BACKGROUND:Sepsis-associated encephalopathy(SAE) is a critical disease caused by sepsis.In addition to high mortality,SAE can also adversely aff ect life quality and lead to significant socioeconomic costs.This review...BACKGROUND:Sepsis-associated encephalopathy(SAE) is a critical disease caused by sepsis.In addition to high mortality,SAE can also adversely aff ect life quality and lead to significant socioeconomic costs.This review aims to explore the development of evaluation animal models of SAE,giving insight into the direction of future research in terms of its pathophysiology and therapy.METHODS:We performed a literature search from January 1,2000,to December 31,2022,in MEDLINE,PubMed,EMBASE,and Web of Science using related keywords.Two independent researchers screened all the accessible articles based on the inclusion and exclusion criteria and collected the relevant data of the studies.RESULTS:The animal models for sepsis are commonly induced through cecal ligation and puncture(CLP) or lipopolysaccharide(LPS) injection.SAE can be evaluated using nervous reflex scores and sepsis evaluation during the acute phase,or through Morris water maze(MWM),openfield test,fear condition(FC) test,inhibitory avoidance,and other tests during the late phase.CONCLUSION:CLP and LPS injection are the most common methods for establishing SAE animal models.Nervous reflexs cores,MWM,FC test,and inhibitory avoidance are widely used in SAE model analysis.Future research should focus on establishing a standardized system for SAE development and analysis.展开更多
BACKGROUND:Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy(SAE)is a major complication.Rosuvastatin may play a neuroprotective role due to its protective effects on the ...BACKGROUND:Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy(SAE)is a major complication.Rosuvastatin may play a neuroprotective role due to its protective effects on the vascular endothelium and its anti-inflammatory functions.Our study aimed to explore the potential protective function of rosuvastatin against SAE.METHODS:Sepsis patients without any neurological dysfunction on admission were prospectively enrolled in the“Rosuvastatin for Sepsis-Associated Acute Respiratory Distress Syndrome”study(SAILS trial,ClinicalTrials.gov number:NCT00979121).Patients were divided into rosuvastatin and placebo groups.This is a secondary analysis of the SAILS dataset.Baseline characteristics,therapy outcomes,and adverse drug events were compared between groups.RESULTS:A total of 86 patients were eligible for our study.Of these patients,51 were treated with rosuvastatin.There were significantly fewer cases of SAE in the rosuvastatin group than in the placebo group(32.1%vs.57.1%,P=0.028).However,creatine kinase levels were significantly higher in the rosuvastatin group than in the placebo group(233[22-689]U/L vs.79[12-206]U/L,P=0.034).CONCLUSION:Rosuvastatin appears to have a protective role against SAE but may result in a higher incidence of adverse events.展开更多
Sepsis-associated encephalopathy （SAE） is a diffuse and acute cerebral dysfunction caused by sepsis. Many sepsis patients exhibit acute deterioration in mental status during the early stage of disease, and central n...Sepsis-associated encephalopathy （SAE） is a diffuse and acute cerebral dysfunction caused by sepsis. Many sepsis patients exhibit acute deterioration in mental status during the early stage of disease, and central nervous system dysfunction has been shown to increase patient mortality. The present study selected 284 sepsis patients who were admitted to the Intensive Care Unit of Beijing Friendship Hospital, Capital Medical University, from January to December 2009. The patients were assigned to SAE and non-SAE patient groups according to SAE occurrence. SAE incidence was 37.68%, and mortality was significantly greater in SAE patients compared with non-SAE patients （41.12% vs. 17.51%, P 〈 0.01）. Univariate analysis and multivariate logistic regression analysis indicated lower arterial partial pressure of oxygen and greater alanine aminotransferase and Acute Physiology and Chronic Health Evaluation II scores in the SAE group compared with the non-SAE group. Arterial partial pressure of oxygen, alanine aminotransferase, and Acute Physiology and Chronic Health Evaluation II scores were determined to be potential risk factors for SAE.展开更多
To investigate the interaction and involvement of sodium hydrosulfide （NaHS）, a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture ...To investigate the interaction and involvement of sodium hydrosulfide （NaHS）, a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture （CLP）-induced sepsis. Adult male Sprague-Dawley rats were randomly divided into four groups： Sham group, CLP group, CLP＋NaHS group and CLP＋aminooxyacetic acid （AOAA, an inhibitor of H2S formation） group. The four groups were observed at 3, 6, 9, 12 h after treatment. We examined hippocampal H2S synthesis and the expression of cystathionine-β-synthetase （CBS）, a major enzyme involved in the H2S synthesis in hippocampus. CBS expression was detected by reverse transcription polymerase chain reaction （RT-PCR）. The concentrations of inflammatory cytokines （TNF-α, IL-1β） were determined in hippocampus by using enzyme-linked immunosorbent assay （ELISA）. Neuronal damage was studied by histological examination of hippocampus. In CLP group, H2S synthesis was significantly increased in hippocampus compared with sham group and it peaked 3 h after CLP （P〈0.05）. Sepsis also resulted in a significantly upregulated CBS mRNA in hippocampus. The levels of TNF-α and IL-1β in the hippocampus were substantially elevated at each time point of measurement （P〈0.05）, and they also reached a peak value at about 3 h. Administration of NaHS significantly aggravated sepsis-associated hippocampus inflammation, as evidenced by TNF-α and IL-1β activity and histological changes in hippocampus. In septic rats pretreated with AOAA, sepsis-associated hippocampus inflammation was reduced. It is concluded that the rats subjected to sepsis may suffer from brain injury and elevated pro-inflammatory cytokines are responsible for the process. Furthermore, administration of H2S can increase injurious effects and treatment with AOAA can protect the brain from injury.展开更多
Background Encephalopathy is a common complication of sepsis, and its onset can occur at any stage of sepsis and implies worse prognosis. However, the incidence, epidemiology, and pathogenesis of sepsis-associated enc...Background Encephalopathy is a common complication of sepsis, and its onset can occur at any stage of sepsis and implies worse prognosis. However, the incidence, epidemiology, and pathogenesis of sepsis-associated encephalopathy remain controversial. The purpose of this study was to investigate the epidemiological features and risk factors for sepsis-associated encephalopathy.展开更多
Background： Despite its high prevalence, morbidity, and mortality, sepsis-associated encephalopathy （SAE） is still poorly understood. The aim of this prospective and observational study was to investigate the clini...Background： Despite its high prevalence, morbidity, and mortality, sepsis-associated encephalopathy （SAE） is still poorly understood. The aim of this prospective and observational study was to investigate the clinical significance of calcium-binding protein A8 （S 100AS） in serum and tumor necrosis factor receptor-associated factor 6 （TRAF6） in peripheral blood mononuclear cells （PBMCs） in diagnosing SAE and predicting its prognosis. Methods： Data of septic patients were collected within 24 h after Intensive Care Unit admission fi-om July 2014 to March 2015. Healthy medical personnel served as the control group. SAE was defined as cerebral dysfhnction in the presence of sepsis that fulfilled the exclusion criteria. The biochemical indicators, Glasgow Coma Scale, Acute Physiology and Chronic Health Evaluation score II, TRAF6 in PBMC, serum S 100A8, S 10013, and neuron-specific enolase were evaluated in SAE patients afresh. TRAF6 and S 100A8 were also measured in the control group. Results： Of the 57 enrolled patients, 29 were diagnosed with SAE. The S 100A8 and TRAF6 concentrations in SAE patients were both significantly higher than that in no-encephalopathy （NE） patients, and higher in NE than that in controls （3.74 ± 3.13 vs. 1.08 ± 0.75 vs. 0.37 ± 0.14 ng/ml, P 〈 0.01 ; 3.18 ± 1.55 vs. 1.02 ± 0.63 vs. 0.47 ± 0.10, P 〈 0.01）. S 100A8 levels of 1.93 ng/ml were diagnostic of SAE with 92.90% specificity and 69.00% sensitivity in the receiver operating characteristic （ROC） curve, and the area under the curve was 0.86 （95% confidence interval [CI]： 0.76-0.95）. TRAF6-relative levels of 1.44 were diagnostic of SAE with 85.70% specificity and 86.20% sensitivity, and the area under the curve was 0.94 （95% CI： 0.88-0.99）. In addition, S 100A8 levels of 2.41 ng/ml predicted 28-day mortality of SAE with 90.00% specificity and 73.70% sensitivity in the ROC curve, and the area under the curve was 0.88. TRAF6 relative levels of 2.94 predicted 28-day mortality of SAE with 80.00% specificity and 68.40% sensitivity, and the area under the curve was 0.77. Compared with TRAF6, the specificity of serum S 100A8 in diagnosing SAE and predicting mortality was higher, although the sensitivity was low. In contrast, the TRAF6 had higher sensitivity for diagnosis. Conclusions： Peripheral blood levels of S 100A8 and TRAF6 in SAE patients were elevated and might be related to the severity of SAE and predict the outcome of SAE. The efficacy and specificity of S 100A8 for SAE diagnosis were superior, despite its weak sensitivity. S100A8 might be a better biomarker for diagnosis of SAE and predicting prognosis.展开更多
Sepsis-associated encephalopathy(SAE),a major cerebral complication of sepsis,occurs in 70%of patients admitted to the intensive care unit(ICU).This condition can cause serious impairment of consciousness and is assoc...Sepsis-associated encephalopathy(SAE),a major cerebral complication of sepsis,occurs in 70%of patients admitted to the intensive care unit(ICU).This condition can cause serious impairment of consciousness and is associated with a high mortality rate.Thus far,several experimental screenings and radiological techniques(e.g.,electroencephalography)have been used for the non-invasive assessment of the structure and function of the brain in patients with SAE.Nevertheless,the pathogenesis of SAE is complicated and remains unclear.In the present article,we reviewed the currently available literature on the epidemiology,clinical manifestations,pathology,diagnosis,and management of SAE.However,currently,there is no ideal pharmacological treatment for SAE.Treatment targeting mitochondrial dysfunction may be useful in the management of SAE.展开更多
BACKGROUND:This study aimed to determine the effects of sepsis on brain integrity,memory,and executive function.METHODS:Twenty sepsis patients who were not diagnosed with sepsis-associated encephalopathy(SAE)but had a...BACKGROUND:This study aimed to determine the effects of sepsis on brain integrity,memory,and executive function.METHODS:Twenty sepsis patients who were not diagnosed with sepsis-associated encephalopathy(SAE)but had abnormal electroencephalograms(EEGs)were included.The control group included twenty healthy persons.A neuropsychological test of memory and executive function and a brain magnetic resonance imaging scan were performed.The volumes of cortex and subcortex were measured using the FreeSurfer software.Acute Physiology and Chronic Health Evaluation II(APACHE II)score was used to determine the disease severity.RESULTS:In the sepsis group,the levels of immediate free recall,immediate cued recall,and delayed cued recall in the California Verbal Learning Test-II(CVLT-II)were significantly lower;the explicit memory(recollection process)in the process dissociation procedure test was lower;and the volumes of the left and right hippocampi were significantly lower compared with the control group.The volume of the presubiculum in the hippocampus of sepsis patients showed statistically signifi cant decrease.In the sepsis group,the volumes of the left and right hippocampi were negatively correlated with the APACHE II score and positively with immediate free recall,immediate cued recall,and delayed cued recall in the CVLT-II;moreover,the hippocampal volume was significantly correlated with recollection but not with familiarity.CONCLUSIONS:Patients with abnormal EEGs during hospitalization but with no SAE still have reduced hippocampal volume and memory defi cits.This fi nding indicates that sepsis leads to damage to specifi c parts of the hippocampus.展开更多
目的探讨脓毒症患者发生脓毒症相关脑病(SAE)的危险因素,建立简便、易用的预测模型并进行验证。方法回顾性分析徐州医科大学附属医院2017年1月至2021年12月入住重症监护病房(ICU)脓毒症患者的临床资料,根据纳入排除标准,确定最终入选病...目的探讨脓毒症患者发生脓毒症相关脑病(SAE)的危险因素,建立简便、易用的预测模型并进行验证。方法回顾性分析徐州医科大学附属医院2017年1月至2021年12月入住重症监护病房(ICU)脓毒症患者的临床资料,根据纳入排除标准,确定最终入选病例,将2017年1月至2019年12月收集的病例作为训练队列组(n=640),将2020年1月至2021年12月收集的病例作为验证队列组(n=300)。将训练队列组患者资料进行Logistic回归分析,确定SAE发生的危险因素,建立回归方程,并可视化为列线图。验证队列组对建立的回归方程进行验证,通过绘制受试者工作特征(receiver operating characteristic,ROC)曲线及计算ROC曲线下面积(area under the curve,AUC)评价模型的区分度,通过Hosmer-Lemeshow检验和校准图评价模型的校准度。结果本研究共纳入940例患者,单因素及多因素Logistic回归结果表明,高龄、使用升压药、高中枢神经特异蛋白(S100β)水平、低脉搏血氧饱和度(SpO_(2))和低蛋白血症5个因素为SAE发病的独立危险因素(P<0.05),纳入预测模型,该预测模型的AUC在训练和验证队列组分别为0.810(95%CI 0.763~0.857)和0.813(95%CI 0.740~0.885),模型的校准曲线在训练和验证队列组均与平面直角坐标系中45°的直线重合度较高,提示该模型的表现良好。结论本研究建立的预测模型可以科学、有效地对SAE的发生进行预测,操作简便、快速,具有重要的临床价值。展开更多
基金supported by the National High Level Hospital Clinical Research Fund (2022-PUMCH-B-109)CAMS Innovation Fund for Medical Sciences (CIFMS)(2021-1-I2M-020)。
文摘BACKGROUND:Sepsis-associated encephalopathy(SAE) is a critical disease caused by sepsis.In addition to high mortality,SAE can also adversely aff ect life quality and lead to significant socioeconomic costs.This review aims to explore the development of evaluation animal models of SAE,giving insight into the direction of future research in terms of its pathophysiology and therapy.METHODS:We performed a literature search from January 1,2000,to December 31,2022,in MEDLINE,PubMed,EMBASE,and Web of Science using related keywords.Two independent researchers screened all the accessible articles based on the inclusion and exclusion criteria and collected the relevant data of the studies.RESULTS:The animal models for sepsis are commonly induced through cecal ligation and puncture(CLP) or lipopolysaccharide(LPS) injection.SAE can be evaluated using nervous reflex scores and sepsis evaluation during the acute phase,or through Morris water maze(MWM),openfield test,fear condition(FC) test,inhibitory avoidance,and other tests during the late phase.CONCLUSION:CLP and LPS injection are the most common methods for establishing SAE animal models.Nervous reflexs cores,MWM,FC test,and inhibitory avoidance are widely used in SAE model analysis.Future research should focus on establishing a standardized system for SAE development and analysis.
基金This research received funding from the CAMS Innovation Fund for Medical Sciences(CIFMS)(2020-I2M-C&T-B-014,2021-I2M-1-020).
文摘BACKGROUND:Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy(SAE)is a major complication.Rosuvastatin may play a neuroprotective role due to its protective effects on the vascular endothelium and its anti-inflammatory functions.Our study aimed to explore the potential protective function of rosuvastatin against SAE.METHODS:Sepsis patients without any neurological dysfunction on admission were prospectively enrolled in the“Rosuvastatin for Sepsis-Associated Acute Respiratory Distress Syndrome”study(SAILS trial,ClinicalTrials.gov number:NCT00979121).Patients were divided into rosuvastatin and placebo groups.This is a secondary analysis of the SAILS dataset.Baseline characteristics,therapy outcomes,and adverse drug events were compared between groups.RESULTS:A total of 86 patients were eligible for our study.Of these patients,51 were treated with rosuvastatin.There were significantly fewer cases of SAE in the rosuvastatin group than in the placebo group(32.1%vs.57.1%,P=0.028).However,creatine kinase levels were significantly higher in the rosuvastatin group than in the placebo group(233[22-689]U/L vs.79[12-206]U/L,P=0.034).CONCLUSION:Rosuvastatin appears to have a protective role against SAE but may result in a higher incidence of adverse events.
基金supported by the Natural Science Foundation of Beijing(HDAC regulation of TLR4-mediated vascular endothelial cell injury in sepsis),No.7102039
文摘Sepsis-associated encephalopathy （SAE） is a diffuse and acute cerebral dysfunction caused by sepsis. Many sepsis patients exhibit acute deterioration in mental status during the early stage of disease, and central nervous system dysfunction has been shown to increase patient mortality. The present study selected 284 sepsis patients who were admitted to the Intensive Care Unit of Beijing Friendship Hospital, Capital Medical University, from January to December 2009. The patients were assigned to SAE and non-SAE patient groups according to SAE occurrence. SAE incidence was 37.68%, and mortality was significantly greater in SAE patients compared with non-SAE patients （41.12% vs. 17.51%, P 〈 0.01）. Univariate analysis and multivariate logistic regression analysis indicated lower arterial partial pressure of oxygen and greater alanine aminotransferase and Acute Physiology and Chronic Health Evaluation II scores in the SAE group compared with the non-SAE group. Arterial partial pressure of oxygen, alanine aminotransferase, and Acute Physiology and Chronic Health Evaluation II scores were determined to be potential risk factors for SAE.
基金supported by a grant from the National Natural Sciences Foundation of China (No. 81071526)
文摘To investigate the interaction and involvement of sodium hydrosulfide （NaHS）, a H2S donor, on hippocampus of rats suffering from sepsis-associated encephalopathy, rats were subjected to cecal ligation and puncture （CLP）-induced sepsis. Adult male Sprague-Dawley rats were randomly divided into four groups： Sham group, CLP group, CLP＋NaHS group and CLP＋aminooxyacetic acid （AOAA, an inhibitor of H2S formation） group. The four groups were observed at 3, 6, 9, 12 h after treatment. We examined hippocampal H2S synthesis and the expression of cystathionine-β-synthetase （CBS）, a major enzyme involved in the H2S synthesis in hippocampus. CBS expression was detected by reverse transcription polymerase chain reaction （RT-PCR）. The concentrations of inflammatory cytokines （TNF-α, IL-1β） were determined in hippocampus by using enzyme-linked immunosorbent assay （ELISA）. Neuronal damage was studied by histological examination of hippocampus. In CLP group, H2S synthesis was significantly increased in hippocampus compared with sham group and it peaked 3 h after CLP （P〈0.05）. Sepsis also resulted in a significantly upregulated CBS mRNA in hippocampus. The levels of TNF-α and IL-1β in the hippocampus were substantially elevated at each time point of measurement （P〈0.05）, and they also reached a peak value at about 3 h. Administration of NaHS significantly aggravated sepsis-associated hippocampus inflammation, as evidenced by TNF-α and IL-1β activity and histological changes in hippocampus. In septic rats pretreated with AOAA, sepsis-associated hippocampus inflammation was reduced. It is concluded that the rats subjected to sepsis may suffer from brain injury and elevated pro-inflammatory cytokines are responsible for the process. Furthermore, administration of H2S can increase injurious effects and treatment with AOAA can protect the brain from injury.
文摘Background Encephalopathy is a common complication of sepsis, and its onset can occur at any stage of sepsis and implies worse prognosis. However, the incidence, epidemiology, and pathogenesis of sepsis-associated encephalopathy remain controversial. The purpose of this study was to investigate the epidemiological features and risk factors for sepsis-associated encephalopathy.
文摘Background： Despite its high prevalence, morbidity, and mortality, sepsis-associated encephalopathy （SAE） is still poorly understood. The aim of this prospective and observational study was to investigate the clinical significance of calcium-binding protein A8 （S 100AS） in serum and tumor necrosis factor receptor-associated factor 6 （TRAF6） in peripheral blood mononuclear cells （PBMCs） in diagnosing SAE and predicting its prognosis. Methods： Data of septic patients were collected within 24 h after Intensive Care Unit admission fi-om July 2014 to March 2015. Healthy medical personnel served as the control group. SAE was defined as cerebral dysfhnction in the presence of sepsis that fulfilled the exclusion criteria. The biochemical indicators, Glasgow Coma Scale, Acute Physiology and Chronic Health Evaluation score II, TRAF6 in PBMC, serum S 100A8, S 10013, and neuron-specific enolase were evaluated in SAE patients afresh. TRAF6 and S 100A8 were also measured in the control group. Results： Of the 57 enrolled patients, 29 were diagnosed with SAE. The S 100A8 and TRAF6 concentrations in SAE patients were both significantly higher than that in no-encephalopathy （NE） patients, and higher in NE than that in controls （3.74 ± 3.13 vs. 1.08 ± 0.75 vs. 0.37 ± 0.14 ng/ml, P 〈 0.01 ; 3.18 ± 1.55 vs. 1.02 ± 0.63 vs. 0.47 ± 0.10, P 〈 0.01）. S 100A8 levels of 1.93 ng/ml were diagnostic of SAE with 92.90% specificity and 69.00% sensitivity in the receiver operating characteristic （ROC） curve, and the area under the curve was 0.86 （95% confidence interval [CI]： 0.76-0.95）. TRAF6-relative levels of 1.44 were diagnostic of SAE with 85.70% specificity and 86.20% sensitivity, and the area under the curve was 0.94 （95% CI： 0.88-0.99）. In addition, S 100A8 levels of 2.41 ng/ml predicted 28-day mortality of SAE with 90.00% specificity and 73.70% sensitivity in the ROC curve, and the area under the curve was 0.88. TRAF6 relative levels of 2.94 predicted 28-day mortality of SAE with 80.00% specificity and 68.40% sensitivity, and the area under the curve was 0.77. Compared with TRAF6, the specificity of serum S 100A8 in diagnosing SAE and predicting mortality was higher, although the sensitivity was low. In contrast, the TRAF6 had higher sensitivity for diagnosis. Conclusions： Peripheral blood levels of S 100A8 and TRAF6 in SAE patients were elevated and might be related to the severity of SAE and predict the outcome of SAE. The efficacy and specificity of S 100A8 for SAE diagnosis were superior, despite its weak sensitivity. S100A8 might be a better biomarker for diagnosis of SAE and predicting prognosis.
基金supported by the National Natural Science Foundation of China(Grant Number:82072209).
文摘Sepsis-associated encephalopathy(SAE),a major cerebral complication of sepsis,occurs in 70%of patients admitted to the intensive care unit(ICU).This condition can cause serious impairment of consciousness and is associated with a high mortality rate.Thus far,several experimental screenings and radiological techniques(e.g.,electroencephalography)have been used for the non-invasive assessment of the structure and function of the brain in patients with SAE.Nevertheless,the pathogenesis of SAE is complicated and remains unclear.In the present article,we reviewed the currently available literature on the epidemiology,clinical manifestations,pathology,diagnosis,and management of SAE.However,currently,there is no ideal pharmacological treatment for SAE.Treatment targeting mitochondrial dysfunction may be useful in the management of SAE.
基金the Shanxi Province Key Scientific and Technological Project(2016YFJH2-05)the Youth Project of the Second Affi liated Hospital of Xi’an Jiaotong University(YJ[QN]201523).
文摘BACKGROUND:This study aimed to determine the effects of sepsis on brain integrity,memory,and executive function.METHODS:Twenty sepsis patients who were not diagnosed with sepsis-associated encephalopathy(SAE)but had abnormal electroencephalograms(EEGs)were included.The control group included twenty healthy persons.A neuropsychological test of memory and executive function and a brain magnetic resonance imaging scan were performed.The volumes of cortex and subcortex were measured using the FreeSurfer software.Acute Physiology and Chronic Health Evaluation II(APACHE II)score was used to determine the disease severity.RESULTS:In the sepsis group,the levels of immediate free recall,immediate cued recall,and delayed cued recall in the California Verbal Learning Test-II(CVLT-II)were significantly lower;the explicit memory(recollection process)in the process dissociation procedure test was lower;and the volumes of the left and right hippocampi were significantly lower compared with the control group.The volume of the presubiculum in the hippocampus of sepsis patients showed statistically signifi cant decrease.In the sepsis group,the volumes of the left and right hippocampi were negatively correlated with the APACHE II score and positively with immediate free recall,immediate cued recall,and delayed cued recall in the CVLT-II;moreover,the hippocampal volume was significantly correlated with recollection but not with familiarity.CONCLUSIONS:Patients with abnormal EEGs during hospitalization but with no SAE still have reduced hippocampal volume and memory defi cits.This fi nding indicates that sepsis leads to damage to specifi c parts of the hippocampus.
文摘目的探讨脓毒症患者发生脓毒症相关脑病(SAE)的危险因素,建立简便、易用的预测模型并进行验证。方法回顾性分析徐州医科大学附属医院2017年1月至2021年12月入住重症监护病房(ICU)脓毒症患者的临床资料,根据纳入排除标准,确定最终入选病例,将2017年1月至2019年12月收集的病例作为训练队列组(n=640),将2020年1月至2021年12月收集的病例作为验证队列组(n=300)。将训练队列组患者资料进行Logistic回归分析,确定SAE发生的危险因素,建立回归方程,并可视化为列线图。验证队列组对建立的回归方程进行验证,通过绘制受试者工作特征(receiver operating characteristic,ROC)曲线及计算ROC曲线下面积(area under the curve,AUC)评价模型的区分度,通过Hosmer-Lemeshow检验和校准图评价模型的校准度。结果本研究共纳入940例患者,单因素及多因素Logistic回归结果表明,高龄、使用升压药、高中枢神经特异蛋白(S100β)水平、低脉搏血氧饱和度(SpO_(2))和低蛋白血症5个因素为SAE发病的独立危险因素(P<0.05),纳入预测模型,该预测模型的AUC在训练和验证队列组分别为0.810(95%CI 0.763~0.857)和0.813(95%CI 0.740~0.885),模型的校准曲线在训练和验证队列组均与平面直角坐标系中45°的直线重合度较高,提示该模型的表现良好。结论本研究建立的预测模型可以科学、有效地对SAE的发生进行预测,操作简便、快速,具有重要的临床价值。
