Carbon monoxide poisoning
- Peter F Clardy, MD
Peter F Clardy, MD
- Assistant Professor of Medicine
- Harvard Medical School
- Scott Manaker, MD, PhD
Scott Manaker, MD, PhD
- Section Editor — Critical Care
- Professor of Medicine
- University of Pennsylvania School of Medicine
- Holly Perry, MD
Holly Perry, MD
- Assistant Professor of Pediatrics
- Tufts University School of Medicine
- Section Editors
- Stephen J Traub, MD
Stephen J Traub, MD
- Section Editor — Toxicology
- Associate Professor of Emergency Medicine
- Mayo Medical School
- Michele M Burns, MD, MPH
Michele M Burns, MD, MPH
- Section Editor — Pediatric Toxicology
- Assistant Professor of Pediatrics
- Harvard Medical School
Carbon monoxide (CO) is an odorless, tasteless, colorless, nonirritating gas formed by hydrocarbon combustion. The atmospheric concentration of CO is generally below 0.001 percent, but it may be higher in urban areas or enclosed environments. CO binds to hemoglobin with much greater affinity than oxygen, forming carboxyhemoglobin (COHb) and resulting in impaired oxygen transport and utilization. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae.
CO poisoning will be reviewed here. A summary table to facilitate emergent management is provided (table 1). Related topics including smoke inhalation and hyperbaric oxygen therapy are presented separately. (See "Hyperbaric oxygen therapy" and "Inhalation injury from heat, smoke, or chemical irritants".)
Carbon monoxide (CO) poisoning is responsible for up to 40,000 emergency department (ED) visits and 5000 to 6000 deaths per year, making it one of the leading causes of poisoning death in the United States [1-3]. Inadvertent CO poisoning likely causes around 500 deaths annually; the number of intentional CO poisonings is perhaps 10 times higher [1,4,5]. The overall case-fatality rate for CO poisoning ranges from 0 to 31 percent [3,6,7].
Unlike intentional poisoning, unintended poisoning demonstrates both seasonal and regional variation, and it is most common during the winter months in cold climates . Morbidity, which is primarily related to late neurocognitive impairment, persists beyond initial stabilization in up to 40 percent of victims [3,6].
Smoke inhalation is responsible for most inadvertent cases of CO poisoning. Other potential sources of CO include poorly functioning heating systems, improperly vented fuel-burning devices (eg, kerosene heaters, charcoal grills, camping stoves , gasoline-powered electrical generators [9,10]), and motor vehicles operating in poorly ventilated areas (eg, ice rinks, warehouses, parking garages). CO poisonings following open air exposure to motorboat exhaust have also been reported . In addition, underground electrical cable fires produce large amounts of CO, which can seep into adjacent buildings and homes . An increase in carbon monoxide exposures has been reported to occur in the immediate aftermath of hurricanes [9,13,14].
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- CLINICAL PRESENTATION
- Symptoms and signs
- Myocardial injury
- Delayed neuropsychiatric syndrome
- Initial treatment and disposition
- Hyperbaric oxygen
- Hyperbaric oxygen and delayed neuropsychiatric syndrome (DNS)
- HBO during pregnancy
- Isocapnic hyperpnea
- PEDIATRIC CONSIDERATIONS
- ADDITIONAL RESOURCES
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS