title: Treatment of diabetic ketoacidosis using normalization of blood 3-hydroxybutyrate concentration as the endpoint of emergency management. A randomized controlled study.
abstract: OBJECTIVE
  To compare the efficacy of an extended insulin regimen using correction of hyperketonemia as endpoint with a more conventional regimen in the treatment of diabetic ketoacidosis.
  
  
  METHODS
  A total of 22 patients admitted to a Belfast teaching hospital with clinical and biochemical features of diabetic ketoacidosis (pH < 7.25 and/or bicarbonate < 16 mmol/l) were randomized to either conventional or extended insulin regimens. In the conventional regimen, insulin was administered at 5 U/h until near-normoglycemia (blood glucose < or = 10 mmol/l) and then administered at a reduced rate until clinical recovery. In the extended regimen, administration of insulin at 5 U/h was continued beyond attainment of normoglycemia, until resolution of hyperketonemia (3-hydroxybutyrate < 0.5 mmol/l). Main outcome measures were 3-hydroxybutyrate and bicarbonate levels during the 24 h after attainment of near-normoglycemia.
  
  
  RESULTS
  After near-normoglycemia, correction of hyperketonemia was achieved earlier with the extended treatment (5.9 +/- 0.8 vs. 21.8 +/- 3.4 h, P = 0.0004 [mean +/- SD]). The area under the curve of 3-hydroxybutyrate against time for 24 h after near-normoglycemia was reduced with the extended treatment (24.9 +/- 3.8 vs. 55.9 +/- 6.7 mmol.l-1.h-1, P = 0.001). These differences remained statistically significant after adjustment for higher baseline levels of 3-hydroxybutyrate at near-normoglycemia in the extended treatment group. Bicarbonate levels at 6 and 12 h after near-normoglycemia were not significantly different between groups.
  
  
  CONCLUSIONS
  The extended insulin regimen, which was easy to implement at ward level, produced a more rapid resolution of ketosis than the conventional regimen.
authors.affiliation: Sir George E Clark Metabolic Unit, Royal Victoria Hospital, Belfast, Northern Ireland, U.K.
authors.forename: M I
authors.initials: MI
authors.lastname: Wiggam
authors.forename: M J
authors.initials: MJ
authors.lastname: O'Kane
authors.forename: R
authors.initials: R
authors.lastname: Harper
authors.forename: A B
authors.initials: AB
authors.lastname: Atkinson
authors.forename: D R
authors.initials: DR
authors.lastname: Hadden
authors.forename: E R
authors.initials: ER
authors.lastname: Trimble
authors.forename: P M
authors.initials: PM
authors.lastname: Bell
mesh_terms: D020155:3-Hydroxybutyric Acid; D000328:Adult; D001639:Bicarbonates / Q000097:blood / Q000378:metabolism; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D016883:Diabetic Ketoacidosis / Q000097:blood / Q000188:drug therapy*; D004573:Electrolytes / Q000097:blood / Q000378:metabolism; D005260:Female; D006801:Humans; D006885:Hydroxybutyrates / Q000097:blood*; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D007275:Injections, Intravenous; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D013997:Time Factors
chemical_list: D001639:Bicarbonates; D004573:Electrolytes; D006885:Hydroxybutyrates; D007004:Hypoglycemic Agents; D007328:Insulin; D020155:3-Hydroxybutyric Acid