A novel stimulating electrode attachment method designed to maintain electromyography-based neuromuscular monitoring detectability during laparoscopic surgery: a single-center randomized, double-blind, controlled pilot study.

PURPOSE: We evaluated the electromyography (EMG)-based neuromuscular monitoring detectability of our novel stimulating electrode attachment method compared to the original Nihon-Kohden (Tokyo, Japan) attachment method. METHODS: This single-center randomized, double-blind, controlled pilot study enrolled 32 patients aged ≥ 18 years, undergoing scheduled laparoscopic surgery. The EMG electrode NM-345Y™ was attached to one forearm using the Nihon-Kohden method (Pattern N-K) and the other forearm using our novel method (Pattern Cross). The allocation to each attachment method was determined post-randomization. In Pattern Cross, the NM-345Y™ was attached such that the line connecting the anode and cathode crosses the ulnar nerve. Patients received 0.9 mg/kg rocuronium after calibration with the forearm in 90-degree supination. Following tracheal intubation, the forearm was positioned in 0-degree pronation. Intraoperatively, 0.2 mg/kg rocuronium was administered if the train-of-four (TOF) count one persisted for 1 min on either side. Post-surgery, the forearm position was returned to 90-degree supination, and rocuronium was antagonized with sugammadex. TOF and post-tetanic count (PTC) were simultaneously measured bilaterally every 15 s and 5 min, respectively, from post-calibration to tracheal extubation. RESULTS: The time to first PTC appearance was significantly shorter by 33 min in the Pattern Cross group than in the Pattern N-K group (95% Confidence interval: 1-66, p = 0.043). Following sugammadex administration, TOF ratios ≥ 0.9 were achieved in 72% of patients in the Pattern N-K group and 97% of those in the Pattern Cross group (p = 0.025). CONCLUSIONS: Crossing the line connecting the anode and cathode with the ulnar nerve stabilizes EMG-based neuromuscular monitoring detectability.

Effect of remimazolam on the incidence of delirium after transcatheter aortic valve implantation under general anesthesia: a retrospective exploratory study.

PURPOSE: Delirium after transcatheter aortic valve implantation (TAVI) should be prevented because it is associated with worse patient outcomes. Perioperative administration of benzodiazepines is a risk factor for postoperative delirium; however, the association between remimazolam, a newer ultrashort-acting benzodiazepine for general anesthesia, and postoperative delirium remains unclear. This study aimed to evaluate whether remimazolam administration during TAVI under general anesthesia affected the incidence of postoperative delirium. METHODS: This single-center retrospective study recruited all adult patients who underwent transfemoral TAVI (TF-TAVI) under general anesthesia between March 2020 and May 2022. Patients were divided into the remimazolam (R) and propofol (P) groups according to the sedative used for anesthesia. In the R group, all patients received flumazenil after surgery. The primary endpoint was the incidence of delirium within 3 days after surgery. Factors associated with delirium after TF-TAVI were examined by multiple logistic regression analysis. RESULTS: Ninety-eight patients were included in the final analysis (R group, n = 40; P group, n = 58). The incidence of postoperative delirium was significantly lower in the R group than in the P group (8% vs. 26%, p = 0.032). Multiple logistic regression analysis revealed that remimazolam (odds ratio 0.17, 95% CI 0.04-0.80, p = 0.024) was independently associated with the incidence of postoperative delirium, even after adjustment for age, sex, preoperative cognitive function, history of stroke, and TF-TAVI approach. CONCLUSION: Remimazolam may benefit TF-TAVI in terms of postoperative delirium; however, its usefulness must be further evaluated in extensive prospective studies.

Association between Enterocyte Injury and Mortality in Patients on Hemodialysis Who Underwent Cardiac Surgery: An Exploratory Study.

BACKGROUND: Intestinal ischemia and enterocyte injury are significant causes of death after cardiac surgery. Hemodialysis is a well-known risk factor for intestinal ischemia. However, the relationship between enterocyte injury and mortality is unclear. This exploratory study assessed the association between intestinal fatty acid-binding protein (I-FABP), a specific marker of enterocyte injury, at intensive care unit (ICU) admission and in-hospital mortality in patients on hemodialysis who underwent cardiac surgery with cardiopulmonary bypass. MATERIALS AND METHODS: Forty-seven consecutive patients on long-term hemodialysis who underwent elective cardiac surgery (median age, 70 y; men, 27 [57%]) were prospectively enrolled. The association between serum I-FABP levels at ICU admission and in-hospital mortality was compared with the associations between serum I-FABP levels and prognostic severity scores, vasoactive-inotropic scores, and lactate levels. RESULTS: Only I-FABP levels at ICU admission were significantly related to in-hospital mortality (odds ratio, 5.54; 95% confidence interval [CI], 1.08-28.43) in the simple logistic regression analysis. Univariate and multiple linear regression analyses indicated prolonged cardiopulmonary bypass (ρ, 0.49; 95% CI, 0.15-0.83), higher mean norepinephrine dose (ρ, 0.07; 95% CI, 0.02-0.12), lower mean dopamine dose (ρ, -0.51; 95% CI, -0.94 to -0.08), and intra-aortic balloon pump use (ρ, 3.63; 95% CI, 1.68-5.59) were significant risk factors for high I-FABP levels. CONCLUSIONS: Enterocyte injury at ICU admission was associated with in-hospital mortality after cardiac surgery for patients on hemodialysis. Intraoperative hidden hypoperfusion of the intestine may impact prognoses. Enterocyte injury prevention, early diagnosis, and intervention for intestinal ischemia might be required to improve outcomes.

Sevoflurane has postconditioning as well as preconditioning properties against hepatic warm ischemia-reperfusion injury in rats.

PURPOSE: Ischemia-reperfusion (IR) injury is inevitable after liver transplantation and liver resection with inflow occlusion. Sevoflurane has been widely used during hepatobiliary surgery and was reported to exhibit preconditioning (PreC) properties against hepatic IR injury; however, its postconditioning (PostC) properties remain unknown. This study examined whether a clinically applicable dose of sevoflurane has PostC and PreC properties against hepatic IR injury and roles of heme oxygenase-1 (HO-1). METHODS: Warm ischemia was induced in male Wistar rats, excluding the sham group, for 1 h, followed by 3 h of reperfusion. Group C received propofol from 60 min before ischemia until the end of the experimental procedure. In the SPreC and SPostC groups, propofol was replaced by 2.5% sevoflurane for 30 min from 35 min before ischemia in the SPreC group and for 30 min from 5 min before reperfusion in the SPostC group. The SPreC+Z and SPostC+Z groups received a HO-1 inhibitor, zinc protoporphyrin (Znpp), 60 min before ischemia, and sevoflurane PreC and PostC were induced. RESULTS: Serum aspartate aminotransferase, alanine aminotransferase, and lactic dehydrogenase levels, and histological damage scores in the SPreC and SPostC groups were significantly lower than those in group C. Inhibiting HO-1 with Znpp partially blocked these protective effects of sevoflurane. Sevoflurane PreC and PostC significantly increased the number of HO-1-positive Kupffer cells in comparison with group C, and Znpp prevented sevoflurane-induced HO-1 expression. CONCLUSION: PostC and PreC by sevoflurane at a clinically applicable dose have equally protective effects against hepatic IR injury by increasing HO-1 expression.

Inhalation of hydrogen gas protects against myocardial stunning and infarction in swine.

OBJECTIVES: The present study was carried out to determine whether inhalation of hydrogen (H(2)) gas protects myocardium against ischemia-reperfusion (I/R) injury in swine. DESIGN: In anesthetized open-chest swine, myocardial stunning was produced by 12-minute occlusion of left anterior descending coronary artery (LAD) followed by 90-minute reperfusion in the first study. Group A inhaled 100% oxygen, and group B inhaled 2% H(2) plus 98% oxygen during ischemia and reperfusion. In the second study, myocardial infarction was produced by 40-minute occlusion of LAD followed by 120-minute reperfusion. Group C inhaled 100% oxygen during ischemia and reperfusion. Group D inhaled 2% H(2) plus 98% oxygen. Group E inhaled 4% H(2) plus 96% oxygen. RESULTS: The change of segment shortening (%SS) from baseline at 90 minutes after reperfusion in group B was 74 ± 13 (mean ± SD) %, which was significantly higher than that in group A (48 ± 15%). Myocardial infarct size in group E (32 ± 10%), but not in group D (40 ± 9%) was smaller than that in group C (46 ± 6%). CONCLUSIONS: Inhalation of 2% H(2) gas improves myocardial stunning, and inhalation of 4% but not 2% H(2) gas reduces myocardial infarct size in swine.

Postischemic infusion of sivelestat sodium hydrate, a selective neutrophil elastase inhibitor, protects against myocardial stunning in swine.

PURPOSE: It seems controversial whether or not neutrophil elastase inhibitors are effective in attenuating myocardial ischemia/reperfusion injury. We thus investigated possible protective effects of sivelestat, a neutrophil elastase inhibitor, against myocardial stunning i.e., prolonged myocardial dysfunction following a brief episode of ischemia. METHODS: Swine were divided into control group (group C), low-dose sivelestat group (group L), and high-dose sivelestat group (group H) (n = 7 for each group). All the swine were subjected to myocardial ischemia through ligation of the left anterior descending (LAD) coronary artery for 12-min, followed by 90-min reperfusion. Sivelestat was infused intracoronally at concentrations of 6 and 60 mg/ml throughout the reperfusion period in groups L and H, respectively, while saline was infused in the group C. Heart rate (HR), left ventricular developed pressure (LVdP), maximum rate of LVdP (LVdP/dt (max)), LV end-diastolic pressure (LVEDP), percentage of segment shortening (%SS, an index of regional myocardial contractility), and coronary venous interleukin-6 concentration in the LAD perfusion area were measured before ischemic induction and during reperfusion. RESULTS: The ischemia/reperfusion insult did not cause any significant changes in HR, LVdP, LVdP/dt (max), and LVEDP in all groups. However, it significantly reduced %SS in the LAD perfusion area and increased the interleukin-6 concentration in group C. Those changes in %SS and the interleukin-6 concentration were both greatly attenuated, but not prevented, in groups L and H. CONCLUSION: Sivelestat presumably attenuates myocardial contractile dysfunction due to myocardial stunning by inhibiting neutrophil-derived elastase, thereby suppressing the production of interleukin-6 in activated neutrophils.