肝硬化患者门静脉系统血栓形成29例分析

目的提高对肝硬化患者门静脉系统血栓（PVT）形成的认识及诊治水平。方法收集我院2007年3月至2009年8月收治的肝硬化合并PVT患者29例进行回顾性分析。结果肝硬化合并PVT临床表现多样且缺乏特异性;D-二聚体及血小板水平的升高或相对升高是肝硬化患者发生PVT的独立危险因素;PVT诊断主要依赖影像学检查;在患者条件允许的前提下,及时、合理地选择各种方法进行抗凝、溶栓是治疗的关键。结论提高对肝硬化合并PVT的认识,及时诊断、合理选择治疗方案是决定本病预后的关键。     

乙肝肝硬化患者门静脉宽度与门静脉血栓形成的关系

背景门静脉血栓(portal vein thrombosis,PVT)的早期诊断仍是临床上一个难题,急需要发现可早期预测诊断的无创指标.目的探讨门静脉宽度与PVT形成之间的关系.方法收集418例乙肝肝硬化患者.根据是否发生PVT分为PVT组(n=66)和非PVT组(n=352)组.比较两组患者的一般资料差异,使用多因素Logistic回顾分析影响PVT发生的危险因素.通过受试者工作特征(receiver operating characteristic,ROC)曲线评估不同危险因素预测PVT的效能.结果与非PVT组患者相比,PVT组患者的Child-Pugh评分更高、Child-Pugh A级比例更低、血小板水平更高、D-二聚体水平更高、门静脉宽度更宽、门静脉血流更慢,上述差异均存在统计学意义(P<0.05).Logistic回归显示门静脉宽度(OR=3.941,P=0.001)、门静脉血流(OR=0.841,P=0.007)、血小板水平(OR=1.024,P=0.008)和D-二聚体水平(OR=2.383,P=0.000)是肝硬化患者发生PVT的独立危险因素.门静脉宽度诊断PVT的ROC曲线下面积最大为0.874,最佳诊断值为>12.5 mm,此时的预测敏感性和特异性分别为78%和82%.结论门静脉直径增加是肝硬化患者PVT发生的危险因素,对PVT诊断具有一定价值.     

肝硬化门静脉高压术后血栓形成的相关危险因素

目的 探讨肝硬化门静脉高压术后血栓形成的相关危险因素.方法 选自我院2006年5月至2010年10月收治的行单纯脾切除、脾切除加分流术及脾切除联合贲门周围血管离断术的患者共123例,其中术后血栓形成者29例,未有血栓形成者94例.对两组患者年龄、性别、身高、体重、体重指数、高血压病史、嗜酒史、是否有肝炎病毒感染史、既往有无腹水、手术时间、术中出血量、血小板计数、D-二聚体、门静脉宽度、脾静脉宽度、肝功能Child分级、凝血酶原时间以及术后抗凝药物的使用情况进行对比,结果进行统计学分析.结果 血栓组29例病人中21例(72.4％)既往有腹水史,非血栓组94例病人中52例(55.3％)既往有腹水史,两组对比有统计学差异(P＜0.05).血栓组门静脉、脾静脉宽度显著增大,血栓组门静脉宽度＞1.3 cm者22例(75.8％),对照组为23例(24.5％),两组对比有统计学差异(P＜0.05).血栓组脾静脉宽度＞0.9 cm者18例(62.1％),对照组为41例(43.6％),两组对比有统计学差异(P＜0.05).两组血小板计数、D-二聚体、术后抗凝药物使用情况对比均有统计学差异(P＜0.05).结论 影响肝硬化门静脉高压术后门静脉血栓形成的危险因素主要包括小板计数升高、腹水、D-二聚体升高、门静脉宽度增宽以及脾静脉宽度增宽,术后动态监测血小板计数以及早期的抗凝药物使用可以防止门静脉血栓的形成.     

肝硬化患者门静脉血栓形成的自然病程和抗凝治疗

门静脉血栓形成(PVT)是肝硬化的常见并发症之一,但其自然病程和治疗管理尚未得到国际指南和会议共识的明确建议。既往研究表明PVT可自发再通,而抗凝治疗明显有利于PVT的再通。由于肝硬化患者本身存在凝血功能受损和门静脉高压带来的出血风险,目前对于肝硬化患者PVT的抗凝治疗存在争议。然而,近年来许多研究表明抗凝治疗对肝硬化...     

肝硬化患者门静脉血栓形成的临床表现和危险因素

目的研究肝硬化患者门静脉血栓(PVT)形成的临床表现及危险因素。方法收集2008年4月-2015年4月宁夏医科大学总医院收治的肝硬化患者资料541例。其中76例肝硬化合并PVT的患者为研究组,同阶段通过匹配患者的性别、年龄及肝功能Child-Pugh分级,76例肝硬化不合并PVT为对照组。对比分析两组患者的临床资料及相关检查指标。计量资料组间比较采用t检验,计数资料组间比较采用χ2检验,并应用非条件Logistic回归模型筛选肝硬化PVT形成的独立危险因素。结果肝硬化PVT患者中,42.1%(32/76)隐匿起病,57.9%(44/76)有明显临床表现。大部分患者肝功能分级为Child-Pugh B和C级。血小板、血糖、中性粒细胞百分比、重度食管胃底静脉曲张、血浆D-二聚体、门静脉宽度、脾脏厚度在两组患者中差异有统计学意义(P值均0.05)。进一步非条件Logistic回归模型分析显示中性粒细胞百分比[比值比(OR)=1.044,P=0.040]、血浆D-二聚体(OR=0.091,P0.001)、门静脉宽度(OR=0.030,P=0.008)、脾脏厚度(OR=0.427,P=0.003)为PVT形成的危险因素。结论肝硬化PVT可隐匿起病,也可伴有不同的临床表现。肝硬化PVT常发生在晚期肝硬化患者中,血浆D-二聚体、门静脉宽度、脾脏厚度、中性粒细胞百分比为肝硬化PVT形成的独立危险因素。     

肝硬化门静脉高压患者行脾切除断流术后早期门静脉血栓形成的原因分析

目的探讨肝硬化门静脉高压接受脾切除断流术后早期门静脉血栓形成的原因。方法对2012年1月-2013年12月首都医科大学附属北京佑安医院收治的83例脾切断流术后患者进行回顾性分析,随访时间3个月,根据是否发生门静脉血栓分为血栓组与对照组,计量资料组间比较采用t检验,计数资料比较采用χ2检验。采用Logistic回归模型进行多因素分析。结果 44例脾切断流术后患者发生门静脉血栓,发生率53.01%;血栓组与对照组间比较,术前门静脉直径、术后门静脉直径、脾脏容积、脾切除前后门静脉流速差差异均有统计学意义(P值分别为0.014、0.017、0.013、0.030),是术后早期门静脉血栓形成危险因素;Logistic回归分析显示手术前后门静脉流速差是术后门静脉血栓形成的独立危险因素(P=0.003);而手术前、后的门静脉血流流速,门静脉压力变化,手术时间,术中出血,血小板最高值与门静脉血栓形成均无关。结论血流动力学因素影响脾切断流术后门静脉血栓形成,抗凝治疗需个体化。     

肝前性非肝硬化性门静脉高压症的诊疗进展

肝前性非肝硬化性门静脉高压是一组由非肝硬化因素导致的门静脉高压性疾病,目前认为这组疾病的病因主要与JAK2突变、血液高凝状态有关。临床表现主要包括静脉曲张破裂出血、脾肿大等,患者肝功能正常或仅有轻微异常。对肝前性非肝硬化性门静脉高压疾病的诊断主要依靠其影像学特点,同时还需排除肝硬化门静脉高压。治疗方面主要采取抗凝治疗和内镜下治疗,患者预后一般较好。本文系统梳理了肝前性非肝硬化性门静脉高压的主要进展。     

门静脉血栓形成对肝硬化病程发展影响

目的探讨门静脉血栓（PVT）形成对肝硬化病程的影响。方法回顾我院2003年～2011年肝硬化伴PVT形成的患者资料。18例肝硬化伴PVT形成患者人选血栓组;随机选择同阶段肝硬化门静脉高压症的无门静脉血栓形成患者19例作为对照组,比较两组患者的门静脉宽度、脾脏厚度、食管胃底静脉曲张、腹水及上消化道大出血发生等情况。结果血栓组的门静脉宽度及脾脏厚度大于对照组,差异有统计学意义（P〈0．05）。血栓组食管胃底重度静脉曲张、上消化道大出血和大量腹水比例两组比较,差异有统计学意义（P〈0．05）。结论脾肿大和门静脉增宽是PVT形成的主要危险因素,PVT形成加重门静脉高压的程度,从而增加上消化道出血几率,使腹水难以消退,增加相关并发症发生率并使相关症状加重,预防门静脉血栓形成有助于延缓肝硬化病情发展。     

肝硬化门静脉高压患者门静脉压力与血流动力学的关系

通过多普勒超声技术，检测肝硬化门静脉高压患者门静脉系统血流动力学状态并分析其与门静脉压力的关系，旨在探讨多普勒超声技术对肝硬化门静脉高压患者门静压力的诊断意义。     

肝硬化门静脉血栓形成37例临床分析

目的探讨门静脉血栓（PVT）形成对肝硬化病程的影响。方法回顾我院2003～2010年肝硬化伴PVT形成的患者资料。18例肝硬化伴PVT形成患者入选血栓组;随机选择同阶段肝硬化门静脉高压症的无门静脉血栓形成患者19例作为对照组,比较两组患者的门静脉宽度及脾脏厚度,食管胃底静脉曲张、腹水及上消化道大出血发生等情况。结果血栓组的门静脉宽度及脾脏厚度大于对照组,差异有统计学意义（P〈0.05）。血栓组患者的上消化道大出血发生率、重度食管胃底静脉曲张程度、大量腹水患者数量明显高于对照组。结论 PVT形成加重门静脉高压的程度,从而增加上消化道出血机率,使腹水难以消退,预防门静脉血栓形成有助于延缓肝硬化病情发展。     

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT.     

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis(PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to:(1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis;(2) describe the principal factors most frequently involved in PVT development; and(3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.     

Portal vein thrombosis in liver cirrhosis简

Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.     

Portal vein thrombosis: Insight into physiopathology, diagnosis, and treatment

Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a pa...     

Portal vein thrombosis in cirrhosis: Controversies and latest developments

Portal vein thrombosis(PVT) is encountered in livercirrhosis, particularly in advanced disease. It has been a feared complication of cirrhosis, attributed to significant worsening of liver disease, poorer clinical outcomes and potential inoperability at liver transplantation; also catastrophic events such as acute intestinal ischaemia. Optimal management of PVT has not yet been addressed in any consensus publication.We review current literature on PVT in cirrhosis; its prevalence, pathophysiology, diagnosis, impact on the natural history of cirrhosis and liver transplantation,and management. Studies were identified by a search strategy using MEDLINE and Google Scholar. The incidence of PVT increases with increasing severity of liver disease: less than 1% in well-compensated cirrhosis, 7.4%-16% in advanced cirrhosis. Prevalence in patients undergoing liver transplantation is 5%-16%.PVT frequently regresses instead of uniform thrombus progression. PVT is not associated with increased risk of mortality. Optimal management has not been addressed in any consensus publication. We propose areas for future research to address unresolved clinical questions.     

肝硬化门静脉血栓形成的临床分析

目的　探讨肝硬化 (LC)门静脉血栓 (PVT)形成对LC病程发展的影响。方法　检索我院自 1 995至 2 0 0 2年肝硬化PVT形成患者 ,血栓诊断依据彩色多普勒和 (或 )CT。 4 8例肝硬化PVT形成患者入选血栓组 ;同阶段LC门脉高压症的非血栓病例中选择 5 2例作为对照组。对两组患者的肝功能Child Pugh分级、凝血功能、门静脉、脾静脉宽度及脾脏面积、厚度进行比较。行t检验 ,χ2 检验 ,Logistic回归分析。结果　肝硬化PVT形成除继发于脾切除等手术后 ,75 .0 %隐匿发病 ,85 .4 %的血栓发生于门静脉主干 ,脾脏增大与门静脉增宽是PVT形成的危险因素 (P =0 .0 0 3、0 .0 1 0 )。血栓组门静脉及脾静脉宽度分别为 (1 .4 8± 0 .2 6 )cm ,(1 .2 3± 0 .38)cm ,与对照组比较差异有显著性 [(1 .37± 0 .2 2 )cm ,(1 .0 5± 0 .30 )cm ,P =0 .0 37,0 .0 31 ]。血栓组脾面积平均值为 (96 .6 4± 33.4 )cm2 ,脾厚径为 (6 .0 7± 1 .2 0 )cm ,分别大于对照组的 (80 .81± 2 8.9)cm2 ,(5 .2 3± 1 .0 8)cm(P =0 .0 36 ,0 .0 0 1 )。血栓组食管胃底静脉曲张程度重于非血栓组 ,大出血、大量腹水比例高 (P <0 .0 5 )。血栓形成后 1年内死亡率为1 6 .6 % ,较非血栓组增高 (P =0 .0 2 3)。两组肝功能Child Pugh分级、凝血功能、血小板计     

Portal vein thrombosis in cirrhosis: Why a well-known complication is still matter of debate

Portal vein thrombosis(PVT)represents a well-known complication during the natural course of liver cirrhosis(LC),ranging from asymptomatic cases to lifethreating conditions related to portal hypertension and hepatic decompensation.Portal flow stasis,complex acquired hypercoagulable disorders and exogenous factors leading to endothelial dysfunction have emerged as key factors for PVT development.However,PVT occurrence remains unpredictable and many issues regarding its natural history,prognostic significance and treatment are still elusive.In particular although spontaneous resolution or disease stability occur in most cases of PVT,factors predisposing to disease progression or recurrence after spontaneous recanalization are not clarified as yet.Moreover,PVT impact on LC outcome is still debated,as PVT may represent itself a consequence of liver fibrosis and hepatic dysfunction progression.Anticoagulation and transjugular intrahepatic portosystemic shunt are considered safe and effective in this setting and are recommended in selected cases,even if the safer therapeutic option and the optimal therapy duration are still unknown.Nevertheless,their impact on mortality rates should be addressed more extensively.In this review we present the most debated questions regarding PVT,whose answers should come from prospective cohort studies and large sample-size randomized trials.     

肝硬化并发门静脉血栓临床表现和诊断进展

正门静脉血栓形成(portal vein thrombosis,PVT)是晚期肝硬化的常见并发症之一~([1])。近年来,文献报道PVT在肝硬化患者的患病率为0.6%～26.0%~([2,3])。PVT的临床表现差异很大,可无症状,也可表现为致命性并发症,如静脉曲张破裂出血、肠梗死等。随着影像学技术的不断提高,越来越多不同程度的PVT被诊断出来~([4～6])。1肝硬化并发PVT的临床特点1.1急性PVT PVT的临床表现取决于血栓形成的