title: Hyperglycemia and insulin resistance in cardiac arrest patients treated with moderate hypothermia.
abstract: BACKGROUND
  It is unknown whether the hyperglycemia that follows cardiac arrest and during therapeutic hypothermia (TH) is due to the arrest or the TH, whether it is associated with adverse outcomes, or whether its treatment affects outcomes.
  
  
  OBJECTIVE
  The objective of the study was to determine the effects of TH on the blood glucose (BG) levels in postcardiac arrest patients and the effects of hyperglycemia on mortality.
  
  
  METHODS
  This was a chart review of 62 patients undergoing TH after cardiac arrest between September 2005 and April 2008. BG levels from 72 hours before the arrest to 48 hours after TH and iv insulin infusion rates were analyzed and correlated with survival to discharge from hospital.
  
  
  METHODS
  The study was conducted at a tertiary, university referral center.
  
  
  METHODS
  PATIENTS undergoing TH after cardiac arrest participated in the study.
  
  
  METHODS
  TH consisted of cooling as rapidly as possible to 33°C, holding that temperature for 24 hours, and then controlled rewarming to 37°C over 8 or 16 hours. Hyperglycemia was managed with iv insulin drip protocols.
  
  
  METHODS
  The relationship of cardiac arrest and hypothermia to hyperglycemia, with a key secondary outcome being the relationship of hyperglycemia to survival to discharge, was measured.
  
  
  RESULTS
  Analysis of glucose patterns showed no independent effect of TH on BG levels. Mean BG levels between cardiac arrest and the initiation of hypothermia were higher in nonsurvivors (253 ± 112 mg/dL, n = 48) than in survivors (192 ± 69 mg/dL, n = 24, P = .016). BG, insulin infusion rates, and insulin resistance during hypothermia, during rewarming, and 24-48 hours after hypothermia were not significantly different between the 2 groups.
  
  
  CONCLUSIONS
  In patients treated with TH, the TH had no independent effect on BG levels. Mortality was associated with increased BG levels after cardiac arrest but before initiation of TH or an insulin drip. Likely, it is the severity of stress from the cardiac arrest that causes the hyperglycemia in these patients.
authors.affiliation: Division of Endocrinology, Metabolism, and Molecular Medicine (M.D.E., A.W., L.A., M.E.M.), Department of Medicine, and Department of Neurology (R.A.B.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; and Department of Internal Medicine (V.A.), University of Illinois at Chicago/Advocate Christ Medical Center, Chicago, Illinois 60453.
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Ettleson
authors.forename: Vanessa
authors.initials: V
authors.lastname: Arguello
authors.forename: Amisha
authors.initials: A
authors.lastname: Wallia
authors.forename: Lester
authors.initials: L
authors.lastname: Arguelles
authors.forename: Richard A
authors.initials: RA
authors.lastname: Bernstein
authors.forename: Mark E
authors.initials: ME
authors.lastname: Molitch
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D005260:Female; D006323:Heart Arrest / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology*; D007036:Hypothermia, Induced / Q000009:adverse effects / Q000379:methods*; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D012189:Retrospective Studies
chemical_list: D001786:Blood Glucose