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Background: Although total joint arthroplasty is the most effective procedures for end-stage arthritis, the incidence of postoperative death and complications remains high. The association of additional peripheral nerve blocks (PNBs) to routine spinal or general anesthesia with major adverse events (including mortality and complication rates) in elective total hip arthroplasty (THA) or total knee arthroplasty (TKA) has been subject to inconclusive findings. Methods: This retrospective observational single institution study included all patients ≧ 18 years undergoing their first elective THA or TKA from January 1, 2012 to December 31, 2021. A 1:2 propensity score matching (PSM) was performed to account for the baseline differences between two groups that were accepted to PNB or not. Kaplan–Meier curves were employed to estimate the effects of PNB on mortality. The associations of PNB and the complications were assessed by logistic regression models. Results: We identified 1328 patients, among whom 197 had PNB and 1131 had not. The 90-day all-cause mortality was significantly reduced in patients with PNBs (0 % vs 2.79 %, P = 0.041) after THA or TKA, when compared to the non-PNB group. PNB was also associated with a lower risk of pulmonary complications (odds ratio [OR], 0.430; 95%confidence interval [CI],0.216–0.857) and deep vein thrombosis (OR, 0.103; 95%CI, 0.011–0.954). Interpretation: The results of this observational, propensity score–matched cohort study suggested a strong association between the addition of PNBs to routine spinal or general anesthesia and decreased risks of major adverse events.

Abstract Background Patients with hemorrhagic shock may develop emerging enterogenic sepsis due to damage to the intestinal mucosal barrier and translocation of intestinal bacteria and endotoxins caused by ischemic injury. Because of the dual effects of anesthesia state and hemorrhagic shock, perioperative emerging enterogenic sepsis is even more rare and insidious. Case presentation We reported a case of 56-year-old man who underwent right hepatectomy for intrahepatic bile duct stones. Severe hemorrhage occurred during the procedure and the hemodynamics neither improved nor worsened after rehydration therapy and vasoactive drug administration. Based on the patient’s history and clinical presentation, a possible enterogenic sepsis was considered. After anti-infective treatment and hormone supplementation, the patient’s circulation improved significantly and he had an uneventful recovery. Conclusion The possibility of emerging enterogenic sepsis in hemorrhagic shock must always be taken into consideration. Familiarity with the risk factors and pathophysiological alterations of enterogenic sepsis is a prerequisite for early recognition and sound clinical decision making.

Summary: Background: Convincing clinical evidence regarding completely opioid-free postoperative pain management using erector spinae plane block (ESPB) in patients undergoing open major hepatectomy (OMH) is lacking. Herein, we aimed to compare the postoperative analgesic efficacy of the visualised continuous opioid-free ESPB (VC-ESPB) and conventional intravenous opioid-based postoperative pain management in hepatocellular carcinoma (HCC) patients undergoing OMH. Methods: This open-label, randomised, controlled, non-inferiority trial enrolled patients with HCC undergone open major hepatectomy in Fujian Provincial Hospital and compared the postoperative analgesic efficacy of VC-ESPB (VC-ESPB group) and conventional intravenous opioid-based pain management regimen (conventional group). Patients were randomly assigned (1:1) to VC-ESPB group and conventional group. Patients were not masked to treatment allocation. The VC-ESPB group was treated with intermittent injections of 0.25% ropivacaine (bilateral, 30 mL each side) given every 12 h through catheters placed in the space of erector spinae and an opioid-free intravenous pump (10-mg tropisetron diluted to 100 mL with 0.9% normal saline [NS]) for postoperative pain management. The conventional group did not receive ESPB and was treated with a conventional intravenous opioid-based pump (2.5-μg/kg sufentanil and 10-mg tropisetron diluted to 100 mL with 0.9% NS). Patients in the VC-ESPB group underwent magnetic resonance imaging (MRI) to identify local anaesthetic diffusion after ESPB was performed under ultrasound guidance. The primary outcome was postoperative analgesic efficacy, which was indicated by the cumulative area under the curve (AUC) of the pain visual analogue scale scores (range, 0–10; a higher score indicates more pain) obtained at rest and at movement until 48 h postoperatively after leaving the post-anaesthesia care unit (PACU). Herein, an AUC of 26.5 was set as the noninferiority margin, which needed to be satisfied for both cumulative AUCPACU-48 h at rest and cumulative AUCPACU-48 h at movement. Per protocol participants were included in primary and safety analyses. This trial was registered with ChiCTR.org.cn (ChiCTR1900026583). Findings: Between October 30, 2019, and May 1, 2023, 106 patients were enrolled and randomly assigned to the VC-ESPB group (n = 53) and the conventional group (n = 53). After the dropout (n = 5), a total of 101 patients (VC-ESPB group, n = 50; conventional group, n = 51) were analysed. Both the level of cumulative AUCPACU-48 h (at rest: 160.08 ± 38.00 vs. 164.94 ± 31.00; difference [90% CI], −4.861 [−16.308, 6.585]) and cumulative AUCPACU-48 h (at movement: 209.64 ± 28.98 vs. 212.59 ± 33.11; difference [90% CI], −2.948 [−13.236, 7.339]) were similar between the VC-ESPB and control groups within the first postoperative 48 h. The upper limit of the 90% CIs for the difference in cumulative ACUPACU-48 h at rest and at movement did not reach the upper inferiority margin (26.5). During the first postoperative 48 h, the rate of nonsteroidal anti-inflammatory drug rescue analgesia was similar between the VC-ESPB group and conventional group (n = 16, 32.0% vs. n = 11, 21.6%; P = 0.236). Treatment-related death was not observed in the VC-ESPB group (n = 0, 0%) and conventional group (n = 0, 0%). In VC-ESPB group, local site paralysis (n = 1, 2.0%) was observed in one patient and rash (n = 1, 2.0%) was observed in another patient. One patient in the conventional group was observed with rash preoperatively (n = 1, 2.0%). The VC-ESPB group had significantly lower rates of postoperative nausea (n = 2, 4.0%, vs. n = 9, 17.6%, P = 0.028), vomiting (n = 1, 2.0% vs. n = 8, 15.7%, P = 0.031) and lower incidence of major complications (n = 4, 8.0% vs. n = 6, 11.8%; P = 0.033). Interpretation: This study demonstrates the noninferiority of VC-ESPB when compared with the conventional opioid-based approach for postoperative pain management after OMH, suggesting that it is feasible to achieve opioid-free postoperative pain management for OMH. Funding: The Joint Funds for the Innovation of Science and Technology, Fujian Province, China; the Youth Scientific Research Project of Fujian Provincial Health Commission; the Fujian Research and Training Grants for Young and Middle-aged Leaders in Healthcare; and the Key Clinical Specialty Discipline Construction Program of Fujian, China.

Cancer-induced bone pain (CIBP) occurs frequently among advanced cancer patients. Voltage-gated sodium channels (VGSCs) have been associated with chronic pain, but how VGSCs function in CIBP is poorly understood. Here, we aimed to investigate the specific role of VGSCs in the dorsal root ganglia (DRGs) in CIBP. A CIBP rat model was generated by the intratibial inoculation of MRMT-1 breast carcinoma cells. Transcriptome sequencing was conducted to assess the gene expression profiles. The expression levels of key genes and differentiated genes related to activated pathways were measured by Western blotting and qPCR. We implanted a catheter intrathecally for the administration of lentivirus and drugs. Then, the changes in the mechanical withdrawal threshold (MWT) were measured. We identified 149 differentially expressed mRNAs (DEmRNAs) in the DRGs of CIBP model rats. The expression of Nav1.6, which was among these DEmRNAs, was significantly upregulated. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the DEmRNAs showed that they were mainly enriched in the mitogen-activated protein kinase (MAPK) pathway. The decrease in MWT induced by bone cancer was attenuated by Nav1.6 knockdown. Western blot analysis revealed that a p38 inhibitor decreased the expression of Nav1.6 and attenuated pain behavior. Our study shows that the upregulation of Nav1.6 expression by p38 MAPK in the DRGs of rats contributes to CIBP.

Patients with cancer, especially breast, prostate, and lung cancer, commonly experience bone metastases that are difficult to manage and are associated with bone cancer pain. Amitriptyline is often used to treat chronic pain, such as neuropathic pain. In this study, the effects of amitriptyline on the mechanical withdrawal threshold and its underlying mechanisms were evaluated in rat models of bone cancer pain. Walker 256 rat mammary gland carcinoma cells were injected into the bone marrow cavity of the right tibia of rats to provoke bone cancer pain. Then, amitriptyline was intraperitoneally administered twice daily from fifth day after the operation. Rats with bone cancer showed an apparent decline in the mechanical withdrawal threshold at day 11 after Walker 256 cells inoculation. The levels of the glutamate-aspartate transporter in the spinal cord dorsal horn decreased remarkably, and the concentration of the excitatory amino acid glutamate in the cerebrospinal fluid increased substantially. Amitriptyline injection could prevent the decline of mechanical withdrawal threshold in bone cancer pain rats. In addition, glutamate-aspartate transporter was upregulated on the glial cell surface, and glutamate levels were reduced in the cerebrospinal fluid. However, amitriptyline injection could not prevent the bone cancer pain-induced reduction in glutamate-aspartate transporter in the glial cell cytosol, it further downregulated cytosolic glutamate-aspartate transporter. Amitriptyline had no significant effect on GLAST messenger RNA expression, and bone cancer pain-invoked protein kinase A/protein kinase C upregulation was prevented. Taken together, these results suggest that the intraperitoneal injection of amitriptyline can prevent the decrease of mechanical withdrawal threshold in bone cancer pain rats, the underlying mechanisms may be associated with the inhibition of protein kinase A/protein kinase C expression, thus promoting glutamate-aspartate transporter trafficking onto the glial cell surface and reducing excitatory amino acid concentrations in the cerebrospinal fluid. [ABSTRACT FROM AUTHOR]