肝硬化门静脉高压自发性脾肾分流患者临床特征分析

目的:分析肝硬化门静脉高压合并自发性脾肾分流患者临床特征。方法:回顾性分析我院17例肝硬化门静脉高压合并脾肾分流患者作为分流组,记录其Child-Pugh评分,门静脉内径、脾静脉内径,总胆红素水平及有无食管胃底静脉曲张、肝性脑病及腹水的发生;随机抽取同期住院20例肝硬化门静脉高压未合并脾肾分流患者作为对照组,分析其临床特征。结果:分流组患者门静脉及脾静脉内径分别为(14.14±0.93)mm、(15.82±1.03)mm,对照组患者分别为(15.35±1.22)mm、(12.56±1.90)mm,两组相比较差异均有统计学意义(P0.05);脾肾分流患者总胆红素水平为(32.94±7.56)μmol/L,总胆红素异常率为88.23%,对照组分别为(37.45±22.61)μmol/L和55.00%,两组总胆红素水平相比无统计学意义(P0.05)。分流组患者总胆红素异常率高于对照组(P0.05);分流组食管胃底静脉曲张、肝性脑病、腹水发生率分别为88.24%、47.06%、23.53%,对照组分别为55.00%、10.00%、30.00%,两组相比较,食管胃底静脉曲张及肝性脑病发生率有统计学意义(P0.05),腹水发生率相比无统计学意义(P0.05)。结论:肝硬化门静脉高压合并脾肾分流患者存在不同程度的总胆红素升高,多合并食管胃底静脉曲张,其肝性脑病的发生率明显升高。     

肝硬化后门静脉血栓形成的临床特点研究

目的研究肝硬化(liver cirrhosis,LC)后门静脉血栓(portal vein thrombosis,PVT)形成的临床特点。方法对9678例LC患者进行回顾性分析,采用腹部B超/腹部增强CT及腹部增强MRI检查门脉主干或左右分支,筛选出LC伴PVT形成者(PVT组),同时将LC后无PVT患者纳为对照组,比较2组的Child-Pugh分级、门静脉及脾静脉宽度、脾脏面积及厚度、腹水、上消化道出血、肝性脑病和肝肾综合征等并发症。结果 LC患者中有396例(4.09%)PVT形成。PVT组中LC的病因主要有乙型肝炎、酒精性及丙型肝炎LC,PVT主要分布在门静脉主干、门静脉右支、肠系膜上静脉、门静脉左支和脾静脉。按Child-Pugh进行分级,PVT组与对照组比较,肝损伤较重(P<0.01)。PVT组合并腹水、上消化道出血、肝性脑病及肝肾综合征等并发症的发病率均较对照组高(P<0.01)。PVT组门静脉和脾静脉宽度分别为(1.50±0.23)cm和(1.25±0.34)cm,对照组为(1.38±0.23)cm和(1.06±0.29)cm。PVT组脾脏面积为(97.48±32.90)cm2,脾脏厚度为(6.09±1.21)cm;对照组分别为(81.19±29.10)cm2和(5.26±0.99)cm。PVT组门静脉及脾静脉宽度和脾脏厚度均大于对照组,差异有统计学意义(P<0.05)。PVT组有侧支循环开放的患者占96.21%,对照组为78.25%,2组比较差异有统计学意义(P<0.05)。结论 LC后PVT形成对LC患者的临床转归有重要影响。     

彩色多普勒检测门静脉高压脐静脉分流量对门静脉右支血流动力学的影响

目的探讨门静脉高压脐静脉开放及分流程度对肝脏门静脉右支血流灌注的影响。方法回顾性分析2012年至2015年我院就诊临床诊断的乙型肝炎肝硬化门静脉高压患者125例,其中脐静脉开放患者78例,依据脐静脉分流量分为轻度分流组38例和重度分流组40例,无脐静脉开放形成患者47例为对照组。应用彩色多普勒技术对3组患者的门静脉主干、门静脉左、右支及脐静脉的内径和血流速度及血流量进行检测,并对3组数据进行比较。结果重度分流组的门静脉左支血流量大,门静脉右支血流量明显减少甚至消失,肝右叶萎缩发生率明显增大(P0.05)。结论脐静脉开放是肝硬化门静脉高压主要的侧支循环之一,其分流程度直接影响门静脉右支对于肝右叶的营养血流灌注,使肝右叶血流灌注不足,加剧肝右叶萎缩的发生。     

CT诊断肝硬化门静脉右后支与下腔静脉自炭分流1例

肝硬化门静脉高压时,内脏的静脉血液不易或不能经肝回流到心脏,而通过肝外门静脉系统与腔静脉之间的交通支或吻合支开放、扩张,使部分内脏血液回流到上、下腔静脉,形成侧支循环,亦称门-腔循环或门-体循环[1].其通路有胃静脉-食管静脉、肠系膜下静脉-髂内静脉、副脐静脉-腹腔静脉、脾-肾、胃-肾吻合支等,笔者遇到一例门脉右后支与下腔静脉自发分流,较罕见,报道如下.     

多层螺旋CT门静脉成像对肝硬化门脉高压侧支循环的诊断价值

目的探讨多层螺旋CT(MSCT)门静脉成像对肝硬化门脉高压侧支循环的诊断价值。方法对109例经临床、肝功能和影像学检查诊断为肝硬化门脉高压患者行腹部三期增强扫描,经图像后处理,获得门静脉系统及侧支血管三维重建图像。结果 CTPV可以直观地显示门静脉系统及侧支循环。109例中,胃左静脉曲张67例(61.5%),食管下段静脉曲张87例(80.0%),胃后/短静脉曲张10例(9.2%),食管旁静脉曲张21例(19.3%),胃/脾-肾静脉分流14例(12.8%),门静脉海绵样变18例(16.5%),附脐静脉、腹壁静脉曲张15例(13.8%),椎旁静脉分流6例(5.5%)。结论 MSCT门静脉成像可精确显示各类侧支循环的部位、程度及走行,可为临床治疗前评估提供可靠的影像依据。     

肝硬化食管胃静脉曲张破裂出血的预防和治疗新进展

肝硬化患者门静脉系统血流受阻导致门静脉及其属支血管内静力压力升高并伴侧支循环形成,临床主要表现为腹水、脾大、肝性脑病以及食管胃静脉曲张破裂出血等.其中,食管胃静脉曲张破裂出血的病死率最高,是最常见的消化系统急症之一.肝硬化患者上消化道出血的原因中,70％是因为静脉曲张破裂出血.     

216例肝硬化门静脉高压症患者CT血管成像门静脉侧支血管表现研究

目的探讨肝硬化患者CT 门静脉血管成像中门静脉侧支血管表现,为临床诊断提供依据。方法回顾性研究2013年1月~2014 年1月本院收治的 216 例临床诊断为肝硬化门静脉高压症患者的临床和CT检查资料,针对患者CT门静脉血管成像和门静脉侧支血管三维重建图像进行分析。结果216例患者中,肝硬化门体分流侧支血管的分布、走行及解剖毗邻关系在CT 门静脉血管成像图像上都能得到良好、直观的显示,其中胃左静脉曲张者172例（79.63%）,食管下段静脉曲张者100例（46.30%）,食管旁静脉曲张者 51例（23.61%）,胃/脾肾静脉分流者50例（23.15%）,附脐静脉及腹壁静脉曲张者36例（16.67%）;胃/脾肾静脉分流患者门静脉和脾静脉直径分别为（12.64±1.12） mm和（18.72±3.48） mm,与无分流患者比较有统计学差异[分别为（19.56±5.64） mm和（13.47±2.35）mm,P<0.05]。结论对肝硬化门脉高压患者行CT 门静脉血管成像检查能够对患者侧支循环的部位、严重程度等进行观察,并作出准确的判断。     

门-体分流程度评估血吸虫病肝硬化上消化道出血的应用

目的探讨门-体静脉分流程度在评估血吸虫病肝硬化上消化道出血中的应用。方法以金山医院经临床证实的33例血吸虫病肝硬化上消化道出血患者,及29例血吸虫病肝硬化非出血患者为研究对象,对其进行上腹部128层螺旋CT扫描。采用薄层块最大强度投影(TSMIP)、多平面重建(MPR)对门静脉系进行血管重建,对两组患者门-体静脉分流程度进行评分和比较,分析各侧支血管分流程度与血吸虫病肝硬化上消化道出血的关系。结果 33例上消化道出血患者中,侧支血管发生率如下:胃左静脉曲张86.4%、胃短静脉曲张68.2%、食管静脉曲张50.0%、食管旁静脉曲张50.0%、胃底静脉曲张37.9%、胃肾静脉69.7%、脾肾静脉51.5%、腹壁静脉曲张25.8%、网膜静脉曲张15.2%、脾周静脉曲张63.6%、附脐静脉曲张34.8%、腹膜后-椎旁静脉40.9%、肠系膜静脉曲张36.4%。出血组食管静脉、食管旁静脉、胃左静脉和胃底静脉的发生率和分流程度均明显大于非出血组(P值均0.05)。结论 CT门静脉系成像可精确显示各类侧支血管的部位、程度及走向。食管静脉、食管旁静脉、胃左静脉和胃底静脉能较准确地预测血吸虫病肝硬化上消化道出血的风险情况,上述侧支血管分流程度越高,上消化道出血危险性就越大。     

多排螺旋CT门静脉造影对肝硬化门脉高压侧支循环血管的显示价值

门静脉高压是肝硬化的临床表现之一,其具体表现为侧支循环形成、脾肿大、腹水、肝性脑病、上消化道出血。门体循环有很多侧支,常见的检测方法如B超、胃镜、上消化道食管钡餐等仅显示间接征象或显示侧支循环的一部分,而多排螺旋CT门静脉血管成像（MDCTPV）可以比较清晰地显示门体之间的侧支循环,对临床诊断肝硬化有很大的价值。本研究应用MDCT技术观察肝硬化侧支循环的表现并评价其临床应用价值。     

CT诊断肝硬化门静脉右后支与下腔静脉自发分流1例

肝硬化门静脉高压时，内脏的静脉血液不易或不能经肝回流到心脏，而通过肝外门静脉系统与腔静脉之间的交通支或吻合支开放、扩张，使部分内脏血液回流到上、下腔静脉，形成侧支循环，亦称门-腔循环或门一体循环。其通路有胃静脉-食管静脉、肠系膜下静脉-髂内静脉、副脐静脉-腹腔静脉、脾-肾、胃-肾吻合支等，笔者遇到一例门脉右后支与下腔静脉自发分流，较罕见，报道如下。     

经颈静脉肝内门体分流术对酒精性肝硬化导致门静脉高压的治疗效果与安全性分析

目的分析经颈静脉肝内门体分流术(TIPS)治疗酒精性肝硬化导致门静脉高压的有效性及安全性。方法回顾性总结2006年6月至2011年6月本院30例接受TIPS治疗的酒精性肝硬化导致门静脉高压的患者资料,记录术前及术后门静脉压力、腹水、脾功能亢进、肝功能等指标。随访终点为术后2 a,观察术后并发症包括消化道再出血、支架堵塞、腹水及肝性脑病发生情况,并分析肝性脑病发生与患者临床参数的关系。穿刺前、后门静脉压力差别采用配对t检验分析;Kaplan-Meier方法用于术后临床参数与肝性脑病发生相关性分析。结果 TIPS手术成功率为100%(30/30),门静脉压力术前(37.27±2.52)cm H2O降为术后(24.6±2.58)cm H2O,差异具有统计学意义(P0.05)。术后2 a内,消化道再出血率为3.3%(1/30);腹水治疗有效率达88.9%(16/18);支架狭窄发生率为6.7%(2/30);肝性脑病发生率为40%(12/30)。Kaplan-Meier分析发现患者术前Child-Pugh分级与术后肝性脑病发生密切相关(P=0.04)。结论 TIPS是治疗酒精性肝硬化门静脉高压相关并发症安全有效的微创方法,术前ChildPugh分级是影响患者肝性脑病发生的重要因素。     

Intrahepatic Portosystemic Venous Shunt: Diagnosis by Color Doppler Imaging

Intrahepatic portosystemic venous shunt is a rare clinical entity; only 33 such cases have been reported. It may be congenital, or secondary to portal hypertension. Five patients with this disorder are presented, each of whom was diagnosed by color Doppler imaging, including waveform spectral analysis. One patient with clinical evidence of cirrhosis and portal hypertension had episodes of hepatic encephalopathy and elevated blood levels of ammonia. This patient had a large tubular shunt between the posterior branch of the portal vein and the inferior vena cava. Shunts of this type are considered to be collateral pathways which develop in the hepatic parenchyma as a result of portal hypertension. The other four patients had no evidence of liver disease, and all four evidenced an ancurysmal portohepatic venous shunt within the liver parenchyma. Shunts of this type are considered congenital. The diagnosis of intrahepatic portosystemic venous shunts was established by color Doppler imaging, which demonstrated a direct communication of color flow signals between the portal vein and hepatic vein, in addition to the characterization of the Doppler spectrum at each sampling point from a continuous waveform signal (portal vein) to a turbulent signal (aneurysmal cavity), and finally, to a biphasic waveform signal (hepatic vein). As demonstrated by the five patients, color Doppler imaging is useful in the diagnosis of an intrahepatic portosystemic hepatic venous shunt, and the measurement of shunt ratio may be useful in the follow-up and determining the therapeutic option.     

Spontaneous porto-systemic shunts in liver cirrhosis: Clinical and therapeutical aspects

Spontaneous porto-systemic shunts(SPSS) are frequent in liver cirrhosis and their prevalence increases as liver function deteriorates, probably as a consequence of worsening portal hypertension, but without achieving an effective protection against cirrhosis' complications. Several types of SPSS have been described in the literature, each one associated with different clinical manifestations. In particular,recurrent or persistent hepatic encephalopathy is more frequent in patients with splenorenal shunt, while the presence of gastric varices and consequently the incidence of variceal bleeding is more common in gastrorenal shunt. In the advanced stage, the presence of large SPSS can lead to the so called"portosystemic shunt syndrome", characterized by a progressive deterioration of hepatic function, hepatic encephalopathy and, sometimes, portal vein thrombosis. The detection of SPSS in patients with liver cirrhosis is recommended in order to prevent or treat recurrent hepatic encephalopathy or variceal bleeding.     

Disappearance of hepatic encephalopathy and improvement of liver function after surgical treatment of portal-systemic shunt in a patient with liver cirrhosis

Large portal-systemic shunts in cirrhotic patients often cause recurrent hepatic encephalopathy and might promote liver dysfunction because of the reduced portal blood flow. We report a case of liver cirrhosis in which hepatic encephalopathy disappeared and liver function improved together with an increase of hepatopetal portal blood flow and liver volume after shunt resection. A 70-year-old woman with liver cirrhosis was admitted because of recurrent disorientation. Serum ammonia levels ranged from 174 to 321 micrograms/dL. Computed tomography demonstrated an atrophic liver and a large shunt. Portography disclosed that this shunt originated from the superior mesenteric vein and flowed into the inferior vena cava, common iliac vein and ovarian vein. Portal blood flow was poor because of the deviation into this shunt. After the surgical resection of the shunt, ammonia levels were normalized and hepatic encephalopathy no longer occurred. Portography and computed tomography after surgery demonstrated that hepatopetal portal blood flow evidently improved and the liver volume increased (before 369; after 574 cm3). Two years after surgery, hepaplastin test and serum albumin level improved from 41 to 76% and from 2.7 to 3.4 g/dL, respectively. This case supports the effectiveness of shunt resection for hepatic encephalopathy and the deteriorated liver function in cirrhotic patients with large portal-systemic shunt.     

Portal-systemic shunting in a patient with normal portal vein pressures and histological evidence of idiopathic portal hypertension

Although idiopathic portal hypertension (IPH) is clinically characterized by portal hypertension and marked splenomegaly, we have experienced a case of spontaneous portal-systemic shunt without splenomegaly in whom the liver histology resembled IPH but with normal portal pressure. We admitted a 64 year old man who had suffered from hepatic encephalopathy for 2 years. Laparoscopy revealed a dark grey liver with a sharp edge and a concave surface. Examination of a liver biopsy specimen revealed peri-portal fibrosis consistent with IPH. A single, large, portal-systemic shunt was identified by percutaneous transhepatic portography. The shunt arose from the left gastric vein and flowed through the left renal vein into the inferior vena cava. No varices were identified. There were no morphological changes in the hepatic or portal veins. Portal vein pressure was normal. There was a slight difference between the portal pressure and the wedged hepatic vein pressure, suggesting a presinusoidal block. This case raises important questions concerning the aetiology of IPH and the relationship between portal hypertension and the development of collateral venous circulation.     

Helicobacter pylori infection does not correlate with plasma ammonia concentration and hepatic encephalopathy in patients with cirrhosis

BACKGROUND/AIMS: In patients with cirrhosis, infection of the stomach with Helicobacter pylori may increase ammonia production and, consequently, the incidence of hepatic encephalopathy. To test this hypothesis a retrospective analysis was performed in patients with a transjugular intrahepatic portosystemic shunt. These patients are regarded to be ideal candidates for such a study since they have a high bioavailability of gut-derived ammonia and many of them develop spontaneous hepatic encephalopathy. METHODOLOGY: In 132 patients (Child-Pugh class A: 24%, B: 49%, C: 27%) with stable transjugular intrahepatic portosystemic shunt function for more than 3 months (mean follow-up: 15.5 +/- 10.8 months) the diagnosis of H. pylori infection was established by a specific and sensitive immunoblot assay for IgG- and IgA-antibodies. During follow-up, hepatic encephalopathy was assessed by clinical examination and a structured questionnaire. Venous plasma ammonia concentration was measured at the time of antibody determination (end of study period). RESULTS: Eighty-four patients (64%) had negative and 48 patients (36%) had positive immunoblots for H. pylori. The groups were comparable with respect to age, gender, etiology of cirrhosis, Child-Pugh class, follow-up after transjugular intrahepatic portosystemic shunt, and shunt function. The ammonia concentrations of the patients without (group 1) and with antibodies against H. pylori (group 2) were 73 +/- 27 and 69 +/- 28 mumol/L (mean +/- SD), respectively. Hepatic encephalopathy occurred in 23 of 84 patients (27%) of group 1 and in 11 of 48 patients (23%) of group 2. CONCLUSIONS: A positive immunoblot for H. pylori antibodies neither correlates with plasma ammonia concentration nor with the incidence of hepatic encephalopathy in patients with cirrhosis of the liver and portosystemic shunt.     

Portal hemodynamics in chronic portal-systemic encephalopathy. Angiographic study in seven cases

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P less than 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P less than 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.     

经颈静脉肝内门腔静脉分流术治疗肝癌合并门静脉高压的临床研究

目的 探讨经颈静脉肝内门腔静脉分流术(TIPS)治疗肝癌合并门静脉高压的有效性、安全性和临床价值.方法 收集肝癌合并门静脉高压患者95例,其中63例行TIPS治疗(TIPS组),观察术后情况并随访生存期资料,其余32例(对照组)行内科支持治疗,随访生存期资料.评估TIPS组术后情况、术后肝性脑病、再出血、死亡原因等.行Kaplan-Meier生存分析比较两组中位生存时间,分析Child-Pugh分级及终末期肝病评估模式(MELD)评分与术后生存时间的关系.结果 TIPS组术后门静脉压力梯度平均降低13.6 cmH2O(1 cmH2O-0.098 kPa),术后6个月肝性脑病和再出血的累积发生率分别为20.6%和26.3%,截至随访结束死亡56例,其中最终死于门静脉高压破裂出血者12例.TIPS组中位生存期较对照组延长.TIPS组中MELD评分≤13分者中位生存时间大于评分>13分者(x2=4.71,P=0.03),Child-Pugh分级A到C级中位生存时间依次缩短(x2=15.6,P=0.00).结论 TIPS是治疗肝癌合并门静脉高压及其并发症安全有效的方法 ,应根据术前肝功能状况选择手术患者.     

The incidence of portal vein thrombosis at liver transplantation.

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt.