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Objective: Recent preclinical and clinical data suggest that thoracic epidural analgesia, a technique primarily aimed at decreasing pain, might exert anti-inflammatory effects, enhance splanchnic and pancreatic blood flow during acute pancreatitis; however, the influence of epidural analgesia on mortality remains under investigated in this setting. This study was therefore designed to assess the impact of epidural analgesia on mortality in ICU patients with acute pancreatitis.Design: Multicenter retrospective, observational, cohort study.Setting: Seventeen French and Belgian ICUs.Patients: All patients admitted to with acute pancreatitis between June 2009 and March 2014.Interventions: The primary exposure was thoracic epidural analgesia versus standard care without epidural analgesia. The primary outcome was 30-day mortality. Propensity analyses were used to control for bias in treatment assignment and prognostic imbalances.Measurements and Main Results: One thousand three ICU patients with acute pancreatitis were enrolled, of whom 212 died within 30 days. Epidural analgesia was used in 46 patients and was associated with reduced mortality in unadjusted analyses (4% vs. 22%; p = 0.003). After adjustment for baseline variables associated with mortality, epidural analgesia was still an independent predictor of 30-day mortality (adjusted odds ratio, 0.10; [95% CI, 0.02-0.49]; p = 0.004). Using propensity score analysis, the risk of all-cause 30-day mortality in patients with acute pancreatitis receiving epidural analgesia was significantly lower than that in matched patients who did not receive epidural analgesia (2% vs. 17%; p = 0.01).Conclusions: Among critically ill patients with acute pancreatitis, mortality at 30 days was lower in patients who received epidural analgesia than in comparable patients who did not. These findings support ongoing research on the use of epidural analgesia as a therapeutic intervention in acute pancreatitis. [ABSTRACT FROM AUTHOR]

An editorial is presented which discusses distinct biological effects of time-controlled adaptive ventilation in pulmonary and extrapulmonary acute respiratory distress syndrome. It mentions that acute respiratory distress syndrome (ARDS) pathogenesis is characterized by severe injury to both the lung epithelium and the vascular endothelium leading to the increased permeability of the alveolar-capillary membrane. It states pathophysiologic features of pulmonary and extrapulmonary ARDS.

The article examines whether the soluble form of the receptor for advanced glycation end products (sRAGE) is a marker of acute lung injury and acute respiratory distress syndrome in the intensive care unit. It is known that the levels of sRAGE are elevated during acute lung injury, but it is unknown if the elevation is linked to alveolar epithelium injury or in systemic inflammation. The results of the study revealed that sRAGE levels are elevated regardless of the presence or absence of severe sepsis.

Keywords: acute respiratory distress syndrome; biomarkers; extracorporeal membrane oxygenation; lung injury and repair; mechanical ventilation; ultra-protective ventilation For example, a recruitment maneuver induced a significant and rapid (within 1 hr) decrease in plasma sRAGE in patients with nonfocal ARDS ([12]), which is possibly consistent with an association between reducing driving pressure and minimizing lung epithelial injury. Acute respiratory distress syndrome, biomarkers, extracorporeal membrane oxygenation, lung injury and repair, mechanical ventilation, ultra-protective ventilation. [Extracted from the article]

Conflicting results have been reported on the influence of Polymyxin-B hemoperfusion treatment on systemic inflammation markers. The aim of the study was to assess in a randomized control trial the influence on plasma cytokine concentrations of Polymyxin-B hemoperfusion in septic shock due to peritonitis. A panel of 10 pro- or anti-inflammatory cytokines was measured in 213 patients with peritonitis-induced septic shock enrolled in the randomized trial ABDOMIX testing the impact of 2 Polymyxin-B hemoperfusion sessions with standard treatment. Gram-negative bacteria were identified in 69% of patients. In the overall population, baseline plasma cytokine concentrations were not different between the two groups. Circulating tumor necrosis factor-α, interleukin (IL)-1β, IL-10, IL-6, and IL-1RA decreased significantly over time in both groups (P <0.0001 for all in controls, and P = 0.0002, 0.003, and <0.0001 in patients treated with Polymyxin-B hemoperfusion). IL-17A decreased significantly in patients treated with Polymyxin B hemoperfusion (P = 0.045) but not in controls. At the end of the second Polymyxin-B hemoperfusion session or at corresponding time in controls, plasma levels of cytokines did not differ between the two groups. Similar results were found in the subgroup of patients with gram-negative peritonitis who completed two Polymyxin-B hemoperfusion sessions. These results do not support a significant influence of Polymyxin-B hemoperfusion on circulating cytokines assessed except for IL-17A which clinical significance remains to be elucidated.