Anterior lumbar interbody fusion: single institutional review of complications and associated variables

BACKGROUND CONTEXTAs more patients undergo anterior lumbar interbody fusion (ALIF) procedures and more devices are created for that purpose, it is important to understand the complications that can arise and the variables that mitigate risk for major and minor complications.PURPOSETo assess complication rates after ALIF with or without posterior instrumentation and variables associated with increased likelihood of postoperative complications. We aim to provide this data as benchmarking to improve patient safety and surgical care.STUDY DESIGNA single-center retrospective cohort study.PATIENT SAMPLEAll adult patients who underwent ALIF between 2017 and 2019 was performedOUTCOME MEASURESPost-operative major and minor complications were evaluated.METHODSComplications were recorded and presented as percentages. Patient demographics, perioperative, and postoperative data were also collected and analyzed between patients who had no complications and those that had any complication. Subgroup analysis of surgical complications were performed by nonparametric Chi-square tests. Continuous variables were compared using Mann-Whitney U tests.RESULTSNinty-five of three hundred sixty-two (26.2%) of patients experienced a minor or major complication. Among the most common complications found were surgical site infections (5.8%), neurological complications (4.1%), vascular complications (3.6%), and urinary tract infections (3.3%). Patients undergoing ALIF alone with post-operative complications had higher mean age, higher BMI, higher ASA status, and experienced higher estimated blood loss. Patients undergoing ALIF and posterior instrumentation with post-operative complications were more likely to have diabetes and had a higher ASA status. Patients with any complications from both groups had longer length of stay, discharge to a non-home setting and were more likely to be readmitted or return to the operating room.CONCLUSIONOur study reveals variables associated with complications at our institution, including age of the patient, BMI, and ASA status leading to higher complications and greater LOS, higher readmission rates, and disposition to skilled facilities.     

重组腺病毒介导LacZ基因在大鼠肺脏的表达

目的探讨重组腺病毒介导的β-半乳糖苷酶(LacZ)基因在大鼠肺脏的转基因表达。方法Wistar大鼠70只,随机分为Ad-Null组和Ad-LacZ组(n=35),分别应用1．67×10~9pfu／ml复制缺陷型重组腺病毒AdCMV和AdCMVLacZ各600μl,经气管导管滴入；各组于滴人病毒后2、5、7、14、21、28和35 d行肺组织X-gal染色。另取大鼠20只,随机分为C组、L组、M组和H组(n=5),分别应用病毒保存液和低滴度(1．67×10~8pfu／ml)、中滴度(1．67×10~9pfu／ml)、高滴度(5×10~9pfu／ml)的AdCMVLacZ各600μl,滴入病毒后7 d行肺组织X-gal染色和HE染色。结果滴入病毒后2 d,Ad-LacZ组肺组织内即有转基因表达,滴人后7 d达高峰,并维持至35 d；转基因表达位于气管、支气管上皮细胞和肺泡细胞。H组、M组转基因阳性细胞率明显高于L组和C组(P＜0．01)。HE染色显示,H组中3只大鼠肺组织有轻度炎性浸润。所有动物均未见远隔器官转基因表达。结论气管内滴人重组腺病毒可呈剂量依赖性介导LacZ基因在大鼠肺内表达,但过高剂量可诱发机体炎性反应。     

利多卡因对N-甲基-D-天冬氨酸抑制大鼠肾上腺嗜铬细胞瘤细胞增殖的影响

目的 观察利多卡因对 N-甲基-D-天冬氨酸(NMDA)抑制大鼠肾上腺嗜铬细胞瘤细胞(PC12细胞)增殖的影响。方法 将体外培养的 PC12细胞分为6组，分别采用正常不含药液的培养基(C组)；含400μmol·L(-1)NMDA 的培养基(N组)；NMDA 分别混合10μmol·L~(-1)(L_1组)、10~2μmol·L~(-1)(L_2组)、10~3μmol·L~(-1)(L_3组)以及10~4μmol·L~(-1)(L_4组)利多卡因的培养基培养5d，应用流式细胞仪测定细胞 DNA 相对含量，解析细胞周期，计算 S 期细胞荧光强度占受测细胞总荧光强度的百分数为 S期分数(SPF)和 S 期与 G_2期细胞荧光强度之和与 M 期细胞荧光强度的比值[(S G_2)/M]。结果 与C 组比较，N、L_1组 SPF 和(S G_2)/M 均降低(P<0.05)，L_4组 SPF 降低(P<0.05)，而 L_2及 L_3组 SPF和(S G_2)/M 差异无统计学意义(P>0.05)。与 N 组比较，L_2、L_3及 L_4组 SPF 和(S G_2)/M 升高(P<0.05)，L_1组 SPF 升高(P<0.05)，而(S G_2)/M 差异无统计学意义(P>0.05)。结论 NMDA 可以通过抑制 PC12细胞 DNA 合成而影响细胞的增殖活性，利多卡因能拮抗 NMDA 对 PC12细胞增殖的抑制作用。     

异丙酚预处理对大鼠离体心脏缺血-再灌注损伤的影响

目的 探讨异丙酚预处理对心肌缺血-再灌注(I-R)损伤的作用及其机制。方法 成年雄性 SD 大鼠18只，随机分为对照组(C组)、I-R 组、50μmol/L 异丙酚预处理组(P组)，每组6只。建立Langendorff 离体心脏灌流模型，平衡35min 后 I-R 组和 P 组均停灌30min，然后复灌120min。其中 P 组停灌前用含50μmol/L 异丙酚的 K-H 液灌流10min，并用无异丙酚的 K-H 液冲洗10min。C 组不停灌，也不用异丙酚处理。灌流结束后，制备心肌组织匀浆，测定 NO 含量、总 NOS 及超氧化物歧化酶(SOD)活性，用免疫组化 SABC 染色检测诱导型 NOS(iNOS)蛋白与血红素氧化酶-1(HO-1)蛋白表达水平，同时行光镜及透射电镜观察。结果病理学显示 C 组正常，I-R 组心肌组织严重损伤，P 组轻度损伤；与C 组相比，I-R 组和 P 组 iNOS、HO-1蛋白表达量和 iNOS 活性均升高，cNOS 活性均降低(P<0.05或0.01)；I-R 组总 NOS 活性和 NO 含量、Cu.Zn-SOD、Mn-SOD 和总 SOD 活性均降低(P<0.05或0.01)，但P 组无变化(P>0.05)。与 I-R 组比较，P 组除 iNOS 活性不变外，其余指标均升高(P<0.05或0.01)。结论 异丙酚预处理对心肌 I-R 损伤具有保护作用，其机制在于抑制或清除氧自由基以降低氧化应激水平，并通过恢复 cNOS 活性而增加 NO 的含量。     

老年患者不同靶浓度罗库溴铵肌松效应的比较

目的比较老年患者不同靶浓度罗库溴铵的肌松效应。方法择期全麻老年患者100例,ASAⅡ级,随机分为4组(n=25),A组、B组和C组麻醉诱导气管插管时效应室靶浓度(Ce)为3μg/ ml,术中维持Ce分别为0.6、0.8、1.0μg/ml;D组麻醉诱导气管插管时Ce为3.3μg/ml,术中维持Ce为0_8μg/ml。记录肌松起效时间、恢复时间和恢复指数。评价气管插管条件和术中肌松程度。记录手术及TCI时间、罗库溴铵总用药量和期间用药量[总用药量,(体重×TCI时间)]。结果4组均可顺利完成气管插管,D组起效时间较A组、B组和C组缩短(P<0.05);A组肌松满意率低,B组、C组和D组均可维持满意肌松,但C组罗库溴铵用量较多,术中肌松程度较大,术后恢复时间较长(P<0.05)。结论麻醉诱导气管插管时罗库溴铵Ce为3.3μg/ml、术中麻醉维持Ce为0.8μg/ml,可产生满意的肌松条件,且有利于术后肌松恢复,是一种适用于老年患者合理的TCI给药方案。     

Fetal anaesthesia for intrauterine treatment

Fetal anaesthesia was performed 5 times in 1 patient to treat pleural effusions, obtain fetal blood sampling, provide albumin infusion, and establish and replace a pleuro-amniotic indwelling shunt catheter under ultrasound guidance. A maternal epidural catheter was placed and used for epidural anaesthesia for the first 4 anaesthetics. Fetal administration of pancuronium 0.15 mg·kg^?1 via the umbilical vein or 0.25 mg·kg^?1 intramuscularly was enough to produce immobilization without maternal effect. However, maternal pretreatment with intravenous diazepam and fentanyl was required for fetal sedation and analgesia, which was necessary for accurate and safe injection, and for suppression of fetal stress.     

左旋精氨酸对体外循环心内直视手术心肌保护作用研究

目的研究左旋精氨酸(L-Arg)对体外循环心内直视手术心肌的保护作用。方法12例风湿性心脏病心脏手术患者随机分对照组(A)和治疗组(B)。常规全身麻醉、中度低温体外循环下手术。体外循环前,A组经颈内静脉注射泵泵入单纯10%葡萄糖注射液,B组泵入含L-Arg10%葡萄糖注射液,两组分别在麻醉前,心肺转流(CPB)前,CPB后30min、1h、2h通过Swan-Ganz导管监测右房压(RAP)、肺动脉平均压(PAMP)、肺毛细血管楔压(PCWP)、平均动脉压(MAP)及心排血量(CO)。结果A组RAP、PAMP和PCWP较CPB前明显升高,MAP和CO明显降低;B组RAP、PAMP和PCWP较CPB前明显降低,MAP和CO明显升高。A、B两组组间RAP、PAMP、PCWP、MAP及CO比较,差异有统计学意义(P<0.05)。结论L-Arg对体外循环心内直视手术心肌有保护作用。     

FNDC5 attenuates adipose tissue inflammation and insulin resistance via AMPK-mediated macrophage polarization in obesity

BackgroundObesity-induced chronic inflammation is critical in the pathogenesis of insulin resistance, and the recruitment and proinflammatory activation of adipose tissue macrophages (ATMs) is important for the development of this process. Here, we examined the effects of fibronectin type III domain-containing 5 (FNDC5) on inflammation and insulin resistance in high-fat diet-induced obese mice.Materials and MethodsMale wild-type (WT) and FNDC5^−/− mice were fed with standard chow (Ctrl) or high fat diet (HFD) for 20 weeks to induce obesity and insulin resistance. Firstly, effects of FNDC5 gene deletion on obesity, insulin resistance, macrophage accumulation and polarization and adipose tissue inflammation were determined in mice. Secondly, the macrophage polarity shift was further examined with flow cytometry in isolated stromal vascular fraction (SVF). Thirdly, the effects of exogenous FNDC5 on lipopolysaccharide (LPS)-induced macrophage polarization, inflammation and the underlying signaling mechanism were investigated in RAW264.7 macrophages and primary mouse peritoneal cavity macrophages (PMs). Finally, the therapeutic effects of FNDC5 overexpression were examined in HFD-induced obese WT and FNDC5^−/− mice.ResultsFNDC5 gene deletion aggravated obesity, insulin resistance, fat accumulation and inflammation accompanied with enhanced AMPK inhibition, macrophages recruitment and M1 polarization in mice fed with HFD. Exogenous FNDC5 inhibited LPS-induced M1 macrophage polarization and inflammatory cytokine production via AMPK phosphorylation in both RAW264.7 macrophages and PMs. FNDC5 overexpression attenuated insulin resistance, AMPK inhibition, M1 macrophage polarization and inflammatory cytokine production in adipose tissue of obese WT and FNDC5^−/− mice.ConclusionsFNDC5 attenuates adipose tissue inflammation and insulin resistance via AMPK-mediated macrophage polarization in HFD-induced obesity. FNDC5 plays several beneficial roles in obesity and may be used as a therapeutic regimen for preventing inflammation and insulin resistance in obesity and diabetes.     

Development and Validation of a Natural Language Processing Tool to Identify Injuries in Infants Associated With Abuse

ObjectivesMedically minor but clinically important findings associated with physical child abuse, such as bruises in pre-mobile infants, may be identified by frontline clinicians yet the association of these injuries with child abuse is often not recognized, potentially allowing the abuse to continue and even to escalate. An accurate natural language processing (NLP) algorithm to identify high-risk injuries in electronic health record notes could improve detection and awareness of abuse. The objectives were to: 1) develop an NLP algorithm that accurately identifies injuries in infants associated with abuse and 2) determine the accuracy of this algorithm.MethodsAn NLP algorithm was designed to identify ten specific injuries known to be associated with physical abuse in infants. Iterative cycles of review identified inaccurate triggers, and coding of the algorithm was adjusted. The optimized NLP algorithm was applied to emergency department (ED) providers’ notes on 1344 consecutive sample of infants seen in 9 EDs over 3.5 months. Results were compared with review of the same notes conducted by a trained reviewer blind to the NLP results with discrepancies adjudicated by a child abuse expert.ResultsAmong the 1344 encounters, 41 (3.1%) had one of the high-risk injuries. The NLP algorithm had a sensitivity and specificity of 92.7% (95% confidence interval [CI]: 79.0%–98.1%) and 98.1% (95% CI: 97.1%–98.7%), respectively, and positive and negative predictive values were 60.3% and 99.8%, respectively, for identifying high-risk injuries.ConclusionsAn NLP algorithm to identify infants with high-risk injuries in EDs has good accuracy and may be useful to aid clinicians in the identification of infants with injuries associated with child abuse.     

乙酰半胱氨酸对兔肝缺血再灌注损伤的保护机制探讨

目的探讨家兔肝脏缺血再灌注损伤的机制及N-乙酰半胱氨酸(NAC)对兔肝组织的保护作用。方法 40只成年兔(3~4周龄),体质量3.5~4.5 kg,随机分为肝缺血再灌注组(IR组)和肝缺血再灌注+NAC组(IR+NAC组),于门静脉阻断前(T0)、门静脉开放即刻(T1)、开放后2 h(T2)、5 h(T3)和7 h(T4)分别采用全自动生化分析仪测定各组血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)水平;黄嘌呤氧化酶法测定血清丙二醛(MDA)和超氧化物岐化酶(SOD)活性;TUNEL法和琼脂糖凝胶电泳法检测肝细胞凋亡并计算凋亡指数。结果与T0比较,2组T1、T2、T3、T4各时间点ALT、AST及MDA显著升高、SOD显著降低;与IR组比较,IR+NAC组T1、T2、T3、T4各时间点ALT、AST及MDA明显下降而SOD明显升高,肝脏病理损伤改善;与IR组比较,IR+NAC组在再灌注后5 h、7 h,凋亡细胞减少及细胞凋亡率明显降低。结论 NAC对家兔肝脏缺血再灌注损伤有明显的保护作用,其可能机制与NAC清除氧自由基从而抑制肝细胞凋亡有关。