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Carbon monoxide poisoning

 
Medical Encyclopedia: Carbon Monoxide Poisoning
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Definition

Carbon monoxide (CO) poisoning occurs when carbon monoxide gas is inhaled. CO is a colorless, odorless, highly poisonous gas that is produced by incomplete combustion. It is found in automobile exhaust fumes, faulty stoves and heating systems, fires, and cigarette smoke. Other sources include woodburning stoves, kerosene heaters, improperly ventilated water heaters and gas stoves, and blocked or poorly maintained chimney flues. CO interferes with the ability of the blood to carry oxygen. The result is headache, nausea, convulsions, and finally death by asphyxiation.

Description

Carbon monoxide, sometimes called coal gas, has been known as a toxic substance since the third century B.C. It was used for executions and suicides in early Rome. Today it is the leading cause of accidental poisoning in the United States. According to the Journal of the American Medical Association, 1,500 Americans die each year from accidental exposure to CO, and another 2,300 from intentional exposure (suicide). An additional 10,000 people seek medical attention after exposure to CO and recover.

Anyone who is exposed to CO will become sick, and the entire body is involved in CO poisoning. A developing fetus can also be poisoned if a pregnant woman breathes CO gas. Infants, people with heart or lung disease, or those with anemia may be more seriously affected. People such as underground parking garage attendants who are exposed to car exhausts in a confined area are more likely to be poisoned by CO. Firemen also run a higher risk of inhaling CO.

— Tish Davidson


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Children's Health Encyclopedia: Carbon Monoxide Poisoning
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Definition

Carbon monoxide (CO) poisoning occurs when carbon monoxide gas is inhaled. CO is a colorless, odorless, highly poisonous gas that is produced by incomplete combustion. It is found in automobile exhaust fumes, faulty stoves and heating systems, fires, and cigarette smoke. Other sources include wood-burning stoves, kerosene heaters, improperly ventilated water heaters and gas stoves, and blocked or poorly maintained chimney flues. CO interferes with the ability of the blood to carry oxygen. The result is headache, nausea, convulsions, and finally death by asphyxiation.

Description

Carbon monoxide, sometimes called coal gas, has been known as a toxic substance since the third century B.C. It was used for executions and suicides in early Rome.

Anyone who is exposed to CO becomes sick, and the entire body is involved in CO poisoning. A developing fetus can also be poisoned if a pregnant woman breathes CO gas. Infants, people with heart or lung disease, or those with anemia may be more seriously affected. People such as underground parking garage attendants who are exposed to car exhausts in a confined area are more likely to be poisoned by CO. Firemen also run a higher risk of inhaling CO.

Demographics

Carbon monoxide is the leading cause of accidental poisoning in the United States. Experts estimate that 1,500 Americans die each year from accidental exposure to CO and another 2,300 from intentional exposure (suicide). An additional 10,000 people seek medical attention after exposure to CO and recover.

Causes and Symptoms

Normally when a person breathes fresh air into the lungs, the oxygen in the air binds with a molecule called hemoglobin (Hb) that is found in red blood cells. This process allows oxygen to be moved from the lungs to every part of the body. When the oxygen/hemoglobin complex reaches a muscle where it is needed, the oxygen is released. Because the oxygen binding process is reversible, hemoglobin can be used over and over again to pick up oxygen and move it throughout the body.

Inhaling carbon monoxide gas interferes with this oxygen transport system. In the lungs, CO competes with oxygen to bind with the hemoglobin molecule. Hemoglobin prefers CO to oxygen and accepts it more than 200 times more readily than it accepts oxygen. Not only does the hemoglobin prefer CO, it holds on to the CO much more tightly, forming a complex called carboxyhemoglobin (COHb). As a person breathes CO contaminated air, more and more oxygen transportation sites on the hemoglobin molecules become blocked by CO. Gradually, there are fewer and fewer sites available for oxygen. All cells need oxygen to live. When they do not get enough oxygen, cellular metabolism is disrupted and eventually cells begin to die.

The symptoms of CO poisoning and the speed with which they appear depend on the concentration of CO in the air and the rate and efficiency with which a person breathes. Heavy smokers can start off with up to 9 percent of their hemoglobin already bound to CO, which they regularly inhale in cigarette smoke. This makes them much more susceptible to environmental CO. The Occupational Safety and Health Administration (OSHA) has established a maximum permissible exposure level of 50 parts per million (ppm) over eight hours.

With exposure to 200 ppm for two to three hours, a person begins to experience headache, fatigue, nausea, and dizziness. These symptoms correspond to 15 to 25 percent COHb in the blood. When the concentration of COHb reaches 50 percent or more, death results in a very short time. Emergency room physicians have the most experience diagnosing and treating CO poisoning.

The symptoms of CO poisoning in order of increasing severity include the following:

  • headache
  • shortness of breath
  • dizziness
  • fatigue
  • mental confusion and difficulty thinking
  • loss of fine hand-eye coordination
  • nausea and vomiting
  • rapid heart rate
  • hallucinations
  • inability to execute voluntary movements accurately
  • collapse
  • lowered body temperature (hypothermia)
  • coma
  • convulsions
  • seriously low blood pressure
  • cardiac and respiratory failure
  • death

In some cases, the skin, mucous membranes, and nails of a person with CO poisoning are cherry red or bright pink. Because the color change does not always occur, it is an unreliable symptom to count on for diagnosis.

Although most CO poisoning is acute, or sudden, it is possible to suffer from chronic CO poisoning. This condition exists when a person is exposed to low levels of the gas over a period of days to months. Symptoms are often vague and include (in order of frequency) fatigue, headache, dizziness, sleep disturbances, cardiac symptoms, apathy, nausea, and memory disturbances. Little is known about chronic CO poisoning, and it is often misdiagnosed.

When to Call the Doctor

A healthcare professional should be consulted whenever more than passing exposure to carbon monoxide is suspected. While waiting for help to arrive, a potentially affected person should be moved outdoors.

Diagnosis

The main reason to suspect CO poisoning is evidence that fuel is being burned in a confined area, for example, a car running inside a closed garage, a charcoal grill burning indoors, or an unvented kerosene heater in a workshop. Under these circumstances, one or more persons suffering from the symptoms listed above strongly suggests CO poisoning. In the absence of some concrete reason to suspect CO poisoning, the disorder is often misdiagnosed as migraine headache, stroke, psychiatric illness, food poisoning, alcohol poisoning, or heart disease.

Concrete confirmation of CO poisoning comes from a carboxyhemoglobin test. This blood test measures the amount of CO that is bound to hemoglobin in the body. Blood is drawn as soon after suspected exposure to CO as possible.

Other tests that are useful in determining the extent of CO poisoning include measurement of other arterial blood gases and pH; a complete blood count; measurement of other blood components such as sodium, potassium, bicarbonate, urea nitrogen, and lactic acid; an electrocardiogram (ECG); and a chest x ray.

Treatment

Immediate treatment for CO poisoning is to remove the victim from the source of carbon monoxide gas and into fresh air. If the victim is not breathing and has no pulse, cardiopulmonary resuscitation (CPR) should be started. Depending on the severity of the poisoning, 100 percent oxygen may be given with a tight fitting mask as soon as it is available.

Taken with other symptoms of CO poisoning, COHb levels of over 25 percent in healthy individuals, over 15 percent in people with a history of heart or lung disease, and over 10 percent in pregnant women usually indicate the need for hospitalization. In the hospital, fluids and electrolytes are given to correct imbalances that have arisen from the breakdown of cellular metabolism.

In severe cases of CO poisoning, individuals are given hyperbaric oxygen therapy. This treatment involves placing the person in a chamber in which the person breathes 100 percent oxygen at a pressure of more than one atmosphere (the normal pressure the atmosphere exerts at sea level). The increased pressure forces more oxygen into the blood. Hyperbaric facilities are specialized and are usually available only at larger hospitals.

Prognosis

The speed and degree of recovery from CO poisoning depends on the length of exposure to the gas and the concentration of carbon monoxide. The half-life of CO in normal room air is four to five hours, which means that in four to five hours half of the CO bound to hemoglobin will be replaced with oxygen. At normal atmospheric pressures, but breathing 100 percent oxygen, the half-life for the elimination of CO from the body is 50 to 70 minutes. In hyperbaric therapy at three atmospheres of pressure, the half-life is reduced to between 20 and 25 minutes.

Although the symptoms of CO poisoning may subside in a few hours, some affected persons show memory problems, fatigue, confusion, and mood changes for two to four weeks after their exposure to the gas.

Prevention

Carbon monoxide poisoning is preventable. Particular care should be paid to situations where fuel is burned in a confined area. Portable and permanently installed carbon monoxide detectors that sound a warning similar to smoke detectors are available for under $50. Specific actions that prevent CO poisoning include the following:

  • Stop smoking. Smokers have less tolerance to environmental CO.
  • Have heating systems and appliances installed by a qualified contractor to assure that they are properly vented and meet local building codes.
  • Inspect and properly maintain heating systems, chimneys, and appliances.
  • Do not use a gas oven or stove to heat the home.
  • Do not burn charcoal indoors.
  • Make sure there is good ventilation if using a kerosene heater indoors.
  • Do not leave cars or trucks running inside the garage.
  • Keep car windows rolled up when stuck in heavy traffic, especially if inside a tunnel.

Parental Concerns

Parents should not allow children to play in areas heated by kerosene space heaters or to use charcoal grills of any kind indoors.

Resources

Books

Braunwald, Eugene, et al, eds. "Hypoxia and Cyanosis." In Harrison's Principles of Internal Medicine, 15th ed. New York: McGraw Hill, 2001, pp. 214–6.

Carbon Monoxide Poisoning: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, CA: Icon Health Publications, 2004.

Penney, David G. Carbon Monoxide Toxicity. Lakeland, FL: CRC Press, 2000.

Robertson, William O. "Chronic Poisoning: Trace Metals and Others." In Cecil Textbook of Medicine, 22nd ed. Edited by Lee Goldman, et al. Philadelphia: Saunders, 2003, pp. 91–9.

Periodicals

Harper A., and J. Croft-Baker. "Carbon monoxide poisoning: undetected by both patients and their doctors." Age and Ageing 33, no. 2 (2004): 105–9.

Huffman, S. M. "Exposure to carbon monoxide from material handling equipment." Journal of Occupational and Environmental Hygiene 1, no. 5 (2004): D54–6.

Piantadosi C. A. "Carbon monoxide poisoning." Undersea and Hyperbaric Medicine 31, no. 1 (2004): 167–77.

Thomassen, O., G. Brattebo, M. Rostrup. "Carbon monoxide poisoning while using a small cooking stove in a tent." American Journal of Emergency Medicine 22, no. 3 (2004): 204–6.

Vacchiano, G., and R. Torino. "Carbon-monoxide poisoning, behavioral changes and suicide: an unusual industrial accident." Journal of Clinical Forensic Medicine 8, no. 2 (2004): 86–92.

Organizations

American Academy of Clinical Toxicology. 777 East Park Drive, PO Box 8820, Harrisburg, PA 17105–8820. Web site: www.clintox.org/index.html.

American Academy of Emergency Medicine. 611 East Wells Street, Milwaukee, WI 53202. Web site: www.aaem.org/.

American Academy of Family Physicians. 11400 Tomahawk Creek Parkway, Leawood, KS 66211–2672. Web site: www.aafp.org/.

American Academy of Pediatrics. 141 Northwest Point Boulevard, Elk Grove Village, IL 60007–1098. Web site: www.aap.org/default.htm.

American Association of Poison Control Centers. 3201 New Mexico Avenue NW, Washington, DC 20016. Web site: www.aapcc.org/.

American College of Emergency Physicians. PO Box 619911, Dallas, TX 75261–9911. Web site: www.acep.org/.

American College of Hyperbaric Medicine. PO Box 25914–130, Houston, Texas 77265. Web site: www.hyperbaricmedicine.org/.

American College of Occupational and Environmental Medicine. 55 West Seegers Road, Arlington Heights, IL 60005. Web site: www.acoem.org/.

American College of Osteopathic Emergency Physicians. 142 E. Ontario Street, Suite 550, Chicago, IL 60611. Web site: www.acoep.org/.

International Congress on Hyperbaric Medicine. 1592 Union Street, San Francisco, CA 94123. Web site: www.ichm.net/.

Undersea and Hyperbaric Medical Society. 10531 Metropolitan Ave, Kensington, MD 20895. Web site: www.uhms.org/.

Web Sites

"A Guide to Prevent Carbon Monoxide Poisoning." Industry Trade Group. Available online at www.carbonmonoxide-poisoning.com/ (accessed November 2, 2004).

"Carbon Monoxide Poisoning." Centers for Disease Control and Prevention. Available online at www.cdc.gov/nceh/airpollution/carbonmonoxide/default.htm (accessed November 2, 2004).

"Carbon Monoxide Poisoning." National Library of Medicine. Available online at www.nlm.nih.gov/medlineplus/carbonmonoxidepoisoning.html (accessed November 2, 2004).

Other

Carbon Monoxide Headquarters. Wayne State University School of Medicine. www.phymac.med.wayne.edu/FacultyProfile/penney/COHQ/co1.htm (accessed November 2, 2004).

[Article by: L. Fleming Fallon Jr., MD, DrPH]


Veterinary Dictionary: carboxyhemoglobinemia
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Excessive concentrations of carbon monoxide in the blood.

Wikipedia: Carbon monoxide poisoning
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Home > Library > Miscellaneous > Wikipedia
This article is about carbon monoxide poisoning. For general information on carbon monoxide, see carbon monoxide.
Carbon monoxide poisoning
Classification and external resources

Spacefilling model of a carbon monoxide molecule
ICD-10 T58.
ICD-9 986
DiseasesDB 2020
MedlinePlus 002804
eMedicine emerg/817
MeSH C21.613.455.245

Carbon monoxide poisoning occurs after enough inhalation of carbon monoxide (CO). Carbon monoxide is a toxic gas, but, being colorless, odorless, tasteless, and non-irritating, it is very difficult for people to detect. Carbon monoxide is a product of combustion of organic matter with insufficient oxygen supply and is often produced in domestic or industrial settings by motor vehicles and other gasoline-powered tools, heaters, and cooking equipment. Exposures at 100 ppm or greater can be dangerous to human health.[1]

Symptoms of mild acute poisoning include headaches, vertigo, and flu-like effects; larger exposures can lead to significant toxicity of the central nervous system and heart, and even death. Following acute poisoning, long-term sequelae often occur. Carbon monoxide can also have severe effects on the fetus of a pregnant woman. Chronic exposure to low levels of carbon monoxide can lead to depression, confusion, and memory loss. Carbon monoxide mainly causes adverse effects in humans by combining with hemoglobin to form carboxyhemoglobin (HbCO) in the blood. This prevents oxygen binding to hemoglobin reducing the oxygen-carrying capacity of the blood leading to hypoxia. Additionally, myoglobin and mitochondrial cytochrome oxidase are thought to be adversly affected. Carboxyhemoglobin can revert to hemoglobin, but the recovery takes time because the HbCO complex is fairly stable.

Treatment of poisoning largely consists of administering 100% oxygen or providing hyperbaric oxygen therapy, although the optimum treatment remains controversial.[2] Oxygen works as an antidote as it increases the removal of carbon monoxide from hemoglobin, in turn providing the body with normal levels of oxygen. The prevention of poisoning is a significant public health issue. Domestic carbon monoxide poisoning can be prevented by early detection with the use of household carbon monoxide detectors. Carbon monoxide poisoning is the most common type of fatal poisoning in many countries.[3] It is also commonly used as a method to commit suicide, usually by deliberately inhaling the exhaust fumes of a running car engine. Carbon monoxide poisoning has also been implicated as the cause of apparent haunted houses. Symptoms such as delirium and hallucinations have led people suffering poisoning to think they have seen ghosts or to believe their house is haunted.[4]

Contents

Sources of carbon monoxide

Carbon monoxide is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Sources of carbon monoxide inside buildings include house fires, faulty furnaces, heaters, wood-burning stoves, internal combustion vehicle exhaust, electrical generators, propane-fueled equipment such as portable stoves, and gasoline-powered tools such as leaf blowers, lawn mowers, high-pressure washers, concrete cutting saws, power trowels, and welders.[5][6][7][8][9][10] Exposure typically occurs when equipment is used in buildings or semi-enclosed spaces.[6] Poisoning may also occur following the use of a self-contained breathing apparatus (SCUBA) due to faulty diving air compressors.[11] Riding in pickup trucks has led to poisoning in children.[12] Idling automobiles with the exhaust pipe blocked by snow has led to the poisoning of car occupants.[13] Generators and propulsion engines on boats, especially houseboats, has resulted in fatal carbon monoxide exposures.[14][15] Another source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers. Dichloromethane is converted into carbon monoxide by the body.[16][17][18]

Sources of carbon monoxide in relation to concentration in parts per million are listed below:

Concentration Source
0.1 ppm Natural atmosphere level (MOPITT)[19]
0.5 to 5 ppm Average level in homes[20]
5 to 15 ppm Near properly adjusted gas stoves in homes[20]
100 to 200 ppm Exhaust from automobiles in the Mexico City central area[21]
5,000 ppm Exhaust from a home wood fire[22]
7,000 ppm Undiluted warm car exhaust without a catalytic converter[22]

Toxicity

Carbon monoxide is toxic to all aerobic forms of life. It is easily absorbed through the lungs.[23] Carbon monoxide is colorless, odorless, tasteless, and non-irritating which makes it difficult for humans to detect.[23] Inhaling even relatively small amounts of the gas can lead to hypoxic injury, neurological damage, and even death. Different people and populations may have a different carbon monoxide tolerance level.[24] On average, exposures at 100 ppm or greater is dangerous to human health.[1] In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm.[25] Carbon monoxide exposure may lead to a significantly shorter lifespan due to heart damage.[26] 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.[27][28][29]

The acute effects produced by carbon monoxide in relation to ambient concentration in parts per million are listed below:[30][31]

Concentration Symptoms
35 ppm (0.0035%) Headache and dizziness within six to eight hours of constant exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours; loss of judgment
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%) Dizziness, nausea, and convulsions within 45 min; insensible within 2 hours
1,600 ppm (0.16%) Headache, tachycardia, dizziness, and nausea within 20 min; death in less than 2 hours
3,200 ppm (0.32%) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in one to two minutes. Convulsions, respiratory arrest, and death in less than 20 minutes.
12,800 ppm (1.28%) Unconsciousness after 2-3 breaths. Death in less than three minutes.

Symptoms

Acute poisoning

The main manifestations of poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart. Symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue.[32] These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis.[6] Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous.[33] Cardiac abnormalities include fast heart rate, low blood pressure, and cardiac arrhythmia.[34][35] The central nervous system is one of the organs most sensitive to poisoning. Symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and even death.[36][37] Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney failure, skin lesions, and visual and auditory problems.[34][38][39][40]

One of the major concerns following acute carbon monoxide poisoning is the severe neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, parkinson's disease-like syndromes, cortical blindness, and a depressed mood.[6][41] Depression may even occur in those who did not have pre-existing depression.[42] These delayed neurological sequelae may occur in up to 50% of poisoned patients after 2 to 40 days.[6] It is difficult to predict who will develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.[43]

Chronic poisoning

Chronic exposure to relatively low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea and vomiting.[7] It is unknown whether low-level chronic exposure may cause permanent neurological damage.[6] Typically, upon removal from exposure to carbon monoxide, symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning.[7] However, one case noted permanent memory loss and learning problems after a 3-year exposure to relatively low levels of carbon monoxide from a faulty furnace.[44] Chronic exposure may worsen cardiovascular symptoms in some people.[7] Long term exposures to carbon monoxide present the greatest risk to persons with coronary heart disease and in people who are pregnant.[45]

Pathophysiology

The precise mechanisms by which the effects of carbon monoxide are induced upon bodily systems are complex and not yet fully understood.[32] Known mechanisms include carbon monoxide binding to hemoglobin, myoglobin and mitochondrial cytochrome oxidase, and carbon monoxide causing brain lipid peroxidation.[36][46][47]

Hemoglobin

Carbon monoxide shifts the oxygen-dissociation curve to the left.

Following absorption carbon monoxide binds to hemoglobin which is the principal oxygen-carrying compound in blood; this produces a compound known as carboxyhemoglobin. The traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood and inhibits the transport, delivery, and utilization of oxygen by the body. The affinity between hemoglobin and carbon monoxide is approximately 230 times stronger than the affinity between hemoglobin and oxygen so carbon monoxide binds to hemoglobin in preference to oxygen.[48][47][49]

Hemoglobin is a tetramer with four oxygen binding sites. The binding of carbon monoxide at one of these sites increases the oxygen affinity of the remaining three sites, which causes the hemoglobin molecule to retain oxygen that would otherwise be delivered to the tissue.[46] This situation is described as carbon monoxide shifting the oxygen dissociation curve to the left.[47] Because of the increased affinity between hemoglobin and oxygen during carbon monoxide poisoning, the blood oxygen content is increased. But because all the oxygen stays in the hemoglobin, none is delivered to the tissues. This causes hypoxic tissue injury.[6] Hemoglobin acquires a bright red color when converted into carboxyhemoglobin, so poisoned patients have been described as looking pink-cheeked and healthy. However this cherry-red appearance is rarely seen in living patients so is not considered a reliable diagnostic sign.[50][47][51]

Myoglobin

Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity for myoglobin, about 60 times greater than that of oxygen.[6] Carbon monoxide bound to myoglobin may impair its ability to utilize oxygen.[47] This causes reduced cardiac output and hypotension, which may result in brain ischemia.[6] A delayed return of symptoms have been reported. This results following a recurrence of increased carboxyhemoglobin levels; this effect may be due to a late release of carbon monoxide from myoglobin, which subsequently binds to hemoglobin.[3]

Cytochrome oxidase

Another mechanism involves effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. Carbon monoxide binds to cytochrome oxidase with less affinity than oxygen, so it is possible that it requires significant intracellular hypoxia before binding.[52] This binding interferes with aerobic metabolism and efficient adenosine triphosphate synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.[53] The rate of dissociation between carbon monoxide and cytochrome oxidase is slow, causing a relatively prolonged impairment of oxidative metabolism.[32]

Poisoning to the central nervous system

The mechanism that is thought to have a significant influence on delayed effects involves formed blood cells and chemical mediators, which cause brain lipid peroxidation (degradation of unsaturated fatty acids). Carbon monoxide causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite.[32] In the brain this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis.[54] The result of these effects is lipid peroxidation, which causes delayed reversible demyelinization of white matter in the central nervous system, which can lead to edema and necrosis within the brain.[46] This brain damage occurs mainly during the recovery period. This may result in cognitive defects, especially affecting memory and learning, and movement disorders. These disorders are typically related to damage to the cerebral white matter and basal ganglia.[54][55] Hallmark pathological changes following poisoning is bilateral necrosis of the white matter, globus pallidus, cerebellum, hippocampus and the cerebral cortex.[6][56][1]

Poisoning during pregnancy

Carbon monoxide poisoning in pregnant women may cause severe adverse fetal effects. Poisoning causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus. Carbon monoxide also crosses the placenta and combines with fetal hemoglobin, causing more direct fetal tissue hypoxia. Additionally, fetal hemoglobin has a 10 to 15% higher affinity for carbon monoxide than adult hemoglobin, causing more severe poisoning in the fetus than in the adult.[3] Elimination of carbon monoxide is slower in the fetus, leading to an accumulation of the toxic chemical.[57] The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so despite mild maternal poisoning or following maternal recovery, severe fetal poisoning or death may still occur.[58]

Diagnosis

As many symptoms of carbon monoxide poisoning also occur with many other types of poisonings and infections (such as the flu), the diagnosis is often difficult.[18][59] A history of potential carbon monoxide exposure, such as being exposed to a residental fire, may suggest poisoning, but the diagnosis is confirmed by measuring the levels of carbon monoxide in the blood. This can be determined by measuring the amount of carboxyhemoglobin compared to the amount of hemoglobin in the blood.[6] Carbon monoxide is produced naturally by the body as a byproduct of converting protoporphyrin into bilirubin. This carbon monoxide also combines with hemoglobin to make carbooxyhemoglobin, but not at toxic levels.[6] The ratio of carboxyhemoglobin to hemoglobin molecules in an average person who is not poisoned is 5%, although cigarette smokers who smoke two packs/day may have levels up to 9%.[60]

Serious toxicity occurs with the carboxyhemoglobin to hemoglobin ratio above 25%, and the risk of fatality is high with levels over 70%. Still, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects.[32] Carboxyhemoglobin levels are more guides to exposure levels than guides to effects, as they do not reliably predict clinical course of action or short- or long-term consequences.[61] Persons poisoned who come to medical facilities a relatively long time after exposure to carbon monoxide may have normal or only slightly elevated levels of carboxyhemoglobin, but still have significant symptoms as levels of carboxyhemoglobin may be well past their peak.[62] For late arriving patients a normal carboxyhemoglobin level does not rule out poisoning.[63] A CO-oximeter may be used to determine carboxyhemoglobin levels.[64][65] Pulse CO-oximeters estimate carboxyhemoglobin with a non-invasive finger clip similar to a pulse oximeter.[66] The use of a pulse oximeter is not effective in the diagnosis of carbon monoxide poisoning as patients suffering from carbon monoxide poisoning may have a normal oxygen saturation level on a pulse oximeter.[67] This is due to the carboxyhemoglobin being misrepresented as oxyhemoglobin on a pulse oximeter.[68]

Differential diagnosis

There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning.[37] The earliest symptoms, especially from low level exposures, are often non-specific and readily confused with other illnesses, typically flu-like viral syndromes, depression, chronic fatigue syndrome, chest pain, and migraine or other headaches.[69] Other conditions included in the differential diagnosis include acute respiratory distress syndrome, altitude sickness, lactic acidosis, diabetic ketoacidosis, meningitis, methemoglobinemia, or opioid or toxic alcohol poisoning.[37]

Prevention

Public concern

Carbon Monoxide detector connected to a North American power outlet

Prevention remains a vital public health issue, requiring public education on the safe operation of appliances, heaters, fireplaces, and internal-combustion engines, as well as increased emphasis on the installation of carbon monoxide detectors.[23] In buildings, carbon monoxide detectors are usually installed around heaters and other equipment. If a relatively high level of carbon monoxide is detected, the device sounds an alarm, giving people the chance to evacuate and ventilate the building.[70][71] Unlike smoke detectors, carbon monoxide detectors do not need to be placed near ceiling level.[72] The Consumer Product Safety Commission has stated, "carbon monoxide detectors are as important to home safety as smoke detectors are," and recommends each home have at least one carbon monoxide detector, and preferably one on each level of the building.[73] These devices, which are relatively inexpensive[71] and widely available, are either battery- or AC-powered, with or without battery backup.[74]

Standardization

The use of carbon monoxide detectors has been standardized in many areas. In the USA, NFPA 720-2009[75], the carbon monoxide detector guidelines published by the National Fire Protection Association, mandates the placement of carbon monoxide detectors/alarms on every level of the residence, including the basement, in addition to outside sleeping areas. In new homes, AC-powered detectors must have battery backup and be interconnected to insure early warning of occupants at all levels.[75] NFPA 720-2009 is the first national carbon monoxide standard to address devices in non-residential buildings. These guidelines, which now pertain to schools, healthcare centers, nursing homes and other non-residential buildings, includes three main points:[75]

1. A secondary power supply (battery backup) must operate all carbon monoxide notification appliances for at least 12 hours,
2. Detectors must be on the ceiling in the same room as permanently installed fuel-burning appliances, and
3. Detectors must be located on every habitable level and in every HVAC zone of the building.

Treatment

First aid

First aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself and obtaining medical treatment. Patients who are unconscious may require CPR on site.[47] The typical medical treatment for carbon monoxide poisoning is administering oxygen to the victim by a non-rebreather mask.[36] Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it into hemoglobin.[76] The half life of carbon monoxide is approximately 320 minutes while breathing normal air, this decreases to 80 minutes while breathing 100% oxygen.[24] Due to the possible severe effects in the fetus, pregnant patients are typically treated with oxygen for longer periods of time than non-pregnant patients.[77]

Hyperbaric oxygen

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin[24] and cytochrome oxidase[78] to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 minutes, compared to 80 minutes for regular oxygen.[24] It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin.[76] 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.[2][79][80][81][82][83] There have been randomized controlled trials in which the two treatment options have been compared;[61][84][85][86][87][88] of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation.[89][90][91] A review of all the literature on carbon monoxide poisoning treatment 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.[2]

Further treatment

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.[47] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[92] Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols.[6] Unless severe, metabolic acidosis is treated with sodium bicarbonate. Treatment with sodium bicarbonate is controversial as acidosis may increase tissue oxygen availability.[93] Treatment of acidosis may only need to consist of oxygen therapy.[6][37] 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.[32][94][95] Extensive follow up and supportive treatment is often required for delayed neurological damage.[36] Outcomes are often difficult to predict following poisoning[96], especially patients who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels.[37] One study reported that approximately 30% of people with severe carbon monoxide poisoning will have a fatal outcome.[18]

Epidemiology

The true number of incidents of carbon monoxide poisoning is unknown, since many non-lethal exposures go undetected.[18][32] From the available data, carbon monoxide poisoning is the most common cause of injury and death due to poisoning worldwide.[97] It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[98] In many industrialized countries carbon monoxide is the cause of more than 50% of fatal poisonings.[3] In the United States, approximately 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[73] Carbon monoxide poisoning contributes to the approximately 5613 smoke inhalation deaths each year in the United States.[99] The CDC reports, "Each year, more than 500 Americans die from unintentional carbon monoxide poisoning, and more than 2,000 commit suicide by intentionally poisoning themselves."[100] For the 10-year period from 1979 to 1988, 56,133 deaths from carbon monoxide poisoning occurred in the United States, with 25,889 of those being suicides, leaving 30244 unintentional deaths.[99] A report from New Zealand showed that 206 people died from carbon monoxide poisoning in the years of 2001 and 2002. In total carbon monoxide poisoning was responsible for 43.9% of deaths by poisoning in that country.[101] In South Korea, 1,950 people had been poisoned by carbon monoxide with 254 deaths from 2001 through 2003.[102] A report from Jerusalem showed 3.53 per 100,000 people were poisoned annually from 2001 through 2006.[103]

Suicide

Before the 1960s most domestic gas supply in the United Kingdom was coal gas (alternatively known as town gas) which in its unburned form contained high levels of carbon monoxide. Carbon monoxide poisoning by intentionally inhaling coal gas was a common suicide method, accounting for nearly half of all suicides in the United Kingdom in the late 1950s.[104] After the British government phased out coal gas in favor of natural gas in the 1960s, the suicide rate in Britain fell by almost a third and has not risen since.[104] The use of coal gas as a suicide method has declined as most domestic gas supply worldwide is now natural gas, which lacks carbon monoxide.[105][106] Until the invention of catalytic converters, suicide has been committed by inhaling the exhaust fumes of a running car engine, particularly in an enclosed space such as a garage.[107][108] Before 1975, motor car exhaust contained up to 25% carbon monoxide; but newer cars have catalytic converters, which eliminate over 99% of the carbon monoxide produced.[109] However even cars with catalytic converters can produce substantial amounts of carbon monoxide if an idling car is left in an enclosed space such as a closed garage.[110]

As carbon monoxide poisoning via car exhaust has become less of a suicide option, there has been an increase in new methods of carbon monoxide poisoning such as burning charcoal or other fossil fuels within a confined space.[111] Such incidents have occurred mostly in connection with group suicide pacts in Asian countries such as Japan, Taiwan, and Hong Kong,[112][113][114][115] but are starting to occur in western countries as well,[116][117] such as the 2007 suicide of Boston lead singer Brad Delp.[118]

Carbon monoxide poisoning and "haunted houses"

Many of the phenomena generally associated with haunted houses, including strange visions and sounds and feelings of dread, can be attributed to carbon monoxide poisoning, as its symptoms include confusion, delirium, emotional disturbances, and hallucinations.[37][119] In one famous case, carbon monoxide poisoning was clearly identified as the cause of an alleged haunting. Dr. William Wilmer, an ophthalmologist, described the experiences of one of his patients in a 1921 article published in the American Journal of Ophthalmology. "Mr. and Mrs. H." moved into a new home, but soon began to complain of headaches and fatigue. They began to hear bells and footsteps during the night, accompanied by strange physical sensations and sightings of mysterious figures. When they began to investigate the symptoms, they discovered the previous residents of the house had similar experiences. An examination of their furnace found it to be severely damaged, resulting in incomplete combustion and forcing most of the fumes, including carbon monoxide, into the house rather than up the chimney.[4]

A report published in 2005 described a 23-year old female victim of carbon monoxide poisoning, found delirious and hyperventilating, who saw a "ghost" while in the shower. A new gas water heater had just been improperly installed in her home, which flooded the house with carbon monoxide when the victim closed all the exterior windows and doors and took a shower.[119]

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See also

v • d • e
Poisonings, toxicities, and overdoses (T36-T65, 960-989) (history)
Inorganic
Lead · Mercury · Cadmium · Silver · Thallium · Tin · Beryllium · Cobalt
Nonmetals/halogen compounds
Other
Organic
CHO
Pharmaceuticals
Biological
(including venom,
toxin,
food poisoning)
Poisonous plants/
derivatives

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