2,833 publications from this institution
Results from some of these cohort studies have provided an indication of how nutrition guidelines have been applied in clinical practice and which areas need to be improved. Others have generated hypotheses that will be (or are already being) tested in randomized studies.
The results of recent large-scale clinical trials have led us to review our understanding of the metabolic response to stress and the most appropriate means of managing nutrition in critically ill patients. This review presents an update in this field, identifying and discussing a number of areas for which consensus has been reached and others where controversy remains and presenting areas for future research. We discuss optimal calorie and protein intake, the incidence and management of re-feeding syndrome, the role of gastric residual volume monitoring, the place of supplemental parenteral nutrition when enteral feeding is deemed insufficient, the role of indirect calorimetry, and potential indications for several pharmaconutrients.
In a large, contemporary, and multicenter sample of patients with sepsis in the emergency department, hourly delays in antibiotic administration were associated with increased odds of hospital mortality even among patients who received antibiotics within 6 hours. The odds increased within each sepsis severity strata, and the increased odds of mortality were greatest in septic shock.
Calcium has a fundamental role in the maintenance of myocardial function and vascular tone. The ionized form of calcium is the most important physiologically, and this form needs to be measured to assess physiologically active calcium levels. Ionized hypocalcemia can occur as a result of various pathophysiological disturbances, and it is seen frequently in critically ill patients. Several investigators have observed a poorer prognosis in those patients with ionized hypocalcemia. It is unclear whether calcium supplementation is beneficial in these patients. It may improve cardiovascular performance, but, in contrast, it may contribute to cellular damage (especially during hypoxia following cardiopulmonary resuscitation). In sepsis, there may be an increased cellular influx of calcium, which may be deleterious to cellular function; indeed, calcium entry blockers in this situation may be protective. We review the role of calcium as an inotropic agent, its interaction with other inotropic agents, and its use during blood transfusion and during cardiopulmonary resuscitation.
Severe sepsis induces Disseminated Intravascular Coagulation (DIG) and organ dysfunction. 50 % of the septic patients have thrombocytopenia related to thrombin generation, which activates platelets, and inflammatory cytokines ( IL-1,TNF) which activate leucocytes and endothelial cells increasing platelet adhesion. We investigate ex vivo the platelets aggregability, adhesiveness and vascular growth factor release of patients with severe sepsis (n=l 1) and septic shock (n=10) at Day 0, 3 and 7. ADP, collagen and thrombin (TRAP) induced platelet rich plasma aggregation were impaired in all the patients by comparison to 10 normal subjects, even in absence of thrombocytopenia. The slope and the percentage of aggregation were decreased after collagen and TRAP but not ADP. Whole blood flow cylometry confirms the aggregation defect. GPIIbllla activation, stained by PAC-1 expression and fibrinogen- FITC fixation, was significantly reduced spontaneously and after activation by collagen and TRAP. In opposit, P selectin (CD62p) and vWF receptor remain unchanged. Adhesion of septic patient's platelet to endothelial cells is under investigation. aggreg ADP ADP collagen collagen TRAP TRAP slope % aggreg slope % aggreg slope % aggreg normal 37.7 ±3.5 73.3 ±5.7 46.4 ±6.4 83.3 ±5.9 64.6 ±5.9 83.6 ±3.4 sepsis 30.1 ±5.8 61.0±14.l 34.5±3.6 70.6+7.9 40.1+12.6 70.5 ±9.7 pvalue 0.679 0.185 0.001 0.014 0.002 0.015 FCM CD62p PAC-1 fibrinogen meanfluo PBS TRAP PBS TRAP PBS TRAP normal 153 626.75 158 505.75 255.5 766 sepsis 115.6 530.9 120.1 275.6 233.9 309.8 pvalue 0.575 0.263 0.045 0.009 0.084 0.002 VEGF and PDGF mesured in the plasma supernatant after TRAP induced platelet aggregation, was differently regulated with an increased release of VEGF (125.99±99 in control vs 376 ±170 in septic p=0.017) and an inhibition of PDGF (2629±491 vs 1959+478 p=0.033). In conclusion severe sepsis is characterized by an impaired platelet aggregation with concerved adhesion and complex angiogenic regulation.
SCOPUS: ed.j
Erasme Hospital; Free University of Brussels; Brussels, Belgium Address requests for reprints to: Jean-Louis Vincent, MD, PhD, Department of Intensive Care, Erasme University Hospital, Route de Lennik 808, B-1070 BRUSSELS, Belgium. E-mail: [email protected]
