title: Tight glycemic control increases metabolic distress in traumatic brain injury: a randomized controlled within-subjects trial.
abstract: OBJECTIVE
  To determine the effects of tight glycemic control on brain metabolism after traumatic brain injury using brain positron emission tomography and microdialysis.
  
  
  METHODS
  Single-center, randomized controlled within-subject crossover observational trial.
  
  
  METHODS
  Academic intensive care unit.
  
  
  METHODS
  We performed a prospective, unblinded randomized controlled within-subject crossover trial of tight (80-110 mg/dL) vs. loose (120-150 mg/dL) glycemic control in patients with severe traumatic brain injury to determine the effects of glycemic control on brain glucose metabolism, as measured by [18F] deoxy-D-glucose brain positron emission tomography. Brain microdialysis was done simultaneously.
  
  
  RESULTS
  Thirteen severely injured traumatic brain injury patients underwent the study between 3 and 8 days (mean 4.8 days) after traumatic brain injury. In ten of these subjects, global brain and gray matter tissues demonstrated higher glucose metabolic rates while glucose was under tight control as compared with loose control (3.2 ± 0.6 vs. 2.4 + 0.4, p = .02 [whole brain] and 3.8 ± 1.4 vs. 2.9 ± 0.8, p = .05 [gray matter]). However, the responses were heterogeneous with pericontusional tissue demonstrating the least state-dependent change. Cerebral microdialysis demonstrated more frequent critical reductions in glucose (p = .02) and elevations of lactate/pyruvate ratio (p = .03) during tight glycemic control.
  
  
  CONCLUSIONS
  Tight glycemic control results in increased global glucose uptake and an increased cerebral metabolic crisis after traumatic brain injury. The mechanisms leading to the enhancement of metabolic crisis are unclear, but delivery of more glucose through mild hyperglycemia may be necessary after traumatic brain injury.
authors.affiliation: Department of Neurology, UCLA School of Medicine, Los Angeles, CA, USA. pvespa@mednet.ucla.edu
authors.forename: Paul
authors.initials: P
authors.lastname: Vespa
authors.forename: David L
authors.initials: DL
authors.lastname: McArthur
authors.forename: Nathan
authors.initials: N
authors.lastname: Stein
authors.forename: Sung-Cheng
authors.initials: SC
authors.lastname: Huang
authors.forename: Weber
authors.initials: W
authors.lastname: Shao
authors.forename: Maria
authors.initials: M
authors.lastname: Filippou
authors.forename: Maria
authors.initials: M
authors.lastname: Etchepare
authors.forename: Thomas
authors.initials: T
authors.lastname: Glenn
authors.forename: David A
authors.initials: DA
authors.lastname: Hovda
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D018592:Cross-Over Studies; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods; D011446:Prospective Studies; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D013312:Stress, Physiological / Q000502:physiology*; D015599:Trauma Severity Indices; D055815:Young Adult
chemical_list: D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D005947:Glucose