Effect of ultrasound-guided stellate ganglion block on cerebral oxygen metabolism and S100B protein during carotid endarterectomy.

OBJECTIVE: To investigate the effect of ultrasound-guided stellate ganglion block (SGB) on cerebral oxygen metabolism and serum S100B during carotid endarterectomy (CEA). METHODS: Patients who were prospectively enrolled to receive CEA under elective general anesthesia were randomized into an SGB group and a control group (ChiCTR2000033385). Before anesthesia, the SGB group underwent ipsilateral SGB under ultrasound guidance, while the control group did not. Ultrasound-guided right subclavian internal jugular vein catheterization was performed under general anesthesia. Mean arterial pressure (MAP) and heart rate (HR) were monitored at various time points (T0-T4). Arterial and internal jugular venous bulb blood were collected for blood gas analysis, determining jugular venous oxygen saturation (SjvO2), arteriovenous oxygen difference (AVDO2), cerebral oxygen extraction ratio (COER), lactate production rate (LPR), and lactate-oxygen index (LOI). The serum concentration of S100B in the internal jugular venous bulb at each time point was measured. RESULTS: The results revealed significantly lower HR during anesthesia induction and surgery in the SGB group, with more stable MAP and HR during endotracheal intubation and surgery compared to the control group (P<0.05). The control group exhibited decreases at T3 and a slight increase at T4. SjvO2 was significantly higher in the SGB group, while AVDO2 and COER gradually decreased over time, but they were significantly higher in the control group (P<0.05). LPR and LOI in both groups peaked at T3 and were significantly different between T4 and T2 (P<0.05). Serum S100B levels in both groups rose and then decreased at each time point, but they were consistently lower in the SGB group (P<0.05). CONCLUSION: SGB before CEA effectively suppresses the stress response, maintains intraoperative hemodynamic stability, improves brain tissue oxygen supply, and demonstrates a neuroprotective effect.

Current Progress on Neuroinflammation-mediated Postoperative Cognitive Dysfunction: An Update.

Postoperative cognitive dysfunction (POCD) is a common complication of the central nervous system (CNS) in elderly patients after surgery, showing cognitive changes such as decreased learning and memory ability, impaired concentration, and even personality changes and decreased social behavior ability in severe cases. POCD may appear days or weeks after surgery and persist or even evolve into Alzheimer's disease (AD), exerting a significant impact on patients' health. There are many risk factors for the occurrence of POCD, including age, surgical trauma, anesthesia, neurological diseases, etc. The level of circulating inflammatory markers increases with age, and elderly patients often have more risk factors for cardiovascular diseases, resulting in an increase in POCD incidence in elderly patients after stress responses such as surgical trauma and anesthesia. The current diagnostic rate of POCD is relatively low, which affects the prognosis and increases postoperative complications and mortality. The pathophysiological mechanism of POCD is still unclear, however, central nervous inflammation is thought to play a critical role in it. The current review summarizes the related studies on neuroinflammation-mediated POCD, such as the involvement of key central nervous cells such as microglia and astrocytes, proinflammatory cytokines such as TNF-α and IL-1ß, inflammatory signaling pathways such as PI3K/Akt/mTOR and NF-κB. In addition, multiple predictive and diagnostic biomarkers for POCD, the risk factors, and the positive effects of anti-inflammatory therapy in the prevention and treatment of POCD have also been reviewed. The exploration of POCD pathogenesis is helpful for its early diagnosis and long-term treatment, and the intervention strategies targeting central nervous inflammation of POCD are of great significance for the prevention and treatment of POCD.

Comparison of adjuvant pharmaceuticals for caudal block in pediatric lower abdominal and urological surgeries: A network meta-analysis.

STUDY OBJECTIVE: Caudal block helps relieve pain after sub-umbilical surgery in pediatric patients; however, the duration for which it exerts its analgesic effect is limited. The addition of certain adjuvant agents to local anesthetics (LAs) that are used to administer caudal block can prolong postoperative analgesia. Therefore, we aimed to compare the efficiencies and side effects of caudal adjuvants in the settings of pediatric lower abdominal and urological surgeries. DESIGN: A network meta-analysis (NMA). PATIENTS: One hundred and twelve randomized controlled trials (RCTs) involving 6800 pediatric patients were included in the final analysis. INTERVENTIONS: Different adjuvant agents, namely clonidine, dexamethasone, dexmedetomidine, fentanyl, ketamine, magnesium, midazolam, morphine, neostigmine, and tramadol. MEASUREMENTS: The primary outcome was the duration of analgesia. The secondary outcomes included the requirement for additional analgesia, analgesic consumption, and postoperative complications. The effects and rankings were evaluated using NMA and the surface under the cumulative ranking curve scores, respectively. RESULTS: Neostigmine, dexmedetomidine, and dexamethasone were found to be the three most effective adjuvants that prolong the duration of analgesia for caudal block, and these adjuvants extended this duration by 8.9 h (95% confidence interval [CI], 7.1-10.7), 7.3 h (95% CI, 6.0-8.6), and 5.9 h (95% CI, 4.0-7.7), respectively. Caudal neostigmine was associated with an increase in the incidence of postoperative nausea and vomiting, whereas dexmedetomidine and dexamethasone showed no postoperative complications. CONCLUSIONS: This NMA provided evidence and suggested that dexmedetomidine and dexamethasone may be the most beneficial adjuvant pharmaceutics adding to LAs for caudal block in children. However, given the off-label status of caudal dexmedetomidine and dexamethasone, further high-quality RCTs are still warranted, especially to determine whether delayed neurological complications will occur.

Mechanical power normalized to predicted body weight is associated with mortality in critically ill patients: a cohort study.

BACKGROUND: Mechanical power (MP), defined as the amount of energy produced by mechanical ventilation and released into the respiratory system, was reportedly a determining factor in the pathogenesis of ventilator-induced lung injury. However, previous studies suggest that the effects of MP were proportional to their involvement in the total lung function size. Therefore, MP normalized to the predicted body weight (norMP) should outperform the absolute MP value. The objective of this research is to determine the connection between norMP and mortality in critically ill patients who have been on invasive ventilation for at least 48 h. METHODS: This is a study of data stored in the databases of the MIMIC-III, which contains data of critically ill patients for over 50,000. The study involved critically ill patients who had been on invasive ventilation for at least 48 h. norMP was the relevant exposure. The major endpoint was ICU mortality, the secondary endpoints were 30-day, 90-day mortality; ICU length of stay, the number of ventilator-free days at day 28. RESULT: The study involved a total of 1301 critically ill patients. This study revealed that norMP was correlated with ICU mortality [OR per quartile increase 1.33 (95% CI 1.16-1.52), p <  0.001]. Similarly, norMP was correlated with ventilator-free days at day 28, ICU length of stay. In the subgroup analysis, high norMP was associated with ICU mortality whether low or high Vt (OR 1.31, 95% CI 1.09-1.57, p = 0.004; OR 1.32, 95% CI 1.08-1.62, p = 0.008, respectively). But high norMP was associated with ICU mortality only in low PIP (OR 1.18, 95% CI 1.01-1.38, p = 0.034). CONCLUSION: Our findings indicate that higher norMP is independently linked with elevated ICU mortality and various other clinical findings in critically ill patients with a minimum of 48 h of invasive ventilation.

Postoperative Neutrophil-to-Lymphocyte Ratio Is Associated with Mortality in Adult Patients After Cardiopulmonary Bypass Surgery: A Cohort Study.

BACKGROUND Cardiopulmonary bypass (CPB) contributes to the development of systemic inflammatory response after cardiothoracic surgery. As a measure of inflammation and immune reaction, the neutrophil-to-lymphocyte ratio (NLR) has been linked to poor outcomes in a variety of diseases. However, it remains to be seen whether postoperative NLR is associated with CPB patient mortality. The purpose of this research was to explore the prognostic role of the postoperative NLR in adult patients undergoing cardiothoracic surgery with cardiopulmonary bypass. MATERIAL AND METHODS This is an analysis of data stored in the databases of the MIMIC-III, which contains data of critically ill patients for over 50,000. The exposure of interest was postoperative NLR. The primary outcomeaThis study incorporates data from the MIMIC III database, which includes more than 50 000 critically ill patients. The variable of interest was postoperative NLR. The primary outcome was 30-day mortality and the secondary outcomes were 90-day mortality, length of intensive care unit stay, and length of hospital stay. was 30-day mortality, the secondary outcome was 90-day mortality, length of hospital stay and length of ICU stay. RESULTS We enrolled 575 CPB patients. The ROC curve for the postoperative NLR to estimate mortality was 0.741 (95% confidence interval [CI]: 0.636-0.847, P<0.001), and the critical value was 7.48. There was a significant difference between different postoperative NLR levels in the Kaplan-Meier curve (P=0.045). Furthermore, elevated postoperative NLR was associated with increased hospital mortality (hazard ratio [HR]: 1.1, 95% CI: 1.0-1.1, P=0.021). However, there was no important relationship in these patients between the postoperative NLR levels and 90-day mortality (HR: 1.1, 95% CI: 1.0-1.5, P=0.465). CONCLUSIONS Our findings suggest that higher postoperative NLR is associated with greater hospital mortality in adult patients undergoing cardiopulmonary bypass surgery.

Postoperative analgesic effects of paravertebral block versus erector spinae plane block for thoracic and breast surgery: A meta-analysis.

BACKGROUND: Paravertebral block (PVB) is the most recognized regional anesthesia technique after thoracic epidural anesthesia for postoperative analgesia in thoracic and breast surgery. Erector spinae plane block (ESPB) is a recently discovered blocking technique, and it has evidenced excellent postoperative analgesia for breast and thoracic surgery with fewer adverse reactions. However, there are controversies about the postoperative analgesic effects of the two analgesic techniques. OBJECTIVE: To assess the analgesic effects of PVB versus ESPB in postoperative thoracic and breast surgery. METHODS: We systematically searched PubMed, Cochrane Library, EMBASE, Web of Science, and ScienceDirect databases up to April 5, 2021. The primary outcome was postoperative pain scores. Secondary outcomes included: opioid consumption, additional analgesia, postoperative nausea and vomiting (PONV) 24 hours post-operation, and the time required for completing block procedure. This study was registered in PROSPERO, number CRD42021246160. RESULTS: After screening relevant, full-text articles, ten randomized controlled trials (RCTs) that met the inclusion criteria were retrieved for this meta-analysis. Six studies involved thoracic surgery patients, and four included breast surgery patients. Thoracic surgery studies included all of the outcomes involved in this meta-analysis while breast surgery did not report pain scores at movement and additional analgesia in 24 hours post-operation. For thoracic surgery, PVB resulted in significant reduction in the following pain scores: 0-1 hours (MD = -0.79, 95% CI: -1.54 to -0.03, P = 0.04), 4-6 hours (MD = -0.31, 95% CI: -0.57 to -0.05, P = 0.02), and 24 hours (MD = -0.42, 95% CI: -0.81 to -0.02, P = 0.04) at rest; significant reduction in pain scores at 4-6 hours (MD = -0.47, 95% CI: -0.93 to -0.01, P = 0.04), 8-12 hours (MD = -1.09, 95% CI: -2.13 to -0.04, P = 0.04), and 24 hours (MD = -0.31, 95% CI: -0.57 to -0.06, P = 0.01) at movement. Moreover, the opioid consumption at 24 hours post-operation (MD = -2.74, 95% CI: -5.41 to -0.07, P = 0.04) and the incidence of additional analgesia in 24 hours of the postoperative course (RR: 0.53, 95% CI: 0.29 to 0.97, P = 0.04) were significantly lower in the PVB group than in the ESPB group for thoracic surgery. However, no significant differences were found in pain scores at rest at various time points postoperatively, and opioid consumption at 24 hours post-operation for breast surgery. The time required for completing block procedure was longer in the PVB group than in the ESPB group for thoracic and breast surgery, and the incidence of PONV between the two groups showed no significant difference. CONCLUSION: The postoperative analgesic effects of PVB versus ESPB are distinguished by the surgical site. For thoracic surgery, the postoperative analgesic effect of PVB is better than that of ESPB. For breast surgery, the postoperative analgesic effects of PVB and ESPB are similar.

Propofol Affects EGF's Activity in Intestinal Cell by Down-Regulating EGFR-Mediated Intracellular Signaling.

Propofol is a commonly used anesthetic drug in clinic. In recent years, a series of non-anesthetic effects of propofol have been discovered. Studies have shown that propofol has many effects on the intestine. Epidermal growth factor (EGF) is one of the most important growth factors that could regulate intestinal growth and development. In the current study, we studied the effect of protocol on the biological activity of EGF on intestinal tissue and cell models. Through flow cytometry, indirect immunofluorescence and Western-blot and other technologies, it was found that propofol reduced the activity of EGF on intestinal cells, which inhibited EGF-induced intestinal cell proliferation and changed the cell behavior of EGF. To further explore the potential mechanism by which propofol down-regulated epidermal growth factor receptor (EGFR)-induced signaling, we carried out a series of related experiments, and found that propofol may inhibit the proliferation of intestinal cells by inhibiting the EGFR-mediated intracellular signaling pathway. The current research will lay the theoretical and experimental basis for further study of the effect of propofol on the intestine.