Cerebral energy metabolism during transient hyperglycemia in patients with severe brain trauma.

Abstract

To study whether transient hyperglycemia adversely affects cerebral energy metabolism in patients with severe traumatic brain lesions. Prospective, nonrandomized study in the neurosurgical intensive care unit of a university hospital. 108 patients treated for severe traumatic brain lesions. All patients were treated according to neurosurgical intensive care routine including monitoring of intracranial pressure. One microdialysis catheter was inserted via a burr hole frontally to that used for the intraventricular catheter ("better" position). In patients with focal lesions one or more catheters were inserted into cerebral cortex surrounding an evacuated focal contusion or underlying an evacuated hematoma ("worse" position). Perfusion rate was 0.3 micro l/min and samples were taken every 30 or 60 min. The levels of glucose, pyruvate, lactate, glutamate, and glycerol were analyzed and displayed bedside. There were 18 episodes of moderate (12-15 mmol/l) and 6 episodes of pronounced (>15 mmol/l) hyperglycemia. Moderate hyperglycemia did not change intracerebral levels of lactate, pyruvate, glutamate, glycerol, or lactate/pyruvate ratio. Lactate concentrations increased during pronounced hyperglycemia. Pronounced cerebral lactic acidosis and a moderate increase in interstitial glycerol concentration indicating cell membrane degradation was observed in a single patient with pronounced, long-lasting hyperglycemia. Cerebral energy metabolism was affected by transient hyperglycemia only at blood glucose concentration above 15 mmol/l as shown by a moderate increase in interstitial lactate level.