Incidence of postoperative hypothermia and shivering and risk factors in patients undergoing malignant tumor surgery: a retrospective study.

BACKGROUND: Perioperative hypothermia and shivering are common and can cause adverse outcomes. The aim of this study was to investigate the incidence of postoperative hypothermia and shivering and their risk factors in patients undergoing malignant tumor surgery. METHODS: This retrospective study collected data from patients with American Society of Anesthesiologists physical status (ASA) I or II who underwent scheduled surgery from November 2020 to March 2021 at Fudan University Shanghai Cancer Center. Each patient's core body temperature was measured at three time points: time point 1 (arrival at the postanesthesia care unit (PACU)), time point 2 (after 30-min care in the PACU), and time point 3 (at discharge from the PACU). At time point 1, if the patient's body temperature was below 36 ℃, we provided an active forced-air warmer. At time point 2, if it was still below 36 ℃, the forced-air warmer was still applied until the patient was discharged from the PACU. If it reached 36 ℃, the forced-air warmer would be switched off. Univariate and multivariate logistic regression combined with stepwise methods and linear regression were used to explore risk factors for postoperative hypothermia and shivering. RESULTS: The numbers (percentage) of 202 patients who developed postoperative hypothermia at the different time points were 52 (25.7%), 37 (18.3%) and 28 (13.9%). Eight patients (4.0%) experienced shivering. Multivariate logistic regression showed that high weight (OR = 0.923, 95% CI: 0.884 to 0.964, P = 0.0003) and low estimated blood loss (OR = 0.252, 95% CI: 0.115 to 0.550, P = 0.0005) were protective factors against hypothermia, while long surgical duration (OR = 3.339, 95% CI: 1.675 to 6.655, P = 0.0006) was an independent risk factor for hypothermia at time point 1. There was no risk factor associated with the occurrence of shivering (P > 0.05). There was a significant difference between the hypothermia and normothermia groups in the median length of stay in the PACU (59.0 vs. 49.0 min, P = 0.0123). CONCLUSIONS: Postoperative hypothermia occurred frequently. Weight, estimated blood loss and surgical duration were significantly associated with hypothermia on arrival at the PACU.

Intraoperative lidocaine infusion in patients undergoing pancreatectomy for pancreatic cancer: a mechanistic, multicentre randomised clinical trial.

BACKGROUND: Intravenous lidocaine has been postulated to improve long-term survival after surgery for pancreatic cancer through anti-inflammatory effects, anti-tumour effects, or both. We investigated whether intraoperative lidocaine improves survival after pancreatectomy for pancreatic cancer and whether lidocaine modified the formation of neutrophil extracellular traps (NETs), high levels of which are associated with poor prognosis. METHODS: Patients undergoing pancreatectomy were randomly assigned to i.v. lidocaine (continuous intraoperative infusion of 2 mg kg-1 h-1, after 1.5 mg kg-1 bolus at induction of anaesthesia) or saline placebo. The co-primary outcomes were survival/disease-free survival 3 yr after surgery. Secondary outcomes (masked to treatment allocation) included intraoperative opioid (sufentanil) dose, postoperative complications, and circulating and tumour-associated NETs (immunofluorescence assay, enzyme-linked immune assay, or both). RESULTS: A total of 563 participants (34.6% female; median age, 64 yr) completed 3 yr of clinical follow-up. Overall, 283 participants were randomised to lidocaine infusion, and 280 participants were randomised to placebo. Infusion of lidocaine did not alter overall (hazard ratio [HR]=0.98; 95% confidence interval [CI], 0.81-1.17; P=0.79) or disease-free survival (HR=0.91; 95% CI, 0.71-1.17; P=0.44). Mean intraoperative sufentanil dose was reduced by lidocaine infusion (47.6 µg [4.6]) compared with placebo (68.4 µg [4.8]; P<0.001), but postoperative complications and length of hospital stay were similar between groups. Circulating NETs were lower after lidocaine infusion up to 3 days after surgery, but tumour-associated NETs were not altered by intraoperative treatment. CONCLUSION: In patients undergoing pancreatectomy for pancreatic cancer, intraoperative infusion of lidocaine did not improve overall or disease-free survival. Reduced formation of circulating NETs was absent in pancreatic tumour tissue. CLINICAL TRIAL REGISTRATION: NCT03245346; updated in Chi-CTR-2000035469.

Association between intraoperative intravenous lidocaine infusion and survival in patients undergoing pancreatectomy for pancreatic cancer: a retrospective study.

BACKGROUND: Intravenous lidocaine has been shown to reduce opioid consumption and is associated with favourable outcomes after surgery. In this study, we explored whether intraoperative lidocaine reduces intraoperative opioid use and length of stay (LOS) and improves long-term survival after pancreatic cancer surgery. METHODS: This retrospective study included 2239 patients who underwent pancreatectomy from January 2014 to December 2017. The patients were divided into non-lidocaine and lidocaine (bolus injection of 1.5 mg kg-1 at the induction of anaesthesia followed by a continuous infusion of 2 mg kg-1 h-1 intraoperatively) groups. The overall use of postoperative rescue analgesia and LOS were recorded. Propensity score matching was used to minimise bias, and disease-free survival and overall survival were compared between the two groups. RESULTS: After propensity score matching, patient characteristics were not significantly different between groups. Intraoperative sufentanil consumption and use of postoperative rescue analgesia in the lidocaine group were significantly lower than those in the non-lidocaine group. The LOS was similar between groups. There was no significant difference in disease-free survival between groups (hazard ratio [HR]=0.913; 95% confidence interval [CI], 0.821-1.612; P=0.316). The overall survival rates at 1 and 3 yr were significantly higher in the lidocaine group than in the non-lidocaine group (68.0% vs 62.6%, P<0.001; 34.1% vs 27.2%, P=0.011). The multivariable analysis indicated that intraoperative lidocaine infusion was associated with a prolonged overall survival (HR=0.616; 95% CI, 0.290-0.783; P=0.013). CONCLUSION: Intraoperative intravenous lidocaine infusion was associated with improved overall survival in patients undergoing pancreatectomy.

Propofol attenuates the adhesion of tumor and endothelial cells through inhibiting glycolysis in human umbilical vein endothelial cells.

Propofol is one of the most commonly used intravenous anesthetics and plays an important role in tumor suppression. In the present study, we aimed to investigate the mechanism by which propofol attenuates tumor endothelial cells (TECs) and tumor cell adhesion to inhibit tumor metastasis in vitro. Human umbilical vein endothelial cells (HUVECs) cultured in Dulbecco's modified Eagle's medium were treated with tumor conditioned medium for 24 h, followed by 4 h of treatment with or without 25 µM of propofol, 10 µM of KN93, 500 µM of MK801, or 20 µM of rapastinel. It was found that propofol inhibited TEC adhesion and the glycolysis level of TECs. Consistently, propofol inhibited the expressions of adhesion molecules (E-selectin, ICAM-1, and VCAM-1) and glycolysis proteins (GLUT1, HK2, and LDHA) in TECs. Moreover, propofol attenuated the expression of HIF-1α, the phosphorylation of AKT and Ca2+/calmodulin-dependent protein kinase II (CaMKII), and the Ca2+ concentration in TECs. MK801, an inhibitor of NMDA receptor, and KN93, an inhibitor of CaMKII, both inhibited the expressions of adhesion molecules and glycolysis proteins, in a manner similar to propofol. Additionally, rapastine, an activator of NMDA receptor, could counteract the effects of propofol. Our results indicated that propofol attenuates intracellular Ca2+ concentration, CaMKII and AKT phosphorylation, and HIF-1α expression, probably via inhibiting the NMDA receptor, thus inhibiting glycolysis and adhesion of tumor and endothelial cells.

Effect of thoracic epidural anesthesia with different concentrations of ropivacaine on arterial oxygenation during one-lung ventilation.

BACKGROUND: Thoracic epidural anesthesia can contribute to facilitate the fast-track approach in lung surgery. However, data regarding the effects of thoracic epidural anesthesia on oxygenation during one-lung ventilation (OLV) are scarce and contradictory. Therefore, the authors conducted a prospective, randomized, double-blinded trial in patients undergoing lung surgery under spectral entropy-guided intravenous anesthesia to evaluate the effects of thoracic epidural anesthesia with different concentrations of ropivacaine on oxygenation, shunt fraction (Qs/Qt) during OLV, and maintenance doses of propofol. METHODS: One hundred twenty patients scheduled for lung surgery were randomly divided into four groups to epidurally receive saline (Group S), 0.25% (Group R0.25), 0.50% (Group R0.50), and 0.75% (Group R0.75) ropivacaine. Ropivacaine was administered intraoperatively (6-8 ml of first bolus + 5 ml/h infusion). Arterial oxygen tension (Pao2) and Qs/Qt were measured before, during, and after OLV. RESULTS: Pao2 was significantly lower in Group R0.75 compared with that in Group S and Group R0.25 10 min (170 +/- 61 vs. 229 +/- 68 mmHg, P = 0.01; 170 +/- 61 vs. 223 +/- 70 mmHg, P = 0.03) and 20 min after OLV (146 +/- 52 vs. 199 +/- 68 mmHg, P = 0.009; 146 +/- 52 vs. 192 +/- 67 mmHg, P = 0.03). During OLV, Qs/Qt was significantly higher in Group R0.75 compared with that in Group S and Group R0.25 (P < 0.05). Maintenance doses of propofol were significantly lower in Group R0.75. Vasopressor requirements were higher in Group R0.75. CONCLUSION: A decrease in oxygenation during OLV occurred only at the highest dose of epidural local anesthetic and not at lower doses. Higher doses of epidural medication required less propofol and more vasopressors.

Protective effect of dexmedetomidine infusion combined with epidural blockade on postoperative complications after surgery: A prospective randomized controlled clinical trial.

OBJECTIVES: This prospective, randomized, controlled study aimed to explore the efficacy of dexmedetomidine combined with epidural blockade on postoperative recovery of elderly patients after radical resection for colorectal cancer. METHODS: Ninety-six elderly patients who underwent radical resection for colorectal cancer were randomly divided into the following four groups: dexmedetomidine, epidural blockade (ropivacaine), combined (dexmedetomidine + epidural blockade), and control (0.9% saline). The Mini-Mental State Examination (MMSE), Visual Analog Scale (VAS), and Ramsay scores at 48 hours, and time to first activity, length of hospital stay, and postoperative complication rates at 3 months were assessed. RESULTS: Twelve hours after surgery, Ramsay scores were higher in the combined compared with the control and epidural blockade groups. Twenty-four hours after surgery, MMSE scores were higher in the combined compared with the other groups. The combined group showed the lowest VAS scores except at 48 hours. Time to first activity and length of hospital stay were significantly shorter in the combined compared with the other groups. There was no difference in total postoperative complication rates among the groups. CONCLUSIONS: A combination of intraoperative dexmedetomidine infusion and epidural blockade could mitigate pain after surgery, improve cognitive dysfunction in early surgery, and facilitate recovery.

Isoflurane preconditioning ameliorates electromagnetic pulse-induced neural damage by shifting microglia polarization toward anti-inflammatory phenotype via upregulation of SOCS1.

With the speedy technological advances during the past few decades, human exposure to the electromagnetic field (EMF) has become increasingly common. Exposure to EMF may induce neural injuries and dysfunction of various organs, likely involving neuroinflammation and activation of microglial cells. Isoflurane preconditioning (IP) is shown to provide neuroprotection in various neurological diseases by inhibiting excessive neuroinflammatory responses. Brain samples harvested from rats exposed to electromagnetic pulse (EMP) with or without IP were subjected to qPCR, Western blot assay, and immunohistochemistry to determine the expression of pro-inflammatory/anti-inflammatory microglia markers and a variety of pro- and anti-inflammatory mediators. Suppressor of cytokine signaling 1 (SOCS1) siRNA was used in cultured N9 microglia cells to examine the roles of SOCS1 in the effect of IP. In both in vivo and in vitro experiments, EMP-exposed microglia were predominantly pro-inflammatory microglia, accompanied by increased expression of pro-inflammatory cytokines and chemokines, and activation of TLR4 pathway, leading to neuronal death. IP reversed the changes induced by EMP and switched the activated microglia to an anti-inflammatory phenotype. SOCS1 siRNA abolished the beneficial effects of IP. IP ameliorates EMP-induced neural injuries by shifting microglia polarization from pro-inflammatory to anti-inflammatory phenotype via upregulation of SOCS1.

Effects of ropivacaine on adhesion molecule CD11b expression and function in human neutrophils.

Local anesthetics possess a wide range of anti-inflammatory properties through their effects on neutrophils. However, limited information is available on the effects of ropivacaine (a new local anesthetic) on neutrophil function. The aim of this study was to investigate anti-inflammatory properties of ropivacaine with regard to its effects on the expression and function of CD11b in human neutrophils. CD11b expression was examined by flow cytometry and its function was determined by measuring adhesion of neutrophils to human umbilical vein endothelial cells (HUVECs). Ropivacaine inhibited CD11b expression in formyl-methionyl-leucyl-phenylalanine (fMLP)-activated neutrophils in a concentration-dependent manner, but not in a time-dependent manner. The inhibitory potency of ropivacaine was similar to that of bupivacaine and levobupivacaine, but was more potent than that of lidocaine. The up-regulation of CD11b induced by platelet-activating factor (PAF) priming was also inhibited by ropivacaine. fMLP increased adhesion of neutrophils to HUVECs, which was inhibited by ropivacaine. In addition, ropivacaine more potently inhibited the fMLP-induced CD11b expression in the presence of ethylene glycol-bis(2-aminoethylether)-N,N,N ,N -tetraacetic acid (EGTA), a chelator of extracellular Ca(2+). However, ropivacaine showed no effect on the fMLP-induced CD11b expression in the presence of butan-1-ol, a blocker of phospholipase D (PLD) pathway, which completely inhibited the fMLP-induced CD11b expression in neutrophils. Our results suggest that ropivacaine exerts anti-inflammatory activity, and this appears to be mediated through inhibiting the expression and function of adhesion molecule CD11b in neutrophils.