Intracerebral microdialysis and bedside biochemical analysis in patients with fatal traumatic brain lesions

Background: Microdialysis with bedside biochemical analysis was used to mon itor cerebral biochemical alterations that precede and accompany increase i n intracranial pressure (ICP), resulting in a complete cessation of cerebra l blood flow. Methods: Seven patients, who died due to an untreatable increase in ICP, we re included. The patients originate from a large, consecutive series of sev erely head injured patients (n: 95) monitored with intracerebral microdialy sis (perfusion rate 0.3 mul/min). One microdialysis catheter was inserted v ia a separate burr hole frontally to that used for the intraventricular cat heter ("better" position) and one catheter was inserted into cerebral corte x surrounding an evacuated focal contusion or underlying an evacuated haema toma ("worse" position). Biochemical analyses of glucose, lactate, glycerol , urea, glutamate, and pyruvate were performed at the bedside. All samples were frozen for subsequent HPLC (high-performance liquid chromatography) an alyses of amino acids and ions. Results: Decreases in glucose and pyruvate and increases in lactate, glycer ol, glutamate, and lactate/ pyruvate (la/py) ratio characterized cerebral i schaemia. The measured markers give information regarding substrate availab ility (glucose), redox state of the tissue (la/py ratio), degradation of gl ycerophospholipids in cell membranes (glycerol), and extracellular concentr ation of excitatory amino acids (glutamate). In the "worse" position bioche mical deterioration occurred before the increase in ICP. In the "better" po sition biochemical deterioration was usually observed after the increase in ICP. Conclusion: Changes of cerebral energy metabolism that accompany cerebral i schaemia follow a certain pattern and may be detected at the bedside by int racerebral microdialysis before the secondary damage causes an increase in ICP.