GLUCOSE MODULATION OF ISCHEMIC BRAIN INJURY - REVIEW AND CLINICAL RECOMMENDATIONS

Ischemic brain injury is the third-leading cause of death among Americ ans and the leading cause of serious disability. Based on studies of a nimal models, a substantial amount of experimental evidence shows that hyperglycemia at the onset of brain ischemia worsens postischemic neu rologic outcome. Consistent with these observations, hyperglycemia als o is associated with a worsening of postischemic brain injury in human s. In humans, however, data are often difficult to interpret because o f problems in determining the timing of hyperglycemia relative to a cr itical ischemic event and in elucidating the effect of coexisting path ophysiologic processes (for example, a stress response) on outcome. Gl ucose modulation of neurologic injury is observed when ischemia is eit her global (for example, that accompanying cardiac arrest or severe sy stemic hypotension) or focal (for example, that accompanying thromboti c or embolic stroke). Toxicity is probably the result of an intracellu lar lactic acidosis. Specifically, the associated hydrogen ions are in jurious to neurons and glia. On the basis of these factors, we recomme nd diligent monitoring of blood glucose concentrations in patients who are at increased risk for new-onset, ongoing, or recurring cerebral i schemia. In such patients, the use of fluid infusions, corticosteroid drugs, and insulin, as well as stress management, should be tailored t o treat preexisting hyperglycemia and prevent new-onset hyperglycemia. Maintenance of normoglycemia is recommended. When one attempts to tre at preexisting hyperglycemia, care should be taken to avoid rapid flui d shifts, electrolyte abnormalities, and hypoglycemia, all of which ca n be detrimental to the brain.