title: Insulin-related decrease in cerebral glucose despite normoglycemia in aneurysmal subarachnoid hemorrhage.
abstract: BACKGROUND
  Hyperglycaemia following aneurysmal subarachnoid hemorrhage (SAH) is associated with complications and impaired neurological recovery. The aim of this study was to determine the effect of insulin treatment for glucose control on cerebral metabolism in SAH patients.
  
  
  METHODS
  This prospective, nonrandomized study was conducted in 31 SAH patients in an intensive care unit (age 52 +/- 10 years, World Federation of Neurological Surgeons grade 2.9 +/- 1.6). A microdialysis catheter was inserted into the vascular territory of the aneurysm after clipping. Blood glucose levels above 140 mg/dl were treated with intravenous insulin and the microdialysates were analyzed hourly for the first 12 hours of infusion.
  
  
  RESULTS
  No hypoglycaemia occurred. Twenty-four patients were treated with insulin for glucose control. Higher age and World Federation of Neurological Surgeons score were risk factors for need for insulin treatment (P < 0.05). Although blood glucose remained stable after initiation of insulin infusion, insulin induced a significant decrease in cerebral glucose at 3 hours after onset of the infusion until the end of the observation period (P < 0.05), reflecting high glucose utilization. The lactate:pyruvate ratio and glutamate did not increase, excluding ischaemia as possible cause of the decrease in glucose. Glycerol tended toward higher values at the end of the observation period (9 to 12 hours), reflecting either tissue damage after SAH or the beginning of cellular distress after insulin infusion.
  
  
  CONCLUSIONS
  Higher SAH grade was among the risk factors for need for insulin. Intensive glycaemic control using insulin induced a decrease of cerebral glucose and a slight increase in glycerol, though blood glucose remained normal. Future studies might detect relevant metabolic derangements when insulin treatment starts at low cerebral glucose levels, and may allow us to design a strategy for avoidance of insulin-induced metabolic crisis in SAH patients.
authors.affiliation: Department of Neurosurgery, Charité Campus Virchow Medical Center, Augustenburger Platz, 13353 Berlin, Germany.
authors.forename: Florian
authors.initials: F
authors.lastname: Schlenk
authors.forename: Daniela
authors.initials: D
authors.lastname: Graetz
authors.forename: Alexandra
authors.initials: A
authors.lastname: Nagel
authors.forename: Maren
authors.initials: M
authors.lastname: Schmidt
authors.forename: Asita S
authors.initials: AS
authors.lastname: Sarrafzadeh
mesh_terms: D001786:Blood Glucose / Q000187:drug effects*; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy / Q000209:etiology*; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use*; D002532:Intracranial Aneurysm / Q000097:blood / Q000150:complications* / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000097:blood / Q000150:complications* / Q000209:etiology
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin