title: Intracerebral microdialysis and bedside biochemical analysis in patients with fatal traumatic brain lesions.
abstract: BACKGROUND
  Microdialysis with bedside biochemical analysis was used to monitor cerebral biochemical alterations that precede and accompany increase in intracranial pressure (ICP), resulting in a complete cessation of cerebral blood flow.
  
  
  METHODS
  Seven patients, who died due to an untreatable increase in ICP, were included. The patients originate from a large, consecutive series of severely head injured patients (n: 95) monitored with intracerebral microdialysis (perfusion rate 0.3 microl/min). One microdialysis catheter was inserted via a separate burr hole frontally to that used for the intraventricular catheter ("better" position) and one catheter was inserted into cerebral cortex surrounding an evacuated focal contusion or underlying an evacuated haematoma ("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) analyses of amino acids and ions.
  
  
  RESULTS
  Decreases in glucose and pyruvate and increases in lactate, glycerol, glutamate, and lactate/pyruvate (la/py) ratio characterized cerebral ischaemia. The measured markers give information regarding substrate availability (glucose), redox state of the tissue (la/py ratio), degradation of glycerophospholipids in cell membranes (glycerol), and extracellular concentration of excitatory amino acids (glutamate). In the "worse" position biochemical deterioration occurred before the increase in ICP. In the "better" position biochemical deterioration was usually observed after the increase in ICP.
  
  
  CONCLUSIONS
  Changes of cerebral energy metabolism that accompany cerebral ischaemia follow a certain pattern and may be detected at the bedside by intracerebral microdialysis before the secondary damage causes an increase in ICP.
authors.affiliation: Department of Clinical Neuroscience, Lund University Hospital, Stockholm, Sweden.
authors.forename: N
authors.initials: N
authors.lastname: Ståhl
authors.forename: P
authors.initials: P
authors.lastname: Mellergård
authors.forename: A
authors.initials: A
authors.lastname: Hallström
authors.forename: U
authors.initials: U
authors.lastname: Ungerstedt
authors.forename: C H
authors.initials: CH
authors.lastname: Nordström
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D007427:Intracranial Pressure; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D019289:Pyruvic Acid / Q000378:metabolism
chemical_list: D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose; D005990:Glycerol