PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48 hours) Continued

II_a. CARBON MONOXIDE TOXICITY Problems

Pathophysiology:

Carbon monoxide toxicity is one of the leading causes of death in fires.^13-15   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 & Diagnosis:

The magnitude of the carbon monoxide toxicity roughly corresponds with the peak percent of the circulating hemoglobin bound by carbon monoxide (CO Hgb).  It is important to remember that the burn victim is typically being treated with oxygen at the scene and during transport.  Therefore, the first CO Hgb obtained may be considerably lower than the peak level which would be that at the time of extrication.

Symptoms of carbon monoxide toxicity are usually not present until carboxyhemoglobin (COHgb) 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 pre-existing coronary artery disease.  In addition, the neurologic dysfunction caused by carbon monoxide exposure 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 ^17-18 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.

*CO Hgb – carboxyhemoglobin

 

Treatment of carbon monoxide toxicity consists of the early displacement of carbon monoxide from hemoglobin by administration of 90% to 100% oxygen.^13-15   The half-life of carboxyhemoglobin in the patient when breathing 20% oxygen is about 120 to 200 mins, whereas the half-life when breathing 90% to 100% high-flow oxygen is 30 mins (i.e., the concentration of carboxyhemoglobin is reduced by –50% every 30 mins if an oxygen concentration of 90% to 100% is used).  Oxygen administration is required for all major burns until carbon monoxide toxicity can be excluded or until carboxyhemoglobin levels return to normal. 

Endotracheal intubation and use of 90% to 100% oxygen with mechanical ventilatory assistance is indicated for those patients with severely impaired neurologic function and a high carboxyhemoglobin. 

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 (i.e., >50%), but no major burns or severe pulmonary injury and the patient is not responding to high-flow oxygen with clearance of symptoms.  However, the vast majority of cases can be successfully managed by simply using 100% oxygen.^13-18

In general, for cyanide poisoning, cardiopulmonary support is usually sufficient treatment, since the liver, via the enzyme rhodenase, will clear the cyanide from circulation.^17-18   Sodium nitrite is used (300 mg iv over 5 to 10 mins) in severe cases, especially in those patients in which the diagnosis is made by blood concentrations.  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.

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