title: Global cerebral edema and brain metabolism after subarachnoid hemorrhage.
abstract: OBJECTIVE
  Global cerebral edema is common among patients with poor-grade subarachnoid hemorrhage and is associated with poor outcome. Currently no targeted therapy exists largely due to an incomplete understanding of the underlying mechanisms.
  
  
  METHODS
  This is a prospective observational study including 39 consecutive patients with poor-grade subarachnoid hemorrhage with multimodal neuromonitoring. Levels of microdialysate lactate-pyruvate ratio, episodes of cerebral metabolic crisis (lactate-pyruvate ratio >40 and brain glucose <0.7 mmol/L), brain tissue oxygen tension, cerebral perfusion pressure, and transcranial Doppler sonography flow velocities were analyzed.
  
  
  RESULTS
  Median age was 54 years (range, 45 to 61 years) and 62% were female. Patients with global cerebral edema on admission (n=24 [62%]) had a higher incidence of metabolic crisis in the first 12 hours of monitoring (n=15 [15% versus 2%], P<0.05) and during the total time of neuromonitoring (20% versus 3%, P<0.001) when compared to those without global cerebral edema. There was no difference in brain tissue oxygen tension or cerebral perfusion pressure between the groups; however, in patients with global cerebral edema, a higher cerebral perfusion pressure was associated with lower lactate-pyruvate ratio (P<0.05). Episodes of metabolic crisis were associated with poor outcome (modified Rankin Scale score 5 or 6, P<0.05).
  
  
  CONCLUSIONS
  In patients with poor-grade subarachnoid hemorrhage, global cerebral edema is associated with early brain metabolic distress.
authors.affiliation: Division of Critical Care Neurology, Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA.
authors.forename: Raimund
authors.initials: R
authors.lastname: Helbok
authors.forename: Sang-Bae
authors.initials: SB
authors.lastname: Ko
authors.forename: J Michael
authors.initials: JM
authors.lastname: Schmidt
authors.forename: Pedro
authors.initials: P
authors.lastname: Kurtz
authors.forename: Luis
authors.initials: L
authors.lastname: Fernandez
authors.forename: H Alex
authors.initials: HA
authors.lastname: Choi
authors.forename: E Sander
authors.initials: ES
authors.lastname: Connolly
authors.forename: Kiwon
authors.initials: K
authors.lastname: Lee
authors.forename: Neeraj
authors.initials: N
authors.lastname: Badjatia
authors.forename: Stephan A
authors.initials: SA
authors.lastname: Mayer
authors.forename: Jan
authors.initials: J
authors.lastname: Claassen
mesh_terms: D001921:Brain / Q000378:metabolism*; D001929:Brain Edema / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000503:physiopathology
chemical_list: D019344:Lactic Acid; D019289:Pyruvic Acid; D005947:Glucose; D010100:Oxygen