Radiomic analysis of abdominal organs during sepsis of digestive origin in a French intensive care unit

Background Sepsis is a severe and common cause of admission to the intensive care unit (ICU). Radiomic analysis (RA) may predict organ failure and patient outcomes. The objective of this study was to assess a model of RA and to evaluate its performance in predicting in-ICU mortality and acute kidney injury (AKI) during abdominal sepsis. Methods This single-center, retrospective study included patients admitted to the ICU for abdominal sepsis. To predict in-ICU mortality or AKI, elastic net regularized logistic regression and the random forest algorithm were used in a five-fold cross-validation set repeated 10 times. Results Fifty-five patients were included. In-ICU mortality was 25.5%, and 76.4% of patients developed AKI. To predict in-ICU mortality, elastic net and random forest models, respectively, achieved areas under the curve (AUCs) of 0.48 (95% confidence interval [CI], 0.43–0.54) and 0.51 (95% CI, 0.46–0.57) and were not improved combined with Simplified Acute Physiology Score (SAPS) II. To predict AKI with RA, the AUC was 0.71 (95% CI, 0.66–0.77) for elastic net and 0.69 (95% CI, 0.64–0.74) for random forest, and these were improved combined with SAPS II, respectively; AUC of 0.94 (95% CI, 0.91–0.96) and 0.75 (95% CI, 0.70–0.80) for elastic net and random forest, respectively. Conclusions This study suggests that RA has poor predictive performance for in-ICU mortality but good predictive performance for AKI in patients with abdominal sepsis. A secondary validation cohort is needed to confirm these results and the assessed model

Protracted immune disorders at one year after ICU discharge in patients with septic shock

Abstract Background Sepsis is a leading cause of mortality and critical illness worldwide and is associated with an increased mortality rate in the months following hospital discharge. The occurrence of persistent or new organ dysfunction(s) after septic shock raises questions about the mechanisms involved in the post-sepsis status. The present study aimed to explore the immune profiles of patients one year after being discharged from the intensive care unit (ICU) following treatment for abdominal septic shock. Methods We conducted a prospective, single-center, observational study in the surgical ICU of a university hospital. Eighty-six consecutive patients admitted for septic shock of abdominal origin were included in this study. Fifteen different plasma biomarkers were measured at ICU admission, at ICU discharge and at one year after ICU discharge. Three different clusters of biomarkers were distinguished according to their functions, namely: (1) inflammatory response, (2) cell damage and apoptosis, (3) immunosuppression and resolution of inflammation. The primary objective was to characterize variations in the immune status of septic shock patients admitted to ICU up to one year after ICU discharge. The secondary objective was to evaluate the relationship between these biomarker variations and patient outcomes. Results At the onset of septic shock, we observed a cohesive pro-inflammatory profile and low levels of inflammation resolution markers. At ICU discharge, the immune status demonstrated decreased but persistent inflammation and increased immunosuppression, with elevated programmed cell death protein-1 (PD-1) levels, and a counterbalanced resolution process, with elevated levels of interleukin-10 (IL-10), resolvin D5 (RvD5), and IL-7. One year after hospital discharge, homeostasis was not completely restored with several markers of inflammation remaining elevated. Remarkably, IL-7 was persistently elevated, with levels comparable to those observed after ICU discharge, and PD-1, while lower, remained in the elevated abnormal range. Conclusions In this study, protracted immune disturbances were observed one year after ICU discharge. The study results suggested the presence of long-lasting immune illness disorders following a long-term septic insult, indicating the need for long-term patient follow up after ICU discharge and questioning the use of immune intervention to restore immune homeostasis after abdominal septic shock

Local and systemic innate immune response to secondary human peritonitis. Influence of micro-organism.

International audienceINTRODUCTION: 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. METHODS: Peritoneal and plasma cytokines (IL-1, tumour necrosis factor alpha [TNFalpha], IL-6, IL-10, and IFN) were measured in 66 patients with secondary peritonitis. RESULTS: The concentration ratio between peritoneal fluid and plasma cytokines varied from 5 [2 - 21] (IFN) to 1310 [145 - 3888] (IL-1). There was no correlation between plasma and peritoneal fluid concentration of any cytokine. In the plasma, TNFalpha, IL-6, IFN, and IL-10 were higher in patients with shock versus no shock, and in nonsurvivors versus survivors (p[less than or equal to]0.03). There was no differential plasma release for any cytokine between community-acquired and postoperative peritonitis. Presence of anaerobes or Enterococcus specie in peritoneal fluid was associated with higher plasma TNFalpha: 50 [37-106] vs 38 [29-66] and 45 [36 - 87] vs 39 [27 - 67] pg/ml, respectively (p=0.02). In the peritoneal compartment, occurrence of shock did not result in any difference in peritoneal cytokines. Peritoneal IL-10 was higher in patients who survived (1505 [450 to 3130] vs 102 [9 to 710] pg/ml; p=0.04). Presence of anaerobes and Enterococcus specie was associated with higher peritoneal IFN: 2 [1-6] vs 10 [5-28] and 7 [2-39] vs 2 [1-6], p=0.01 and 0.05 respectively). CONCLUSIONS: Peritonitis triggers an acute systemic and peritoneal innate immune response with a simultaneous release of pro and anti-inflammatory cytokines. Greater 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

Additional file 1: Table S1. of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

p Values of the two-way ANOVA comparing cellular counts over time between survivors and nonsurvivors. (DOC 21 kb

Additional file 4: of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Figure S4. In-ICU early death cumulative incidence of abdominal (n=99) and extra-abdominal (n=31) septic shock groups Figure S5. Cumulative incidence of death for patients alive at day 5 and still hospitalized in ICU according to the variation from Day 1-to-5 of NLCR. (DOC 21 kb

Additional file 3: of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Table S3. Neutrophils, lymphocytes counts and NLCR variations according to the septic origin ( abdominal vs extra-abdominal) and death timing. (DOC 21 kb

Additional file 2: Table S2. of Reversal of neutrophil-to-lymphocyte count ratio in early versus late death from septic shock

Area under the receiver operating characteristic (ROC) curve for cellular counts to predict death. (DOC 21 kb