• Top
• Objective
• Design
• Interventions
• Measurements ...
• Conclusions

Objective

To study whether transient hyperglycaemia adversely affects cerebral energy metabolism in patients with severe traumatic brain lesions.

Design

Prospective, nonrandomised study.

Interventions

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 the cerebral cortex surrounding an evacuated focal contusion or underlying an evacuated haematoma ('worse' position). The perfusion rate was 0.3 μl/min and samples were taken every 30 or 60 min. The levels of glucose, pyruvate, lactate, glutamate, and glycerol were analysed and displayed bedside.

Measurements and main results

In 108 patients, 18 episodes of moderate (12–15 mmol/l) and six episodes of pronounced (> 15 mmol/l) hyperglycaemia occurred. Moderate hyperglycaemia did not change intracerebral levels of lactate, pyruvate, glutamate, glycerol or lactate/pyruvate ratio. During pronounced hyperglycaemia lactate concentration increased. A 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 hyperglycaemia.

Conclusions

Cerebral energy metabolism was affected by transient hyperglycaemia only at blood glucose concentration above 15 mmol/l as shown by a moderate increase in interstitial lactate level.

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