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Objectives: To investigate national mortality trends over a 12-year period for patients with severe acute pancreatitis (SAP) admitted to Dutch ICUs. Additionally, an assessment of outcome in SAP was undertaken to differentiate between early (< 14 d of ICU admission) and late (> 14 d of ICU admission) mortality.Design: Data from the Dutch National Intensive Care Evaluation and health insurance companies' databases were extracted. Outcomes included 14-day, ICU, hospital, and 1-year mortality. Mortality before and after 2010 was compared using mixed logistic regression and mixed Cox proportional-hazards models. Sensitivity analyses, excluding early mortality, were performed to assess trends in late mortality.Setting: Not applicable.Patients: Consecutive adult patients with SAP admitted to all 81 Dutch ICUs between 2007 and 2018.Interventions: Not applicable.Measurements and Main Results: Among 4,160 patients treated in 81 ICUs, 14-day mortality was 17%, ICU mortality 17%, hospital mortality 23%, and 1-year mortality 33%. After 2010 in-hospital mortality adjusted for age, sex, modified Marshall, and Acute Physiology and Chronic Health Evaluation III scores were lower (odds ratio [OR], 0.76; 95% CI, 0.61-0.94) than before 2010. There was no change in ICU and 1-year mortality. Sensitivity analyses excluding patients with early mortality demonstrated a decreased ICU mortality (OR, 0.45; 95% CI, 0.32-0.64), decreased in-hospital (OR, 0.48; 95% CI, 0.36-0.63), and decreased 1-year mortality (hazard ratio, 0.81; 95% CI, 0.68-0.96) after 2010 compared with 2007-2010.Conclusions: Over the 12-year period examined, mortality in patients with SAP admitted to Dutch ICUs did not change, although after 2010 late mortality decreased. Novel therapies should focus on preventing early mortality in SAP. [ABSTRACT FROM AUTHOR]

Introduction: Concern for loss of physical performance and Health-Related Quality of Life (HRQoL) may raise doubts regarding the meaningfulness of an Intensive Care (ICU) admission in elderly patients. We evaluated self-perceived long-term recovery and satisfaction in elderly surviving an abdominal sepsis related ICU-admission and related this to objective measures of HRQoL. Methods: A cross-sectional survey study was performed in all ICU-survivors with age ≥70 admitted with abdominal sepsis. HRQoL, frailty and self-perceived long-term recovery were measured using the EQ-5D-3L, Groningen Frailty Indicator, and a self-developed questionnaire, respectively. Results: Of 144 patients admitted, 48 were alive at follow up (2.42 [0.92; 3.83] years), and 29 (60%) returned the survey. Eleven patients out of 29 (38%) recovered to baseline functioning, and reported higher HRQoL compared to unrecovered patients (0.861 [0.807; 1.000] and 0.753 [0.499; 0.779] respectively, p=0.005). Of the unrecovered patients, 53% were satisfied with their functioning, and 94% were willing to return to ICU. Conclusions: Mortality in elderly patients with abdominal sepsis is high and ICU-admission should be weighed carefully. However, despite substantial functional decline in survivors, it does not necessarily cause self-perceived unsatisfactory functioning, poor HRQoL and unwillingness to receive life-sustaining therapy again. Caution is advised to use an anticipated loss of functioning as an argument to deny an ICU-admission. [ABSTRACT FROM AUTHOR]

Background: Postprandial rise of plasma essential amino acids (EAAs) determines the anabolic effect of dietary protein. Disturbed gastrointestinal function could impair the anabolic response in critically ill patients. Aim was to investigate the postprandial EAA response in critically ill patients and its relation to small‐intestinal function. Methods: Twenty‐one mechanically ventilated patients and 9 healthy controls received a bolus containing 100 ml of a formula feed (Ensure) and 2 g of 3‐O‐Methyl‐d‐glucose (3‐OMG) via postpyloric feeding tube. Fasting and postprandial plasma concentrations of EAAs, 3‐OMG, total bile salts, and the gut‐released hormone fibroblast growth factor 19 (FGF19) were measured over a 4‐hour period. Changes over time and between groups were assessed with linear mixed‐effects analysis. Early (0–60 minutes) and total postprandial responses are summarized as the incremental area under the curve (iAUC). Results: At baseline, fasting EAA levels were similar in both groups: 1181 (1055–1276) vs 1150 (1065–1334) μmol·L−1, P =.87. The early postprandial rise in EAA was not apparent in critically ill patients compared with healthy controls (iAUC60, −4858 [−6859 to 2886] vs 5406 [3099–16,853] µmol·L−1·60 minutes; P =.039). Impaired EAA response did not correlate with impaired 3‐OMG response (Spearman ρ 0.32, P =.09). There was a limited increase in total bile salts but no relevant FGF19 response in either group. Conclusion: Postprandial rise of EAA is blunted in critically ill patients and unrelated to glucose absorption measured with 3‐OMG. Future studies should aim to delineate governing mechanisms of macronutrient malabsorption. [ABSTRACT FROM AUTHOR]

Background: Hypoxia and inflammation are hallmarks of critical illness, related to multiple organ failure. A possible mechanism leading to multiple organ failure is hypoxia- or inflammation-induced down-regulation of the detoxifying glyoxalase system that clears dicarbonyl stress. The dicarbonyl methylglyoxal (MGO) is a highly reactive agent produced by metabolic pathways such as anaerobic glycolysis and gluconeogenesis. MGO leads to protein damage and ultimately multi-organ failure. Whether detoxification of MGO into D-lactate by glyoxalase functions appropriately under conditions of hypoxia and inflammation is largely unknown. We investigated the effect of inflammation and hypoxia on the MGO pathway in humans in vivo. Methods: After prehydration with glucose 2.5% solution, ten healthy males were exposed to hypoxia (arterial saturation 80-85%) for 3.5 h using an air-tight respiratory helmet, ten males to experimental endotoxemia (LPS 2 ng/kg i.v.), ten males to LPS+hypoxia and ten males to none of these interventions (control group). Serial blood samples were drawn, and glyoxalase-1 mRNA expression, MGO, methylglyoxal-derived hydroimidazolone-1 (MG-H1), D-lactate and L-lactate levels, were measured serially. Results: Glyoxalase-1 mRNA expression decreased in the LPS (ß (95%CI); -0.87 (-1.24; -0.50) and the LPS+hypoxia groups; -0.78 (-1.07; -0.48) (P<0.001). MGO was equal between groups, whereas MG-H1 increased over time in the control group only (P=0.003). D-Lactate was increased in all four groups. L-Lactate was increased in all groups, except in the control group. Conclusion: Systemic inflammation downregulates glyoxalase-1 mRNA expression in humans. This is a possible mechanism leading to cell damage and multi-organ failure in critical illness with potential for intervention. [ABSTRACT FROM AUTHOR]

Sepsis is a global health care problem with a high mortality. Early death seems common; however, data are sparse. The objective of the present study was to report causes and influencing factors of early death in sepsis and septic shock. All septic ICU patients were included from 2012 to 2017. Early death was predefined as occurring within 48 h. Causes and factors leading up to death were reported by a panel of four intensivists, independently reviewing the medical files. Following factors were assessed: (1) delay in ICU admission; (2) futile ICU treatment; (3) missed diagnosis or inadequate treatment on the ICU. Fleiss kappa was used to assess inter-observer agreement. 1107 septic patients (APACHE II score 25 ± 8) were included. 344 patients died of which 97 (28%) within 48 h. In 33% an autopsy was performed. Primary causes of early death were multiple organ failure, mesenteric ischaemia and death after cardio-pulmonary resuscitation (CPR). Delay in ICU admission was scored in 32% of early deaths with slight agreement (κ = 0.180), futile ICU treatment in 29% with moderate agreement (κ = 0.415) and missed diagnosis or treatment in 7% of cases with slight agreement (κ = 0.122). Early death after ICU admission in sepsis is common and primarily caused by multiple organ failure, mesenteric ischaemia and death after unsuccessful CPR. Influencing factors were delay in ICU admission and futile ICU admission. Fleiss kappa indicates substantial variability in clinical judgement between intensivists, strengthening the necessity for shared decision making. [ABSTRACT FROM AUTHOR]