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Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy
Abstract
Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15–40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.
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“Severe CO poisoning can result in brain (e.g., cognitive dysfunction, neurological deficits, neuronal necrosis and apoptosis) and myocardial injury (Rose et al., 2017).”
From Low-dose carbon monoxide inhalation to increase total hemoglobin mass and endurance performance: scientific evidence and implications (2024) · cites this paper as Rose et al., 2017
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“CO poisoning includes both, tissue hypoxia and direct cellular changes through various mechanisms, e.g., mitochondrial inhibition, free radical generation, apoptosis, immune-mediated injury, inflammatory effects (Hampson et al., 2012; Rose et al., 2017).”
From Low-dose carbon monoxide inhalation to increase total hemoglobin mass and endurance performance: scientific evidence and implications (2024) · cites this paper as Rose et al., 2017
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Metadata
- Authors
- Rose, J. J., Wang, L., Xu, Q., McTiernan, C. F., Shiva, S., Tejero, J., & Gladwin, M. T.
- Affiliations
- Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-03-01
- Volume
- 195
- Issue
- 5
- Pages
- 596-606
- ISSN
- 1073-449X
- 1535-4970
- Cited by
- 735
- References
- 4
- Language
- en
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