Anesthesiology最新文献

Background: Midazolam is a short-acting benzodiazepine frequently used in the perioperative setting. This study aimed to investigate the potential impact of intraoperative midazolam on postoperative delirium (POD) in older patients undergoing non-cardiac surgery.

Methods: This study included patients aged ≥ 65 years who received general anaesthesia between April 2020 and April 2022 in multiple hospitals across China. POD occurring within 7 days was assessed using the 3-minute Diagnostic Interview for Confusion Assessment Method (3D-CAM). Univariable and multivariable logistic regression models based on the random effects were used to determine the association between midazolam administration and the occurrence of POD, presented as risk ratio (RR) and 95% confidence intervals (CI). Kaplan-Meier cumulative incidence curve was plotted to compare the distribution of time to POD onset between patients who received midazolam and those who did not. Subgroup analyses based on specific populations were performed to explore the relationship between midazolam and POD.

Results: In all, 5,663 patients were included, of whom 723 (12.8%) developed POD. Univariate and multivariable logistic regression analyses based on random effects of different hospitals showed no significant association between midazolam medication and POD among older population (unadjusted RR=0.96, 95% CI: 0.90-1.30, P=0.38; adjusted RR=1.09, 95% CI: 0.91-1.33, P=0.35). Kaplan-Meier curve showed no difference in the distribution of time to POD onset (Hazard ratio [HR]=1.02, 95%CI: 0.88-1.18, P=0.82). The results of subgroup analyses found that intraoperative midazolam treatment was not associated with POD in the specific subgroups of patients.

Conclusions: Intraoperative administration of midazolam may not be associated with an increased risk of POD in older patients undergoing non-cardiac surgery.

Background: Recent evidence indicates that general anesthesia and sleep-wake behavior share some overlapping neural substrates. GABAergic neurons in the central amygdala (CeA) have a high firing rate during wakefulness and play a role in regulating arousal-related behaviors. The objective of this study is to investigate whether CeA GABAergic neurons participate in the regulation of isoflurane general anesthesia and uncover the underlying neural circuitry.

Methods: Fiber photometry recording was used to determine the changes in calcium signals of CeA GABAergic neurons during isoflurane anesthesia in Vgat-Cre mice. Chemogenetic and optogenetic approaches were used to manipulate the activity of CeA GABAergic neurons, and a righting reflex test was used to determine the induction and emergence from isoflurane anesthesia. Cortical electroencephalogram (EEG) recording was used to assess the changes in EEG spectral power and burst-suppression ratio during 0.8% and 1.4% isoflurane anesthesia, respectively. Both male and female mice were used in this study.

Results: The calcium signals of CeA GABAergic neurons decreased during the induction of isoflurane anesthesia and was restored during the emergence. Chemogenetic activation of CeA GABAergic neurons delayed induction time (mean ± SD, vehicle vs. clozapine-N-oxide: 58.75±5.42 s vs. 67.63±5.01 s; n=8, P=0.0017) and shortened emergence time (385.50±66.26 s vs. 214.60±40.21 s; n=8, P=0.0017) from isoflurane anesthesia. Optogenetic activation of CeA GABAergic neurons produced a similar effect. Furthermore, optogenetic activation decreased EEG delta power (Pre-stim vs. Stim: 46.63%±4.40% vs. 34.16%±6.47%; n=8, P=0.0195) and burst-suppression ratio (83.39%±5.15% vs. 52.60%±12.98%; n=8, P=0.0002). Moreover, optogenetic stimulation of terminals of CeA GABAergic neurons in the basal forebrain (BF) also promoted cortical activation and accelerated behavioral emergence from isoflurane anesthesia.

Conclusions: Our results suggest that CeA GABAergic neurons play a role in general anesthesia regulation, which facilitates behavioral and cortical emergence from isoflurane anesthesia through the GABAergic CeA-BF pathway.

Background: Diaphragm dysfunction is common in intensive care unit and associated with weaning failure and mortality. Diagnosis gold standard is the transdiaphragmatic or tracheal pressure induced by magnetic phrenic nerve stimulation. However, the equipment is not commonly available and requires specific technical skills. We aimed to evaluate ultrasound guided transcutaneous phrenic nerve stimulation for daily bedside assessment of diaphragm function by targeted electrical phrenic nerve stimulation.

Methods: In this randomized cross-over study we compared a new method of ultrasound guided transcutaneous electrical phrenic nerve stimulation (SONOTEPS method) using a peripheral nerve stimulator, with the magnetic phrenic nerve stimulation. Intensive care unit adult patients under mechanical ventilation with a Richmond-Agitation-Sedation-Scale score of -4 or -5 were included. Each patient received the two methods of stimulation, in a randomized order. The primary outcome was the tracheal pressure (Ptrach) induced by stimulation.

Results: We analyzed 232 measures of Ptrach from 116 patients of whom 77 presented a diaphragm dysfunction (Ptrach < 11 cmH2O) and 50 a severe diaphragm dysfunction (Ptrach < 8 cmH2O). The Passing-Bablok regression showed no significant differences (intercept A of -0.03 [CI95:-0.83-0.52] and slope B of 0.98 [CI95:0.90-1.05]) between SONOTEPS method and magnetic stimulation which were positively correlated (R²=0.639). The mean bias was -1.08 (CI95 5.02, -7.18) cmH2O. The receiver operating curves showed an excellent performance for the diagnosis of diaphragm dysfunction and severe diaphragm dysfunction with respectively an area under curve of 0.90 (CI95 0.83-0.97) and 0.88 (CI95 0.82-0.95). This performance was not significantly affected by the body mass index or the presence of a neck catheter.

Conclusions: The SONOTEPS method is a simple and accurate tool for bedside assessment of diaphragm function with ultrasound guided transcutaneous phrenic nerve stimulation in sedated patients with no or minimal spontaneous respiratory activity.