Hyperglycemia exacerbates brain damage in acute severe carbon monoxide poisoning.

It is hypothesized that hyperglycemia naturally induced by stress and/or produced by intravenous trauma therapy adversely effects neurologic outcome following acute severe carbon monoxide poisoning, and the higher the blood glucose the greater the degree of brain dysfunction. Increased availability of glucose presumably increases cerebral glycolytic flux, and elevates intracellular and interstitial lactate level, which in turn induces acidosis and edema, resulting in brain damage. In a retrospective study of blood glucose and other data obtained from patients upon hospital admission for CO poisoning, a mean value of 409 mg/dL was associated with "brain death", a value of 215 mg/dL with "minimal to substantial brain damage," and a value of 165 mg/dL with "normal" recovery.