title: Insulin differentially influences brain glucose and lactate in traumatic brain injured patients.
abstract: BACKGROUND
  Hypo- and hyperglycemia must be avoided to prevent additional brain damage following traumatic brain injury (TBI). However, the optimal blood glucose range requiring insulin remains unknown. Cerebral microdialysis is helpful in unmasking signs of metabolic impairment, thereby identifying deleterious blood glucose levels.
  
  
  METHODS
  A retrospective analysis of prospectively collected cerebral microdialysis samples obtained from 20 non-diabetic patients with severe TBI treated at the trauma surgical intensive care unit at the University Hospital Zürich, Switzerland.
  
  
  RESULTS
  The impact of different arterial blood glucose values and concomitant insulin administration on cerebral interstitial glucose and lactate levels was investigated. In addition, energetic impairment was determined by calculating lactate-to-glucose ratios. Insulin administration was associated with significantly reduced cerebral glucose concentrations and significantly increased lactate-to-glucose ratios with arterial blood glucose levels <5 mM. At arterial blood glucose levels >7 mM, insulin administration was associated with significantly increased interstitial glucose values, significantly decreased lactate concentrations, and markedly diminished lactate-to-glucose ratios.
  
  
  CONCLUSIONS
  Insulin exerts differential effects that depend strongly on the underlying arterial blood glucose concentrations. To avoid energetic impairment, insulin should not be administered at arterial blood glucose levels <5 mM. However, at arterial blood glucose levels >7-8 mM, insulin administration appears to be encouraged to increase extracellular glucose concentrations and decrease energetic impairment reflected by reduced interstitial brain lactate and decreased lactate-to-glucose ratios. Nevertheless, frequent analysis is required to minimize the risk of inducing impaired brain metabolism.
authors.affiliation: Surgical Intensive Care, University Hospital Zürich, Zürich, Switzerland.
authors.forename: M
authors.initials: M
authors.lastname: Béchir
authors.forename: R
authors.initials: R
authors.lastname: Meierhans
authors.forename: G
authors.initials: G
authors.lastname: Brandi
authors.forename: J
authors.initials: J
authors.lastname: Sommerfeld
authors.forename: M
authors.initials: M
authors.lastname: Fasshauer
authors.forename: S R
authors.initials: SR
authors.lastname: Cottini
authors.forename: R
authors.initials: R
authors.lastname: Stocker
authors.forename: J F
authors.initials: JF
authors.lastname: Stover
mesh_terms: D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001923:Brain Chemistry / Q000187:drug effects*; D001930:Brain Injuries / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D019344:Lactic Acid; D005947:Glucose