Billeklitgaard0560

Acidosis and higher lactate predict worse outcomes in cardiogenic shock (CS) patients. We sought to determine whether overall acidosis severity on admission predicted in-hospital mortality in CS patients.

This retrospective descriptive analysis included CS patients admitted to a single academic tertiary cardiac intensive care unit from 2007 to 2015. Admission arterial pH, base excess and anion gap values were used to generate a Composite Acidosis Score (range 0 to 5, with a score ≥2 defining Severe Acidosis). Adjusted in-hospital mortality was analyzed using multivariable logistic regression.

We included 1065 patients with median age of 68.9 (59.0, 77.2) years (36.4% females). Concomitant diagnoses included cardiac arrest in 38.1% and acute coronary syndrome in 59.1%. Severe Acidosis was present in 35.2%, and these patients had worse shock and more organ failure. In-hospital mortality occurred in 34.1% and was higher among patients with Severe Acidosis (54.9% vs. 22.4%, adjusted OR 2.01, 95% CI 1.43-2.83, p < 0.001). Increasing Composite Acidosis Score was associated with higher in-hospital mortality (adjusted OR 1.25 per point, 95% CI 1.11-1.40, p < 0.001). Severe Acidosis was associated with higher hospital mortality at every level of shock severity and organ failure (all p < 0.05). Admission lactate level had equivalent discrimination for in-hospital mortality as the Composite Acidosis Score (0.69 vs. 0.66; p = 0.32 by De Long test).

Given its incremental association with higher in-hospital mortality among CS patients beyond shock severity and organ failure, we propose severe acidosis as a marker of hemometabolic shock. Lactate levels performed as well as a composite measure of acidosis for predicting mortality.

Given its incremental association with higher in-hospital mortality among CS patients beyond shock severity and organ failure, we propose severe acidosis as a marker of hemometabolic shock. Lactate levels performed as well as a composite measure of acidosis for predicting mortality.

The impact of albumin resuscitation on sepsis outcomes is debated, particularly in the initial phase of resuscitation. We aimed to investigate the association between albumin use in the initial six hours of resuscitation and subsequent outcomes in adult septic patients.

This single-center, retrospective, propensity score-matched cohort study included adult patients admitted to intensive care units (ICUs) with sepsis or septic shock from January 1, 2006, to May 4, 2018, at a tertiary referral hospital. We compared two groups based on albumin receipt within the initial six resuscitation hours (albumin group vs. non-albumin group). We performed a 12 propensity score matching to assess shock-free time in ICU as the primary outcome.

Of 2,732 patients with medical sepsis, 286 cases in the albumin group were matched with 549 individuals in the non-albumin group. Compared to the non-albumin group, the albumin group required more intravenous fluids and had higher net fluid balance, lower mean arterial pressure, and lower serum base excess level in the initial 6 and 24 hours of resuscitation. Shock-free time, ICU and hospital length of stay, and 28-day mortality were not different between albumin and non-albumin groups (56 vs. 66 hours, P = 0.18; 3.5 vs. 3.7 days, P = 0.61; 9.1 vs. 9.5 days, P = 0.27; 36 vs. 32%, P = 0.25, respectively).

Using albumin during the initial six hours of resuscitation was not associated with benefits in clinical outcomes of patients with medical sepsis.

Using albumin during the initial six hours of resuscitation was not associated with benefits in clinical outcomes of patients with medical sepsis.

Extracorporeal membrane oxygenation (ECMO) use in patients with cardiac arrest is increasing. Utilization remains variable between centers using ECMO as a rescue therapy or early protocolized extracorporeal cardiopulmonary resuscitation.

Single-center, retrospective evaluation of cardiac arrest with cardiopulmonary resuscitation and rescue ECMO support from 2011 through 2019. Study objectives included survival, non-neurologic, and neurologic outcomes; validation of the SAVE and modified SAVE (mSAVE) scores for survival and favorable neurologic outcome; and predictive factor identification in cardiac arrest with ECMO rescue therapy.

89 patients were included. In-hospital survival was 38.2% and median CPC score was 2. Survivors had lower BMI (27.9 ± 4.2 kg/m2 vs 32.3 ± 7.5 kg/m2, p = 0.003), less obesity (BMI ≥30 kg/m2) (26.5% vs. 49.1%, p = 0.035), shorter CPR duration (35.5 ± 31.7m vs. AS-703026 datasheet 58.0 ± 49.5m, p = 0.019), more tracheostomy (38.2% vs. 7.3%, p < 0.001) and less renal replacement therapy (RRT) (17.6% vs. 38.2%, p = 0.031). Patients with a favorable neurologic outcome had lower body weight (86.2 ± 17.9 kg vs. 98.1 ± 19.4 kg, p = 0.010), lower BMI (28.1 ± 4.5 kg/m2 vs. 33.9 ± 7.9 kg/m2, p < 0.001), and less obesity (29.7% vs. 56.3%, p = 0.026). mSAVE score predicted in-hospital survival (OR 1.11; 95%CI 1.03-1.19; p = 0.004) and favorable neurologic outcome (OR 1.11; 1.03-1.20; p = 0.009). Multivariate analysis for in-hospital survival included mSAVE, BMI, CPR-time, Tracheostomy, and RRT (c-statistic 0.864). Favorable neurologic outcome included mSAVE and BMI (c-statistic 0.805).

mSAVE, BMI, RRT, and tracheostomy are predictors of in-hospital survival and mSAVE and BMI are predictors of favorable neurologic outcome in cardiac arrest with ECMO rescue therapy.

mSAVE, BMI, RRT, and tracheostomy are predictors of in-hospital survival and mSAVE and BMI are predictors of favorable neurologic outcome in cardiac arrest with ECMO rescue therapy.

To explore the role of LBP in metabolism and optimize sepsis treatment.

A sepsis model was established by injecting LPS into LBP-/- rats and WT rats and observing changes in the liver over time (0 h, 1 h, 6 h, and 24 h).

Detecting liver inflammation and injury. Optimizing the treatment of sepsis.

WT rats and LBP-/- rats.

We established a sepsis model by injecting LPS intravenously.

First, we induced sepsis in WT and LBP-/- rats with LPS. The rats were sacrificed, and serum and liver samples were collected at 1 h, 6 h and 24 h after LPS injection. We found that the deletion of LBP reduced LPS-induced liver inflammation and injury at 1 h and 6 h. Ballooning degeneration was clearly present in LBP-/- rat livers at 24 h after LPS injection. We found that mitochondrial damage and ROS levels were higher in LBP-/- rat livers than in WT rat livers at 24 h after LPS injection. According to the transcriptomic results, the PPAR pathway may be the reason for lesions in LBP-/- rats. To further investigate the function of PPARα in sepsis, we inhibited mTOR with rapamycin and examined mitochondrial injury and ROS levels.