Carbon monoxide poisoning

Carbon monoxide (CO) is an odorless, colorless gas, and poisoning can cause hypoxia, cell damage, and death. Approximately 1% to 3% of all poisonings are fatal.

Poisoning can occur following exposure from incomplete combustion that includes smoke inhalation from fire, motor vehicle exhaust and other engine exhausts in poorly ventilated spaces, and various industrial sources.

Early symptoms are nonspecific and include headache, dizziness, and nausea.

If symptoms of CO poisoning are suspected, individuals should leave the building or space immediately and call the emergency medical services.

More severe exposure results in cardiovascular manifestations that can include myocardial ischemia, myocardial infarction, cardiac dysfunction, dysrhythmias, and cardiac arrest.

Patients with moderate to severe CO poisoning should be assessed for cardiac involvement with an ECG and measurement of cardiac biomarkers to identify acute myocardial injury, as this can predict poor long-term outcomes.

Neurologic symptoms include acute stroke-like symptoms, altered mental status, confusion, coma, and syncope.

Up to 40% of survivors of CO poisoning suffer from delayed neurocognitive deficits that can become permanent.

Diagnosis is based on a clinical triad: history of CO exposure, elevated carboxyhemoglobin levels, and symptoms consistent with CO poisoning.

High-flow oxygen therapy, hyperbaric oxygen, and supportive therapy are the key treatments.

Issues with hyperbaric treatment include difficulty caring for critically ill patients at some centers, and logistical barriers for timely transfer to facilities offering hyperbaric therapy.

Complications of hyperbaric therapy include seizures related to oxygen toxicity, pulmonary edema, and ear barotrauma.

Carbon monoxide (CO) poisoning is the most common human poisoning.[1]Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017 Mar 1;195(5):596-606. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5363978 http://www.ncbi.nlm.nih.gov/pubmed/27753502?tool=bestpractice.com [2]Hampson NB, Piantadosi CA, Thom SR, et al. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. Am J Respir Crit Care Med. 2012 Dec 1;186(11):1095-101. http://www.atsjournals.org/doi/full/10.1164/rccm.201207-1284CI#.VXHCJ8-jMyo http://www.ncbi.nlm.nih.gov/pubmed/23087025?tool=bestpractice.com CO is formed by incomplete combustion, with fire smoke inhalation, motor vehicles, and other engine exhausts being the most prevalent sources of exposure.[1]Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017 Mar 1;195(5):596-606. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5363978 http://www.ncbi.nlm.nih.gov/pubmed/27753502?tool=bestpractice.com The increased affinity of CO with hemoglobin results in decreased systemic oxygen delivery and the effects of CO on cytochrome c oxidase results in impairment of cellular respiration.

The symptoms of CO poisoning vary widely and are mostly nonspecific. Symptoms can range from headache, nausea, and dizziness, to severe cardiovascular and neurologic symptoms, depending on the dose and duration of the exposure. Mortality of acute CO poisoning is approximately 1% to 3%.[3]Hampson NB. U.S. Mortality due to carbon monoxide poisoning, 1999-2014. Accidental and intentional deaths. Ann Am Thorac Soc. 2016 Oct;13(10):1768-74. https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.201604-318OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed http://www.ncbi.nlm.nih.gov/pubmed/27466698?tool=bestpractice.com Those at highest risk for mortality are those who: are of an older age; are exposed to fire as a source of CO; experience loss of consciousness; and those with very high carboxyhemoglobin levels and respiratory failure.[4]Hampson NB, Hauff NM. Risk factors for short-term mortality from carbon monoxide poisoning treated with hyperbaric oxygen. Crit Care Med. 2008 Sep;36(9):2523-7. http://www.ncbi.nlm.nih.gov/pubmed/18679118?tool=bestpractice.com Survivors of CO poisoning have a higher long-term mortality rate than their nonpoisoned counterparts, and 15% to 40% suffer from near-permanent neurocognitive sequelae.[5]Hopkins RO, Weaver LK, et al.; Undersea & Hyperbaric Medical Society 2008 Annual Scientific Meeting. Cognitive outcomes 6 years after acute carbon monoxide poisoning [abstract]. June 2008 [internet publication]. http://archive.rubicon-foundation.org/xmlui/handle/123456789/7822 [6]Hsiao CL, Kuo HC, Huang CC. Delayed encephalopathy after carbon monoxide intoxication--long-term prognosis and correlation of clinical manifestations and neuroimages. Acta Neurol Taiwan. 2004 Jun;13(2):64-70. http://www.ncbi.nlm.nih.gov/pubmed/15478677?tool=bestpractice.com [7]Weaver LK, Hopkins RO, Churchill SK, et al.; Undersea & Hyperbaric Medical Society 2008 Annual Scientific Meeting. Neurological outcomes 6 years after acute carbon monoxide poisoning [abstract]. June 2008 [internet publication]. http://archive.rubicon-foundation.org/xmlui/handle/123456789/7823 [8]Hampson NB, Rudd RA, Hauff NM. Increased long-term mortality among survivors of acute carbon monoxide poisoning. Crit Care Med. 2009 Jun;37(6):1941-7. http://www.ncbi.nlm.nih.gov/pubmed/19384195?tool=bestpractice.com