Abstract
Although well supported by animal studies, it remains unproven whether lowering hyperglycemia during acute cerebral infarction will improve outcomes. Further support for this therapeutic approach comes from clinical studies in acute myocardial infarction and in ventilated postsurgical patients, where lowering hyperglycemia improved outcomes. Animal studies support the hypothesis that hyperglycemia during acute brain ischemia augments the brain injury, but only in models with reperfusion. The available human studies to date are all observational and they usually find an association between hyperglycemia during acute cerebral infarction and worse outcome. Also, there is evidence that hyperglycemia during acute cerebral infarction is detrimental only with reperfusion. This association appears to be linear in the glucose ranges tested (normal to high). In addition, there is an association between admission hyperglycemia and hemorrhagic conversion of an acute cerebral infarct when thrombolytics are used. Sufficient evidence has accumulated to proceed to clinical efficacy trials to see if tight glycemic control compared with persistent hyperglycemia during acute cerebral infarction will improve outcomes. If such therapy proves beneficial, the increased cost, effort, and risk associated with tight glycemic control during acute cerebral infarction could be justified. Randomized clinical trials to test this hypothesis are currently in progress.
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