The aim of this study was to evaluate an association between nutritional biomarkers and prognosis in septic patients. We retrospectively searched the association between nutritional biomarkers including serum albumin (Alb), total protein (TP), total cholesterol (T-chol), and cholinesterase (ChE), and prognosis for septic patients treated in the ICU for >7 days. We used time-dependent Cox proportional hazard regression analysis to resolve the difference of the statistical weight of each day's data for all 14 consecutive days among individual sepsis patients. The covariates were based on the minimum moving values determined from 1 day, 3 days, 7 days, and 14 days of serial data. The values of these covariates and ICU survival were considered as outcomes. We included 136 septic patients. The decreases in the values of Alb, TP, T-chol, and ChE were significantly associated with the risk of death in the septic patients (p < .05). Especially, the daily changes of Alb were significantly associated with mortality during the ICU stay (p < .05). We found that the changes in serial data of the nutritional markers of Alb, TP, T-chol, and ChE reflected the higher risk of death in patients with prolonged sepsis.

Cerebral oximetry (rSO2) may be useful in assessing the probability of return of spontaneous circulation (ROSC). However, the potential of assessing the trend in the rSO2 value has not been discussed when determining the probability of ROSC. This was a retrospective study of out-of-hospital cardiac arrest (OHCA) patients with continuous rSO2 values recorded during cardiopulmonary arrest. We used logistic regression analysis at each time point to investigate the best subsets of rSO2-related variables for ROSC, which included rSO2 (baseline), the baseline value of rSO2; amount of maximum rise, the maximum difference of rSO2 from rSO2 (baseline) over t minutes; ΔrSO2 (t):(amount of maximum rise)/rSO2 (baseline) over t minutes after hospital arrival. Among the 90 included patients, 35 achieved ROSC. Area under the curve (AUC) analysis revealed that ΔrSO2 over a 16-min measurement period was significantly higher than ΔrSO2 measured over 4-, 8-, 12-, and 20-min periods. During this 16-min period, the subset showing the best AUC value was interaction of the amount of maximum rise and rSO2 (baseline) rather than the amount of maximum rise or ΔrSO2 alone (AUC = 0.91). The combination of rSO2 (baseline) with the amount of maximum rise in rSO2 value over time might be a new index for the prediction of ROSC that could be useful in guiding cardiopulmonary resuscitation. Further studies are needed to validate these findings.

Deep vein thrombosis (DVT) is a major complication in critical care. There are various methods of prophylaxis, but none of them fully prevent DVT, and each method has adverse effects. Electrical muscle stimulation (EMS) could be a new effective approach to prevent DVT in intensive care unit (ICU) patients. We hypothesized that EMS increases the venous flow of the lower limbs and has a prophylactic effect against the formation of DVT. This study included 26 patients admitted to a single ICU. We enrolled patients who could not move themselves due to spinal cord injury, head injury, central nervous system abnormalities, and sedation for mechanical ventilation. The patients were randomly allocated to either the EMS group or the control group. Patients in the EMS group received 30-min sessions of EMS applied to the bilateral lower extremities on arbitrary days within 14 days after admission. The control patients received no EMS. The peak flow velocity and diameter of the popliteal vein (Pop.V) and common femoral vein (CFV) were measured by ultrasound and then the volumes of venous flow were calculated using a formula. There were no statistically significant differences in patient characteristics between the two groups except for the mortality rate. In the EMS group, the median and interquartile range (IQR, 25th–75th percentile) of velocities of the Pop.V and CFV were higher during EMS compared with at rest: 10.6 (8.0–14.8) vs 24.5 (15.1–37.8) cm/s and 17.0 (12.3–23.8) vs 24.3 (17.0–33.0) cm/s, respectively (p < 0.05). The median (IQR) of volumes of venous flow of the Pop.V and CFV at rest and during EMS were 4.2 (2.7–7.2) vs 8.6 (5.4–16.1) cm3/s and 12.9 (9.7–21.4) vs 20.8 (12.3–34.1) cm3/s, respectively (p < 0.05). There were no major complications related to EMS. EMS increased the venous flow of the lower limbs. EMS could be one potential method for venous thromboprophylaxis. UMIN000013642

The proportion of adult patients with return of spontaneous circulation (ROSC) following out-of-hospital cardiac arrest (OHCA) remains unchanged since 2012. A better resuscitation strategy is needed. This study evaluated the effectiveness of a regional cerebral oxygen saturation (rSO₂)-guided resuscitation protocol without rhythm check based on our previous study. Because defibrillation is the definitive therapy that should be performed without delay for shockable rhythm, the study subjects were OHCA patients with non-shockable rhythm on hospital arrival at three emergency departments. They were divided into three groups based on their baseline rSO₂ value (%): ≥50, ≥40 to <50, or <40. Continuous chest compression without rhythm checks was performed for 16 minutes or until a maximum increase in rSO₂ of 10%, 20%, or 35% was achieved in each group, respectively. This intervention cohort was compared with a historical control cohort regarding the probability of ROSC using inverse probability of treatment weighting (IPTW) with propensity score. The control and intervention cohorts respectively included 86 and 225 patients. The rate of ROSC was not significantly different between the groups (adjusted OR 0.91 [95% CI, 0.64-1.29], P = 0.60), but no serious adverse events occurred. Sensitivity analyses 1 and 2 showed a significant difference or positive tendency for higher probability of ROSC (adjusted OR 1.63 [95% CI, 1.22-2.17], P < 0.001) (adjusted OR 1.25 [95% CI, 0.95-1.63], P = 0.11). This trial suggested that a new cardiopulmonary resuscitation protocol with different rhythm check timing could be created using the rSO₂ value. Clinical trial number: UMIN000025684.

Background: Cardiac arrest (CA) can lead to neuronal degeneration and death through various pathways, including oxidative, inflammatory, and metabolic stress. However, current neuroprotective drug therapies will typically target only one of these pathways, and most single drug attempts to correct the multiple dysregulated metabolic pathways elicited following cardiac arrest have failed to demonstrate clear benefit. Many scientists have opined on the need for novel, multidimensional approaches to the multiple metabolic disturbances after cardiac arrest. In the current study, we have developed a therapeutic cocktail that includes ten drugs capable of targeting multiple pathways of ischemia–reperfusion injury after CA. We then evaluated its effectiveness in improving neurologically favorable survival through a randomized, blind, and placebo-controlled study in rats subjected to 12 min of asphyxial CA, a severe injury model. Results: 14 rats were given the cocktail and 14 received the vehicle after resuscitation. At 72 h post-resuscitation, the survival rate was 78.6% among cocktail-treated rats, which was significantly higher than the 28.6% survival rate among vehicle-treated rats (log-rank test; p = 0.006). Moreover, in cocktail-treated rats, neurological deficit scores were also improved. These survival and neurological function data suggest that our multi-drug cocktail may be a potential post-CA therapy that deserves clinical translation. Conclusions: Our findings demonstrate that, with its ability to target multiple damaging pathways, a multi-drug therapeutic cocktail offers promise both as a conceptual advance and as a specific multi-drug formulation capable of combatting neuronal degeneration and death following cardiac arrest. Clinical implementation of this therapy may improve neurologically favorable survival rates and neurological deficits in patients suffering from cardiac arrest.

Mitochondrial transplantation (MTx) has emerged as a potential therapeutic approach for diseases associated with mitochondrial dysfunction, yet its scalability and cross-species feasibility remain underexplored. This study aimed to evaluate the dose-dependent uptake and molecular effects of xenogeneic mitochondrial transplantation (xeno-MTx) using rat-derived mitochondria in mouse neuronal systems. HT-22 hippocampal neuronal cells and a murine model of cardiac arrest-induced global cerebral ischemia were used to assess mitochondrial uptake, gene expression, and mitochondrial DNA presence. Donor mitochondria were isolated from rat pectoralis muscle and labeled with MitoTracker dyes. Flow cytometry and confocal microscopy revealed a dose-dependent increase in donor mitochondrial uptake in vitro. Quantitative PCR demonstrated a corresponding increase in rat-specific mitochondrial DNA and upregulation of Mfn2 and Bak1, with no changes in other fusion, fission, or apoptotic genes. Inhibitor studies indicated that mitochondrial internalization may involve actin-dependent macropinocytosis and cholesterol-sensitive endocytic pathways. In vivo, rat mitochondrial DNA was detected in mouse brains post–xeno-MTx, confirming donor mitochondrial delivery to ischemic tissue. These findings support the feasibility of xeno-MTx and its dose-responsive biological effects in neuronal systems while underscoring the need for further research to determine long-term functional outcomes and clinical applicability.