title: Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury.
abstract: OBJECTIVE
  To determine that intensive glycemic control does not reduce microdialysis glucose concentration brain metabolism of glucose.
  
  
  METHODS
  Prospective monitoring followed by retrospective data analysis of cerebral microdialysis and global brain metabolism.
  
  
  METHODS
  Single center, academic neurointensive care unit.
  
  
  METHODS
  Forty-seven moderate to severe traumatic brain injury patients.
  
  
  METHODS
  A nonrandomized, consecutive design was used for glycemic control with loose insulin (n=33) for the initial 2 yrs or intensive insulin therapy (n=14) for the last year.
  
  
  RESULTS
  In 14 patients treated with intensive insulin therapy, there was a reduction in microdialysis glucose by 70% of baseline concentration compared with a 15% reduction in 33 patients treated with a loose insulin protocol. Despite this reduction in microdialysis glucose, the global metabolic rate of glucose did not change. However, intensive insulin therapy was associated with increased incidence of microdialysis markers of cellular distress, namely elevated glutamate (38+/-37% vs. 10+/-17%, p<.01), elevated lactate/pyruvate ratio (38+/-37% vs. 19+/-26%, p<.03) and low glucose (26+/-17% vs. 11+/-15%, p<.05, and increased global oxygen extraction fraction. Mortality was similar in the intensive and loose insulin treatment groups (14% vs. 15%, p=.9), as was 6-month clinical outcome (p=.3).
  
  
  CONCLUSIONS
  Intensive insulin therapy results in a net reduction in microdialysis glucose and an increase in microdialysis glutamate and lactate/pyruvate without conveying a functional outcome advantage.
authors.affiliation: UCLA Division of Neurosurgery, Los Angeles, CA, and Barrows Neurologic Institute, Phoenix, AZ, USA.
authors.forename: Paul
authors.initials: P
authors.lastname: Vespa
authors.forename: Robert
authors.initials: R
authors.lastname: Boonyaputthikul
authors.forename: David L
authors.initials: DL
authors.lastname: McArthur
authors.forename: Chad
authors.initials: C
authors.lastname: Miller
authors.forename: Maria
authors.initials: M
authors.lastname: Etchepare
authors.forename: Marvin
authors.initials: M
authors.lastname: Bergsneider
authors.forename: Thomas
authors.initials: T
authors.lastname: Glenn
authors.forename: Neil
authors.initials: N
authors.lastname: Martin
authors.forename: David
authors.initials: D
authors.lastname: Hovda
mesh_terms: D000328:Adult; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications*; D018849:Controlled Clinical Trials as Topic; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000517:prevention & control*; D007003:Hypoglycemia / Q000139:chemically induced / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage* / Q000009:adverse effects; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D015999:Multivariate Analysis; D012044:Regression Analysis; D012189:Retrospective Studies
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D005947:Glucose