脓毒症相关肝损伤临床特点及预后分析
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摘要
目的分析脓毒症相关肝损伤(SRLI)的发生率、临床特点以及预后。方法收集2013年1月至2014年12月中国医科大学附属第一医院重症医学科脓毒症患者的临床资料,记录基本信息、导致脓毒症的感染部位、是否急诊手术、住ICU时间、入ICU首个24 h APACHEⅡ和SOFA评分、是否接受机械通气、机械通气时间、是否发生多器官功能障碍综合征(MODS)、营养支持方式、住ICU期间血清总胆红素及氨基转移酶、肝功能异常的发生时间及肝功能异常持续时间。采用秩和检验比较年龄、APACHEⅡ评分、SOFA评分、住ICU时间、机械通气时间;采用卡方检验比较患者来源、手术类型、是否MODS、营养支持的方式等计数资料;死亡相关性因素采用Logistic回归分析。结果共纳入341例脓毒症患者,其中SRLI 96例。以氨基转移酶升高为主要表现17例(17.71%),总胆红素升高为主要表现31例(32.29%),总胆红素及氨基转移酶均升高48例(50%);脓毒症患者平均在入ICU 3.22 d (1～40 d)时开始出现肝损伤,肝损伤发生在1～3 d内的患者66例(68.75%)。SRLI患者MODS发生率为70.83%,病死率为33.33%;SRLI的病死率、机械通气时间、住ICU时间与非肝功能损伤者相比较差异有统计学意义;不同预后患者的APACHEⅡ评分、SOFA评分,机械通气时间和MODS发生率差异有统计学意义,进一步Logistic回归分析,脓毒症伴MODS是此类患者死亡独立危险因素。不同严重程度SRLI患者的持续时间、住ICU时间、预后差异有统计学意义。结论 SRLI发病率较高,且多数发生于脓毒症早期,男性更易患病,腹腔为最常见的感染部位。多数以结合胆红素升高为特点,APACHEⅡ评分、机械通气时间及发生MODS是患者发生SRLI的独立危险因素。
Objective To analyze the incidence, clinical characteristics and prognosis of sepsis-related liver injury(SELI). Methods The data of septic patients in the department of Critical Care Medicine of the First Affiliated Hospital of China Medical University from January 2013 to December 2014 were collected and the basic information, infection site, emergency operation and residence were recorded. Also, the duration of ICU, the first 24 h APACHE II and SOFA score, mechanical ventilation, MODS, nutritional support, serum total bilirubin and aminotransferase, the duration of liver dysfunction and the duration of liver dysfunction during ICU stay were recorded. Rank sum test was used to compare age, APACHE II score, SOFA score, length of stay in ICU, duration of mechanical ventilation; Chi square test was used to compare the patient's source, type of operation, whether MODS, and nutritional support; The logistic regression analysis was used to analyze the related factors of death. Results A total of 341 septic patients with sepsis were included in the study, including 96 patients with septis-related liver dysfunction. The main manifestations were elevated transaminase in 17 cases(17.71%), elevated bilirubin in 31 cases(32.29%), elevated bilirubin and transaminase in 48 cases(50%) and liver injury in 66 cases(68.75%) of sepsic patients occurred within 1-3 days of ICU 3.22 days(1-40 days). The morbidity and mortality of MODS in sepsis-related liver injury patients were 70.83% and 33.33%. Statistically differences in APACHE II scores, SOFA scores, mechanical ventilation duration, and MODS in patients with different prognosis were revealed. Further logistic regression analysis showed that sepsis with MODS was an independent risk factor for death. There were statistical difference in duration of symptoms, duration of ICU stay and prognosis. Conclusion The morbidity of SELI is high, mostly in the early stage of sepsis, men are more prone to the disease. The abdominal cavity is the most common site of infection. High APACHEII score, prolonged mechanical ventilation and MODS are independent risk factors for SELI.
Objective To analyze the incidence, clinical characteristics and prognosis of sepsis-related liver injury(SELI). Methods The data of septic patients in the department of Critical Care Medicine of the First Affiliated Hospital of China Medical University from January 2013 to December 2014 were collected and the basic information, infection site, emergency operation and residence were recorded. Also, the duration of ICU, the first 24 h APACHE II and SOFA score, mechanical ventilation, MODS, nutritional support, serum total bilirubin and aminotransferase, the duration of liver dysfunction and the duration of liver dysfunction during ICU stay were recorded. Rank sum test was used to compare age, APACHE II score, SOFA score, length of stay in ICU, duration of mechanical ventilation; Chi square test was used to compare the patient's source, type of operation, whether MODS, and nutritional support; The logistic regression analysis was used to analyze the related factors of death. Results A total of 341 septic patients with sepsis were included in the study, including 96 patients with septis-related liver dysfunction. The main manifestations were elevated transaminase in 17 cases(17.71%), elevated bilirubin in 31 cases(32.29%), elevated bilirubin and transaminase in 48 cases(50%) and liver injury in 66 cases(68.75%) of sepsic patients occurred within 1-3 days of ICU 3.22 days(1-40 days). The morbidity and mortality of MODS in sepsis-related liver injury patients were 70.83% and 33.33%. Statistically differences in APACHE II scores, SOFA scores, mechanical ventilation duration, and MODS in patients with different prognosis were revealed. Further logistic regression analysis showed that sepsis with MODS was an independent risk factor for death. There were statistical difference in duration of symptoms, duration of ICU stay and prognosis. Conclusion The morbidity of SELI is high, mostly in the early stage of sepsis, men are more prone to the disease. The abdominal cavity is the most common site of infection. High APACHEII score, prolonged mechanical ventilation and MODS are independent risk factors for SELI.
引文
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[13]Levi M, van der Poll T. Inflammation and coagulation[J]. Crit Care Med, 2010, 38(2Suppl):S26-34.
[14]Kim TH, Lee SH, Lee SM. Role of Kupffer cells in pathogenesis of sepsis-induceddrugmetabolizingdysfunction[J].FEBSJ,2011,278(13):2307-2317.
[15]WoznicaEA,InglotM,WoznicaRK,etal.Liverdysfunctionin sepsis[J]. Adv Clin Exp Med, 2018, 27(4):547-551.
[16]Li X, Klintman D, Liu Q, et al. Critical role of CXC chemokines in endotoxemic liver injury in mice[J]. J Leukoc Biol, 2004, 75(3):443-452.
[17]Venkatesha RT, Ahamed J, Nuesch C, et al. Platelet-activating factorinduced chemokine gene expression requires NF-kappaB activation andCa2+/calcineurinsignalingpathways.Inhibitionbyreceptor phosphorylation and beta-arrestin recruitment[J]. J Biol Chem, 2004,279(43):44606-44612.
[18]LiJ,XiaK,XiongM,etal.Effectsofsepsisonthemetabolismof sphingomyelin and cholesterol in mice with liver dysfunction[J]. Exp Ther Med, 2017, 14(6):5635-5640.
[19]Gaddam RR, Fraser R, Badiei A, et al. Differential Effects of Kupffer CellInactivationonInflammationandTheLiverSieveFollowing Caecal-Ligation and Puncture-Induced Sepsis in Mice[J]. Shock, 2017,47(4):480-490.
[20]MinemuraM,TajiriK,ShimizuY.Liverinvolvementinsystemic infection[J]. World J Hepatol, 2014, 6(9):632-642.
[21]DuroD,MitchellPD,KalishLA,etal.Riskfactorsforparenteral nutrition-associatedliverdiseasefollowingsurgicaltherapyfor necrotizing enterocolitis:A Glaser Pediatric Research Network Study[corrected][J]. J Pediatr Gastroenterol Nutr, 2011, 52(5):595-600.
[2]AngusDC,Linde-ZwirbleWT,LidickerJ,etal.Epidemiologyof severe sepsis in the United States:analysis of incidence, outcome, and associated costs of care[J]. Crit Care Med 2001, 29(7):1303-1310.
[3]Yan J, Li S, Li S. The role of the liver in sepsis[J]. Int Rev Immunol,2014, 33(6):498-510.
[4]Chand N, Sanyal AJ. Sepsis-induced cholestasis[J]. Hepatology, 2007,45(1):230-241.
[5]Kobashi H, Toshimori J, Yamamoto K. Sepsis-associated liver injury:Incidence, classification and the clinical significance[J]. Hepatol Res,2013, 43(3):255-266.
[6]Nesseler N, Launey Y, Aninat C, et al. Clinical review:The liver in sepsis[J]. Crit Care, 2012, 16(5):235.
[7]刘一娜,马晓春.脓毒症相关肝损伤49例临床分析[J].中国实用外科杂志, 2012, 32(11):916-918.
[8]Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine[J]. Chest, 1992,101(6):1644-1655.
[9]AithalGP,WatkinsPB,AndradeR J,etal.Casedefinitionand phenotypestandardizationindrug-inducedliverinjury[J].Clin Pharmacol Ther, 2011, 89(6):806-815.
[10]Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure-definition,outcomemeasures,animalmodels,fluidtherapyandinformation technology needs:the Second International Consensus Conference of the Acute Dialysis Quality Initiative(ADQI)Group[J]. Crit Care,2004, 8(4):R204-212.
[11]栾正刚,马晓春.脓毒症相关肝功能损伤[J].中国实用外科杂志, 2012, 32(11):959-965.
[12]BulgerEM,MayS,KerbyJD,etal.Out-of-hospitalhypertonic resuscitationaftertraumatichypovolemicshock:arandomized,placebo controlled trial[J]. Ann Surg, 2011, 253(3):431-441.
[13]Levi M, van der Poll T. Inflammation and coagulation[J]. Crit Care Med, 2010, 38(2Suppl):S26-34.
[14]Kim TH, Lee SH, Lee SM. Role of Kupffer cells in pathogenesis of sepsis-induceddrugmetabolizingdysfunction[J].FEBSJ,2011,278(13):2307-2317.
[15]WoznicaEA,InglotM,WoznicaRK,etal.Liverdysfunctionin sepsis[J]. Adv Clin Exp Med, 2018, 27(4):547-551.
[16]Li X, Klintman D, Liu Q, et al. Critical role of CXC chemokines in endotoxemic liver injury in mice[J]. J Leukoc Biol, 2004, 75(3):443-452.
[17]Venkatesha RT, Ahamed J, Nuesch C, et al. Platelet-activating factorinduced chemokine gene expression requires NF-kappaB activation andCa2+/calcineurinsignalingpathways.Inhibitionbyreceptor phosphorylation and beta-arrestin recruitment[J]. J Biol Chem, 2004,279(43):44606-44612.
[18]LiJ,XiaK,XiongM,etal.Effectsofsepsisonthemetabolismof sphingomyelin and cholesterol in mice with liver dysfunction[J]. Exp Ther Med, 2017, 14(6):5635-5640.
[19]Gaddam RR, Fraser R, Badiei A, et al. Differential Effects of Kupffer CellInactivationonInflammationandTheLiverSieveFollowing Caecal-Ligation and Puncture-Induced Sepsis in Mice[J]. Shock, 2017,47(4):480-490.
[20]MinemuraM,TajiriK,ShimizuY.Liverinvolvementinsystemic infection[J]. World J Hepatol, 2014, 6(9):632-642.
[21]DuroD,MitchellPD,KalishLA,etal.Riskfactorsforparenteral nutrition-associatedliverdiseasefollowingsurgicaltherapyfor necrotizing enterocolitis:A Glaser Pediatric Research Network Study[corrected][J]. J Pediatr Gastroenterol Nutr, 2011, 52(5):595-600.