Purpose of review: Alterations of blood glucose levels are secondary insults with detrimental consequences for the injured brain. Here, we review various aspects of brain glucose metabolism and analyze the evidence on glycemic control during acute brain injury.
Recent findings: An essential component in the overall management of acute brain injury, especially during the acute phase, is maintaining adequate and appropriate control of serum glucose. This is one of the few physiological parameters that is modifiable. Hypoglycemia should be rigorously avoided. However, intensive insulin therapy is associated with unacceptable rates of hypoglycemia and metabolic crisis, and does not necessarily provide benefit. Hyperglycemia is harmful to the injured brain as it compromises microcirculatory blood flow, increases blood-brain barrier permeability, and promotes inflammation. In addition, it triggers osmotic diuresis, hypovolemia, and immunosuppression.
Summary: Glucose is the primary energy substrate for the brain. During injury, the brain increases its needs and is vulnerable to glucose deficit. In these situations, alternative fuel can be lactate, which has potential implications for future research. In this review, various pathophysiological aspects of glucose metabolism during acute brain injury, as well as the risks, causes, and consequences of glucose deficiency or excess, will be discussed.