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CARBON MONOXIDE TOXICITY

Carbon monoxide toxicity is one of the leading causes of death in fires. While oxygen is being used during combustion, carbon monoxide is being released, since it is a basic by-product of combustion. Carbon monoxide is rapidly transported across the alveolar membrane and preferentially binds with the hemoglobin molecule in place of oxygen. In addition, carbon monoxide shifts the hemoglobin-oxygen curve to the left, thereby impairing oxygen unloading at the tissue level. The result is a major impairment in oxygen delivery, since 98% of oxygen is carried to the tissues on hemoglobin. With prolonged exposure, carbon monoxide can also saturate the cell, binding to cytochrome oxidase, thereby further impairing mitochondrial function and adenosine triphosphate (ATP) production.

Symptoms of carbon monoxide toxicity are usually not present until carboxyhemoglobin exceeds 15%, i.e., 15% of the hemoglobin is bound to carbon monoxide rather than oxygen. Symptoms are those of decreased tissue oxygenation, with initial manifestations being neurologic due to the impairment in cerebral oxygenation. Major myocardial dysfunction can also develop, with evidence of myocardial ischemia or even infarction, especially with preexisting coronary artery disease. In addition, the neurologic dysfunction caused by carbon monoxide expo9sure can lead to a progressive and permanent cerebral dysfunction. Frequently, a patient will awaken transiently after severe inhalation injury only to have progressive neurologic deterioration 24 to 48 hours later. Cyanide toxicity presents in a very similar fashion to carbon monoxide, with severe metabolic acidosis and obtundation in severe cases. Diagnosis, however, is more difficult because cyanide levels are not always readily available or very reliable.

Carbon Monoxide Toxicity Table

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Rapid displacement of the CO on hemoglobin using oxygen is essential. The half life of CO-H₈b breathing room air is 90 minutes, whereas the half-life when breathing 90 to 100% high-flow oxygen is 30 minutes, i.e., the concentration of carboxyhemoglobin is reduced by approximately 50% every 30 minutes if an oxygen concentration of 90 to 100% is used.

Oxygen administration is required for all major burns until carbon monoxide toxicity can be ruled out or until carboxyhemoglobin levels return to normal.

Hyperbaric oxygen (2 to 3 atm) produces an even more rapid displacement and is most useful in cases of prolonged exposure, when carbon monoxide is also present in the mitochondria, since the carbon monoxide is more difficult to displace from the cytochrome system. The drawback of hyperbaric oxygen use is the inability to "get to the patient" during this crucial period of hemodynamic and pulmonary instability. Hyperbaric oxygen is best used in cases in which the patient has severe neurologic compromise with high carboxyhemoglobin, but no major burns and is not responding to high-flow oxygen with clearance of symptoms.

Endotracheal intubation and use of 90 to 100% oxygen with mechanical ventilator assist is indicated for those patients with impaired neurologic function and a high carboxyhemoglobin. This patient group not only needs a more aggressive attempt at displacing the carboxyhemoglobin using positive pressure at a high Fi0₂, but is also at a high risk for aspiration, as any neurologically impaired patient would be.

Cyanide management remains controversial. In general, cardiopulmonary support is usually sufficient treatment, since the liver via the enzyme rhodenase will clear the cyanide from the circulation. Sodium nitrite is used (300mg intravenously over 5 to 10 minutes) in severe cases, especially those in which the diagnosis is made by blood levels. Methemoglobin is produced by the nitrite, which, in turn, binds the cyanide. However, methemoglobin does not transport oxygen and a tissue hypoxia can develop, which is similar to the original cyanide effect. Ordinarily, thiosulfate is also given, which, in turn, binds the cyanide to form thiocyanate. One must be reasonably sure of the diagnosis of cyanide toxicity before giving sodium nitrite.