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Objectives To develop evidence-based recommendations for clinicians caring for adults with acute or acute on chronic liver failure in the ICU. Design The guideline panel comprised 29 members with expertise in aspects of care of the critically ill patient with liver failure and/or methodology. The Society of Critical Care Medicine standard operating procedures manual and conflict-of-interest policy were followed throughout. Teleconferences and electronic-based discussion among the panel, as well as within subgroups, served as an integral part of the guideline development. Setting The panel was divided into nine subgroups: cardiovascular, hematology, pulmonary, renal, endocrine and nutrition, gastrointestinal, infection, perioperative, and neurology. Interventions We developed and selected population, intervention, comparison, and outcomes questions according to importance to patients and practicing clinicians. For each population, intervention, comparison, and outcomes question, we conducted a systematic review aiming to identify the best available evidence, statistically summarized the evidence whenever applicable, and assessed the quality of evidence using the Grading of Recommendations Assessment, Development, and Evaluation approach. We used the evidence to decision framework to facilitate recommendations formulation as strong or conditional. We followed strict criteria to formulate best practice statements. Measurements and main results In this article, we report 29 recommendations (from 30 population, intervention, comparison, and outcomes questions) on the management acute or acute on chronic liver failure in the ICU, related to five groups (cardiovascular, hematology, pulmonary, renal, and endocrine). Overall, six were strong recommendations, 19 were conditional recommendations, four were best-practice statements, and in two instances, the panel did not issue a recommendation due to insufficient evidence. Conclusions Multidisciplinary international experts were able to formulate evidence-based recommendations for the management acute or acute on chronic liver failure in the ICU, acknowledging that most recommendations were based on low-quality indirect evidence.

Objective To assess the prevalence of acute kidney injury in patients with subarachnoid hemorrhage patients. Design Retrospective analysis of all subarachnoid hemorrhage admissions. Settings Neurocritical care unit. Patients All patients with a diagnosis of subarachnoid hemorrhage between 2009 and 2014. Interventions None. Measurements and main results Of 1,267 patients included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (changes in creatinine only). Compared to patients without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes mellitus (21.2% vs 9.8%; p Conclusions Critically ill patients with subarachnoid hemorrhage show a strong association between hyperchloremia and acute kidney injury as well as acute kidney injury and mortality.

To assess the reversibility of acute kidney injury-induced neutrophil dysfunction and to identify involved mechanisms.Controlled laboratory experiment and prospective observational clinical study.University laboratory and hospital.C57BL/6 wild-type mice.Patients with septic shock with or without acute kidney injury.Murine acute kidney injury was induced by intraperitoneal injections of folic acid (nephrotoxic acute kidney injury) or by IM injections of glycerol (rhabdomyolysis-induced acute kidney injury). After 24 hours, we incubated isolated neutrophils for 3 hours in normal mouse serum or minimum essential medium buffer. We further studied the effects of plasma samples from 13 patients with septic shock (with or without severe acute kidney injury) on neutrophilic-differentiated NB4 cells.Experimental acute kidney injury significantly inhibited neutrophil migration and intracellular actin polymerization. Plasma levels of resistin, a proinflammatory cytokine and uremic toxin, were significantly elevated during both forms of acute kidney injury. Incubation in serum or minimum essential medium buffer restored normal neutrophil function. Resistin by itself was able to induce acute kidney injury-like neutrophil dysfunction in vitro. Plasma resistin was significantly higher in patients with septic shock with acute kidney injury compared with patients with septic shock alone. Compared with plasma from patients with septic shock, plasma from patients with septic shock and acute kidney injury inhibited neutrophilic-differentiated NB4 cell migration. Even after 4 days of renal replacement therapy, plasma from patients with septic shock plus acute kidney injury still showed elevated resistin levels and inhibited neutrophilic-differentiated NB4 cell migration. Resistin inhibited neutrophilic-differentiated NB4 cell migration and intracellular actin polymerization at concentrations seen during acute kidney injury, but not at normal physiologic concentrations.Acute kidney injury-induced neutrophil dysfunction is reversible in vitro. However, standard renal replacement therapy does not correct this defect in patients with septic shock and acute kidney injury. Resistin is greatly elevated during acute kidney injury, even with ongoing renal replacement therapy, and is sufficient to cause acute kidney injury-like neutrophil dysfunction by itself.

Objective: Despite progress in renal replacement therapy and critical care medicine, acute renal failure (ARF) still carries a very high mortality rate. Neutrophil infiltration has been recognized as a hallmark in postischemic renal injury. Neutrophil recruitment requires adhesion molecules including E-selectin, which mediates leukocyte rolling and adhesion. This study aims to identify the role of E-selectin in ischemia-reperfusion-induced severe ARF. Design: Prospective, controlled, experimental study. Setting: University animal research laboratory. Subjects: C57BU6 wild-type mice or C57BU6 mice gene-deficient for E-selectin. Interventions: Mice underwent 32-min bilateral renal ischemia or identical sham operations. After 4, 12, 24, or 48 hrs, kidneys were harvested and blood samples were taken. A separate group of wild-type mice received either antineutrophil serum or control serum 18 hrs before ischemia. Another group of wild-type mice was injected with function-blocking monoclonal E-selectin antibody or with control antibody 10 mins after reperfusion. Blood samples were taken 24 hrs later. Measurements and Main Results: Blood creatinine and urea nitrogen concentrations, as well as renal myeloperoxidase activity indicating neutrophil infiltration, were measured. Reducing neutrophil counts by antineutrophil serum showed that in this model, organ failure strongly depends on neutrophil counts at time of ischemia. E-selectin deficient mice showed lower creatinine and blood urea nitrogen concentrations than wild-type mice at 24 and 48 hrs (a reduction of 60% to 80%). Kidneys of E-selectin deficient mice also revealed a lower myeloperoxidase activity maximum (75% reduction) at 24 hrs. Western blot analysis showed maximum E-selectin expression 24 hrs after ischemia-reperfusion. Immunostaining localized E-selectin to the endothelium of the peritubular capillary plexus. Compared with control antibody, postischemic injection of anti-E-selectin antibody gave lower creatinine concentrations at 24 hrs, similar to that seen in E-selectin deficient mice. Conclusions: In this model, blocking E-selectin even after onset of reperfusion protects from severe ARF, presumably by reducing postischemic neutrophil infiltration into the kidney. This suggests a new potential therapeutic perspective.