Carbon monoxide poisoning
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Carbon monoxide poisoning occurs after the inhalation of carbon monoxide gas. Carbon monoxide (CO) is a product of combustion of organic matter under conditions of restricted oxygen supply, which prevents complete oxidation to carbon dioxide. Carbon monoxide is colorless, odorless, tasteless, and non-irritating, making it difficult for people to detect.
Common sources of CO which may lead to poisoning include house fires, furnaces/heaters, wood-burning stoves, motor vehicle exhausts, and propane-fuelled equipment such as portable camping stoves, ice resurfacers, and forklifts. CO poisoning can also occur in scuba diving due to faulty or badly sited diving air compressors. (See under Effects of relying on breathing equipment while underwater for more information) or following exposure to the organic solvent methylene chloride, (methylene chloride is metabolized to CO by the body).
Epidemiology
Carbon monoxide poisoning is the most common type of fatal poisoning in France and the United States. It has been estimated that more than 40,000 people per year seek medical attention for carbon monoxide poisoning in the United States. In many industrialized countries carbon monoxide may be the cause of greater than 50% of fatal poisonings.
Suicide
As the availability of other poisons such as cyanide and arsenic were placed under increasingly stringent legal restrictions, the carbon monoxide in town gas became the principal method of suicide by poisoning. Suicide was also often committed by inhaling exhaust fumes of running car engines. In the past motor car exhausts may have contained up to 25% carbon monoxide. However, newer cars have catalytic converters which can eliminate >99% of carbon monoxide produced. Even cars with catalytic converters can produce substantial carbon monoxide if an idling car is left in an enclosed space, this is due to reduced oxygen availability and therefore less efficient combustion.
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 fuel within a confined space, such as a small room, tent, or car. Such incidents have occurred mostly in connection with group suicide pacts in both Japan and Hong Kong, but are starting to occur in western countries as well.
Symptoms
Acute
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, and migraine or other headaches. Often this makes the diagnosis of carbon monoxide poisoning difficult. If suspected the diagnosis can be confirmed by measurement of blood carboxyhemoglobin.
The main manifestations of poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The clinical manifestations include tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, confusion, convulsions, and unconsciousness. CO poisoning may also produce myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, hyperglycemia, muscle necrosis, acute renal failure, skin lesions, visual and auditory problems, and respiratory arrest.
One of the major concerns following CO poisoning is the severe neurological manifestations that may occur days or even weeks after an acute poisoning. Common problems encountered are difficulty with higher intellectual functions and short-term memory, dementia, irritability, gait disturbance, speech disturbances, parkinson-like syndromes, cortical blindness, and depression (depression can occur in those accidentally exposed). These delayed sequelae occur in approximately 15 percent of severely poisoned patients after an interval of 2 to 28 days. 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.
Chronic
Long term, repeat exposures present a greater risk to persons with coronary heart disease and in pregnant patients. Chronic exposure may increase the incidence of cardiovascular symptoms in some workers i.e. motor vehicle examiners, firefighters, and welders. Patients often complain of persistent headaches, lightheadedness, depression, confusion, and nausea. Upon removal from exposure the symptoms usually resolve.
Toxicity
Carbon monoxide is a significantly toxic gas, although patients may demonstrate varied clinical manifestations with different outcomes, even under similar exposure conditions. Toxicity is also increased by several factors including: increased activity and rate of ventilation, pre-existing cerebral or cardiovascular disease, reduced cardiac output, anemia or other hematological disorders, decreased barometric pressure, and high metabolic rate.
Carboxyhemoglobin
Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin; carboxyhemoglobin is a stable complex of carbon monoxide and hemoglobin that forms in red blood cells. Carbon monoxide is produced normally in the body, establishing a low background carboxyhemoglobin saturation. Carbon monoxide also functions as a neurotransmitter. Normal carboxyhemoglobin levels in an average person are less than 5%, whereas cigarette smokers (two packs/day) may have levels up to 9%.
Serious toxicity is often associated with carboxyhemoglobin levels above 25%, and the risk of fatality is high with levels over 70%. Although, no consistent dose response relationship has been found between carboxyhemoglobin levels and clinical effects. 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.
Toxic mechanism
The precise mechanisms by which toxic effects are induced by CO are not fully understood.
Carbon monoxide binds to hemoglobin (reducing oxygen transportation), myoglobin (decreasing its oxygen carrying capacity), and mitochondrial cytochrome oxidase (inhibiting cellular respiration).
Hemoglobin
Carbon monoxide has a significant affinity to the iron (or copper) sites in hemoglobin, the principal oxygen-carrying compound in blood. The affinity between carbon monoxide and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.
CO binds to the hemoglobin, producing carboxyhemoglobin (HbCO); the traditional, belief is that carbon monoxides toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen carrying capacity of the blood, inhibiting transport, delivery, and utilization of oxygen. Hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would be otherwise be delivered to the tissue. This phenomenon is known as the Haldane effect.
Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left. Oxygen blood 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. However, despite CO affecting oxygen availability, other mechanisms may contribute to the crucial effects of CO poisoning.
A sufficient exposure to carbon monoxide can reduce the amount of oxygen taken up by the brain to the point that the victim becomes unconscious, and can suffer brain damage or even death from anoxia. The brain regulates breathing based upon carbon dioxide levels in the blood, rather than oxygen, so a victim can succumb to anoxia without ever noticing anything up to the point of collapse.
Hemoglobin acquires a bright red colour when converted to carboxyhemoglobin, so a casualty of CO poisoning is described in textbooks as looking pink-cheeked and healthy. However, this "classic" cherry-red appearance is very uncommon - it has only been noted in 2% of cases so care should be taken not to overlook the diagnosis even if this colour is not present.
Myoglobin
Carbon monoxide also has a high affinity for myoglobin. CO bound to myoglobin may impair cardiac output and result in cerebral ischemia. A delayed return of symptoms has been reported and appears to result folowing a recurrence of increased carboxyhemoglobin levels, this effect may be due to late release of CO from myoglobin, which subsequently binds to hemoglobin.
Cytochrome Oxidase
A second mechanism involves co effects on the mitochondrial respiratory enzyme chain which is responsible for effective tissue utilization of oxygen. CO does not bind to cytochrome oxidase with the same affiity as oxygen so it likely requires significant intracellular hypoxia before binding. This binding interfers with aerobic metabolism and efficient adenosine triphosphate (ATP) synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death.
Other mechanisms
Another mechanism, (thought to have a significant influence on delayed effects) involves formed blood cells and chemical mediators which cause brain lipid peroxidation.
CO causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite. In the brain this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis. The end result is lipid peroxidation (degradation of unsaturated fatty acids) which causes delayed reversible demyelinization of white matter in the central nervous system, and can lead to edema and focal areas of necrosis within the brain.
This brain damage occurs mainly during the recovery period and results in cognitive defects (especially affecting memory and learning) and movement disorders. The movement disorders are related to a predilection of CO to damage the basal ganglia. These delayed neurological effects may develop over days following the initial acute poisoning.
Pregnancy
Carbon monoxide poisoning can have a significant effect on the fetus. CO causes fetal tissue hypoxia by decreasing the release of maternal oxygen to the fetus, and by carbon monoxide crossing the placenta and combining with fetal hemoglobin, which has a 10 to 15% higher affinity for CO than adult hemoglobin. Elimination of carbon monoxide is also slower in the fetus, leading to an accumulation of CO. The level of fetal morbidity and mortality in acute carbon monoxide poisoning is significant, even despite maternal wellbeing, severe fetal poisoning can still occur. Due to these effects, pregnant patients are treated with normal or hyperbaric oxygen for longer periods of time than non-pregnant patients.
Treatment
First aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself, call for help, and applying CPR if needed. The main medical treatment for carbon monoxide poisoning is 100% oxygen, oxygen hastens the dissociation of carbon monoxide from hemoglobin, improving tissue oxygenation by reducing its biological half-life. Hyperbaric oxygen is also used in the treatment of CO poisoning, hyperbaric oxygen also increases carboxyhemoglobin dissociation and does so to a greater extent than normal oxygen. Hyperbaric oxygen may also facilitate the dissociation of CO from cytochrome oxidase.
A significant controversy in the medical literature is whether or not hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen in terms of increased survival or improved long term outcomes. There have been clinical trials in which the 2 treatment options have been compared; of the six performed, 4 found hyperbaric oxygen improved outcome and 2 found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation. A recent robust review of all the literature on carbon monoxide 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.
Further specific treatment for other complications such as seizure, cardiac abnormalities, pulmonary edema, and acidosis may be required. The delayed development of neuropsychiatric impairment is one of the most serious complications of poisoning, with extensive follow up and treatment often being required.
Prevention
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 alarms. Carbon monoxide alarms are usually installed in homes around heaters and other equipment. If a high level of CO is detected, the device sounds an alarm, giving people in the area a chance to ventilate the area or safely leave the building
References
See also
Resources
- [Website about carbon monoxide poisoning and prevention]
- [2003 report of a group suicide via charcoal-produced carbon monoxide poisoning, in Japan]
- [2005 report of a group suicide via charcoal-produced carbon monoxide poisoning, in the UK]
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