Background: Sepsis is a deadly disease worldwide. Effective treatment strategy of sepsis remains limited. There still was a controversial about association between preadmission metformin use and mortality in sepsis patients with diabetes. We aimed to assess sepsis-related mortality in patients with type 2 diabetes (T2DM) who were preadmission metformin and non-metformin users.Methods: The patients with sepsis and T2DM were included from Medical Information Mart for Intensive Care -III database. Outcome was 30-day mortality. We used multivariable Cox regression analyses to calculate adjusted hazard ratio (HR) with 95% CI.Results: We included 2,383 sepsis patients with T2DM (476 and 1,907 patients were preadmission metformin and non-metformin uses) between 2001 and 2012. The overall 30-day mortality was 20.1% (480/2,383); it was 21.9% (418/1,907), and 13.0% (62/476) for non-metformin and metformin users, respectively. After adjusted for potential confounders, we found that preadmission metformin use was associated with 39% lower of 30-day mortality (HR = 0.61, 95% CI: 0.46–0.81, p = 0.007). In sensitivity analyses, subgroups analyses, and propensity score matching, the results remain stable.Conclusions: Preadmission metformin use may be associated with reduced risk-adjusted mortality in patients with sepsis and T2DM. It is worthy to further investigate this association.
BackgroundHemodynamic management is of paramount importance in patients with acute kidney injury (AKI). Central venous pressure (CVP) has been used to assess volume status. We intended to identify the optimal time window in which to obtain CVP to avoid the incidence of adverse outcomes in patients with AKI.MethodsThe study was based on the Medical Information Mart for Intensive Care (MIMIC) IV database. The primary outcome was in-hospital mortality. Secondary outcomes included the number of ICU-free days and norepinephrine-free days at 28 days after ICU admission, and total fluid input and fluid balance during the first and second day. A time–dose–response relationship between wait time of CVP measurement and in-hospital mortality was implemented to find an inflection point for grouping, followed by propensity-score matching (PSM), which was used to compare the outcomes between the two groups.ResultsTwenty Nine Thousand and Three Hundred Thirty Six patients with AKI were enrolled, and the risk of in-hospital mortality increased when the CVP acquisition time was >9 h in the Cox proportional hazards regression model. Compared with 8,071 patients (27.5%) who underwent CVP measurement within 9 h and were assigned to the early group, 21,265 patients (72.5%) who delayed or did not monitor CVP had a significantly higher in-hospital mortality in univariate and multivariate Cox regression analyses. After adjusting for potential confounders by PSM and adjusting for propensity score, pairwise algorithmic, overlap weight, and doubly robust analysis, the results were still stable. The HRs were 0.58–0.72, all p < 0.001. E-value analysis suggested robustness to unmeasured confounding.ConclusionsAmong adults with AKI in ICU, increased CVP wait time was associated with a greater risk of in-hospital mortality. In addition, early CVP monitoring perhaps contributed to shortening the length of ICU stays and days of norepinephrine use, as well as better fluid management.
Background: the optimal timing of Transthoracic echocardiography (TTE) performance for patients with septic shock remains unexplored. Methods: a retrospective cohort study included patients with septic shock in the MIMIC-Ⅲ database. Risk-adjusted restricted cubic splines modeled the 28-day mortality according to time elapsed from ICU admission to receive TTE. The cut point when a smooth curve inflected was selected to define early and delayed group. We applied propensity score matching (PSM) to ensure our findings were reliable. Causal mediation analysis was used to assess the intermediate effect of fluid balance within 72 h after ICU admission. Results: 3264 participants were enrolled and the risk of 28-day mortality increased until the wait time was around 10 h (Early group) and then was relatively flat afterwards (Delayed group). A beneficial effect of early TTE in terms of the 28-day mortality was observed (HRs 0.73–0.78, all p < 0.05) in the PSM. The indirect effect brought by the fluid balance on day 2 and 3 was significant (both p = 0.006). Conclusion: early TTE performance might be associated with lower risk-adjusted 28-day mortality in patients with septic shock. Better fluid balance may have mediated this effect. A wait time within 10 h after ICU may represent a threshold defining progressively increasing risk.
Background: Acute kidney injury (AKI) is a major health problem affecting millions of people worldwide. Effective preventative and therapeutic treatments remain to be produced. We aim to determine the association between blood glucose and mortality in critical patients with AKI. Method: This cohort study included 18,703 patients with AKI. The exposure of interest was baseline blood glucose. The outcome was 30-day mortality. Multivariable Cox regression analyses and smooth curve fitting were adopted to assess the independent association between blood glucose and 30-day mortality. Results: We identified 18,703 consecutive individuals with AKI. The average age of the participants was 66.8 ± 16.0 years, and about 42.7% of them were female. The overall 30-day mortality was 16.9%. Through the multivariate COX regression model and smooth curve fitting, we observed that the correlation between blood glucose and 30-day mortality is nonlinear. An inflection point was found at about 5.93 mmol/L. On the left side of inflection point, the effect size was 0.81 (HR: 0.81, 95% CI 0.74-0.89, p < 0.001). On the right side of inflection point, the effect size was 1.02 (HR: 1.02,95% CI 1.01-1.03, p < 0.001). Conclusion: Our study suggested that, among patients with AKI, there was a nonlinearity relationship between blood glucose and mortality in patients with AKI. The optimal of blood glucose associated with the lowest risk of 30-day mortality was around 5.93 mmol/L.
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