Strictly speaking, CO is an exogenous toxin, but it is considered here because it produces a characteristic cerebral injury and is frequently associated with delayed neurologic deterioration. The extreme affinity of CO for hemoglobin (more than 200 times that of oxygen) drastically reduces the oxygen content of blood and subjects the brain to prolonged hypoxia and acidosis. Cardiac toxicity and hypotension generally follow. Whether CO also has a direct toxic action on neuronal components is not settled. The effects on the brain for the most part simulate those caused by cardiac arrest. Neurologists are likely to encounter instances of CO poisoning in burn units and in patients who have attempted suicide or have been exposed accidentally to a faulty furnace or to car exhaust in a closed garage. A contemporary review of the subject has been given by Weaver.
Early symptoms include headache, nausea, dyspnea, confusion, dizziness, and clumsiness. These occur when the carboxyhemoglobin level reaches 20 to 30 percent of total hemoglobin. Exposure to relatively low levels of CO from faulty furnaces and gasoline engines should be suspected as the cause of recurrent headaches and confusion that clear upon hospitalization or other change of venue. A cherry-red color of the skin may appear, but is actually an infrequent finding; cyanosis is more common. At slightly higher levels of carboxyhemoglobin, blindness, visual field defects, and papilledema develop, and levels of 50 to 60 percent are associated with coma, decerebrate or decorticate posturing, seizures in a few patients, and generalized slowing of the EEG rhythms. The initial CT or MRI is normal or shows mild cerebral edema; later scans may show a characteristic lesion in the pallidum, as described below. Only if there has been associated hypotension does one see the same types of vascular border-zone infarctions that appear after cardiac arrest.
Delayed neurologic deterioration 1 to 3 weeks (sometimes much longer) after CO exposure occurs more frequently than with other forms of cerebral hypoxia. In Choi’s survey, this feature was observed in 3 percent of 2,360 cases of CO poisoning and in 12 percent of those ill enough to be admitted to a hospital. Extrapyramidal features (parkinsonian gait and bradykinesia) predominated. Three-quarters of such patients were said to recover within a year. Discrete lesions centered in the globus pallidus bilaterally and sometimes the inner portion of the putamina are characteristic of CO poisoning that had produced coma (Fig. 39-5), but similar focal destruction may be seen after drowning, strangulation, and other forms of anoxia. The common feature among the delayed-relapse patients is a prolonged period of pure anoxia (before the occurrence of ischemia). Basal ganglia lesions may be quite prominent on CT even when delayed neurologic sequelae do not occur but they are invariably present between 1 and 4 weeks in patients who develop the delayed extrapyramidal syndrome. In less-severely affected patients we have seen such lesions resolve entirely on CT and MRI and there is no resultant movement disorder.
The initial treatment for carbon monoxide exposure is with inspired oxygen. Because the half-life of CO (normally 5 h) is greatly reduced by the administration of hyperbaric oxygen at 2 or 3 atmospheres, this additional treatment is recommended when the carboxyhemoglobin concentration is greater than 40 percent or in the presence of coma or seizures (Myers et al). According to a trial conducted by Weaver and colleagues, this treatment reduces the incidence of cognitive sequelae from 46 to 25 percent. They administered 3 hyperbaric sessions in the first 24 h after exposure to CO.