Introduction: Although most of clinical studies suggest that hyperglycemia is associated with poor clinical outcome in acute stroke patients, there still are many theoretical and practical doubts that are reflected in some differences in treatment recommendations from clinical guidelines developed in Europe (European Stroke Initiative, Croatian Association for Neurovascular Disorders) and in the USA (American Stroke Association).
Purpose: To point to the most important acts and doubts related to the acute treatment of hyperglycemia in stroke patients.
Methods: On literature review, the following databases were used: Medline (1976-2006), National Guideline Clearinghouse and Stroke Trials Registry-Internet Stroke Center. Selection of the articles depended on clinical experience and knowledge of the authors.
Results: The most important facts indicating a high prevalence of glucose regulation disturbances in stroke patients are highlighted, along with data on the reactive and iatrogenic pathophysiological mechanisms leading to hyperglycemia. Literature data that undoubtedly suggest an association of hyperglycemia with poor clinical outcome and the unfavorable effect of hyperglycemia on the outcome of thrombolysis are pointed out. Some contradictory data on the postulated pathophysiological mechanisms by which hyperglycemia causes cerebral damage are reviewed, especially regarding the role of tissue lactic acidosis induced by hyperglycemia. The favorable results of insulin therapy in critically ill patients are presented, along with the fact that there is still no definitive evidence that strict control of hyperglycemia can improve the outcome in stroke patients.
Discussion: At present, it is not possible to claim whether hyperglycemia contributes to the poor outcome of acute stroke as an independent factor or it is just a marker of the disease severity. It seems that the unfavorable effect of hyperglycemia is not only associated with the level of the brain lactic acidosis. Rather, a complex interaction of several different mechanisms appears to be involved. The threshold of blood glucose concentration at which it becomes a predictor of unfavorable outcome has not yet been exactly established. The different levels of hyperglycemia recommended to be treated with insulin partly reflect different evaluation of the guidelines regarding the potential risks of insulin-induced hypoglycemia and further iatrogenic metabolic disorders. It might be expected that the results of ongoing randomized controlled trials should contribute to developing of more precise and more harmonized clinical guidelines for the treatment of hyperglycemia in stroke patients.