title: Brain tissue oxygen-directed management and outcome in patients with severe traumatic brain injury.
abstract: OBJECTIVE
  The object of this study was to determine whether brain tissue oxygen (PbtO(2))-based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)-based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI).
  
  
  METHODS
  Seventy patients with severe TBI (postresuscitation GCS score < or = 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO(2) monitor (mean age 40 +/- 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 +/- 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO(2) monitors also had therapy to maintain PbtO(2) > 20 mm Hg.
  
  
  RESULTS
  Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO(2) monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO(2)-directed care (25.7%) than in those who received conventional ICP and CPP-based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP-guided management and 64.3% of those receiving PbtO(2)-guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO(2)-directed therapy, mortality was associated with lower mean daily PbtO(2) (p < 0.05), longer durations of compromised brain oxygen (PbtO(2) < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO(2) < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO(2) (p < 0.001), and less successful treatment of compromised PbtO(2) (p = 0.03).
  
  
  CONCLUSIONS
  These results suggest that PbtO(2)-based therapy, particularly when compromised PbtO(2) can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.
authors.affiliation: Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
authors.forename: Alejandro M
authors.initials: AM
authors.lastname: Spiotta
authors.forename: Michael F
authors.initials: MF
authors.lastname: Stiefel
authors.forename: Vicente H
authors.initials: VH
authors.lastname: Gracias
authors.forename: Alicia M
authors.initials: AM
authors.lastname: Garuffe
authors.forename: W Andrew
authors.initials: WA
authors.lastname: Kofke
authors.forename: Eileen
authors.initials: E
authors.lastname: Maloney-Wilensky
authors.forename: Andrea B
authors.initials: AB
authors.lastname: Troxel
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Levine
authors.forename: Peter D
authors.initials: PD
authors.lastname: Le Roux
mesh_terms: D000328:Adult; D001921:Brain / Q000503:physiopathology*; D001930:Brain Injuries / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy*; D005260:Female; D006801:Humans; D002534:Hypoxia, Brain / Q000401:mortality / Q000503:physiopathology / Q000628:therapy; D007427:Intracranial Pressure; D008297:Male; D008991:Monitoring, Physiologic; D010100:Oxygen / Q000378:metabolism*; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D010100:Oxygen