慢性肝病与门静脉血栓形成

门静脉血栓形成与肝硬化，肝癌等慢性肝病关系密切，临床上并非少见但容易被忽视。充分认识门静脉血栓形成的发病机制和临床特点，有助于早期诊断和及时治疗。     

肝硬化脾切除术后1年广泛门静脉血栓形成1例

病例：患者 男,37岁,乙型肝炎肝硬化病史两年,一年前因“食管静脉曲张破裂出血”于当地医院行“脾切除＋断流手术”。     

肝硬化门静脉高压脾切除术后门静脉血栓形成的研究进展

门静脉血栓形成(PVT)是指门静脉或其分支、脾静脉和肠系膜上静脉内形成的血栓。PVT是门静脉高压症脾切除术后的一种常见并发症,往往可能会导致肝损伤、上消化道出血、肝昏迷,甚至是缺血性肠坏死。因而,早期发现PVT并进行有效干预,对降低PVT患者的病死率有十分重要的意义。对肝硬化脾切除术后PVT危险因素和治疗进行了综述,指出PVT应及早进行有效干预。     

日本血吸虫病的超声诊断

1 超声诊断的基本概念 高于可听声频率(20Hz—20kHz)的声学技术在医学领域中的应用称为超声医学,包括超声诊断学、超声治疗学和生物医学超声工程。应用超声的物理特性,诊断人体疾病的科学叫超声诊断学。超声诊断仪器包括发射、扫查、接收、信     

D-二聚体在诊断肝硬化门静脉血栓形成中的应用价值

目的探讨D-二聚体在肝硬化门静脉血栓形成中的预测价值。方法选我院自2005年1月至2008年12月所收肝硬化剔除不符合标准者共有83例入组,据螺旋CT增强扫描是否合并PVT分为血栓组和对照组,观测其D-二聚体水平。结果血栓组D-二聚体水平显著高于对照组。结论 D-二聚体水平异常升高可提示门静脉血栓的形成。     

B型超声、胃镜和脾门静脉核素显像对门静脉高压症的量化诊断研究

目的 将B型超声、胃镜和脾门静脉核素显像三种检查方法的结果进行量化，建立判别式，以探讨其在肝硬化门静脉高压症诊断中的临床意义。方法 分别对40例肝硬化门静脉高压症、10例慢性肝病、12例非肝病患者进行B型超声、胃镜和脾门静脉核素显像检查。结果 经逐步回归分析，筛选出诊断肝硬化门静脉高压症的影像学指标是：门体分流指数（X1）、脾静脉宽度（X2）、肝脏回声分级（X3）、食管静脉曲张程度（X4），将其分别建立判别式为：Y1=-36．912＋15．650X1＋67．289X2-0．425X3-1．651X4，Y0=-23．193＋10．697X1＋61．425X2-3．251X3-2．758X4或Y1=-35．828＋15．857X1＋62．390X2＋0．228X3，Y0=-20．167＋11．042X1＋53．241X2-3．581X3，若Y1〉Y0，即为肝硬化门静脉高压症，其诊断肝硬化门静脉高压症的敏感度均为95％，特异度分别为96％、91％，明显优于B超或胃镜定性检查的78％、75％（P〈0．05）。结论 B型超声和脾门静脉核素显像联合定量检测并建立判别式，可以显著提高对肝硬化门静脉高压症的诊断敏感度。     

肝硬化门脉高压脾切除术后门脉血栓形成15例

因肝硬化门脉高压脾功能亢进症而进行脾切除的患者,术后近期门静脉压力降低,但部分发现术后合并门脉血栓。我院自1995-2004年观察肝硬化门脉高压脾切除术后患者59例,合并门脉血栓者15例。     

断流术后门静脉系统血栓形成及其防治

目的 目的 探讨肝硬化门静脉高压症断流术后门静脉系统血栓的发生情况及其防治。方法 方法 回顾性分析113例肝 硬化门静脉高压症断流术后患者的临床资料, 患者肝硬化均由晚期血吸虫病和乙肝导致, 分析其术后门静脉系统血栓形 成的时间、 部位, 并探讨预防和治疗方法。结果 结果 113例患者中, 33例断流术后门静脉系统血栓形成, 血栓形成发生率为 29.2%。血栓形成时间为术后2～15 d, 中位时间为术后6 d; 单纯脾静脉和门静脉血栓各19例和10例, 另4例脾静脉和门 静脉均有血栓形成。经溶栓治疗后, 30例血栓消失。结论 结论 多数患者断流术后门静脉系统血栓形成位于脾静脉。术中 避免钳夹脾静脉主干、 术后早期采取全身抗凝治疗能有效预防血栓形成。     

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     

门静脉血栓的研究进展

近年来,随着诊断技术的进步,门静脉血栓检出率明显提高,而且在门静脉血栓的危险因素、对门脉系统的影响、临床表现、诊断方法及治疗等方面均有了新的认识,本文就以上几方面的研究进展做一综述。     

Extrahepatic portal vein thrombosis

Noncirrhotic, nontumoral portal vein thrombosis (PVT) is the second most-frequent cause of portal hypertension in the world. General thrombophilic factors can be identified in approximately 60% of patients. PVT may manifest as an acute process. However, the acute episode more frequently is asymptomatic or paucisymptomatic and portal vein thrombosis is misdiagnosed until the development of complications secondary to portal hypertension, such as variceal bleeding or portal biliopathy. Although no randomized controlled trials have been performed, after the diagnosis of acute PVT early initiation of anticoagulation (within 30 days of the onset of symptoms) is recommended to achieve recanalization. In patients with portal cavernoma, anticoagulation is aimed to prevent the progression and recurrence of thrombosis. Because of the lack of data in this specific population, variceal bleeding is managed as in cirrhotic patients. Ursodeoxycholic acid has been proposed empirically for the treatment of patients with symptomatic portal biliopathy. Choledocholithiasis might be present, complicating a bile duct stenosis. Accordingly, an endoscopic retrograde cholangiopancreatography with sphincterotomy, extraction with balloon catheter, and stent placement is indicated. Mortality among patients with PVT is low (5-year mortality rate of 5 to 10%) and is mainly related to associated diseases rather than to complications of portal hypertension.     

Changing perspectives in portal vein thrombosis

The aetiology of portal vein thrombosis (PVT) is heterogeneous. Important primary risk factors for PVT are cirrhosis, hepatobiliary malignancies and pancreatitis. Newly discovered thrombotic risk factors, such as latent myeloproliferative disorders and prothrombotic genetic defects, have also been identified as major risk factors for PVT. At least one-third of PVT patients demonstrate a combination of thrombotic risk factors. PVT, which does not have a detrimental effect on liver function, usually becomes manifest as a variceal haemorrhage in the oesophagus months to years after the development of thrombosis. Owing to intact coagulation variceal bleeding has a better prognosis among patients with PVT than cirrhotics. Endoscopic sclerotherapy or band ligation is the primary therapeutic option for variceal bleeding in patients with PVT. It is questionable whether anticoagulant therapy should be started, since it has not proven beneficial for most PVT patients. Therapy with anticoagulants is only recommended for those with acute PVT (especially in association with mesenteric vein thrombosis), those who recently underwent a portosystemic shunt procedure, and those with other thrombotic manifestations, particularly in case of proven hypercoagulability. Mortality of patients with PVT may be associated with concomitant medical conditions which lead to the PVT or with manifestations of portal hypertension, such as variceal haemorrhage. Multivariate analysis of a large Dutch PVT population has shown that age, malignancy, ascites and the presence of mesenteric vein thrombosis are independently related to survival. Death due to a variceal haemorrhage is rare. Poor outcome of PVT thus appears to be associated primarily with concomitant diseases which lead to PVT, and not the complications of portal hypertension. It is therefore uncertain whether surgical portosystemic shunting affects survival favourably.     

Nonmalignant portal vein thrombosis in adults

Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT. Acute PVT usually presents as abdominal pain. When the thrombus extends to the mesenteric venous arches, intestinal infarction can occur. Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy. Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease. Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively. A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT. For patients with either form of PVT, permanent anticoagulation therapy should be considered if they have a permanent risk factor. In patients with large varices, beta-adrenergic blockade or endoscopic therapy seems to prevent bleeding as a result of portal hypertension, even in patients on anticoagulation therapy. In patients with jaundice or recurrent biliary symptoms caused by cholangiopathy, insertion of a biliary endoprosthesis is the first treatment option. Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.