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Clinical endocrinology · Feb 2006
Intravenous glucose intake independently related to intensive care unit and hospital mortality: an argument for glucose toxicity in critically ill patients.
- Peter H J der Voort, Rieneke A Feenstra, Andries J Bakker, Loek Heide, E Christiaan Boerma, and Iwan C C van der Horst.
- Department of Intensive Care, Medical Centre Leeuwarden, Leeuwarden, the Netherlands. phjvdvoort@chello.nl
- Clin. Endocrinol. (Oxf). 2006 Feb 1;64(2):141-5.
ObjectiveIt is assumed that the toxic effects of glucose play a role in the outcome of critically ill patients. We studied the impact of the amount of infused glucose as a determinant of mortality.DesignA retrospective cohort study design was used as blood glucose levels in critically ill patients are nowadays tightly controlled.PatientsLong-stay critically ill patients (7-30 days).MeasurementsThe association between the mean amount of glucose infusion and both intensive care unit (ICU) and hospital mortality was determined. We corrected for the mean glucose serum concentration, the mean dosage of insulin and for severity of illness, using the acute physiology and chronic health evaluation (APACHE II) score.ResultsOf the 2,042 admitted patients, 273 met the inclusion criteria. The mean length of stay was 14.4 days [interquartile range (IQR) 9-18]. Hospital mortality was significantly lower for patients with a mean glucose level below 8 mmol/l (30/79; 38%) compared to patients with a level above 8 mmol/l (104/194; 54%, P=0.023). Logistic stepwise multivariate regression analysis for both ICU and hospital mortality as dependent variables showed that APACHE II score and the mean daily amount of infused glucose were associated with mortality.ConclusionIn long-stay ICU patients without blood glucose level control, the ICU and hospital mortality was independently related to the mean amount of infused glucose. In addition, mortality in patients with a mean glucose level above 8.0 mmol/l was higher. Both these determinants of mortality can exert their effects by insulin-independent uptake of glucose with subsequent toxic intracellular effects.
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