Critical care : the official journal of the Critical Care Forum
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Our aim was to describe inflammatory cytokines response in the peritoneum and plasma of patients with peritonitis. We also tested the hypothesis that scenarios associated with worse outcome would result in different cytokine release patterns. Therefore, we compared cytokine responses according to the occurrence of septic shock, mortality, type of peritonitis and peritoneal microbiology. ⋯ Peritonitis triggers an acute systemic and peritoneal innate immune response with a simultaneous release of pro and anti-inflammatory cytokines. Higher levels of all cytokines were observed in the plasma of patients with the most severe conditions (shock, non-survivors), but this difference was not reflected in their peritoneal fluid. There was always a large gradient in cytokine concentration between peritoneal and plasma compartments highlighting the importance of compartmentalization of innate immune response in peritonitis.
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Randomized Controlled Trial
Effects of thoracic epidural anaesthesia on survival and microcirculation in severe acute pancreatitis: a randomized experimental trial.
Severe acute pancreatitis is still a potentially life threatening disease with high mortality. The aim of this study was to evaluate the therapeutic effect of thoracic epidural anaesthesia (TEA) on survival, microcirculation, tissue oxygenation and histopathologic damage in an experimental animal model of severe acute pancreatitis in a prospective animal study. ⋯ TEA led to improved survival, enhanced microcirculatory perfusion and tissue oxygenation and resulted in less histopathologic tissue-damage in an experimental animal model of severe acute pancreatitis.
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Observational Study
Prospective observational evaluation of the particle immunofiltration anti-platelet factor 4 rapid assay in MICU patients with thrombocytopenia.
Heparin-induced thrombocytopenia (HIT) results from antibodies to PF4/heparin complexes and clinical diagnosis is difficult. We evaluated the particle immunofiltration anti-platelet factor 4 (PIFA) rapid assay, in conjunction with a clinical risk score, in the diagnosis of HIT. ⋯ While thrombocytopenia in our population is common, the prevalence of HIT is low. The combination of a low to intermediate pretest probability with a negative PIFA test can rapidly exclude the presence of platelet activating anti-PF4/heparin antibodies and, therefore, HIT as the cause of the thrombocytopenia. Since a positive PIFA result has a low positive predictive value, a positive PIFA is not diagnostic of HIT and additional evaluation is warranted.
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Current hemodynamic monitoring of critically ill patients is mainly focused on monitoring of pressure-derived hemodynamic variables related to systemic circulation. Increasingly, oxygen transport pathways and indicators of the presence of tissue dysoxia are now being considered. In addition to the microcirculatory parameters related to oxygen transport to the tissues, it is becoming increasingly clear that it is also important to gather information regarding the functional activity of cellular and even subcellular structures to gain an integrative evaluation of the severity of disease and the response to therapy. ⋯ This complexity of information requires integration of the variables being monitored, which requires mathematical models based on physiology to reduce the complexity of the information and provide the clinician with a road map to guide therapy and assess the course of recovery. In this paper, we review the state of the art of these developments and speculate on the future, in which we predict a physiological monitoring environment that is able to integrate systemic hemodynamic and oxygen-derived variables with variables that assess the peripheral circulation and microcirculation, extending this real-time monitoring to the functional activity of cells and their constituents. Such a monitoring environment will ideally relate these variables to the functional state of various organ systems because organ function represents the true endpoint for therapeutic support of the critically ill patient.
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Cuthbertson and colleagues demonstrate that survivors of severe sepsis face, in general continued ongoing high mortality and quite poor quality of life. This cohort caps the initial, problem-definition stage on long-term outcomes after critical illness. Having compellingly demonstrated the opportunities for improvements in outcomes, epidemiologic and behavioral research must now to turn to understanding the mechanisms by which these outcomes can be improved. Such fundamental research will provide the evidence base to drive informed and successful interventional trials.