Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
-
Clinical Trial
Postoperative vasopressin and copeptin levels in noncardiac surgery patients: a prospective controlled trial.
Further information on the endogenous arginine vasopressin (AVP) response in patients with postoperative systemic inflammatory response syndrome (SIRS) and vasodilatory shock would provide more insight into the pathophysiology of SIRS-associated cardiovascular failure and help indicate AVP therapy. Patients after uncomplicated abdominal surgery without SIRS (n = 10), critically ill patients after noncardiac surgery with SIRS (n = 9), and patients with SIRS plus vasodilatory shock (n = 22) were included in this prospective trial. Plasma AVP (radioimmunoassay) and copeptin (immunoluminometric assay) concentrations together with clinical parameters were documented daily during the first 7 days postoperative. ⋯ In patients without hemofiltration, copeptin levels predicted 28-day mortality with high sensitivity and specificity. The postoperative AVP response in noncardiac surgery patients seems well maintained. The possibility that AVP plays a contributory role in the failure to restore vascular tone in patients with vasodilatory shock cannot be excluded but seems less important than in septic or postcardiotomy shock.
-
Severe sepsis and septic shock, often complicated by acute kidney injury (AKI), are the most common causes of mortality in noncoronary intensive care units (ICUs). This study investigates the outcomes of critically ill patients with sepsis and elucidates the association between prognosis and risk of renal failure, injury to the kidney, failure of kidney function, loss of kidney function, and end-stage renal failure (RIFLE) classification. A total of 121 sepsis patients were admitted to ICU from June 2003 to January 2004. ⋯ Cumulative survival rates at 6-month follow-up after hospital discharge significantly (P < 0.05) differed between non-AKI versus RIFLE injury, non-AKI versus RIFLE failure (RIFLE-F), and RIFLE risk versus RIFLE F. At 6-month follow-up, full recovery of renal function was noted in 85% of surviving patients with AKI (RIFLE risk, RIFLE injury, and RIFLE-F). In conclusion, these findings are consistent with a role for RIFLE classification in accurately predicting in-hospital mortality and short-term prognosis in ICU sepsis patients.
-
This study compares the effectiveness of the Pitt bacteremia score, the Charlson weighted index of comorbidity, and the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring systems for the prediction of mortality in intensive care unit (ICU) patients with sepsis using the retrospective observational method on 134 patients with ICU-acquired sepsis. The statistical analyses show several important findings. ⋯ Third, the Pitt bacteremia score and the APACHE II scores are positively related to mortality in patients with ICU-acquired sepsis. As the result of the analyses, the mortality rate in patients with sepsis in the ICU is better predicted with the Pitt bacteremia score because it provides better estimation of sensitivity and specificity than the APACHE II scoring system and the Charlson weighted index of comorbidity.
-
To examine the effects of anticoagulants and the role of thrombin on neutrophil-platelet-endothelial cell interactions in septic shock. Controlled experiments using phase-contrast microscopy to study neutrophil, platelet, and endothelial cell interactions in flowing cell suspensions under simulated physiologic conditions. University research laboratory. ⋯ In addition, thrombin attenuated the effects of each of these agents on platelet-neutrophil aggregation, platelet activation, and neutrophil activation. These data suggest that H, A, ATIII, and rhAPC decrease sepsis-induced neutrophil-endothelial cell interactions. The reversal of this effect by thrombin suggests that these agents alter neutrophil-endothelial interactions through their anticoagulant effects and the resulting decrease in thrombin activity.