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  • Poster presentation
  • Open Access

Decreased intravenous glucose intake safely prevents hyperglycemia in postsurgical children

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Critical Care201115 (Suppl 1) :P400

  • Published:


  • Hyperglycemia
  • Hypoglycemia
  • Glucose Intake
  • Intensive Insulin Therapy
  • Craniosynostosis


Critical illness induced hyperglycemia in critically ill children can be treated with intensive insulin therapy, but hypoglycaemia is a potential serious side effect. We have investigated whether decreasing intravenous glucose intake, as an alternative method, improves plasma glucose levels without affecting glucose production and protein balance in postsurgical children.


Eight children (age 9.8 ± 1.9 months, weight 9.5 ± 1.1 kg) admitted to the pediatric ICU after surgical correction for nonsyndromal craniosynostosis were studied in a randomized blinded cross-over setting to receive standard glucose (SG, 5.0 mg/kg/minute) or low glucose (LG, 2.5 mg/kg/minute). A 10-hour stable isotope tracer protocol was conducted 6 hours after surgery to study glucose and protein metabolism.


During SG, hyperglycemia (>110 mg/dl) was present, while LG resulted in normoglycemia (LG 105 ± 10 vs. SG 133 ± 30 mg/dl; P = 0.02), but not in hypoglycemia. Endogenous glucose production increased during LG (LG 2.6 ± 1.5 vs. SG 1.1 ± 1.4 mg/kg/minute; P = 0.05). Whole body protein balance was slightly negative in both groups and was not affected by glucose intake.


Standard glucose intake in postsurgical children induced hyperglycemia. Decreasing the intake by one-half of current standards resulted in normoglycemic levels, with increased endogenous glucose production. Patients were in a slight catabolic state and decreasing glucose intake did not deteriorate this. Decreasing glucose intake is a safe method to prevent hyperglycemia in critically ill postsurgical children.

Authors’ Affiliations

Erasmus MC, Rotterdam, the Netherlands
Baylor College of Medicine, Houston, TX, USA
Academic Medical Centre University of Amsterdam/VU Medical Centre, Amsterdam, the Netherlands


© De Betue et al. 2011

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.