Batzi1, E Koutsoumi...
 
Batzi1, E Koutsoumi1, A Paradimitriou1, M Varveri1, A Karabinis1 1ICU, General
Batzi1, E Koutsoumi1, A Paradimitriou1, M Varveri1, A Karabinis1 1ICU, General
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Batzi1, E Koutsoumi1, A Paradimitriou1, M Varveri1, A Karabinis1 1ICU, General Hospital G. Gennimatas, Athens, Greece; 2Department of Endocrinology, General Hospital G. Gennimatas, Athens, Greece Critical Care 2006, 10(Suppl 1):P253 (doi: 10.1186/cc4600) Introduction The influence of the plasma glucose levels on the prognosis of infection is unclear. The aim of this clinical trial is to study the impact of the plasma glucose levels at the onset of bacteremia (PGLOB) on the prognosis of bacteremia in ICU patients. Methods We studied retrospectively 202 bacteremic ICU patients (143 men, 59 women). Mean age: 49.3 ?16.9 years. Mean stay: 25.2 ?11.1 days. Underlying diseases: multiple trauma 131, complicated surgery 52, other 19. All were mechanically ventilated and developed a nosocomial infection (NI) with at least one positive blood culture. From 202 patients, 34 (16.8 ) were diabetic. The PGLOB (at the exact moment of the first positive blood culture) was measured and was related to prognosis of NI. Results In diabetic patients the mean PGLOB was 244.5 ?103.4 mg , while in nondiabetic patients it was 141.3 ?58.4 mg . Global mortality rates (MR): 48/202 = 23.8 . From 48 patients who died, in 37 death was associated with NI with bacteremia; they had mean PGLOB 158.3 ?91.1 mg . The other 11 nonsurvivors had 153.4 ?74.3 PR-39 mg . The related MR to NI and bacteremia according to PGLOB were: 200 mg , MR 27.1 (P = 0.32). Conclusion There was no significant relationship between PGLOB and mortality attributed to NI and bacteremia. Multiple organ dysfunction syndrome was observed more frequently in patients with PGLOB >200 mg , but not significantly. MR was similar in both diabetic and nondiabetic patients.P252 Expression of glucose transporters in critical illnessL Langouche, S Vander Perre, P Wouters, G Van den Berghe Katholieke Universiteit Leuven, Belgium Critical Care 2006, 10(Suppl 1):P252 (doi: 10.1186/cc4599) Stress-induced hyperglycemia is a PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27509597 significant problem in critically ill patients, for whom the severity of hyperglycemia and insulin resistance reflects the risk of death. We recently demonstrated that strict maintenance of normoglycemia with intensive insulin therapy during intensive care reduced the morbidity and mortality of surgical ICU patients [1]. Normal cells respond to hyperglycemia by downregulating the insulin-independent glucose transporters (GLUT1, GLUT2 and GLUT3), thereby protecting themselves against passive glucose overload. Insulin is known to upregulate muscle GLUT4 expression, required for controlled glucose uptake in the muscle. We investigated expression levels of these four GLUTs in critical illness and assessed the impact of intensive insulin therapy. We examined mRNA expression levels with real-time RT-PCR in muscle and liver tissue of 36 nonsurvivors, who had been randomized to intensive (normoglycemic) or conventional (hyperglycemic) insulin therapy and who were comparable for age and severity, duration and type of critical illness. The mean PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/10692555 blood glucose levels were 5.6 ?0.4 and 9.9 ?0.9 mmol/l (P < 0.001) on a median daily insulin dose of 44.2 and 14.4 IU (P = 0.005), respectively. For comparison, we studied tissue harvested from patients undergoing acute surgical stress as well as tissue from healthy controls. We demonstrated that in both the liver and muscle of patients with prolonged critical illness, the high-affinity insulin-independent glucos.

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