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Smoke inhalation victims may have concomitant carbon monoxide and cyanide poisoning.
Clinical signs and symptoms of carbon monoxide poisoning are notoriously nonspecific and correlate poorly with carboxyhemoglobin values.
Carbon monoxide poisoning should be considered for an illness affecting more than one member of a family or group from a common environment.
Cyanide poisoning is marked by rapid onset of central nervous system and cardiovascular dysfunction.
Key laboratory features of cyanide poisoning include marked acidemia, striking lactate elevation, and a diminished arterial–venous O2 difference.
Hydroxycobalamin is the antidote of choice for cyanide poisoning and early administration may be life saving.
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Carbon monoxide (CO) is the leading cause of toxin-related morbidity and mortality in North America, with tens of thousands of exposures and thousands of deaths each year in the United States. While most of these deaths represent suicides, the majority of pediatric fatalities result from smoke inhalation or misadventures involving combustion of fossil fuels with inadequate ventilation. In contrast, cyanide is rarely an agent of deliberate harm and is most often encountered in smoke inhalation victims.1,2 The pathophysiology of smoke inhalation is complex. From a toxicological perspective, carbon monoxide and cyanide poisoning may coexist.1,2 Critical interventions for the management of both of these poisonings include removal from the source of exposure, meticulous supportive care, and, for patients with concomitant cyanide poisoning, timely antidote administration.
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Carbon monoxide (CO) is an insidious poison. It is an imperceptible gas produced by the incomplete combustion of carbon-based compounds such as wood, charcoal, gasoline, or kerosene. In children, CO poisoning is typically unintentional and most often results from malfunctioning home heating systems or proximity to inadequately ventilated generators, charcoal grills, or motor vehicles.3 Rarely, CO poisoning results from inhalation or ingestion of methylene chloride, a hydrocarbon commonly found in paint stripping products and metabolized to CO by the liver.4
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The pathophysiology of CO poisoning is complex and incompletely understood. It is rapidly absorbed through the alveoli and binds to heme iron with an affinity roughly 240 times that of oxygen, resulting in the formation of carboxyhemoglobin (COHb).5,6 This produces a functional anemia as well as a conformational change in the structure of the hemoglobin molecule that shifts the oxyhemoglobin dissociation curve to the left. Collectively, these effects reduce the oxygen carrying capacity of blood and impair the release of oxygen to tissues.
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In addition, CO produces a host of other cellular effects that contribute to toxicity by interfering with oxygen utilization and promoting inflammation.5 Notably, it binds to myoglobin and other heme-containingstructures including mitochondrial cytochromes, impairing cellular respiration and ATP generation.5,7 Predictably, the most prominent effects of CO poisoning involve the myocardium and brain, tissues with little ability to tolerate cellular asphyxia.6,8 The tissue-specific effects ...