Dose-Response Study of Norepinephrine Infusion for Maternal Hypotension in Preeclamptic Patients Undergoing Cesarean Delivery Under Spinal Anesthesia.

BACKGROUND AND OBJECTIVE: Spinal anesthesia remains the preferred mode of anesthesia for preeclamptic patients during cesarean delivery. We investigated the incidence of maternal hypotension under spinal anesthesia during cesarean delivery, by comparing different prophylactic infusion rates of norepinephrine with normal saline. METHODS: We randomly allocated 180 preeclamptic patients (45 in each groups) aged 18-45 scheduled for cesarean delivery to receive one of four prophylactic norepinephrine infusions at doses of 0 (normal saline group), 0.025 (0.025 group), 0.05 (0.05 group), or 0.075 (0.075 group) µg/kg/min following spinal anesthesia. The primary endpoint was the incidence of maternal hypotension (systolic blood pressure < 80% of baseline). RESULTS: The incidence of maternal hypotension was reduced with different prophylactic infusion rates of norepinephrine (26.7%, 15.6%, and 6.7%) compared with normal saline (37.8%) with a significant decreasing trend (p = 0.002). As the infusion doses of norepinephrine increased, there is a significant decreasing trend in deviation of systolic blood pressure control (median performance error; median absolute performance error) from baseline (p < 0.001; p < 0.001) and need for rescue norepinephrine boluses (p = 0.020). The effective dose 50 and effective dose 90 of prophylactic norepinephrine infusion were - 0.018 (95% confidence interval - 0.074, 0.002) µg/kg/min and 0.065 (95% confidence interval 0.048, 0.108) µg/kg/min, respectively. CONCLUSIONS: Prophylactic infusion of norepinephrine, as compared to no preventive measures, can effectively reduce the incidence of maternal hypotension in preeclamptic patients under spinal anesthesia during cesarean delivery, without increasing other adverse events for either the mother or neonate. REGISTRATION: Clinical trials.gov identifier number NCT04556370.

Association between muscular tissue desaturation and acute kidney injury in older patients undergoing major abdominal surgery: a prospective cohort study.

PURPOSE: Present study was designed to investigate the association between muscular tissue desaturation and acute kidney injury (AKI) in older patients undergoing major abdominal surgery. METHOD: A total of 253 patients (≥ 65 years old) who underwent abdominal surgery with expected duration ≥ 2 h were enrolled. Muscular tissue oxygen saturation (SmtO2) was monitored at quadriceps and bilateral flanks during surgery. Muscular desaturation was defined as SmtO2 < 90% baseline lasting for > 60 s. The primary outcome was the incidence of AKI within postoperative 7 days. The association between muscular desaturation and AKI was analyzed by multivariable logistic regression model. The secondary outcomes indicated the other complications within postoperative 30 days. RESULTS: Among 236 patients, 44 (18.6%) of them developed AKI. The incidence of muscular desaturation at quadriceps was 28.8% (68/236). Patients with muscular desaturation had higher incidence of AKI than those without desaturation (27.9% [19/68], vs. 14.9% [25/168], P = 0.020). After adjustment of confounders, multivariable analysis showed that muscular desaturation at quadriceps was significantly associated with an increased risk of AKI (OR = 2.84, 95% CI 1.21-6.67, P = 0.016). Muscular desaturations at left and right flank were also associated with an increased risk of AKI (OR = 6.38, 95% CI 1.78-22.89, P = 0.004; OR = 8.90, 95% CI 1.42-45.63; P = 0.019, respectively). Furthermore, patients with muscular desaturation may have a higher risk of pulmonary complications, sepsis and stroke at 30-day follow-up. CONCLUSION: Muscular desaturation was associated with postoperative AKI in older patients undergoing major abdominal surgery which may serve as a predictor of AKI.

The activation impact of lactobacillus-derived extracellular vesicles on lipopolysaccharide-induced microglial cell.

Perioperative neurocognitive dysfunction (PND) emerges as a common postoperative complication among elderly patients. Currently, the mechanism of PND remains unclear, but there exists a tendency to believe that inflammation plays a significant role in PND. Alterations in the abundance of intestinal microbiota can increase the permeability of the intestinal mucosal barrier and incite extraintestinal inflammatory responses. Metabolites from these microbiota can be absorbed by the intestinal mucosa into the bloodstream, exerting influence upon the central nervous system (CNS). Lactobacillus (Lac), serving as an intestinal probiotic bacterium, possesses the capacity to modulate emotional behavior and cognitive functions. Extracellular vesicles (EVs) are recognized as novel therapeutic carriers for targeted delivery to regulate physiology and pathogenesis. While the mechanism governing the primary function of Lac-EVs in the CNS remains uncertain. Therefore, we established an in vitro neuroinflammation model to induce PND and then treated the mice with Lac-EVs to observe the effect of these EVs on neuroinflammation, particularly on microglial (MG) polarization. Our research unveils that Lac-EVs reduced inflammation induced by LPS in microglia and the activation of related proteins, including the mRNA expression of M1 labeled protein (iNOS). Moreover, the mRNA expression of M2-labeled protein (Arg1) increased. In addition, flow cytometry revealed that the ratio of M1/M2 microglia also changed significantly. Therefore, Lac-EVs promoted the differentiation of M2 microglia by inducing the preferential expression of specific markers related to M2 macrophages and inflammation. In terms of inflammatory cytokine expression, Lac-EVs decreased the secretion of proinflammatory cytokines (IL-1ß and IL-6) and increased IL-10 production after lipopolysaccharide (LPS) stimulation. Therefore, Lac-EVs induce the activation of M2 microglial cells without inducing cellular harm in vitro, and they demonstrate anti-inflammatory effects against lipopolysaccharide-induced neuroinflammation. This finding suggested that it is an effective anti-inflammatory strategy for alleviating inflammation-driven PNDs.

Association of preoperative neutrophil-lymphocyte ratios with the emergence delirium in pediatric patients after tonsillectomy and adenoidectomy: an observational prospective study.

PURPOSE: The study aimed to investigate potential risk factors for emergence delirium (ED) in pediatric patients after tonsillectomy and adenoidectomy (T&A). METHODS: This prospective, single-center observational study enrolled children aged 3-7 years who underwent T&A under general anesthesia. ED was assessed according to DSM-IV or V criteria. Receiver operating characteristic curve analysis was performed to evaluate the predicative and cut-off values of risk factors, including age, preoperative anxiety level, postoperative pain and neutrophil-lymphocyte ratio (NLR) for ED. Univariate and multivariate logistic regression analyses were performed to investigate risk factors for ED. RESULTS: 94 pediatric patients who underwent T&A were enrolled and 19 developed ED (an incidence of 25.3%). Receiver operating characteristic analysis indicated that preoperative NLR was a significant predictor of ED with a cut-off value of 0.8719 and an area under the curve (AUC) of 0.671 (95% confidence interval (CI) 0.546-0.796, P = 0.022). Preoperative NLR (< 0.8719) and postoperative pain were independent risk factors associated with ED (odds ratio: 0.168, 95% CI 0.033-0.858, P = 0.032; odds ratio: 7.298, 95% CI 1.563-34.083, P = 0.011) according to multivariate logistic regression analysis. CONCLUSIONS: Preoperative NLR level and postoperative pain were independent risk factors for ED in pediatric patients undergoing T&A.

Anesthesia and surgery induce changes in endogenous brain protective protein (RNF146) and delirium-like behavior in aged rats.

BACKGROUND: Postoperative delirium (POD) is a common complication after anesthesia and surgery, especially in the elderly. RNF146 has neuroprotective effects in cerebral ischemia, hypoxia, and chronic neurological diseases. However, whether RNF146 expression is related to the occurrence and development of POD remains unclear. Therefore, in this study, we aimed to determine whether RNF146 is involved in the occurrence of POD. METHODS: (Sprague-Dawley) male rats (18 months old) were splenectomized under sevoflurane anesthesia. The cognitive function of rats at 1, 3, and 7 d after anesthesia and surgery was evaluated. Changes in the expression of neuroinflammatory cytokines, IL-6 and IL-10, and RNF146 were measured in the hippocampus in both control group (con) and anesthesia (AS) group. We examined cognitive outcomes and expression of inflammatory factors and RNF146 in con and AS mice using cluster analysis. RESULTS: The cognitive ability and mobility of rats after anesthesia and surgery at day 1, 3, and 7 decreased, especially at day 3. Similarly, the expression of neuroinflammatory factors and RNF146 increased after anesthesia and surgery at day 1, 3, and 7, and the increase was highest at day 3. The clustering and correlation analysis of RNF146 expression in the hippocampi of elderly rats revealed a correlation between POD and neuroinflammation resulting from anesthesia and surgery. CONCLUSION: Anesthesia and surgery can lead to POD and neuroinflammation. The expression of RNF146 correlates with delirium and neuroinflammation caused by anesthesia and surgery.

Comparison of crystalloid and colloid co-load combined with norepinephrine prophylaxis on post-spinal anesthesia hypotension during cesarean delivery: a randomized sequential allocation dose-finding study.

Background: Fluid loading is an essential component of treatment for reducing the incidence of post-spinal anesthesia hypotension and is necessary to maintain intravascular volume, perfuse tissues, and control spinal anesthesia hypotension after sympathetic blockade. We performed a randomized sequential allocation dose-finding study to compare the effects of 10 mL/kg crystalloid and 6% hydroxyethyl starch (130/0.4) co-load on the ED90 of prophylactic norepinephrine infusion for preventing post-spinal anesthesia hypotension during cesarean delivery. Methods: Eighty patients were randomly allocated to receive either a 10 mL/kg crystalloid (Crystalloid Group, n = 40) or 6% hydroxyethyl starch (130/0.4) (Colloid Group, n = 40) co-load combined with prophylactic norepinephrine infusion during spinal anesthesia for cesarean delivery. The first patient received an initial prophylactic norepinephrine infusion rate of 0.025 µg/kg/min. Subsequent patients received a 0.005 µg/kg/min gradient dose of prophylactic norepinephrine. This dose was administered as a gradient based on its effectiveness for preventing post-spinal anesthesia hypotension (defined as SBP < 80% of baseline value) and determined by the up-and-down sequential allocation methodology. The primary study outcome was the ED90 of prophylactic norepinephrine infusion. Secondary outcomes included the incidence of post-spinal anesthesia hypotension, bradycardia, hypertension, Apgar scores, and umbilical artery blood gas values were also measured. Results: The ED90 values of prophylactic norepinephrine infusion for preventing post-spinal anesthesia hypotension during cesarean delivery were 0.063 µg (95% CI: 0.050 to 0.064) and 0.062 µg (95% CI: 0.045 to 0.064) using isotonic regression analysis, and 0.068 µg (95% CI: 0.056 to 0.353) and 0.060 µg (95% CI: 0.050 to 3.590) using probit regression analysis in the Crystalloid Group and Colloid Group, respectively. The secondary outcomes were comparable between the two groups. Conclusion: The administration of a 10 mL/kg 6% hydroxyethyl starch (130/0.4) does not provide additional benefits compared to crystalloid co-load in reducing the ED90 of prophylactic norepinephrine infusion for preventing post-spinal anesthesia hypotension during cesarean delivery.

Maresin1 ameliorates postoperative cognitive dysfunction in aged rats by potentially regulating the NF-κB pathway to inhibit astrocyte activation.

Postoperative cognitive dysfunction (POCD) is one of the most serious postoperative complications in the elderly population. Perioperative central neuroinflammation is considered to be an important pathological mechanism of POCD, with the activation of astrocytes playing a key role in central neuroinflammation. Maresin1 (MaR1) is a specific pro-resolving mediator synthesized by macrophages in the resolution stage of inflammation, and provides unique anti-inflammatory and pro-resolution effects by limiting excessive neuroinflammation and promoting postoperative recovery. However, the question remains whether MaR1 can have a positive effect on POCD. The objective of this study was to investigate the protective effect of MaR1 on POCD cognitive function in aged rats after splenectomy. Morris water maze test and IntelliCage test showed that splenectomy could cause transient cognitive dysfunction in aged rats; however, the cognitive impairment of rats was significantly mitigated when MaR1 pretreatment was administered. MaR1 significantly alleviated the fluorescence intensity and protein expression of glial fibrillary acidic protein and central nervous system specific protein in the cornu ammonis 1 region of the hippocampus. Simultaneously, the morphology of astrocytes was also severely altered. Further experiments showed that MaR1 inhibited the mRNA and protein expression of several key proinflammatory cytokines-interleukin-1ß, interleukin-6, and tumor necrosis factor-α in the hippocampus of aged rats following splenectomy. The molecular mechanism underlying this process was explored by evaluating expression of components of the nuclear factor κB (NF-κB) signaling pathway. MaR1 substantially inhibited the mRNA and protein expression of NF-κB p65 and κB inhibitor kinase ß. Collectively, these results suggest that MaR1 ameliorated splenectomy-induced transient cognitive impairment in elderly rats, and this neuroprotective mechanism may occur through regulating the NF-κB pathway to inhibit astrocyte activation.

Neuroprotective effects of different doses of Maresin1 pretreatment in aged rats after anesthesia/surgery.

OBJECTIVE: The study is to investigate the neuroprotective effect of different doses of Maresin1 pretreatment in aged rats after anesthesia/surgery and the related mechanisms. METHODS: Aged male rats were randomly divided into a control group, an anesthesia/surgery group, and low, medium, and high-dose Maresin1 pretreatment groups, and the hippocampus was taken for study. The Morris water maze was performed to detect the cognitive ability of rats. Western blot and immunofluorescence were used to detect the expression of glial fibrillary acidic protein (GFAP) and central nervous system-specific protein (S100ß). The ultrastructure of astrocytes was observed by a transmission electron microscope. Quantitative real-time PCR was used to detect the relative expression of IL-1ß, IL-6, and TNF-α mRNA. RESULTS: Compared with the control group, the cognition of rats in the anesthesia/surgery group was significantly reduced. The expression of astrocyte markers (GFAP and S100ß) in the hippocampus of rats in the anesthesia/surgery group was increased. The levels of hippocampal inflammatory cytokines (TNF-α, IL-1ß, and IL-6) were also higher in the anesthesia/surgery group than in the control group. After pretreatment with different doses of Maresin1, the cognitive impairment of rats was alleviated to varying degrees. Maresin1 pretreatment decreased the expression of astrocyte markers and inflammatory factors in the hippocampus of rats after anesthesia/surgery, and improve the microstructures of activated astrocytes, especially in the medium-dose group. CONCLUSION: Pretreatment with Maresin1 (especially at medium-dose) showed neuroprotective effects in aged rats after anesthesia/surgery, which may be related to the inhibition of astrocyte activation.

Effects of dexmedetomidine on oxygenation and inflammatory factors in patients undergoing uvulopalatopharyngoplasty: a prospective, randomized, placebo-controlled trial.

PURPOSE: Uvulopalatopharyngoplasty (UPPP) can aggravate lung inflammatory reactions in patients with obstructive sleep apnoea syndrome (OSAS). Dexmedetomidine (Dex) is a selective α-2 adrenoreceptor agonist that can alleviate lung injury. This study was designed to investigate the effects of Dex on oxygenation and inflammatory factors in patients undergoing UPPP in the early perioperative period. METHODS: Patients with OSAS undergoing UPPP were randomly allocated to the Dex Group or Control Group. Arterial blood gas analyses were performed, and the respiratory index (RI) and oxygenation index (OI) were calculated upon entering the operating room (T0) and immediately after surgery (T3). The inflammatory factors tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) were measured at T0 and T3. RESULTS: A total of 44 patients with OSAS were randomized. There was no significant difference in basic patient characteristics between the two groups. The preoperative RI and OI were not significantly different between the two groups, but they were altered immediately after surgery relative to the corresponding preoperative value (p < 0.05). Compared with the Control Group, the RI was significantly lower at T3 in the Dex Group (p < 0.001). However, there was no significant difference in the OI between the two groups (p = 0.128). The inflammatory factors TNF-α (p < 0.001) and IL-6 (p = 0.018) were lower, while IL-10 was higher in the Dex Group than in the Control Group (p < 0.001). CONCLUSION: Dexmedetomidine can improve the oxygenation and inhibit the inflammatory response in patients undergoing UPPP in the early perioperative period. TRIAL REGISTRATION: The present clinical study has been registered at Clinical Trials under number NCT03612440.

Association of electroencephalogram epileptiform discharges during cardiac surgery with postoperative delirium: An observational study.

Background: Delirium is a frequent and serious complication following cardiac surgery involving cardiopulmonary bypass (CPB). Electroencephalography reflects the electrical activity of the cerebral cortex. The impact of electroencephalographic epileptiform discharges during cardiac surgery on postoperative delirium remains unclear. This study was designed to investigate the relationship between intraoperative epileptiform discharges and postoperative delirium in patients undergoing cardiac surgery. Methods: A total of 76 patients who underwent cardiac surgery under CPB were included. The baseline cognitive status was measured before surgery. Electroencephalograms were monitored continuously from entry into the operating room to the end of surgery. The presence of delirium was assessed through the Confusion Assessment Method or the Confusion Assessment Method for the Intensive Care Unit on the first 3 days after surgery. Univariate and multivariate logistic regression analyses were performed to evaluate the association between epileptiform discharges and delirium. Results: Delirium occurred in 31% of patients and epileptiform discharges were present in 26% of patients in the study. Patients with delirium had a higher incidence of epileptiform discharges (52.63% vs. 13.95%, P < 0.001) and longer durations of anesthesia and CPB (P = 0.023 and P = 0.015, respectively). In addition, patients with delirium had a longer length of hospital stay and a higher incidence of postoperative complications. Multivariate logistic regression analysis showed that age and epileptiform discharges were significantly associated with the incidence of postoperative delirium [odds ratio, 4.75 (1.26-17.92), P = 0.022; 5.00 (1.34-18.74), P = 0.017, respectively]. Conclusions: Postoperative delirium is significantly related to the occurrence of epileptiform discharges during cardiac surgery.

Transcutaneous Electrical Acupoint Stimulation Decreases the Incidence of Postoperative Nausea and Vomiting After Laparoscopic Non-gastrointestinal Surgery: A Multi-Center Randomized Controlled Trial.

Importance: Postoperative nausea and vomiting (PONV) gives patients a bad experience and negates their good recovery from surgery. Objective: This trial aims to assess the preventive effectiveness of transcutaneous electrical acupoint stimulation (TEAS) on the incidence of PONV in high-risk surgical patients. Design: The large sample size, multicenter, evaluator-blinded, and randomized controlled study was conducted between September 3, 2019 to February 6, 2021. Setting: The 12 hospitals were from different Chinese provinces. Participants: After obtaining ethics approval and written informed consent, 1,655 patients with Apfel score ≥ 3 points were enrolled for selective laparoscopic non-gastrointestinal surgery under general anesthesia. Interventions: Patients were randomly allocated into the TEAS and Sham group with a 1:1 ratio. The TEAS group was stimulated on bilateral Neiguan and Zusanli acupoints after recovery from anesthesia on the surgical day and the next morning for 30 min, while the Sham group received an identical setting as TEAS but without currents delivered. Electronic patient self-reported scale was used to evaluate and record the occurrence of PONV. Main Outcomes and Measures: Primary clinical end point is the incidence of PONV which was defined as at least one incidence of nausea, retching, or vomiting after operation within postoperative 24 h. Results: Compared with the Sham treatment, the TEAS lowered the PONV incidence by 4.8% (29.4 vs. 34.2%, P = 0.036) and vomiting incidence by 7.4% (10.4 vs. 17.8%, P < 0.001). TEAS also lowered persistent nausea incidence and PONV scores and decreased PONV related complications and Quality of Recovery-40 scores (P < 0.05). TEAS lowered the 24 h PONV risk by 20% (OR, 0.80, 95% CI, 0.65 -0.98; P = 0.032), and lowered hazard ratio by 17% (HR, 0.83, 95% CI, 0.70-0.99; P = 0.035). Both TEAS and palonosetron were the independent PONV risk protective factors for 24 h PONV incidence and cumulative PONV incidence. The combination of TEAS and palonosetron was the most effective strategy to reduce the PONV incidence (P < 0.001). Conclusions and Relevance: TEAS attenuated the PONV incidence and severity in high-risk surgical patients and may be applied clinically as a complement therapy to prevent PONV. Clinical Trial Registration: https://clinicaltrials.gov/ct2/show/NCT04043247, identifier: NCT04043247.

Development and validation of a nomogram to predict chronic postoperative pain in elderly orthopedic patients.

BACKGROUND: At present, there is no nomogram for predicting chronic postoperative pain (CPSP) in elderly orthopedic patients. This study aimed to develop and validate a predictive nomogram of CPSP in elderly orthopedic patients, in order to analyze the risk factors of CPSP in elderly patients undergoing orthopedic surgery and provide support for the clinical prediction of the CPSP in elderly orthopedic patients. METHODS: A total of 1,227 elderly patients undergoing elective orthopedic surgery were enrolled. The demographic and clinical data of patients were collected from the hospital electronic case system, and CPSP was diagnosed 3 months after surgery by telephone questionnaire based on the standards of the International Association for the Study of Pain (IASP). Patients were divided into two groups according to whether or not they had CPSP, and a predictive nomogram was developed using multivariate logistic regression analysis, followed by internal and external validation. RESULTS: Six variables were selected as independent predictors of CPSP in elderly patients undergoing orthopedic surgery: spouse or not, preoperative pain at surgical site, preoperative pain at non-surgical site, type of surgery, postoperative hospital stay, and acute postoperative pain (APSP) or not (P<0.05). The area under the curve (AUC) of this nomogram was 0.815 [95% confidence interval (CI): 0.783-0.847], showing good calibration and clinical practicability. CONCLUSIONS: The predictive nomogram of CPSP in this study has good prediction ability and accuracy, and can play an important auxiliary role in screening high-risk elderly patients with CPSP undergoing orthopedic surgery.

Propofol Regulates the TLR4/NF-κB Pathway Through miRNA-155 to Protect Colorectal Cancer Intestinal Barrier.

Surgery for colorectal cancer (CRC) can cause damage to the intestinal mucosal barrier and lead to bacterial invasion. This study mainly analyzed whether propofol (PPF) could protect the intestinal mucosal barrier damage caused by CRC surgery, and explored its molecular mechanism. A mouse CRC model was constructed using azomethane and dextran sulfate sodium. During anesthesia, continuous intravenous injection of PPF was used for intervention. The influences of PPF on intestinal mucosal permeability and bacterial invasion were detected. The levels of microRNA (miR)-155, Toll-like receptor 4 (TLR4)/NF-κB in the intestinal mucosa, and the location of miR-155 were detected by fluorescence in situ hybridization (FISH). Mouse macrophages were used to analyze the regulation of miR-155 on the secretion of inflammatory cytokines through the TLR4/NF-κB pathway. PPF treatment promoted the expression of tight junction protein in the intestinal mucosa, protected the intestinal barrier, inhibited the translocation of intestinal bacteria, and increased the level of the beneficial bacterium Lactobacillus on the mucosal surface. In addition, PPF treatment could inhibit the expression of miR-155, TLR4/NF-KB, and reverse inflammatory response. miR-155 was expressed in macrophages of intestinal mucosa tissue. Overexpression of miR-155 promoted the nuclear translocation of NF-κB and the expression of inflammatory cytokines in macrophages. The use of VIPER to inhibit TLR4 reversed the pro-inflammatory effects of miR-155. PPF might inhibit the activation of the NF-κB pathway by downregulating miR-155 expression, thereby reducing the secretion of inflammatory cytokines. This might be the mechanism by which PPF protected the intestinal barrier of CRC surgical model mice.

Prophylactic norepinephrine infusion for postspinal anesthesia hypotension in patients undergoing cesarean section: A randomized, controlled, dose-finding trial.

STUDY OBJECTIVE: Prophylactic norepinephrine infusion effectively lowers the incidence of postspinal anesthesia hypotension. The optimal prophylactic dose of norepinephrine remains undefined. The purpose of this study was to investigate the optimal prophylactic dose of norepinephrine to prevent postspinal anesthesia hypotension in patients undergoing cesarean section. DESIGN: Prospective, double-blind, randomized, controlled, dose-finding trial. SETTING: Operating room from March 2020 to June 2020. PATIENTS: Ninety nine primipara or multipara women 18 - 40 years of age, singleton pregnancy ≥ 37 weeks, American Society of Anesthesiologists' physical status 1 or 2, scheduled for elective cesarean section under spinal anesthesia were included in this study. INTERVENTION: Patients were randomly assigned into groups to receive normal saline (NS) or one of four different prophylactic doses (0.025 [NE25], 0.05 [NE50], 0.075 [NE75], and 0.1 [NE100] ug/kg/min) of norepinephrine. The primary end point was the incidence of postspinal anesthesia hypotension (systolic blood pressure [SBP] < 80% of baseline) within 15 min after spinal anesthesia. Secondary outcomes included the overall stability of SBP control versus baseline (median performance error [MDPE] and median absolute performance error [MDAPE]), the dose that would be effective in preventing postspinal anesthesia hypotension in 50% (effective dose, ED 50) and 90% (ED90) of patients, other adverse events (bradycardia, nausea, vomiting, hypertension, and the total additional bolus of norepinephrine and atropine), and neonatal outcomes (blood gas values and Apgar scores). MEASUREMENTS AND MAIN RESULTS: The incidence of postspinal anesthesia hypotension in NS, NE25, NE50, NE75, and NE100 groups was 68.42% (13/19), 40.00% (8/20), 20.00% (4/20), 15.00% (3/20), and 10.00% (2/20), respectively. With increasing prophylactic doses of norepinephrine, the incidence of postspinal anesthesia hypotension decreased (p < 0.001), SBP was maintained closer to the baseline (MDPE, p < 0.001; MDAPE, p = 0.001), and the total additional bolus of norepinephrine decreased (p < 0.001). The ED50 and ED90 values of norepinephrine were 0.016 (95% CI: -0.014 - 0.033) and 0.088 (95% CI: 0.068 - 0.133) ug/kg/min, respectively. Other adverse effects, neonatal outcomes, and the total additional bolus of atropine did not differ among the five groups. CONCLUSIONS: A prophylactic dose of 0.05 or 0.075 µg/kg/min norepinephrine prevents postspinal anesthesia hypotension in patients undergoing cesarean section.

Anesthetic consideration for airway management in patient undergoing tracheal resection and reconstruction for severe postintubation tracheal stenosis: a case report.

Introduction Severe postintubation tracheal stenosis (PITS) is a rare iatrogenic complication after endotracheal intubation.Case presentation A case of PITS in a 51-year-old male undergoing partial pericardiectomy with a principal diagnosis of tuberculous constrictive pericarditis. Within 6 hours of extubation, a second emergency intubation lasting 120 hours was performed. The patient reported exertional dyspnea 30 days after discharge. High-resolution tracheobronchial tree computed tomography with three-dimensional reconstruction revealed constriction of the tracheal lumen of more than 80% at the thyroid planar upper third of the trachea. Flexible bronchoscopy revealed a tracheal stenosis located 3-4 cm from the glottis that could not be passed prior to general anesthesia. Mechanical ventilation with a ProSeal laryngeal mask airway (PLMA) and preparation for extracorporeal circulation as a final rescue option were performed to maximize patient safety. The patient underwent a tracheal resection and reconstruction without complications.Conclusion A supraglottic airway mode may be a practical and worthwhile alternative for patients with severe PITS.

Norepinephrine prophylaxis for postspinal anesthesia hypotension in parturient undergoing cesarean section: a randomized, controlled trial.

OBJECTIVE: To investigate the efficacy and safety of prophylactic infusion of norepinephrine (NE) versus normal saline in patients undergoing cesarean section. METHODS: Patients (n = 97) were randomized to receive a bolus of NE (6 µg) immediately following spinal anesthesia with maintenance NE (0.05 µg/kg/min IV) or normal saline (n = 98). The primary endpoint was the incidence of postspinal anesthesia hypotension [systolic blood pressure (SBP) < 80% of baseline] at 1-20 min following spinal anesthesia. Secondary outcomes were the overall stability of SBP control versus baseline, inferior vena cava collapsibility index (IVC-CI), other adverse events (bradycardia, nausea, vomiting, and hypertension), and neonatal outcomes (blood gas values and Apgar scores). RESULTS: The rates of postspinal anesthesia hypotension and severe postspinal anesthesia hypotension (SBP < 60% of the baseline) were significantly lower in the NE group (17.5% vs. 62.2%, p < 0.001; 7.2% vs. 17.4%, p = 0.031). In the NE group, SBP remained more stable and closer to baseline (p < 0.001), and IVC-CI values were lower 5 min after spinal anesthesia and 5 min after fetal delivery (p = 0.045; p < 0.001, respectively). Other adverse effects and neonatal outcomes were not different between the two groups. CONCLUSION: Prophylactic NE infusion effectively lowers the incidence of postspinal anesthesia hypotension and does not increase other adverse events in patients or neonates.

Mild hypothermia protects neurons against oxygen glucose deprivation via poly (ADP-ribose) signaling.

OBJECTIVE: Hypothermia is a neuroprotective mechanism that has been validated for use in alleviating neonatal hypoxic-ischemic (HI) brain injury. Nevertheless, it is unclear whether poly (ADP-ribose) (PAR) signaling is involved in hypothermia-induced neuroprotection. In this study, we investigated whether mild hypothermia rescues oxygen glucose deprivation (OGD)-induced cell death by modifying PAR-relative protein expression, such as AIF, PARP-1, and PAR polymer, in primary-cultured hippocampal neurons. METHODS: We analyzed neuronal morphology and related protein expression of PAR signaling after OGD followed by mild hypothermia in primary-cultured newborn hippocampal neurons. RESULTS: Hypothermic treatment resulted in improved neuronal viability and alleviated DNA damage. Results from the protein assay showed that hypothermia attenuated nuclear translocation of apoptosis-inducing factor (AIF), inhibited overactivation of poly(ADP-ribose) polymerase-1 (PARP-1), and decreased production of PAR polymer induced by PARP-1 activation after OGD. CONCLUSIONS: These results showed that mild hypothermia partially protects immature hippocampal neurons against OGD injury in part by interfering with the PAR signaling pathway.

Barotrauma after liquid nitrogen ingestion: a case report and literature review.

A 25-year-old man developed a gastric perforation after ingesting a homemade drink containing liquid nitrogen. Surgical repair had to be postponed to seek consultations with experts because the available practitioners in this case, including emergency physicians, surgeons, and anesthesiologists, had little experience and knowledge about the source of the patient's pneumothorax and subcutaneous emphysema. The patient ultimately underwent exploratory laparotomy with general anesthesia, considering that delaying the operation would lead to a longer duration of bacterial peritonitis and delay the standard treatment of postoperative systemic infectious complications. Our literature review revealed that barotrauma is the unique injury mechanism underlying liquid nitrogen ingestion. Injuries to the airway and esophagus are rare.

Suppression of Inner Mitochondrial Membrane Peptidase 2-Like (IMMP2L) Gene Exacerbates Hypoxia-Induced Neural Death Under High Glucose Condition.

It is known that diabetes hyperglycemia enhances cerebral ischemia and reperfusion induced damage. We have previously shown that mutation of inner mitochondrial membrane peptidase 2-like (IMMP2L) increases brain damage caused by transient cerebral ischemia. In this study, we attempt to examine the impact of IMMP2L deficiency on an in vitro model that mimics the diabetic hypoxic conditions. Normal IMMP2L wild type and IMMP2L gene deleted HT22 cells were cultured. Hypoxia was induced under high glucose and acidic conditions with 4 h of oxygen deprivation. Cell viability was assessed by CCK-8 assay and cell death was determined using Annexin V/7-AAD assay. Superoxide production was measured using dihydroethidium staining and mitochondrial membrane potential was detected using JC-1 probe. Suppression of IMMP2L reduced the cell viability, increased the ROS production and decreased the mitochondrial membrane potential. In conclusion, our study demonstrated that deficiency of IMMP2L in cells, cultured under hypoxia, high glucose and acidic conditions, exacerbated neuronal death under a condition that mimics in vivo cerebral ischemia in diabetic condition.