We could not find a published consensus defining significant toxicity. In these instances, point-of-care evaluation of laboratory markers can guide clinicians in their decision-making. While appropriate for EMS, physicians may have to apply stricter triage criteria in mass casualty events with limited supply of medication or decide which patients require additional antidotal therapy. There is no inclusion of point-of-care testing parameters. Patients who show evidence of smoke inhalation (e.g., soot around mouth or nose), confusion, or abnormal vital signs are advocated to receive cyanide antidote. As the focus of this algorithm is directed to pre-hospital providers, the decision to administer antidote is based on vital signs and mental status. In their work, they divided patients into four categories: mild, moderate, and severe smoke inhalation, and cardiac arrest. published an excellent review of cyanide toxicity, with a proposed algorithm on the empiric management of cyanide toxicity in the pre-hospital setting. Ideally, the treatment for cyanide toxicity is initiated in the field due to the time-sensitive nature of this condition. After circulation, airway, and breathing have been assessed and stabilization has been initiated as appropriate, the pre-hospital provider must decide whether to administer an antidote for cyanide toxicity. The approach to resuscitation for critically ill patients is similar for the treatment of victims of smoke inhalation. What Are the Published Indications for Antidotal Therapy in Cyanide Toxicity from Smoke Inhalation? Despite sublethal levels of either toxicant, fatalities have been reported in humans and demonstrated in animal trials. Not surprisingly, carbon monoxide and cyanide act synergistically to inhibit cellular respiration. Like cyanide, it also binds to cytochrome a3 of cytochrome c oxidase and inhibits its function. This toxicant tightly binds to hemoglobin, thereby inhibiting oxygen delivery to tissues. Īnother asphyxiant produced in house fires is carbon monoxide. 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). Organs highly susceptible to ATP depletion (brain, heart) are primarily affected. Affected cells are subsequently forced into anaerobic metabolism. 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. The cyanide ion has a high affinity for metalloproteins and can affect up to 40 different enzyme systems. Hydrogen cyanide gas is a cellular asphyxiant which quickly dissociates into both hydrogen and cyanide ions when dissolved. What Is the Pathophysiology of Cyanide Toxicity? Cyanide is detectable in the blood of almost 60 % of fire-related fatalities and 50 % of survivors of enclosed-space fires. Experts suspect that the amount of hydrogen cyanide in fire-related smoke has increased over the past decades due to use of novel, synthetic building and furnishing materials. Both gases are cellular asphyxiants, respectively competing for oxygen binding sites on hemoglobin or inhibiting cytochrome c oxidase in mitochondrial oxidative phosphorylation. While the composition of smoke is highly variable and depends on fuel available for pyrolysis, temperature, and oxygen availability, two common inhalational toxicants found in smoke are carbon monoxide and hydrogen cyanide. On average, there are 2580 deaths and 13,280 injuries per year associated with fires in the USA, most of them due to the inhalation of smoke. Frequently, both building occupants and firefighters experience inhalation exposure to smoke. While only 29.1 % of fires involve private homes, they represent 75.7 and 79.1 % of all fire-related fatalities and injuries, respectively. How Common Is Cyanide Toxicity After Smoke Inhalation?įire departments in the USA respond to approximately 1,389,500 fires annually.
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