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Carbon monoxide poisoning
Other namesCarbon monoxide intoxication, carbon monoxide toxicity, carbon monoxide overdose
A carbon atom (shown as a grey ball) tripled bonded to an oxygen atom (shown as a red ball).
Carbon monoxide
SpecialtyToxicology, emergency medicine
SymptomsHeadache, dizziness, weakness, vomiting, chest pain, confusion[1]
ComplicationsLoss of consciousness, arrhythmias, seizures[1][2]
CausesBreathing in carbon monoxide[3]
Diagnostic methodCarboxyl-hemoglobin level:
3% (nonsmokers)
10% (smokers)[2]
Differential diagnosisCyanide toxicity, alcoholic ketoacidosis, aspirin poisoning, upper respiratory tract infection[2][4]
PreventionCarbon monoxide detectors, venting of gas appliances, maintenance of exhaust systems[1]
TreatmentSupportive care, 100% oxygen, hyperbaric oxygen therapy[2]
PrognosisRisk of death 1–31%.[2]
Frequency>20,000 emergency visits for non-fire related cases per year (US)[1]
Deaths>400 non-fire related a year (US)[1]

Carbon monoxide poisoning typically occurs from breathing in carbon monoxide (CO) at excessive levels.[3] Symptoms are often described as "flu-like" and commonly include headache, dizziness, weakness, vomiting, chest pain, and confusion.[1] Large exposures can result in loss of consciousness, arrhythmias, seizures, or death.[1][2] The classically described "cherry red skin" rarely occurs.[2] Long term complications may include feeling tired, trouble with memory, and movement problems.[5] In those exposed to smoke, breathing in carbon monoxide (CO) at excessive levels.[3] Symptoms are often described as "flu-like" and commonly include headache, dizziness, weakness, vomiting, chest pain, and confusion.[1] Large exposures can result in loss of consciousness, arrhythmias, seizures, or death.[1][2] The classically described "cherry red skin" rarely occurs.[2] Long term complications may include feeling tired, trouble with memory, and movement problems.[5] In those exposed to smoke, cyanide toxicity should also be considered.[2]

Carbon monoxide poisoning can occur accidentally, as an attempt to end one's own life, or as an attempt to end another's life.[6][7] CO is a colorless and odorless gas which is initially non-irritating.[5] It is produced during incomplete burning of organic matter.[5] This can occur from motor vehicles, heaters, or cooking equipment that run on carbon-based fuels.[1] It can also occur from exposure to methylene chloride.[8] Carbon monoxide primarily causes adverse effects by combining with hemoglobin to form carboxyhemoglobin (HbCO) preventing the blood from carrying oxygen.[5] Additionally, myoglobin and mitochondrial cytochrome oxidase are affected.[2] Diagnosis is based on a HbCO level of more than 3% among nonsmokers and more than 10% among smokers.[2]

Efforts to prevent poisoning include carbon monoxide detectors, proper venting of gas appliances, keeping chimneys clean, and keeping exhaust systems of vehicles in good repair.[1] Treatment of poisoning generally consists of giving 100% oxygen along with supportive care.[2][5] This should generally be carried out until symptoms are no longer present and the HbCO level is less than 10%.[2] While hyperbaric oxygen therapy is used for severe poisonings, the benefit over standard oxygen delivery is unclear.[2][6] The risk of death among those affected is between 1 and 30%.[2]

Carbon monoxide poisoning is relatively common, resulting in more than 20,000 emergency room visits a year in the United States.[1][9] It is the most common type of fatal poisoning in many countries.[10] In the United States, non-fire related cases result in more than 400 deaths a year.[1] Poisonings occur more often in the winter, particularly from the use of portable generators during power outages.[2]attempt to end one's own life, or as an attempt to end another's life.[6][7] CO is a colorless and odorless gas which is initially non-irritating.[5] It is produced during incomplete burning of organic matter.[5] This can occur from motor vehicles, heaters, or cooking equipment that run on carbon-based fuels.[1] It can also occur from exposure to methylene chloride.[8] Carbon monoxide primarily causes adverse effects by combining with hemoglobin to form carboxyhemoglobin (HbCO) preventing the blood from carrying oxygen.[5] Additionally, myoglobin and mitochondrial cytochrome oxidase are affected.[2] Diagnosis is based on a HbCO level of more than 3% among nonsmokers and more than 10% among smokers.[2]

Efforts to prevent poisoning include carbon monoxide detectors, proper venting of gas appliances, keeping chimneys clean, and keeping exhaust systems of vehicles in good repair.[1] Treatment of poisoning generally consists of giving 100% oxygen along with supportive care.[2][5] This should generally be carried out until symptoms are no longer present and the HbCO level is less than 10%.[2] While hyperbaric oxygen therapy is used for severe poisonings, the benefit over standard oxygen delivery is unclear.[2][6] The risk of death among those affected is between 1 and 30%.[2]

Carbon monoxide poisoning is relatively common, resulting in more than 20,000 emergency room visits a year in the United States.[1][9] It is the most common type of fatal poisoning in many countries.[10] In the United States, non-fire related cases result in more than 400 deaths a year.[1] Poisonings occur more often in the winter, particularly from the use of portable generators during power outages.[2][8] The toxic effects of CO have been known since ancient history.[11] The discovery that hemoglobin is affected by CO was made in 1857.[11]

Carbon monoxide is not toxic to all forms of life. Its harmful effects are due to binding with hemoglobin so its danger to organisms that do not use this compound is doubtful. It thus has no effect on photosynthesising plants.[12] It is easily absorbed through the lungs.[13] Inhaling the gas can lead to hypoxic injury, nervous system damage, and even death. Different people and populations may have different carbon monoxide tolerance levels.[14] On average, exposures at 100 ppm or greater is dangerous to human health.[15] In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period;[16][17] in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached.[18] Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage.[19] The carbon monoxide tolerance level for any person is altered by several factors, including activity level, rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other hematological disorders, barometric pressure, and metabolic rate.[20][21][22]

Effects of carbon monoxide in relation to the concentration in parts per million in the air:[23][24]
Concentration Symptoms
35 ppm (0.0035%), (0.035‰) Headache and dizziness within six to eight hours of constant exposure
100 ppm (0.01%), (0.1‰) Slight headache in two to three hours
200 ppm (0.02%), (0.2‰) Slight headache within two to three hours; loss of judgment
400 ppm (0.04%), (0.4‰) Frontal headache within one to two hours
800 ppm (0.08%), (0.8‰) Dizziness, nausea, and convulsions within 45 min; insensible within 2 hours
1,600 ppm (0.16%), (1.6‰) Headache, increased heart rate, dizziness, and nausea within 20 min; death in less than 2 hours
3,200 ppm (0.32%), (3.2‰) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
6,400 ppm (0.64%), (6.4‰) Headache and dizziness in one to two minutes. Convulsions, respiratory arrest, and death in less than 20 minutes.
12,800 ppm (1.28%), (12.8‰) Unconsciousness after 2–3 breaths. Death in less than three minutes.

Acute poisoning

A person within a hyperbaric oxygen chamber

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin[14] and cytochrome oxidase[109] to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 (~80/3 minutes) minutes, compared to 80 minutes for oxygen at regular atmospheric pressure.[14] It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin.[107] However, it is controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen, in terms of increased survival or improved long-term outcomes.[110][111][112][113][114][115] There have been randomized controlled trials in which the two treatment options have been compared;[116][117][118][119][120][121] of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen.[110] Some of these trials have been criticized for apparent flaws in their implementation.[122][123][124][125] A review of all the literature concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.[110]

Other

Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support.[38] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[126] Further treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity and seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support.[38] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[126] Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols.[26] If severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability.[127] Treatment of acidosis may only need to consist of oxygen therapy.[26][31] The delayed development of neuropsychiatric impairment is one of the most serious complications of carbon monoxide poisoning. Brain damage is confirmed following MRI or CAT scans.[25][128][129] Extensive follow up and supportive treatment is often required for delayed neurological damage.[30] Outcomes are often difficult to predict following poisoning,[130] especially people who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels.[31] One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.[69] It has been reported that electroconvulsive therapy (ECT) may increase the likelihood of delayed neuropsychiatric sequelae (DNS) after carbon monoxide (CO) poisoning.[131] A device that also provides some carbon dioxide to stimulate faster breathing (sold under the brand name ClearMate) may also be used.[132]

Epidemiology