Sepsis-associated encephalopathy (SAE) is a diffuse neurological injury that results from severe sepsis, and its underlying pathophysiological mechanisms remain largely unknown. This study aimed to elucidate the pathological basis of SAE and identify potential diagnostic biomarkers by integrating analyses of the intestinal microbiome, plasma metabolomics, and circulating microRNAs (miRNAs). We analyzed data from 50 patients who were divided into SAE or non-SAE groups. The results revealed significant differences in microbial composition between these groups, with a marked decrease in Bacteroides abundance and an increase in Enterococcus abundance in SAE patients. Compared with non-SAE patients, SAE patients presented notable alterations in LysoPC 18:3, linoleic acid, and miRNA PC-3p-535_63045 levels. Multiomics association analysis revealed positive correlations between Enterococcus and LysoPC 18:3, whereas Bacteroides and PC-3p-535_63045 were negatively correlated with linoleic acid. Gene prediction analysis indicated that PC-3p-535_63045 was enriched in PIK3R1, and a KEGG pathway analysis underscored the role of the PI3K‒Akt signaling pathway. PC-3p-535_63045 exhibited strong diagnostic performance, with an AUC of 0.850 (specificity of 0.867, sensitivity of 0.800). Comparative ROC analysis revealed no significant difference between PC-3p-535_63045 alone and the multiomics model. The integrated results from multiomics LASSO regression and random forest analyses suggest that PC-3p-535_63045 is a promising biomarker for the diagnosis of SAE. In conclusion, our multiomics analysis revealed a significant association among Bacteroides, PC-3p-535_63045, and linoleic acid, which suggests that the PI3K-Akt signaling pathway may play an important role in SAE progression. These findings deepen our understanding of the pathophysiological mechanisms underlying SAE and may ultimately enhance diagnostic and predictive capabilities for this condition.

Abstract Sepsis-associated acute kidney injury (SA-AKI) presents a significant diagnostic challenge in intensive care units (ICUs), largely due to the limitations of current biomarkers. This study utilized early metabolic signatures of sepsis—specifically pre-AKI metabolic features in sepsis—to identify characteristic metabolites capable of predicting the occurrence of SA-AKI within 48 h. Using non-targeted metabolomics, serum samples from 50 sepsis patients were analyzed, including 28 patients in the SA-AKI group and 22 in the sepsis-non-AKI group. Machine learning integration of the least absolute shrinkage and selection operator (LASSO) regression and Boruta algorithms identified diagnostic metabolites. Subsequently, molecular docking was employed to explore potential metabolite-protein interactions. Among 634 detected metabolites, five key biomarkers were identified: Sebacic acid, 1-(β-D-Ribofuranosyl)-1,4-dihydronicotinamide (1-RDN), Threonic acid, Methyl acetate, and Acylcarnitine 10:2. Using leave-one-out cross-validation (LOOCV), where one patient was designated as the test set in each iteration repeated 50 times, the support vector machine (SVM) prediction model achieved an AUC value of 0.89 in the validation cohort. Molecular docking predicted stable binding between 1-RDN and phenylalanine hydroxylase (binding energy = −7.9 kcal/mol), suggesting a potential interaction and crosstalk between fatty acid metabolism and phenylalanine pathway dysregulation. This integrated metabolomics and machine learning approach, complemented by in silico molecular docking, successfully delineated early metabolic signatures of SA-AKI, provided a predictive model for early clinical intervention, and generated testable hypotheses regarding the molecular interactions linking metabolic dysregulation to renal injury.

Background:Sepsis-associated encephalopathy (SAE), a devastating complication of sepsis, lacks specific biomarkers and clear pathophysiological understanding, particularly regarding the gut-brain axis. While gut dysbiosis is implicated in SAE, the underlying mechanisms remain elusive. Methods:This study employed an integrated multiomics approach (16S rDNA and fecal miRNA sequencing) to dissect the gut microenvironment in SAE patients (n = 10) compared to sepsis patients without encephalopathy (SP, n = 20). Results:Although α- and β-diversity indices showed no significant differences, distinct compositional shifts in the gut microbiota were observed in SAE patients, characterized by increased abundance of Neisseria, Haemophilus, Lautropia, Enterococcus, Parabacteroides, and decreased Fusobacterium, Phocaeicola, Bacteroides, among others. Concurrently, 12 fecal miRNAs were differentially expressed (DE) in SAE, with 11 upregulated (e.g., miR-106a-5p, miR-181a-5p, miR-223-5p, miR-30e-3p) and 1 downregulated (miR-222-3p). Crucially, correlation network analysis revealed significant interactions between 10 DE miRNAs and 15 bacterial genera, establishing a complex gut microbiota-miRNA interplay in SAE. Machine learning (LASSO and elastic net regression) identified miR-30e-3p and miR-223-5p as the most promising combined diagnostic biomarkers, achieving an area under the curve (AUC) of 0.893. Functional exploration via ceRNA network analysis indicated miR-30e-3p targets inflammation and apoptosis-related genes (e.g., IL1B, RPS6KB1, AKT1), while miR-223-5p primarily targets immune-regulatory genes (e.g., IGF1, AR). Experimental validation confirmed significantly elevated serum IL-1β levels in SAE patients (p < 0.001), supporting the predicted inflammatory pathway. Conclusion:This study provides the first evidence of a fecal miRNA-gut microbiota interaction network in SAE pathogenesis, highlighting miR-30e-3p and miR-223-5p as pivotal mediators and potential diagnostic/therapeutic targets.

AIMS:Post-cardiac arrest brain injury (PCABI) is a leading cause of death in cardiac arrest/cardiopulmonary resuscitation (CA/CPR) victims and long-term disability in CA/CPR survivors. Despite previous evidence indicating that the microbiota-gut-brain axis is critically involved in many neurological disorders, no research has hitherto established a connection between the gut microbiota and PCABI through this axis. This study aims to explore the biological roles of microbial tryptophan metabolites in the progression of PCABI. METHODS:To achieve this, we pretreated rats with a cocktail of broad-spectrum antibiotics (Abx) to eradicate the gut microbiota before establishing a 7-min asphyxia-CA/CPR model. RESULTS:Remarkably, the 24-h survival rate and neurological outcomes improved in Abx/CPR rats. Fecal 16s rDNA sequencing and PICRUSt2 analysis revealed that Abx reshaped the microbial community and elevated the proportion of microbial tryptophan metabolism in rats. Metabolomic profiling suggested that Abx shifted the phenotype of microbial tryptophan metabolism from the indole pathway to the kynurenine pathway, thereby increasing the levels of the neuroprotective metabolite kynurenine in the feces, circulation, and ultimately the brain. Furthermore, the hippocampal expression of aryl hydrocarbon receptor (AhR), an endogenous receptor of kynurenine, was upregulated in Abx/CPR rats. In vitro experiments further demonstrated that the neuroprotective effects of kynurenine are AhR-dependent and that AhR activation could negatively regulate the NLRP3 protein expression. Supporting this, results from qRT-PCR, immunohistochemistry, and immunofluorescence in the rat cerebral cortex exhibited that L-kynurenine inhibited NLRP3-induced pyroptosis. CONCLUSIONS:Our study provides a direct clue to the essential participation of the microbiota-gut-brain axis in the progression of PCABI. It demonstrates that kynurenine might attenuate PCABI by inhibiting NLRP3-induced pyroptosis.

Stroke is a major healthcare problem worldwide, particularly in the elderly population. Despite limited research on the development of prediction models for mortality in elderly individuals with ischemic stroke, our study aimed to address this knowledge gap. By leveraging data from the Medical Information Mart for Intensive Care IV database, we collected comprehensive raw data pertaining to elderly patients diagnosed with ischemic stroke. Through meticulous screening of clinical variables associated with 28-day mortality, we successfully established a robust nomogram. To assess the performance and clinical utility of our nomogram, various statistical analyses were conducted, including the concordance index, integrated discrimination improvement (IDI), net reclassification index (NRI), calibration curves and decision curve analysis (DCA). Our study comprised a total of 1259 individuals, who were further divided into training (n = 894) and validation (n = 365) cohorts. By identifying several common clinical features, we developed a nomogram that exhibited a concordance index of 0.809 in the training dataset. Notably, our findings demonstrated positive improvements in predictive performance through the IDI and NRI analyses in both cohorts. Furthermore, calibration curves indicated favorable agreement between the predicted and actual incidence of mortality (P > 0.05). DCA curves highlighted the substantial net clinical benefit of our nomogram compared to existing scoring systems used in routine clinical practice. In conclusion, our study successfully constructed and validated a prognostic nomogram, which enables accurate short-term mortality prediction in elderly individuals with ischemic stroke.

ABSTRACT Introduction: The present study aimed to explore the clinical features and long-term outcomes associated with neurologic impairment in patients with cardiac arrest (CA) who received extracorporeal cardiopulmonary resuscitation (ECPR). Methods: A total of 37 adult CA patients who underwent venoarterial extracorporeal membrane oxygenation and were admitted to our department between January 2015 and February 2022 were divided according to neurologic impairment. Baseline and CPR- and ECMO-related characteristics were compared between the two groups. Long-term neurologic outcomes were collected via telephone follow-ups. Results: Twenty-four (64.9%) ECPR-supported patients developed neurologic impairments. The two groups differed significantly in median age ( P = 0.026), proportion of intra-aortic balloon pump (IABP) support ( P = 0.011), proportion of continuous renal replacement therapy ( P = 0.025), and median serum creatinine (Cr) level ( P = 0.012) pre-ECMO. The 28-day mortality ( P = 0.001), hospital mortality ( P = 0.003), median duration from CA to restoration of spontaneous circulation ( P = 0.029), proportion of patients with nonpulsatile perfusion (NP) >12 hours ( P = 0.040), and median ECMO duration ( P = 0.047) were higher in the neurologic impairment group. In contrast, the group without neurologic impairment exhibited a longer median intensive care unit length of stay ( P = 0.047), longer median hospital LOS ( P = 0.031), and more successful ECMO weaning ( P = 0.049). Moreover, NP >12 hours combined with IABP support (odds ratio [OR], 14.769; 95% confidence interval [CI], 1.417~153.889; P = 0.024) and serum Cr level (OR, 1.028; 95% CI, 1.001~1.056; P = 0.043) were independent risk factors for neurologic impairment. Furthermore, neurologic impairment was associated with significantly worse 90-day survival (hazards ratio, 4.218; 95% CI, 1.745~10.2; P = 0.0014). Conclusions: The incidence of neurologic impairment was higher in patients who received ECPR and was closely related to 28-day mortality and discharge survival. NP >12 hours combined with IABP support and serum Cr levels were independent risk factors for neurologic impairments in ECPR-supported patients. Neurologic impairment significantly adversely affected the long-term outcomes of ECPR-supported patients after discharge.

Sepsis-associated encephalopathy (SAE) is an acute neurological deficit caused by severe sepsis without signs of direct brain infection, characterized by the systemic inflammation and disturbance of the blood-brain barrier. SAE is associated with a poor prognosis and high mortality in patients with sepsis. Survivors may exhibit long-term or permanent sequelae, including behavioral changes, cognitive impairment, and decreased quality of life. Early detection of SAE can help ameliorate long-term sequelae and reduce mortality. Half of the patients with sepsis suffer from SAE in the intensive care unit, but its physiopathological mechanism remains unknown. Therefore, the diagnosis of SAE remains a challenge. The current clinical diagnosis of SAE is a diagnosis of exclusion; this makes the process complex and time-consuming and delays early intervention by clinicians. Furthermore, the scoring scales and laboratory indicators involved have many problems, including insufficient specificity or sensitivity. Thus, a new biomarker with excellent sensitivity and specificity is urgently needed to guide the diagnosis of SAE. MicroRNAs have attracted attention as putative diagnostic and therapeutic targets for neurodegenerative diseases. They exist in various body fluids and are highly stable. Based on the outstanding performance of microRNAs as biomarkers for other neurodegenerative diseases, it is reasonable to infer that microRNAs will be excellent biomarkers for SAE. This review explores the current diagnostic methods for sepsis-associated encephalopathy (SAE). We also explore the role that microRNAs could play in SAE diagnosis and if they can be used to make the SAE diagnosis faster and more specific. We believe that our review makes a significant contribution to the literature because it summarizes some of the important diagnostic methods for SAE, highlighting their advantages and disadvantages in clinical use, and could benefit the field as it highlights the potential of miRNAs as SAE diagnostic markers.

目的 设计腰大池引流定位定量报警装置并验证其应用效果.方法 腰大池引流定位定量报警装置由升降调节杆、重量报警装置、激光笔、刻度尺、腰大池引流袋、侧面板、主面板等组成.选取杭州市某三级甲等医院危重症医学科2022年5月—9月的21例卧床留置腰大池引流管患者为试验组,使用腰大池引流定位定量报警装置;2022年1月—4月的21例卧床留置腰大池引流管患者为对照组,使用传统工具定位.比较两组患者定位时间、定位高度差值、护理人员满意度及每日引流量的差异.结果 试验组腰大池引流袋定位时间为(12.32±2.93)s,短于对照组(33.24±8.84)s,差异具有统计学意义(t=38.298,P＜0.001);试验组定位高度差值为(1.25±0.21)mm,小于对照组(7.03±1.92)mm,差异具有统计学意义(t=20.456,P＜0.001);试验组护理人员满意度(100％)高于对照组(28.57％),差异具有统计学意义(P＜0.05).试验组每日引流量为(162±13)ml,对照组为(165±37)ml,目标准确度高于对照组.结论 腰大池引流定位定量报警装置可节约定位测量时间,减小定位高度误差,提高护理人员满意度.

BackgroundGut–microbiota–brain axis links the relationship between intestinal microbiota and sepsis-associated encephalopathy (SAE). However, the key mediators between them remain unclear.MethodsMemory test was determined by Water maze. Intestinal flora was measured by 16S RNA sequencing. Neurotransmitter was detected by high-performance liquid chromatography (HPLC). Histopathology was determined by H&E, immunofluorescence (IF), and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining. Flow cytometry was employed to determine the proportion of macrophages.ResultsFecal microbiota transplantation (FMT) relieved hippocampus impairment of SAE rats by inhibiting inflammation cytokine secretion, the expression of IBA-1 and neurotransmitter disturbance, and cell apoptosis and autophagy, accompanied by the reduced M1 polarization and M1 pro-inflammation factors produced by macrophages in mesenteric lymph nodes (MLNs). Actually, M1 polarization in SAE rats depended on intestinal epithelial cell (IEC)-derived exosome. GW4869-initiated inhibition of exosome secretion notably abolished M1 polarization and the secretion of IL-1β. However, GW4869-mediated improvement of hippocampus impairment was counteracted by the delivery of recombinant interleukin (IL)-1β to hippocampus. Mechanistically, IEC-derived exosome induced the excessive circulating IL-1β produced by CP-R048 macrophages, which subsequently induced damage and apoptosis of hippocampal neurons H19-7 in an autophagy-dependent manner. And reactivation of autophagy facilitates intestinal IL-1β-mediated hippocampal neuron injury.ConclusionCollectively, intestinal flora disturbance induced the exosome release of IECs, which subsequently caused M1 polarization in MLNs and the accumulation of circulating IL-1β. Circulating IL-1β promoted the damage and apoptosis of neurons in an autophagy-dependent manner. Possibly, targeting intestinal flora or IEC-derived exosome contributes to the treatment of SAE.

总结体外膜肺氧合技术在院内"999"急救中的应用及管理体会.完善院内体外膜肺氧合急救护理团队管理;制订"999"急救后启动体外膜肺氧合程序流程与应急预案;改进用物管理,缩短准备时间;强调医护抢救配合,注重心肺复苏质量与体外膜肺氧合置管效率;做好院内转运管理等.对10例"前IC U期"的心搏骤停患者成功建立体外膜肺氧合,从患者第1次发生心搏骤停至体外膜肺氧合成功转机时间38～74 min,平均(49.5±6.2)min;10例均成功行院内转运至IC U,未发生严重不良事件.经过整体治疗与护理,5例成功撤离体外膜肺氧合治疗后康复出院,随访3个月未有脑功能障碍等相关并发症;3例体外膜肺氧合治疗>14 d,心功能无法逆转,家属提出自动出院;2例体外膜肺氧合治疗48 h内,再次出现心搏骤停合并严重的多脏器功能衰竭死亡.

Background The main objective of this study was to investigate the role of a multimodal neurological monitoring (MNM)-guided protocol in the precision identification of neural impairment and long-term neurological outcomes in venoarterial extracorporeal membrane oxygenation (VA-ECMO) supported patients. Methods We performed a cohort study that examined adult patients who underwent VA-ECMO support in our center between February 2010 and April 2021. These patients were retrospectively assigned to the “with MNM group” and the “without MNM group” based on the presence or absence of MNM-guided precision management. The differences in ECMO-related characteristics, evaluation indicators (precision, sensitivity, and specificity) of the MNM-guided protocol, and the long-term outcomes of the surviving patients were measured and compared between the two groups. Results A total of 63 patients with VA-ECMO support were retrospectively assigned to the without MNM group (n = 35) and the with MNM group (n = 28). The incidence of neural impairment in the without MNM group was significantly higher than that in the with MNM group (82.1 vs. 54.3%, P = 0.020). The MNM group exhibited older median ages [52.5 (39.5, 65.3) vs. 31 (26.5, 48.0), P = 0.008], a higher success rate of ECMO weaning (92.8 vs. 71.4%, P = 0.047), and a lower median duration of building ECMO [40.0 (35.0, 52.0) vs. 58.0 (48.0, 76.0), P = 0.025] and median ECMO duration days [5.0 (4.0, 6.2) vs. 7.0 (5.0, 10.5), P = 0.018] than the group without MNM. The MNM-guided protocol exhibited a higher precision rate (82.1 vs. 60.0%), sensitivity (95.7 vs. 78.9%), and specificity (83.3 vs. 37.5%) in identifying neural impairment in VA-ECMO support patients. There were significant differences in the long-term outcomes of survivors at 1, 3 and 6 months after discharge between the two groups (P < 0.05). However, the results showed no significant differences in ICU length of stay (LOS), hospital LOS, survival to discharge, or 28-day mortality between the two groups (P > 0.05). Conclusion The MNM-guided protocol is conducive to guiding intensivists in the improvement of cerebral protection therapy for ECMO-supported patients to detect and treat potential neurologic impairment promptly, and then improving long-term neurological outcomes after discharge.

目的 探讨乳酸及乳酸清除率对静脉-动脉体外膜肺氧合(VA-ECMO)治疗心源性休克(CS)患者预后的评估价值.方法 回顾性分析2012年6月至2020年3月浙江大学附属杭州市第一人民医院收治的CS患者60例,收集VA-ECMO病例及临床资料,记录VA-ECMO上机前和上机后6?h、24?h、48?h、72?h患者血乳酸水平,根据28?d预后存活分组,分析确定与28?d病死率的相关变量.进一步按乳酸清除率水平高低分组,比较各时间点乳酸清除率在VA-ECMO治疗CS患者的预后评估中的效能.结果 60例CS患者经VA-ECMO治疗后48?h乳酸水平降至正常,其中48例(80％)成功脱离体外膜肺氧合(ECMO),43例(71.7％)在ECMO治疗后28?d仍存活,48?h血乳酸水平高于1.35?mmol/L是28?d全因病死率的最佳单项预测指标(P=0.014),RCO曲线下面积(AUC)为0.704.在ECMO支持后6?h、48?h和72?h测得的乳酸清除率表明,高乳酸清除率(≥10％)组的ICU住院时间、机械通气时间更长(P<0.05).结论 及早恢复患者的乳酸水平可改善预后,乳酸及乳酸清除率对VA-ECMO治疗CS患者有重要预后评估价值.

目的 探讨体外膜肺氧合(ECMO)对心脏骤停患者神经功能预后的影响因素.方法 纳入2012年1月至2020年6月因心脏骤停入住浙江大学医学院附属杭州市第一人民医院重症医学科且行ECMO治疗的22例患者.以脑功能分类(CPC)量表评价患者出院时神经功能情况,并将其分为CPC良好组(12例,CPC 1～2分)和CPC不佳组(10例,CPC 3～5分).比较两组患者的一般资料、心脏骤停病因、基础疾病、疾病严重程度、心脏骤停相关情况、神经系统相关情况、ECMO相关情况及肌钙蛋白I、白蛋白等生化指标.采用二分类Logistic回归分析ECMO治疗心脏骤停患者对其神经功能预后的影响因素.结果 22例接受ECMO治疗的心脏骤停患者中,14例存活出院且12例神经功能良好.CPC不佳组患者肌钙蛋白Ⅰ[47.0(26.8,80.0)μg/L vs.13.6(3.3,32.6)μg/L,U=20.000,P=0.017]水平较 CPC 良好组显著升高,白蛋白[(27±7)g/L vs.(33±6)g/L,t=2.485,P=0.022]水平较CPC良好组显著降低.此外,CPC不佳组患者第3天ECMO流量[(3.6±0.8)L/min vs.(3.0±0.7)L/min,t=2.091,P=0.050]高于 CPC 良好组,但两组比较差异无统计学意义.Logistic回归分析结果显示,较低的白蛋白浓度[优势比(OR)=0.755,95％置信区间(CJ)(0.576,0.990),P=0.042]是ECMO治疗心脏骤停患者神经功能预后不佳的独立危险因素.结论 较低的白蛋白浓度是ECMO治疗的心脏骤停患者神经功能预后不佳的独立危险因素.

Sepsis-associated encephalopathy(SAE) caused by infections outside the central nervous system always presents extensive brain damage.It is common in clinical practice and associated with a poor prognosis.There are problems in the assessing and diagnosing of SAE.Many factors,such as sedation and mechanical ventilation,make it difficult to assess SAE,while electrophysiological examination may play a role in the assessment.We reviewed the studies of electrophysiological techniques such as electroencephalography and somatosensory evoked potentials for monitoring SAE,hoping to provide certain evidence for the clinical evaluation and diagnosis of SAE.

Background: The aim of study was to summarize the clinical characteristics and experience of extracorporeal membrane oxygenation (ECMO) in pregnant and postpartum patients.Methods and Results: We retrospectively reviewed 131 consecutive ECMO patients at our center from May 2015 to May 2021. A total of 10 Chinese patients were pregnant or postpartum at the time of ECMO initiation. Patients ranged in age from 25 to 36 years (median age 30.5 years). The ECMO duration ranged from 3 to 31 days (median duration 8 days). There was a stabilizing trend of acid-base balance and decreasing lactic acid over the 3 days following ECMO initiation. Seven (70%) patients survived at least 48 h after weaning from ECMO. Four (40%) patients survived until discharge, and four (40%) fetuses survived until discharge.Conclusion: ECMO provides a suitable temporary cardiopulmonary support for pregnant and postpartum patients. ECMO shows a favorable effect on short-term stability in critical obstetric patients.

Background/aim: Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis that affects upwards of half of all sepsis patients. Few studies have examined the etiology and risk factors of SAE among elderly patients. This study was designed to explore the epidemiology of SAE and the risk factors associated with its development in elderly populations. Materials and methods: This was a retrospective analysis of elderly sepsis patients admitted to our intensive care unit between January 2017 and January 2022. We then compared non-SAE and SAE groups concerning baseline clinicopathological findings, underlying diseases, infection site, disease type, disease severity, biochemical findings, and 28-day mortality. We further stratified patients in the SAE group based on whether or not they survived for 28 days, and we compared the above data between these groups. Results: Of the 222 elderly sepsis patients, 132 (59.46%) had SAE. SAE patients were found to be significantly older than non-SAE patients. Both age and blood sodium concentrations were found to be associated with SAE risk, while elderly sepsis patients without underlying chronic obstructive pulmonary disease (COPD) have a relatively higher risk of developing SAE. The SAE group also had a significantly higher rate of 28-day mortality, and sequential organ failure assessment (SOFA) scores were a risk factor associated with 28-day mortality. Conclusion: Among elderly sepsis patients, SAE risk increases with advancing age, higher blood sodium concentrations, and without underlying COPD. SAE incidence is associated with a poorer prognosis, and SOFA scores are independent predictors of increased mortality among elderly SAE patients.

目的 动态观察序贯器官功能衰竭(sequential organ failure assessment,SOFA)评分、血清降钙素原(procalci-tonin,PCT)在脓毒症患者中的变化,分析两者联合检测对脓毒症患者病情及预后的评估.方法 选取2016年12月-2019年12月浙江大学医学院附属杭州市第一人民医院重症医学科收治的脓毒症患者40例,据病情严重程度及中国脓毒症/脓毒性休克急诊治疗指南(2018)将患者分为脓毒症组、脓毒性休克组,根据人院28 d是否存活分为存活组和死亡组,比较各组SOFA及PCT的变化,用受试者工作特征曲线(ROC曲线)下面积分析SOFA联合PCT对脓毒症患者病情及预后的预测价值.结果 脓毒症组患者第1、5天SOFA评分与脓毒性休克组比较差异有统计学意义(均P ＜0.01);经过治疗脓毒症组SOFA评分改善更明显,PCT下降更明显.存活组患者第5天SOFA为(8.36±1.87)分,死亡组第5天SOFA为(13.22 ± 2.84)分,两者比较差异有统计学意义(P＜0.01);存活患者第5天PCT与死亡组比较差异有统计学意义(P＜0.01).据ROC曲线分析,SOFA及PCT的曲线下面积(AUC)分别为0.607、0.814;SOFA及PCT联合的AUC为0.875.结论 SOFA和PCT联合检测对脓毒症患者的病情及预后有预测意义.

Background: Drowning is an important cause of accidental death in humans. The main cause of death following drowning is pulmonary oedema or lung injury, eventually leading to acute respiratory distress syndrome. The present study aimed to determine the protective effects of Ulinastatin on freshwater-induced acute drowning lung injury. Methods: Rabbits were randomly divided into a control, freshwater, freshwater + small-dose Ulinastatin, freshwater + medium-dose Ulinastatin, freshwater + large-dose Ulinastatin group. The arterial blood gas analysis was performed before modelling (baseline) and at various time points after freshwater instillation. And then, the wet-to-dry weight ratio lung permeability index were measured to detect the effect of Ulinastatin on lung endothelial permeability. Furthermore, histopathological staining and ELISAs were used to analyse the histological changes and inflammatory cytokines expression resulted from lung injury, respectively. Western blotting and Quantitative real-time polymerase chain reaction were used to measure the protein and mRNA levels of Hypoxia inducible factor-lα (HIF-1α)/ Vascular endothelial growth factor (VEGF) in the lung tissues. Results: By inhibiting the HIF-1α/VEGF pathway, treatment with Ulinastatin at a large dose could markedly attenuate changes in the PaO2/FiO2 (P/F), lung endothelial permeability, histopathology, and the expression of inflammatory cytokines induced by freshwater instillation. Conclusion: Ulinastatin is a potential candidate treatment for freshwater drowning-induced acute lung injury that targets the HIF-1α/VEGF pathway.

Background: To explore the epidemiology, clinical features, risk indicators, and long-term outcomes of neurological complications caused by veno-arterial extracorporeal membrane oxygenation (V-A ECMO). Methods: We retrospectively analyzed 60 adult patients who underwent V-A ECMO support in our unit from February 2012 to August 2020. These patients were separated into the neurological complications group (NC group) and the non-neurological complications group (nNC group). The differences in basic data and ECMO data between the two groups were compared. The data of long-term neurological prognosis were collected by telephone follow-up. Results: Thirty-nine patients (65.0%) had neurological complications. There were significant differences between the two groups in terms of median age, hypertension, median blood urea nitrogen, median troponin I (TNI), median lactic acid, pre-ECMO percutaneous coronary intervention, continuous renal replacement therapy (CRRT), median Sequential Organ Failure Assessment score, median Acute Physiology and Chronic Health Evaluation II score, median peak inspiratory pressure, median positive end expiratory pressure, and median fresh frozen plasma (P < 0.05). The median Intensive Care Unit length of stay (ICU LOS), 28-day mortality, median post-ECMO vasoactive inotropic score, non-pulsate perfusion (NP), and median ECMO duration of the NC group were significantly higher than those of the nNC group (P < 0.05). Furthermore, multiple logistic regression analysis revealed that TNI (P = 0.043), CRRT (P = 0.047), and continuous NP > 12 h (P = 0.043) were independent risk indicators for neurological complications in patients undergoing ECMO. Forty-four patients (73.3%) survived after discharge, and 38 patients (63.3%) had Cerebral Performance Category score of 1–2. And there were significant differences between the two groups in long-term neurological outcomes after discharge for 6 months (P < 0.05). Conclusion: The incidence of neurological complications was higher in patients undergoing V-A ECMO and was closely related to adverse outcomes (including ICU LOS and 28-day mortality). TNI, CRRT, and continuous NP > 12 h were independent risk indicators for predicting neurological complications in ECMO supporting patients. And the neurological complications of patients during ECMO support had significant adverse effect on long-term surviving and neurological outcomes of patients after discharge for 6 months.

目的 分析脓毒症相关性脑病(SAE)28 d病死的影响因素.方法 选取2015年1月至2019年12月浙江大学医学院附属杭州市第一人民医院收治的127例SAE患者为研究对象,按28 d生存结局分为存活组、病死组.比较两组患者临床资料,并采用多因素logistic回归分析SAE患者28 d病死的影响因素.结果 127例SAE患者28 d存活73例(57.5％),病死54例(42.5％).存活组与病死组在年龄、合并糖尿病比例、降钙素原水平、心功能分级Ⅲ～Ⅳ级比例、序贯器官衰竭(SOFA)评分、急性生理与慢性健康评估(APACHE)Ⅱ评分等方面比较,差异均有统计学意义(均P<0.05);进一步作多因素logistic回归分析显示,SOFA评分(OR=1.198)、APACHEⅡ评分(OR=1.168)是SAE患者28 d病死的独立影响因素(均P<0.05).结论 SOFA评分、APACHEⅡ评分是预测SAE患者28 d病死的独立影响因素.