title: Biochemical indications of cerebral ischaemia and mitochondrial dysfunction in severe brain trauma analysed with regard to type of lesion.
abstract: The study focuses on three questions related to the clinical usefulness of microdialysis in severe brain trauma: (1) How frequently is disturbed cerebral energy metabolism observed in various types of lesions? (2) How often does the biochemical pattern indicate cerebral ischaemia and mitochondrial dysfunction? (3) How do these patterns relate to mortality?
  
  
  
  The study includes 213 consecutive patients with severe brain trauma (342 intracerebral microdialysis catheters). The patients were classified into four groups according to the type of lesion: extradural haematoma (EDH), acute subdural haematoma (SDH), cerebral haemorrhagic contusion (CHC) and no mass lesion (NML). Altogether about 150,000 biochemical analyses were performed during the initial 96 h after trauma.
  
  
  
  Compromised aerobic metabolism occurred during 38 % of the study period. The biochemical pattern indicating mitochondrial dysfunction was more common than that of ischaemia. In EDH and NML aerobic metabolism was generally close to normal. In SDH or CHC it was often severely compromised. Mortality was increased in SDH with impaired aerobic metabolism, while CHC did not exhibit a similar relation.
  
  
  
  Compromised energy metabolism is most frequent in patients with SDH and CHC (32 % and 49 % of the study period, respectively). The biochemical pattern of mitochondrial dysfunction is more common than that of ischaemia (32 % and 6 % of the study period, respectively). A correlation between mortality and biochemical data is obtained provided the microdialysis catheter is placed in an area where energy metabolism reflects tissue outcome in a large part of the brain.
authors.affiliation: Department of Neurosurgery, Odense University Hospital, Odense, Denmark. carl-henrik.nordstrom@med.lu.se.
authors.forename: Carl-Henrik
authors.initials: CH
authors.lastname: Nordström
authors.affiliation: Department of Neurosurgery, Odense University Hospital, Odense, Denmark.
authors.forename: Troels Halfeld
authors.initials: TH
authors.lastname: Nielsen
authors.affiliation: Department of Neurosurgery, Lund University Hospital, Lund, Sweden.
authors.forename: Wilhelm
authors.initials: W
authors.lastname: Schalén
authors.affiliation: Department of Neurosurgery, Lund University Hospital, Lund, Sweden.
authors.forename: Peter
authors.initials: P
authors.lastname: Reinstrup
authors.affiliation: Department of Neurosurgery, Lund University Hospital, Lund, Sweden.
authors.forename: Urban
authors.initials: U
authors.lastname: Ungerstedt
mesh_terms: D000328:Adult; D000070642:Brain Injuries, Traumatic / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D002544:Cerebral Infarction / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000378:metabolism*; D019289:Pyruvic Acid / Q000378:metabolism
chemical_list: D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose
keywords: Cytoplasmatic redox; Ischaemia; Lactate; Microdialysis; Mitochondrial dysfunction; Pyruvate; Traumatic brain injury