title: Nutritional support and brain tissue glucose metabolism in poor-grade SAH: a retrospective observational study.
abstract: BACKGROUND
  We sought to determine the effect of nutritional support and insulin infusion therapy on serum and brain glucose levels and cerebral metabolic crisis after aneurysmal subarachnoid hemorrhage (SAH).
  
  
  METHODS
  We used a retrospective observational cohort study of 50 mechanically ventilated poor-grade (Hunt-Hess 4 or 5) aneurysmal SAH patients who underwent brain microdialysis monitoring for an average of 109 hours. Enteral nutrition was started within 72 hours of admission whenever feasible. Intensive insulin therapy was used to maintain serum glucose levels between 5.5 and 7.8 mmol/l. Serum glucose, insulin and caloric intake from enteral tube feeds, dextrose and propofol were recorded hourly. Cerebral metabolic distress was defined as a lactate to pyruvate ratio (LPR)>40. Time-series data were analyzed using a general linear model extended by generalized estimation equations (GEE).
  
  
  RESULTS
  Daily mean caloric intake received was 13.8±6.9 cal/kg and mean serum glucose was 7.9±1 mmol/l. A total of 32% of hourly recordings indicated a state of metabolic distress and <1% indicated a state of critical brain hypoglycemia (<0.2 mmol/l). Calories received from enteral tube feeds were associated with higher serum glucose concentrations (Wald=6.07, P=0.048), more insulin administered (Wald=108, P<0.001), higher body mass index (Wald=213.47, P<0.001), and lower body temperature (Wald=4.1, P=0.043). Enteral feeding (Wald=1.743, P=0.418) was not related to brain glucose concentrations after accounting for serum glucose concentrations (Wald=67.41, P<0.001). In the presence of metabolic distress, increased insulin administration was associated with a relative reduction of interstitial brain glucose concentrations (Wald=8.26, P=0.017), independent of serum glucose levels.
  
  
  CONCLUSIONS
  In the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Further study is needed to understand how nutritional support and insulin administration can be optimized to minimize secondary injury after subarachnoid hemorrhage.
authors.affiliation: Columbia University, Department of Neurology, Milstein Hospital, 177 Fort Washington, Suite 8-300, New York, NY 10032, USA. mjs2134@columbia.edu
authors.forename: J Michael
authors.initials: JM
authors.lastname: Schmidt
authors.forename: Jan
authors.initials: J
authors.lastname: Claassen
authors.forename: Sang-Bae
authors.initials: SB
authors.lastname: Ko
authors.forename: Hector
authors.initials: H
authors.lastname: Lantigua
authors.forename: Mary
authors.initials: M
authors.lastname: Presciutti
authors.forename: Kiwon
authors.initials: K
authors.lastname: Lee
authors.forename: E Sander
authors.initials: ES
authors.lastname: Connolly
authors.forename: Stephan A
authors.initials: SA
authors.lastname: Mayer
authors.forename: David S
authors.initials: DS
authors.lastname: Seres
authors.forename: Neeraj
authors.initials: N
authors.lastname: Badjatia
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism*; D015331:Cohort Studies; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D017551:Microdialysis / Q000379:methods; D008875:Middle Aged; D018529:Nutritional Support / Q000379:methods*; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000378:metabolism* / Q000628:therapy*
chemical_list: D005947:Glucose