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.

Health hazard evaluation report: evaluation of exposures and respiratory health at a coffee roasting and packaging facility.

“…These gases are released during and after roasting and grinding by a process called off-gassing [Anderson et al 2003]. High exposures to CO and CO 2 can cause headache, dizziness, fatigue, nausea, altered mentation, rapid breathing, impaired consciousness, coma, and death [Newton 2002;Nishimura et al 2003;Langford 2005;CDC 2013a;Raffel and Thompson 2013;Rose et al 2017]. Occupational exposure limits for CO and CO 2 are listed in Table 1.…”

Health hazard evaluation report: evaluation of exposures and respiratory health at a coffee roasting and packaging facility and attached retail cafe.

“…These gases are released during and after roasting and grinding, a process called off-gassing [Anderson et al 2003]. High exposures to CO and CO 2 can cause headache, dizziness, fatigue, nausea, confusion, rapid breathing, impaired consciousness, coma, and death [Newton 2002;Nishimura et al 2003;Langford 2005;CDC 2013a;Raffel and Thompson 2013;Rose et al 2017]. Occupational exposure limits for CO and CO 2 are listed in Table 1.…”

Multiple Victims of Carbon Monoxide Poisoning in the Aftermath of a Wildfire: A Case Series

“…4 Inhaled CO can cause toxicity through several mechanisms by both hypoxic stress from binding to haemoglobin and intracellular sites, as well as non-hypoxic pathways such as oxidative stress, endothelial leukocyte adhesion, and lipid peroxidation. 5 There is a large spectrum of clinical features due to CO poisoning ranging from nausea and dizziness to coma, with death occurring in about 1% -3%. 6 Interestingly, initial carboxyhemoglobin (COHb) level does not correlate with exhibited symptoms.…”