Association of preoperative coronavirus disease 2019 with mortality, respiratory morbidity and extrapulmonary complications after elective, noncardiac surgery: An observational cohort study.

STUDY OBJECTIVE: To assess the impact of preoperative infection with the contemporary strain of severe acute respiratory coronavirus 2 (SARS-CoV-2) on postoperative mortality, respiratory morbidity and extrapulmonary complications after elective, noncardiac surgery. DESIGN: An ambidirectional observational cohort study. SETTING: A tertiary and teaching hospital in Shanghai, China. PATIENTS: All adult patients (≥ 18 years of age) who underwent elective, noncardiac surgery under general anesthesia at Huashan Hospital of Fudan University from January until March 2023 were screened for eligibility. A total of 2907 patients were included. EXPOSURE: Preoperative coronavirus disease 2019 (COVID-19) positivity. MEASUREMENTS: The primary outcome was 30-day postoperative mortality. The secondary outcomes included postoperative pulmonary complications (PPCs), myocardial injury after noncardiac surgery (MINS), acute kidney injury (AKI), postoperative delirium (POD) and postoperative sleep quality. Multivariable logistic regression was used to assess the risk of postoperative mortality and morbidity imposed by preoperative COVID-19. MAIN RESULTS: The risk of 30-day postoperative mortality was not associated with preoperative COVID-19 [adjusted odds ratio (aOR), 95% confidence interval (CI): 0.40, 0.13-1.28, P = 0.123] or operation timing relative to diagnosis. Preoperative COVID-19 did not increase the risk of PPCs (aOR, 95% CI: 0.99, 0.71-1.38, P = 0.944), MINS (aOR, 95% CI: 0.54, 0.22-1.30; P = 0.168), or AKI (aOR, 95% CI: 0.34, 0.10-1.09; P = 0.070) or affect postoperative sleep quality. Patients who underwent surgery within 7 weeks after COVID-19 had increased odds of developing delirium (aOR, 95% CI: 2.26, 1.05-4.86, P = 0.036). CONCLUSIONS: Preoperative COVID-19 or timing of surgery relative to diagnosis did not confer any added risk of 30-day postoperative mortality, PPCs, MINS or AKI. However, recent COVID-19 increased the risk of POD. Perioperative brain health should be considered during preoperative risk assessment for COVID-19 survivors.

Bumetanide attenuates sevoflurane-induced neuroapoptosis in the developing dentate gyrus and impaired behavior in the contextual fear discrimination learning test.

INTRODUCTION: Sevoflurane acts as a gamma-aminobutyric acid subtype A receptor agonist and can induce widespread apoptosis of immature dentate granule cells in postnatal day 21 mice. The dentate granule cells of postnatal day 21 mice undergo a developmental stage when gamma-aminobutyric acid (GABA) shifts from inducing the depolarization of neurons to causing hyperpolarization. However, it is unclear whether sevoflurane induces apoptosis of immature granule cells by facilitating the depolarization or hyperpolarization of neurons. METHODS: We utilized bumetanide, an Na+ -K+ -2Cl- cotransporter isoform 1 (NKCC1) antagonist, to determine whether the NKCC1-mediated GABA depolarization of neurons plays a role in sevoflurane-induced neuroapoptosis. We also investigated whether sevoflurane exposure is related to long-term cognitive dysfunction in postnatal day 21 mice and explored the possible protective effects of bumetanide. RESULTS: Bumetanide attenuated the sevoflurane-induced apoptosis of dentate granule cells in postnatal day 21 mice. Exposure to sevoflurane at postnatal day 21 mice did not affect their motor ability or anxiety level, and it had no effect on spatial learning or memory functions. However, sevoflurane exposure at postnatal day 21 impaired the pattern separation ability in the contextual fear discrimination test; bumetanide mitigated this effect of sevoflurane as well. CONCLUSION: Bumetanide attenuates sevoflurane-induced apoptosis and is a promising prospect for protecting against anesthesia-induced neurotoxicity in the developing brain.

The efficacy of dexmedetomidine for the prevention of catheter-related bladder discomfort: A systematic review and meta-analysis.

BACKGROUND: The effective therapy to reduce postoperative catheter-related bladder discomfort (CRBD) remained unknown. OBJECTIVE: We attempted to manage the systematic review and a meta-analysis to clarify the efficacy of dexmedetomidine (DEX) in potential prevention on CRBD. METHODS: We performed the meta-analysis on randomized clinical trials (RCTs), and searched the databases from Web of Sciences, Embase and referred Cochrane Library published from October 2016 to September 2020. Data extraction was carefully conducted by 2 authors, respectively. Meta-analysis that was applied synthetically concerns the incidence and severity of CRBD and the treatment effect of DEX on CRBD. RESULTS: We acquired 5 RCTs with interventions of DEX on CRBD. Meta-analysis showed DEX has significantly reduced the incidence and severity of CRBD compared with control at 0 hour (risk ratios [RR] = 0.40, 95% CI = 0.53-0.29, P < .01), 1 hour (RR = 0.44, 95% CI = 0.34-0.57, P < .01), and 2 hours (RR = 0.43, 95% CI = 0.32-0.58, P < .01) and 6 hours (RR = 0.43, 95% CI = 0.29-0.63, P < .01). DEX was also associated with lower incidence of moderate to severe CRBD at 0, 1, and 6 hours after surgery. There were no significant differences in adverse events other than bradycardia, hypotension, and hypertension. CONCLUSION: The 5 RCTs showed great effectiveness in reducing the incidence and severity of the early and later postoperative CRBD. Meta-analysis showed that DEX interventions were useful in preventing the early and later postoperative CRBD without significant side effects.

Comparing remifentanil and sufentanil in stress reduction during neurosurgery: a randomised controlled trial.

Background In most scenarios, anaesthesiologists titrate opioids to control nociceptive surgical stress based on intraoperative haemodynamic changes. Remifentanil was reported to cause more profound cardiovascular depression than sufentanil. A concern is that this direct cardiovascular depression might counteract the hypertension and tachycardia caused by surgical manipulation and mask inadequate analgesia. Objective To compare remifentanil and sufentanil, titrated to maintain a comparable haemodynamic range (within 20% of baseline) and combined with the same propofol regimen, in stress reduction measured as plasma levels of putative mediators of surgical stress. Setting Huashan Hospital of Fudan University, Shanghai, China. Method Forty-five patients undergoing supratentorial glioma resection were randomised to the remifentanil group or the sufentanil group. Main outcome measures Plasma concentrations of cortisol, epinephrine, norepinephrine, interleukin-6, interleukin-10 and lymphocyte counts were analysed before anaesthesia, 1 h after incision, at the end of surgery and 24 h after incision using enzyme-linked immunosorbent assay and an automatic haematology analyser. Recovery profiles during emergence from anaesthesia were also compared. Results Except for a lower epinephrine concentration in the remifentanil group 24 h after incision (median [interquartile range], 4.2 [3.4-6.1] vs. 8.4 [4.8-12.5] ng/ml; P = 0.003), stress biomarkers were not significantly different between the two groups. Patients in the sufentanil group had lower grades in coughing, restlessness (P = 0.001 and < 0.001, respectively) and a lower incidence of postoperative shivering (P = 0.007). Conclusion Compared to that of sufentanil, the direct cardiovascular depression of remifentanil does not mask the clinical manifestation of inadequate analgesia when both drugs are titrated according to haemodynamic variables in neurosurgery.

Novel circular RNAs expressed in brain microvascular endothelial cells after oxygen-glucose deprivation/recovery.

Circular RNAs (circRNAs) are generated by head-to-tail splicing and are ubiquitously expressed in all multicellular organisms. Their important biological functions are increasingly recognized. Cerebral ischemia reperfusion injury-induced brain microvascular endothelial cell dysfunction is an initial stage of blood-brain barrier disruption. The expression profile and potential function of circRNAs in brain microvascular endothelial cells is unknown. Rat brain microvascular endothelial cells were extracted and cultured in glucose-free medium for 4 hours with 5% CO2 and 95% N2, and the medium was then replaced with complete growth medium for 6 hours. The RNA in these cells was then extracted. The circRNA was identified by Find_circ and CIRI2 software. Functional and pathway enrichment analysis of genes that were common to differentially expressed mRNAs and circRNA host genes was performed by the Database for Annotation, Visualization and Integrated Discovery Functional Annotation Tool. Miranda software was used to predict microRNAs that were potentially spong-ed by circRNAs. Furthermore, cytoscape depicted the circR-NA-microRNA interaction network. The results showed that there were 1288 circRNAs in normal and oxygen-glucose deprived/recovered primary brain microvascular endothelial cells. There are 211 upregulated and 326 downregulated differentially expressed circRNAs. The host genes of these differentially expressed circRNAs overlapped with those of differentially expressed mRNAs. The shared genes were further studied by functional enrichment analyses, which revealed that circRNAs may contribute to calcium ion function and the cyclic guanosine 3',5'-monophosphate (CAMP) dependent protein kinase (PKα) signaling pathway. Next, quantitative reverse transcription polymerase chain reaction assays were performed to detect circRNA levels transcribed from the overlapping host genes. Eight out of the ten circRNAs with the highest fold-change identified by sequencing were successfully verified. Subsequently, the circRNA-microRNA interaction networks of these eight circRNAs were explored by bioinformatic analysis. These results demonstrate that altered circRNAs may be important in the pathogenesis of cerebral ischemia reperfusion injury and consequently may also be potential therapeutic targets for cerebral ischemia diseases. All animal experiments were approved by the Chongqing Medical University Committee on Animal Research, China (approval No. CQMU20180086) on March 22, 2018.