Hyperglycemia is associated with a worsened outcome after ischemic cerebral injury. In conditions of insufficient oxygen supply, cellular energy requirements may be partially met by anaerobic glycolysis which leads to an accumulation of lactic acid. Since this is virtually all ionized at physiological pH an intracellular acidosis develops, leading to deregulation of ionic membrane pumps and the formation of other mediators of neuronal injury. This intracellular acidosis is the probable mechanism of the adverse effects of hyperglycemia in brain injury, although the evidence in focal ischemia is not as clear. Thus hyperglycemia enhances injury in the ischemic core, whereas damage in the penumbra may be reduced due to collateral flow. Significant hyperglycemia (> 10 mmol/l) should always be corrected with insulin infusion in neurosurgical patients.
Normal brain is almost totally dependent upon a continuous delivery of exogenous glucose for maintenance of cellular energy requirements. Therefore glucose levels should be monitored routinely and maintained between 4 and 8 mmol/l.
The administration of glucose-containing solutions does not produce a significant increase in blood glucose, but may predispose patients to a worsened outcome. Therefore it seems prudent to withhold glucose-containing solutions from neurosurgical patients, except those in whom the onset of hypoglycemia may be rapid and have severe consequences such as diabetics. Hyperglycemia should be corrected prior to a likely ischemic event so as not to exacerbate it.
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