Estimated plasma volume status as a simple and accessible predictor of 28-day mortality in septic shock: insights from a retrospective study of the MIMIC-IV database.

Background: Assessing volume status in septic shock patients is crucial for tailored fluid resuscitation. Estimated plasma volume status (ePVS) has emerged as a simple and effective tool for evaluating patient volume status. However, the prognostic value of ePVS in septic shock patients remains underexplored. Methods: The study cohort consisted of septic shock patients admitted to the ICU, sourced from the MIMIC-IV database. Patients were categorized into two groups based on 28-day survival outcomes, and their baseline characteristics were compared. According to the ePVS (6.52 dL/g) with a hazard ratio of 1 in the restricted cubic spline (RCS) analysis, patients were further divided into high and low ePVS groups. A multivariable Cox regression model was utilized to evaluate the association between ePVS and 28-day mortality rate. The Kaplan-Meier survival curve was plotted, and all-cause mortality was compared between the high and low groups using the log-rank test. Results: A total of 7,607 septic shock patients were included in the study, among whom 2,144 (28.2%) died within 28 days. A J-shaped relationship was observed between ePVS at ICU admission and 28-day mortality, with an increase in mortality risk noted when ePVS exceeded 6.52 dL/g. The high ePVS group exhibited notably higher mortality rates compared to the low ePVS group (28-day mortality: 26.2% vs. 30.2%; 90-day mortality: 35% vs. 42.3%). After adjustment for confounding factors, ePVS greater than 6.52 dL/g independently correlated with an increased risk of 28-day mortality (HR: 1.20, 95% CI: 1.10-1.31, p < 0.001) and 90-day mortality (HR: 1.25, 95% CI: 1.15-1.35, p < 0.001). Kaplan-Meier curves demonstrated a heightened risk of mortality associated with ePVS values exceeding 6.52 dL/g. Conclusion: A J-shaped association was observed between ePVS and 28-day mortality in septic shock patients, with higher ePVS levels associated with increased risk of mortality.

The Importance of Venous Reflux Status Evaluation in the Intensive Care Unit.

The current management approach for critically ill patients emphasizes maintaining adequate cardiac output and mean arterial pressure. Recently, researchers have increasingly emphasized the clinical significance of venous reflux. Bedside venous Doppler ultrasonography offers continuous, dynamic, and quantifiable assessment of the venous reflux status. In this review, we explore the pertinent literature on assessing the venous reflux status in critically ill patients. We propose a bedside ultrasonographic evaluation method that starts with the hepatic veins and progresses to the portal, renal and intrarenal, femoral, and pulmonary veins. The clinical significance of venous reflux status evaluation is discussed in terms of its effect on right ventricular function, the functioning of other organs, and the guidance of fluid therapy. Overall, we underscore the importance of venous reflux status evaluation in critically ill patients and highlight the benefits of incorporating bedside ultrasonography for the continuous monitoring of venous return.

A new sight for paraquat poisoning from immunology.

Paraquat (methyl viologen, PQ) is highly toxic to humans. Pulmonary fibrosis is the most common cause of death after PQ poisoning. However, no effective therapy is available. The current treatment dilemma and pathology suggest that we should reconsider how to treat the poisoning using other methods, such as immunization. Some clues indicate that immune mechanisms may play important roles in the pathology of PQ poisoning. We implemented a simple experiment to test the hypothesis that activated innate immunity was involved in acute lung injury induced by PQ. Six rats were randomly distributed to two groups: PQ poisoning group and Immunosuppression group (cyclophosphamide pretreatment). Forty-eight hours after PQ administration, rats were anesthetized. The right lungs were excised for histopathology. The experimental results confirmed that in the set of immune deficiency, the inflammatory response in Immunosuppression group could not be effectively triggered so the lung pathology was much better than PQ poisoning group. The immunopathogenic mechanism of PQ poisoning may be essentially a sterile inflammation triggered and amplified by damage-associated molecular patterns (DAMPs). If the hypothesis is established, it may change the therapeutic regimen of PQ poisoning and the prognosis of patients.