Articles Carbon Monoxide Poisoning: Dangers, Diagnosis and Treatment Methods

Carbon monoxide (CO) poisoning is one of the most common causes of morbidity and mortality worldwide due to inhalation poisoning, whether accidental or intentional (suicidal). It is estimated to be responsible for approximately 31% of all poisonings in our country. In Turkey, CO poisonings are more prevalent during the winter months and windy weather conditions. Deaths due to accidental exposure occur more frequently in winter, whereas suicides can occur throughout the year.

Carbon monoxide affects cellular functions in conjunction with endogenously produced CO and nitric oxide during hemoglobin catabolism in humans. Endogenously produced CO binds to approximately 0.4-0.7% of human hemoglobin, forming carboxyhemoglobin (COHb), which acts as a neurotransmitter. However, environmental exposure can result in COHb levels of 1-3%, and in smokers, levels of 6-15%. Exogenous CO is produced when carbonaceous compounds such as coal, oil, fertilizers, dung, and natural gas do not burn completely. Other sources include exhaust gases from motor vehicles, heaters, methylene chlorides, and fires. Deadly COHb levels can be reached within 10 minutes in closed garages.

CO is a colorless, odorless, non-irritating toxic gas easily absorbed by the lungs. It is primarily eliminated unchanged by the lungs, with less than 1% converting to carbon dioxide, 10-15% binding to proteins like myoglobin and cytochrome-c oxidase, and less than 1% remaining in solution. CO competes with oxygen binding to hemoglobin, binding 200-250 times more strongly than oxygen. This impairs oxygen transport capacity, causes impaired oxygen release at the tissue level, and leads to cellular hypoxia. Small amounts of dissolved free CO in the blood play a significant role. CO’s direct effect on cells and the resulting impairment of oxygen transport capacity suggest its importance in tissue hypoxia. CO binds strongly to cardiac myoglobin, causing myocardial depression, hypotension, and arrhythmias. Oxygenation damage begins in the central nervous system after tissue hypoxia, leading to advanced mitochondrial damage, capillary leakage, leukocyte accumulation, and cell destruction. Ultimately, reversible demyelination occurs in the brain due to high oxygen consumption, primarily affecting the basal ganglia.

Exposure to carbon monoxide during pregnancy can have serious harmful effects on the fetus. Because the fetus is more sensitive to CO, fetal COHb levels exceed maternal levels. Prolonged exposure to CO increases COHb levels in tissues, leading to late cardiac and neurological symptoms. Severe headaches, signs of Parkinson’s disease, heart attacks, hyperthyroidism, and especially hypothyroidism, and irregularities in reproductive hormones in men and women are more likely to be detected in patients.

The severity of poisoning clinically depends on CO concentration and exposure time. Children, the elderly, those with heart disease, anemics, those with lung disease, and pregnant women are at higher risk. CO poisoning can be acute or chronic, with varying clinical findings. Low-dose and short-term exposure may cause headaches, weakness, dizziness, lethargy, difficulty in thinking, chest pain, palpitations, nausea, and complaints of diarrhea. In acute poisonings, neurological and cardiologic signs are more prominent. Unconsciousness, balance and gait disturbances, hypotension, heart attacks, arrhythmias, and metabolic acidosis may occur. Unconsciousness is the most common neurological sign. Additionally, syncope, seizures, memory loss, stupor, cognitive disorders, balance and gait disturbances, tachycardia, tachypnea, headache, nausea, vomiting, lethargy, and other non-specific symptoms are common and can be confused with viral infections. In long-term exposures to CO, COHb levels increase significantly. Consequently, late cardiac and neurological symptoms appear. Severe headaches, signs of Parkinson’s disease, heart attacks, hyperthyroidism, and more hypothyroidism are more common.

The most important diagnostic tool is the physician’s suspicion of CO poisoning. A thorough history should be taken in suspected cases of CO poisoning. The use of stoves, heaters, closed garages, etc., at home and in the workplace should be questioned. Particularly, the cause of the incident, exposure time to CO, even transient loss of consciousness, chest pain, other poisoning possibilities such as cyanide or drugs should be investigated. If there is suspicion, COHb levels in venous or arterial blood gas should be measured. The most important finding in diagnosis is the measurement of COHb levels in blood. COHb levels below 10% may not be related to the patient’s symptoms, but levels above 10% can be diagnostic. At COHb levels of 10-30%, symptoms such as headache, mild shortness of breath, and gastroenteritis may occur, while COHb levels of 40% and above can cause severe symptoms such as coma, convulsions, and cardiac arrest. Metabolic acidosis in blood gas is considered severe poisoning. In addition, lactate levels are also important.

During neurological examination of patients, consciousness functions, power loss, balance, walking, and speech should be evaluated. Hypoglycemia in the emergency room can be confused with CO poisoning, so care should be taken. Brain computed tomography should be performed in case of altered consciousness. Lesions at the level of the globus pallidum are most commonly seen in CO poisoning. In addition, magnetic resonance imaging should be performed for abnormalities in white matter. Delayed neuropsychiatric disease can occur weeks to months (3-240 days) after acute poisoning symptoms have improved. It is estimated that this syndrome occurs in 10-30% of patients. These patients may present with personality changes such as impaired consciousness, aggression, violence, sudden reaction, irritability, Parkinsonism, urinary incontinence, dementia, and psychosis. Improvement in delayed neuropsychiatric syndromes is seen in 50-75% of patients within 1 year.

Electrocardiography should be performed in all cases of carbon monoxide poisoning. Ischemic changes, ST depression, ST elevation can be seen despite normal coronary arteries. If ST elevation is present in CO poisoning, thrombolysis is likely not appropriate because the cause is myocardial toxicity rather than thrombotic occlusion of epicardial coronary arteries. ECG monitoring should be performed for arrhythmia monitoring.

The basis of treatment in CO poisoning is the removal of CO, which binds reversibly to hemoglobin and tissue proteins faster than oxygen. The half-life of COHb varies but is usually 4-6 hours. Therefore, oxygen should be given to all patients with CO poisoning until COHb levels drop below 5%. Hyperbaric oxygen therapy is highly beneficial in severe cases. Lactic acidosis should not be corrected unless the pH is <7.15, as it facilitates tissue oxygen diffusion. In addition to shortening the COHb half-life, hyperbaric oxygen therapy has positive effects such as reducing oxygen free radical production and levels, inhibiting lipid peroxidation, correcting impaired mitochondrial functions, and correcting capillary disturbed platelet adhesion. Currently accepted hyperbaric oxygen therapy includes unconsciousness, neurological or consciousness abnormalities, cardiac ischemic findings on electrocardiography, COHb levels above 20%, and pregnancy.

Prevention is crucial in reducing the sequelae and deaths caused by CO poisoning. Public education on the dangers of CO is important. Emphasis should be placed on this education through the media during the winter months. Regular maintenance of heating systems at home and in the workplace, adequate ventilation of environments, and cleaning of chimneys can prevent CO poisoning at home and at work. CO sensors can be alerting against acute and chronic poisoning. Catalytic converters can reduce CO content in exhaust gases from vehicles, thereby reducing the severity of CO exposure.

Assoc. Prof. Dr. Abuzer COŞKUN

Bağcılar Training and Research Hospital

Emergency Medicine Clinic
Educational Responsible