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Erector spinae plane block, a novel ultrasound-guided fascial plane block, has become popular for perioperative pain management. This randomized controlled trial tested the hypothesis that preoperative bilateral erector spinae plane block improves the quality of recovery in patients undergoing posterior lumbar interbody fusion.Eighty-four patients scheduled for elective posterior lumbar interbody fusion were enrolled. Patients were randomly administered either ultrasound-guided bilateral erector spinae plane blocks using 20 ml of 0.375% ropivacaine on each side (ESPB group, n = 42) or no block (control group, n = 42) after anesthesia induction. The primary outcome was the quality of recovery 24 h postoperatively, assessed using the 15-item quality of recovery questionnaire.The global postoperative 24-h quality of recovery-15 score was 117 [114-121] in the erector spinae plane block group and 108 [105-111] in the control group, with a median difference of 9 (95% confidence interval 7-12, P 0.001). Compared with the control group, preoperative bilateral erector spinae plane blocks reduced the area under the curve of the numeric rating scale pain scores over 48 h, prolonged the time to first rescue analgesia, lessened postoperative 24 h morphine consumption, decreased the occurrence of postoperative nausea and vomiting, and improved patient satisfaction with postoperative analgesia. There were no block-related adverse events.We found that preoperative bilateral erector spinae plane blocks provided superior early quality of recovery, postoperative analgesia, and patient satisfaction scores in patients undergoing posterior lumbar interbody fusion.Chinese Clinical Trial Registry, ChiCTR1900027186, 4/11/2019.

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.

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.

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 Na

Study objective Intraoperative systemic lidocaine has become widely accepted as an adjunct to general anesthesia, associated with opioid-sparing and enhanced recovery. We hypothesized that perioperative systemic lidocaine improves postoperative pain and enhances the quality of recovery (QoR) in patients following video-assisted thoracic surgery (VATS). Design Prospective, single-center, double-blind, randomized placebo-controlled clinical trial. Setting Single institution, tertiary university hospital. Patients Adult patients aged 18 to 65 undergoing VATS were eligible for participation. Interventions Patients enrolled in this study were randomized to receive either system lidocaine (a bolus of 1.5 mg kg−1, followed by an infusion of 2 mg kg−1 h−1 until the end of the surgical procedure) or identical volumes and rates of 0.9% saline. Measurements The primary outcome was a global QoR-15 score 24 h after surgery. Secondary outcomes included postoperative pain score, cumulative opioid consumption, emergence time, length of PACU stay, adverse events, and patient satisfaction. Main results There was no difference in the global QoR-15 scores at 24 h postoperatively between the lidocaine and saline groups (median 117, IQR 113.5–124, vs. median 116, IQR 111–120, P = 0.067), with a median difference of 3 (95% CI 0 to 6, P = 0.507). Similarly, postoperative pain scores, postoperative cumulative opioid consumption, PACU length of stay, the occurrence of PONV, and patient satisfaction were comparable between the two groups (all P > 0.05). Conclusions Our current findings do not support using perioperative systemic lidocaine as a potential strategy to improve postoperative pain and enhance QoR in patients undergoing VATS. Trial registration Chinese Clinical Trial Registry (identifier: ChiCTR1900027515).

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.