title: Brain energy metabolism in patients with spontaneous subarachnoid hemorrhage and global cerebral edema.
abstract: BACKGROUND
  Previous studies of spontaneous subarachnoid hemorrhage (SAH) have shown that global cerebral edema on the first computed tomography scan is associated with a more severe initial injury and is an independent predictor of poor outcome. Effects of secondary ischemic events also influence outcome after SAH.
  
  
  OBJECTIVE
  This study demonstrates that early global edema is related to markers of an increased cerebral energy metabolism as measured with intracerebral microdialysis, which could increase vulnerability to adverse events.
  
  
  METHODS
  Fifty-two patients with microdialysis monitoring after spontaneous SAH were stratified according to the occurrence of global cerebral edema on the first computed tomography scan taken a median of 2 hours after the initial bleed. Microdialysis levels of glucose, lactate, and pyruvate were compared between the global edema (n = 31) and no global edema (n = 21) groups. Clinical outcome was assessed with the Glasgow Outcome Scale score at >/= 6 months.
  
  
  RESULTS
  Patients with global edema showed significantly elevated lactate and pyruvate levels 70 to 79 hours after SAH and marginally significantly higher levels of lactate 60 to 69 hours and 80 to 89 hours after SAH. There was a trend toward worse outcome in the edema group.
  
  
  CONCLUSIONS
  Patients with global cerebral edema have higher interstitial levels of lactate and pyruvate. The edema group may have developed a cerebral hypermetabolism to meet the increased energy demand in the recovery phase after SAH. This stress would make the brain more vulnerable to secondary insults, increasing the likelihood of energy failure.
authors.affiliation: Department of Neuroscience, Neurosurgery, Uppsala University Hospital, Uppsala, Sweden. maria.zetterling@telia.com
authors.forename: Maria
authors.initials: M
authors.lastname: Zetterling
authors.forename: Lena
authors.initials: L
authors.lastname: Hallberg
authors.forename: Lars
authors.initials: L
authors.lastname: Hillered
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Karlsson
authors.forename: Per
authors.initials: P
authors.lastname: Enblad
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Ronne Engström
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D001923:Brain Chemistry / Q000502:physiology; D001929:Brain Edema / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D045604:Extracellular Fluid / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D017551:Microdialysis; D010085:Oxidative Phosphorylation; D011237:Predictive Value of Tests; D019289:Pyruvic Acid / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000175:diagnosis / Q000378:metabolism*; D014057:Tomography, X-Ray Computed; D015854:Up-Regulation / Q000502:physiology
chemical_list: D015415:Biomarkers; D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose