiric treatment with hydroxocobalamin for fire smoke victims have been reported in the literature. On the basis of a literature review and a panel discussion, a group of European experts has proposed emergency management protocols for cyanide toxicity in fire smoke victims.

Physiologically based pharmacokinetic modeling of hydrogen cyanide levels in human breath

“…In another review, baud suggested 1 mg/l to be toxic and 2.7 mg/l to be potentially lethal (baud 2007). Geldner et al (2013) proposed 200 μmol/l (5.2 mg/l), whereas Anseeuw et al (2013) suggested 3 mg/l (111 μmol/l) as being lethal. since cyanide continues to break down postmortem, the divergence of the reported values may be explained by difficulties in relating measured blood cyanide levels to actual concentrations at the time of death.…”

Pink skin, urine and effluent fluid after cyanide poisoning

“…It should be mentioned again that the diagnosis is very difficult in case of smoke inhalation. A group of European experts has recently acknowledged hydroxocobalamin as a valid empiric treatment for fire smoke victims [7]. For cyanide salt intoxication, as it occurred in present case, Thompson et al, [8] reviewed the available pharmacological data on hydroxycobalamin and concluded that it was an effective antidote.…”

Case Files of the University of Massachusetts Toxicology Fellowship: Does This Smoke Inhalation Victim Require Treatment with Cyanide Antidote?

“…Affected cells are subsequently forced into anaerobic metabolism. Organs highly susceptible to ATP depletion (brain, heart) are primarily affected [5]. From rodent studies, it is further believed that cyanide also alters neurotransmitter concentrations in the brain, mainly increasing glutamate and dopamine while decreasing γ-aminobutyric acid (GABA) [6].…”

“…The cyanide ion has a high affinity for metalloproteins and can affect up to 40 different enzyme systems [5]. When bound to the ferric iron (Fe 3+ ) in cytochrome a3, a heme group within cytochrome c oxidase, non-competitive inhibition results in arrest of oxidative phosphorylation.…”