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==Diagnosis==
==Diagnosis==


As many of the clinical signs and symptoms of carbon monoixde poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.<ref name="Varon"/> A history of potential carbon monoxide exposure, such as being exposed to a residental fire, may suggest poisoning but the diagnosis is most reliably confirmed by measuring levels of carbon monoxide found in the blood. This can be determined by measuring [[carboxyhemoglobin]], which is a stable complex of carbon monoxide and [[hemoglobin]] that forms in [[red blood cells]].<ref name="goldfranks"/> Carbon monoxide is produced normally in the body as a degradation product of [[protoporphyrin]] to [[bilirubin]] establishing a low background carboxyhemoglobin saturation.<ref name="goldfranks"/> Normal carboxyhemoglobin levels in an average person are typically less than 5%, although cigarette smokers (two packs/day) may have levels up to 9%.<ref name="Clinical toxicology2001-ford">{{cite book | editor = Ford MD, Delaney KA, Ling LJ, Erickson T | title = Clinical toxicology | year = 2001 | page=1046|publisher = WB Saunders Company | isbn = 0-7216-5485-1}}</ref>
As many of the clinical signs and symptoms of carbon monoixde poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.<ref name="Varon"/><ref>{{cite journal |author=Bennetto L, Powter L, Scolding NJ |title=Accidental carbon monoxide poisoning presenting without a history of exposure: A case report|journal=Journal of Medical Case Reports|volume=2 |issue= |pages=118 |year=2008 |month=April |pmid=18430228|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18430228}}</ref> A history of potential carbon monoxide exposure, such as being exposed to a residental fire, may suggest poisoning but the diagnosis is most reliably confirmed by measuring levels of carbon monoxide found in the blood. This can be determined by measuring [[carboxyhemoglobin]], which is a stable complex of carbon monoxide and [[hemoglobin]] that forms in [[red blood cells]].<ref name="goldfranks"/> Carbon monoxide is produced normally in the body as a degradation product of [[protoporphyrin]] to [[bilirubin]] establishing a low background carboxyhemoglobin saturation.<ref name="goldfranks"/> Normal carboxyhemoglobin levels in an average person are typically less than 5%, although cigarette smokers (two packs/day) may have levels up to 9%.<ref name="Clinical toxicology2001-ford">{{cite book | editor = Ford MD, Delaney KA, Ling LJ, Erickson T | title = Clinical toxicology | year = 2001 | page=1046|publisher = WB Saunders Company | isbn = 0-7216-5485-1}}</ref>


Serious toxicity is often associated with carboxyhemoglobin levels 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.<ref name="JToxClinTox1994-hardy">{{cite journal | author=Hardy KR, Thom SR | title=Pathophysiology and treatment of carbon monoxide poisoning | journal=Journal of Toxicology. Clinical Toxicology | year=1994 | pages=613–29 | volume=32 | issue=6 | pmid=7966524 | doi=10.3109/15563659409017973 | issn=0731-3810}}</ref> Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.<ref name="MedJAust1999-Scheinkestel">{{cite journal | author=Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV | title=Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial | journal=[[The Medical Journal of Australia]] | year=1999 | pages=203–10 | volume=170 | issue=5 | pmid=10092916 | month=Mar | issn=0025-729X | url=http://www.mja.com.au/public/issues/mar1/scheink/scheink.html | format=Free full text}}</ref> Additionally, people poisoned who present to medical facilities a long time after exposure may have normal or only slightly elevated levels of carboxyhemoglobin but still have significant symptoms as levels may be well past their peak.<ref>{{cite journal |author=Myers RA, Britten JS |title=Are arterial blood gases of value in treatment decisions for carbon monoxide poisoning? |journal=Critical Care Medicine|volume=17 |issue=2 |pages=139-42 |year=1989 |month=Feb |pmid=2644066|doi=}}</ref> In late presenting patients a normal carboxyhemoglobin level cannot be used to rule out poisoning.<ref>{{cite journal |author=Keleş A, Demircan A, Kurtoğlu G |title=Carbon monoxide poisoning: how many patients do we miss? |journal=European Journal of Emergency Medicine: Official Journal of the European Society for Emergency Medicine |volume=15 |issue=3 |pages=154–7 |year=2008 |month=June |pmid=18460956 |doi=10.1097/MEJ.0b013e3282efd519 |issn=0969-9546}}</ref> The use of a [[co-oximeter]] is recommended to determine carboxyhemoglobin levels.<ref name="pmid455674">{{cite journal |author=Rodkey FL, Hill TA, Pitts LL, Robertson RF |title=Spectrophotometric measurement of carboxyhemoglobin and methemoglobin in blood |journal=Clinical Chemistry |volume=25 |issue=8 |pages=1388–93 |year=1979 |month=August |pmid=455674 |doi= |url=http://www.clinchem.org/cgi/pmidlookup?view=long&pmid=455674 |accessdate=2009-07-17 |issn=0009-9147}}</ref><ref name="pmid7361284">{{cite journal |author=Rees PJ, Chilvers C, Clark TJ |title=Evaluation of methods used to estimate inhaled dose of carbon monoxide |journal=Thorax |volume=35 |issue=1 |pages=47–51 |year=1980 |month=January |pmid=7361284 |pmc=471219 |doi= 10.1136/thx.35.1.47|url=http://thorax.bmj.com/cgi/pmidlookup?view=long&pmid=7361284 |issn=0040-6376}}</ref> Pulse co-oximeters have made it possible to estimate carboxyhemoglobin with a non-invasive finger clip similar to a [[pulse oximeter]].<ref name="pmid18500075">{{cite journal |author=Coulange M, Barthelemy A, Hug F, Thierry AL, De Haro L |title=Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning |journal=Undersea & Hyperbaric Medicine |volume=35 |issue=2 |pages=107–11 |year=2008 |pmid=18500075 |doi= |url= http://archive.rubicon-foundation.org/8084 |month=Mar |issn=1066-2936}}</ref> 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]] reading on a pulse oximeter.<ref>{{cite journal |author=Vegfors M, Lennmarken C |title=Carboxyhaemoglobinaemia and pulse oximetry |journal=British Journal of Anaesthesia |volume=66 |issue=5 |pages=625–6 |year=1991 |month=May |pmid=2031826 |doi= 10.1093/bja/66.5.625|issn=0007-0912}}</ref> This due to the carboxyhemoglobin being misinterpreted as oxyhemoglobin on pulse oximetry.<ref>{{cite journal |author=Barker SJ, Tremper KK |title=The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2 |journal=Anesthesiology|volume=66 |issue=5 |pages=677-9 |year=1987 |month=May |pmid=3578881|doi=}}</ref>
Serious toxicity is often associated with carboxyhemoglobin levels 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.<ref name="JToxClinTox1994-hardy">{{cite journal | author=Hardy KR, Thom SR | title=Pathophysiology and treatment of carbon monoxide poisoning | journal=Journal of Toxicology. Clinical Toxicology | year=1994 | pages=613–29 | volume=32 | issue=6 | pmid=7966524 | doi=10.3109/15563659409017973 | issn=0731-3810}}</ref> Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.<ref name="MedJAust1999-Scheinkestel">{{cite journal | author=Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV | title=Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial | journal=[[The Medical Journal of Australia]] | year=1999 | pages=203–10 | volume=170 | issue=5 | pmid=10092916 | month=Mar | issn=0025-729X | url=http://www.mja.com.au/public/issues/mar1/scheink/scheink.html | format=Free full text}}</ref> Additionally, people poisoned who present to medical facilities a long time after exposure may have normal or only slightly elevated levels of carboxyhemoglobin but still have significant symptoms as levels may be well past their peak.<ref>{{cite journal |author=Myers RA, Britten JS |title=Are arterial blood gases of value in treatment decisions for carbon monoxide poisoning? |journal=Critical Care Medicine|volume=17 |issue=2 |pages=139-42 |year=1989 |month=Feb |pmid=2644066|doi=}}</ref> In late presenting patients a normal carboxyhemoglobin level cannot be used to rule out poisoning.<ref>{{cite journal |author=Keleş A, Demircan A, Kurtoğlu G |title=Carbon monoxide poisoning: how many patients do we miss? |journal=European Journal of Emergency Medicine: Official Journal of the European Society for Emergency Medicine |volume=15 |issue=3 |pages=154–7 |year=2008 |month=June |pmid=18460956 |doi=10.1097/MEJ.0b013e3282efd519 |issn=0969-9546}}</ref> The use of a [[co-oximeter]] is recommended to determine carboxyhemoglobin levels.<ref name="pmid455674">{{cite journal |author=Rodkey FL, Hill TA, Pitts LL, Robertson RF |title=Spectrophotometric measurement of carboxyhemoglobin and methemoglobin in blood |journal=Clinical Chemistry |volume=25 |issue=8 |pages=1388–93 |year=1979 |month=August |pmid=455674 |doi= |url=http://www.clinchem.org/cgi/pmidlookup?view=long&pmid=455674 |accessdate=2009-07-17 |issn=0009-9147}}</ref><ref name="pmid7361284">{{cite journal |author=Rees PJ, Chilvers C, Clark TJ |title=Evaluation of methods used to estimate inhaled dose of carbon monoxide |journal=Thorax |volume=35 |issue=1 |pages=47–51 |year=1980 |month=January |pmid=7361284 |pmc=471219 |doi= 10.1136/thx.35.1.47|url=http://thorax.bmj.com/cgi/pmidlookup?view=long&pmid=7361284 |issn=0040-6376}}</ref> Pulse co-oximeters have made it possible to estimate carboxyhemoglobin with a non-invasive finger clip similar to a [[pulse oximeter]].<ref name="pmid18500075">{{cite journal |author=Coulange M, Barthelemy A, Hug F, Thierry AL, De Haro L |title=Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning |journal=Undersea & Hyperbaric Medicine |volume=35 |issue=2 |pages=107–11 |year=2008 |pmid=18500075 |doi= |url= http://archive.rubicon-foundation.org/8084 |month=Mar |issn=1066-2936}}</ref> 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]] reading on a pulse oximeter.<ref>{{cite journal |author=Vegfors M, Lennmarken C |title=Carboxyhaemoglobinaemia and pulse oximetry |journal=British Journal of Anaesthesia |volume=66 |issue=5 |pages=625–6 |year=1991 |month=May |pmid=2031826 |doi= 10.1093/bja/66.5.625|issn=0007-0912}}</ref> This due to the carboxyhemoglobin being misinterpreted as oxyhemoglobin on pulse oximetry.<ref>{{cite journal |author=Barker SJ, Tremper KK |title=The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2 |journal=Anesthesiology|volume=66 |issue=5 |pages=677-9 |year=1987 |month=May |pmid=3578881|doi=}}</ref>

Revision as of 04:33, 27 September 2009

Carbon monoxide poisoning
SpecialtyEmergency medicine Edit this on Wikidata

Carbon monoxide poisoning occurs after the inhalation of carbon monoxide (CO). Carbon monoxide is a significantly toxic gas, but, being colorless, odorless, tasteless, and non-irritating, it is very difficult for people to detect.[1] 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.[2] In the United States, OSHA limits long-term workplace exposure levels to 50 ppm.[3]

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.[4] 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.[5] 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.[6]

Sources

Carbon monoxide is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide (CO2). Common sources of carbon monoxide that may lead to poisoning include house fires, faulty furnaces, heaters, or wood-burning stoves, motor vehicle exhaust, propane-fueled equipment such as kitchen and portable camping stoves, and gasoline-powered tools such as leaf blowers, lawn mowers, high-pressure washers, concrete cutting saws, power trowels, and welders.[7][8][9][10][11] Exposure typically occurs when equipment is used in buildings or semi-enclosed spaces.[8] Poisoning can also occur following use of self-contained breathing apparatus, such as recreational scuba diving, due to faulty or badly sited diving air compressors.[12] Children riding in the back of pickup trucks has led to poisoning[13] while idling automobiles with the exhaust pipe blocked by snow has lead to the poisoning of the cars occupants.[14] Generators and propulsion engines on boats, especially houseboats, have resulted in fatal carbon monoxide exposures.[15][16] Another source of poisoning in humans is exposure to the organic solvent dichloromethane, most commonly found in paint strippers, it is metabolized to carbon monoxide by the body.[17][18][19]

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

Concentration Source
0.1 ppm Natural background atmosphere level (MOPITT)[20]
0.5 to 5 ppm Average background level in homes[21]
5 to 15 ppm Levels near properly adjusted gas stoves in homes[21]
100 to 200 ppm Mexico City central area from automobiles[22]
5,000 ppm Chimney of a home wood fire[23]
7,000 ppm Undiluted warm car exhaust, without catalytic converter[23]

Toxicity

Carbon monoxide is significantly toxic to all aerobic forms of life and is easily absorbed through the lungs.[1] Patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions.[24] Inhaling even relatively small amounts can lead to hypoxic injury, neurological damage, and possibly death. One report concluded that carbon monoxide exposure can lead to significant loss of lifespan after exposure due to damage to the heart muscle.[25] Toxicity is also increased by several factors, including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia, sickle cell disease or other hematological disorders, decreased barometric pressure, and high metabolic rate.[26][27][28]

The acute effects produced by carbon monoxide in relation to ambient concentration in parts per million are listed below:[29][30]

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

The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. Early symptoms of acute carbon monoxide poisoning are nonspecific and include headaches, nausea, and fatigue; these early symptoms are often mistaken for a viral syndrome such as influenza or other illnesses such as food poisoning or gastroenteritis.[8] Headache is one of the most common symptoms and is often described as dull, frontal, and continuous.[31] Further systemic symptoms include cardiac abnormalities such as tachycardia, hypertension, and ECG changes.[32] The central nervous system is one of the organ systems most sensitive to poisoning and symptoms displayed include delirium, hallucinations, dizziness, ataxia, confusion, convulsions, unconsciousness, respiratory arrest, and even death.[33][34] Less common symptoms following poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, and visual and auditory problems.[32]

One of the major concerns following acute poisoning is the severe neurological manifestations that may occur after poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, amnesia, psychosis, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression,[8][35] which can even occur in those accidentally exposed who did not have pre-existing depression.[36] These delayed neurological sequelae may occur in up to 50 percent of symptomatic poisoned patients after an interval of 2 to 40 days.[8] It is difficult to predict who may develop delayed sequelae; however, advancing age, loss of consciousness while poisoned, and initial neurological abnormalities may indicate a greater chance of developing delayed symptoms.[37]

Chronic

Chronic exposure to low levels of carbon monoxide may cause persistent headaches, lightheadedness, depression, confusion, memory loss, and nausea and vomiting.[9] It is unclear if chronic exposure can cause permanent neurological damage.[8] Typically, upon removal from exposure, the symptoms usually resolve themselves unless there has been an episode of severe acute poisoning.[9] However, one case noted permanant memory and learning problems after a 3-year exposure to low level carbon monoxide from a faulty furnace.[38] Chronic exposure may increase the incidence of cardiovascular symptoms in some workers, such as motor vehicle examiners, firefighters, and welders.[9] It appears long term, repeated exposures present the greatest risk to persons with coronary heart disease and in pregnant patients.[39]

Pathophysiology

The precise mechanisms by which toxic effects are induced are not fully understood. Known mechanisms include carbon monoxide binding to hemoglobin reducing oxygen transportation, binding to myoglobin decreasing its oxygen storage capacity, binding to mitochondrial cytochrome oxidase inhibiting cellular respiration, and brain lipid peroxidation.[33][40][41]

Hemoglobin

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

Carbon monoxide has a significant affinity to the iron sites in hemoglobin, the principal oxygen-carrying compound in blood. The affinity between hemoglobin and carbon monoxide is about 230 times stronger than the affinity between hemoglobin and oxygen.[42] Carbon monoxide binds to hemoglobin, producing carboxyhemoglobin (COHb); the traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.[41][43]

Hemoglobin is a tetramer with four oxygen binding sites, and binding of carbon monoxide at one of these sites also increases the oxygen affinity of the remaining 3 sites, which therefore causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.[40] Levels of oxygen available for tissue use are decreased. This situation is described as carbon monoxide shifting the oxygen dissociation curve to the left.[41] Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes tissue hypoxic injury.[8] Hemoglobin acquires a bright red color when converted to carboxyhemoglobin, so a casualty of poisoning is patients being described as looking pink-cheeked and healthy. However, this cherry-red appearance is rarely seen in living patients[44] and therefore has limited value as a diagnostic criterion.[41][45]

Myoglobin

Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity for myoglobin being about 60 times greater than that of oxygen.[8] Carbon monoxide bound to myoglobin may impair its ability to utilize oxygen.[41] This causes impaired cardiac output and hypotension which may result in brain ischemia.[8] A delayed return of symptoms has been reported and this appears to result following a recurrence of increased carboxyhemoglobin levels; this effect may be due to late release of CO from myoglobin, which subsequently binds to hemoglobin.[5]

Cytochrome oxidase

Another mechanism involves effects on the mitochondrial respiratory enzyme chain that is responsible for effective tissue utilization of oxygen. Carbon monoxide does not bind to cytochrome oxidase with the same affinity as oxygen, so it likely requires significant intracellular hypoxia before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate (ATP) synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.[46]

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.[47] In the brain, this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis.[48] The end 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.[40] This brain damage occurs mainly during the recovery period and results 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.[48] Hallmark pathological changes following poisoning is bilateral necrosis of the white matter, globus pallidus, cerebellum, hippocampus and the cerebral cortex.[8][49][2]

Pregnancy

Carbon monoxide poisoning in pregnant women can 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, typically causing more severe poisoning in the fetus.[5] Elimination of carbon monoxide is also slower in the fetus, leading to an accumulation of carbon monoxide.[50] The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, so even despite mild maternal poisoning or following maternal recovery, severe fetal poisoning or death can still occur.[51]

Diagnosis

As many of the clinical signs and symptoms of carbon monoixde poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.[19][52] A history of potential carbon monoxide exposure, such as being exposed to a residental fire, may suggest poisoning but the diagnosis is most reliably confirmed by measuring levels of carbon monoxide found in the blood. This can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells.[8] Carbon monoxide is produced normally in the body as a degradation product of protoporphyrin to bilirubin establishing a low background carboxyhemoglobin saturation.[8] Normal carboxyhemoglobin levels in an average person are typically less than 5%, although cigarette smokers (two packs/day) may have levels up to 9%.[53]

Serious toxicity is often associated with carboxyhemoglobin levels 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.[47] Therefore, carboxyhemoglobin levels are more guides to exposure levels than effects as they do not reliably predict clinical course or short- or long-term outcome.[54] Additionally, people poisoned who present to medical facilities a long time after exposure may have normal or only slightly elevated levels of carboxyhemoglobin but still have significant symptoms as levels may be well past their peak.[55] In late presenting patients a normal carboxyhemoglobin level cannot be used to rule out poisoning.[56] The use of a co-oximeter is recommended to determine carboxyhemoglobin levels.[57][58] Pulse co-oximeters have made it possible to estimate carboxyhemoglobin with a non-invasive finger clip similar to a pulse oximeter.[59] 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 reading on a pulse oximeter.[60] This due to the carboxyhemoglobin being misinterpreted as oxyhemoglobin on pulse oximetry.[61]

Differential diagnosis

There are many conditions to be considered in the differential diagnosis of carbon monoxide poisoning.[34] 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.[62] 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.[34]

Prevention

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.[1] Carbon monoxide detectors are usually installed in homes around heaters and other equipment. If a high level of carbon monoxide is detected, the device sounds an alarm, giving people a chance to ventilate the area or safely leave the building.[63][64] Unlike smoke detectors, they do not need to be placed near ceiling level.[65] The Consumer Product Safety Commission has stated that "carbon monoxide detectors are as important to home safety as smoke detectors are", and recommends that each home should have at least one carbon monoxide detector.[66] These devices, which are inexpensive[64] and widely available, can either be battery-operated or AC powered with or without a battery backup.[67]

The use of detectors has been standardized in many areas; in the USA the 2009 edition of NFPA 720, the carbon monoxide detector guidelines published by the National Fire Protection Association (NFPA), 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, electrically powered detectors must have battery backup and be interconnected to assure early warning of occupants at all levels. NFPA 720-2009 is also 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, include three main points: 1) A secondary power supply 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, 3) Detectors must be located on every habitable level and in every HVAC zone of the building.[68]

Treatment

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.[41] The main medical treatment for carbon monoxide poisoning is administering oxygen by a non-rebreather mask.[33] Oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing carbon monoxides biological half-life.[69] The half life of carbon monoxide is approximately 320 minutes while breathing normal air, this decreases to 80 minutes when breathing 100% oxygen.[24] Due to possible severe effects in the fetus, pregnant patients are typically treated with oxygen for longer periods of time than non-pregnant patients.[70]

Hyperbaric oxygen is also used in the treatment of poisoning, as it increases dissociation of CO from carboxyhemoglobin[24] and from cytochrome oxidase[71] to a greater extent than normal oxygen. Hyperbaric oxygen at 3-times atmospheric pressure reduces the half life of carbon monoxide to 23 minutes.[24] It also enhances oxygen transport to the tissues by the plasma, partially bypassing the normal transfer through hemoglobin.[69] However, it is still controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen in terms of increased survival or improved long term outcomes.[4][72][73][74][75][76] There have been randomized controlled trials[54][77][78][79][80][81] in which the two treatment options have been compared; 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.[82][83][84] 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 clinically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.[4]

Further specific treatment for other complications such as seizure, hypotension, cardiac abnormalities, pulmonary edema, and acidosis may be required. Increased muscle activity or seizures should be treated with dantrolene or diazepam; diazepam should only be given with appropriate respiratory support.[41] Hypotension requires treatment with intravenous fluids; vasopressors may be required to treat myocardial depression.[85] Cardiac dysrhythmias are treated with standard advanced cardiac life support protocols.[8] Unless its is severe, treatment of metabolic acidosis with sodium bicarbonate is controversial as acidosis may actually increase tissue oxygen availability. Treatment of acidosis may only need to consist of oxygen therapy.[8][34] The delayed development of neuropsychiatric impairment is one of the most serious complications of poisoning. Brain damage is usually confirmed following magnetic resonance imaging (MRI) or computerized tomography (CT) scans.[47][86][87] Extensive follow up and supportive treatment is often required for delayed neurological damage.[33] Outcomes are difficult to predict following poisoning[88] but patients who have symptoms of cardiac arrest, coma, metabolic acidosis, or have high carboxyhemoglobin levels are associated with a poor prognosis.[34] One study reported that approximately 30% of people with severe poisoning will have a fatal outcome.[19]

Epidemiology

The true incidence of carbon monoxide poisoning is not known, since many non-lethal exposures go undetected.[19] From the available data it appears to be the most common cause of injury and death due to poisoning worldwide.[89] It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States.[90] In many industrialized countries, carbon monoxide may be the cause of greater than 50% of fatal poisonings.[5] In the U.S., about 200 people die each year from carbon monoxide poisoning associated with home fuel-burning heating equipment.[66] While carbon monoxide poisoning is thought to contribute to the approximate 5613 smoke inhalation deaths each year in the USA.[91] 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."[92] A report from New Zealand covering poisoning deaths in the years 2001 and 2002 showed that 206 people died from carbon monoxide, in total it was responsible for 43.9% of poisoning deaths in that country.[93]

Suicide

In the past the most common method of suicide by carbon monoxide poisoning was by intentionally inhaling town gas as it contains high levels of carbon monoxide. However, this method has been declining as most domestic gas supply is now natural gas which lacks carbon monoxide.[94][95] Suicide has additionally often been committed by inhaling the exhaust fumes of a running car engine, particularly in an enclosed space such as a garage.[96][97] In the past, motor car exhaust may have contained up to 25% carbon monoxide; but newer cars have catalytic converters, which can eliminate over 99% of carbon monoxide produced.[98] However, even cars with catalytic converters can produce substantial amounts of carbon monoxide if an idling car is left in an enclosed space.[99]

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, such as a small room, tent, or car.[100] Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong,[101][102][103] but are starting to occur in Western countries as well, such as the 2007 suicide of Boston lead singer Brad Delp.[104]

Carbon monoxide poisoning and "haunted houses"

Symptoms of carbon monoxide poisoning may include confusion, delirium, depression, emotional disturbances, and hallucinations.[34] 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.[105] 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.[6]

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 installed in her home, apparently improperly, which flooded the house with carbon monoxide when the victim closed all the exterior windows and doors and took a shower.[105]

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See also

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