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。     

三维多层螺旋CT对肝硬化门脉高压患者侧支循环的诊断价值

目的　了解多层螺旋CT门体侧支循环的显示情况,并探讨其临床意义。方法　对2003 -04 ~2003-12北京友谊医院43例肝硬化门脉高压病人分别进行胃镜和多层螺旋CT门脉成像。了解食管胃底静脉曲张及门体侧支循环形成情况并加以比较,同时分析其与肝功能之间的相关性。结果　多层螺旋CT能清晰地显示门静脉及其侧支血管,胃镜显示食管静脉曲张38 /43(88. 4% ),胃底静脉曲张23 /43 (53 .5% ),螺旋CT显示食管静脉曲张37 /43(86% ),胃底静脉曲张25 /43(58 .1% )。对食管胃底静脉曲张的显示与胃镜有高度一致性,Kappa值分别为0 .876和0. 903。结论　多层螺旋CT结合多种三维重建技术进行图像后期处理,能产生高质量的血管图像,三维多层螺旋CT门脉造影,能显示肝硬化病人门体侧支血管,可能是这个领域中理想的血管成像技术。     

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。     

螺旋CT门静脉造影对门脉高压侧支循环的研究

目的探讨多排螺旋CT门静脉造影(CT portal venography,CTPV)显示肝硬化门脉高压侧支循环血管的临床应用价值。方法对92例肝硬化门脉高压的患者分别进行CT门脉造影,获得门脉侧支循环血管的清晰图像,测量门静脉主干和胃左静脉直径,将胃镜与CT门静脉造影两种技术进行比较。结果应用CT门静脉造影能清晰显示和测量门脉侧支循环的血管。CT门静脉造影与胃镜两种方法对食管和胃底曲张静脉的显示能力具有一致性,Kappa值分别为0.502和0.478。结论应用多排螺旋CT门静脉造影能很好显示和测量门体间侧支循环血管。联合应用多排螺旋CT门静脉造影与胃镜两种方法,对于肝硬化门静脉高压患者的诊断、病情判断和估计预后有帮助。     

肝硬化非常见侧支循环临床特点研究

目的 探讨肝硬化患者门体循环之间非常见侧支循环形成的临床特点及意义。方法 对临床确诊为肝硬化的患者运用64排螺旋CT和三维血管成像结合电子胃镜检查,观察其门体循环之间非常见侧支循环的形成。结果 ①700例肝硬化患者中118例(16.86%)存在非常见侧支循环,依次为脾肾静脉分流、胃肾静脉分流、椎旁静脉分流、腹膜后静脉分流、胃脾分流和心膈角静脉分流。②非常见侧支循环形成与肝硬化Child-Pugh分级相关(P<0.01)。③与常见侧支循环形成组比较,非常见侧支循环组较少出现重度食管和(或)胃底静脉曲张、重度门静脉高压性胃病及大量腹水(P<0.01)。④非常见侧支循环组中肝性脑病和慢性血氨升高的发生率高于常见侧支循环组(P<0.01)。结论 ①肝硬化患者中非常见侧支循环并不"非常见";②非常见侧支循环形成与肝功能Child-Pugh分级有关;③非常见侧支循环形成可缓解门静脉高压引起的相关并发症,但增大了肝性脑病和慢性血氨升高的发病率。     

食管胃底静脉曲张血供与侧支的研究

目的通过多层螺旋CT(multi—detecter row computed tomography，MDCT)了解食管胃底静脉曲张及与之相关的侧支循环，为食管胃底静脉曲张破裂出血治疗方案的选择和预后的判断提供客观依据。方法选择51例临床证实的肝硬化门静脉高压患者，其中胃镜显示食管静脉曲张51例，伴胃底静脉曲张31例。对所有患者进行MDCT血管成像，重点观察食管胃底静脉曲张及相关侧支循环。结果MDCT血管成像能清晰地显示肝硬化门体侧支血管，并显示所有食管静脉曲张。MDCT显示胃底静脉曲张32例(62．7％)，与胃镜检查结果(31／51，60．8％)比较，两者具有高度一致性，Kappa值为0．876。食管曲张静脉几乎全部由胃左静脉供血，30例(58．8％)单纯由胃左静脉前支供血，21例(41．2％)伴有食管旁静脉；24例(75％)胃底曲张静脉为单纯胃左静脉供血，3例(9．4％)由胃短(胃后)静脉供血，5例(15．6％)为胃短(胃后)和胃左静脉双重供血，双重供血者因胃底静脉曲张和食管静脉曲张常相互交通，所以这些病例胃短(胃后)静脉也同时参与食管静脉曲张的形成。结论MDCT能较清晰地显示食管胃底静脉曲张侧支循环。食管静脉曲张主要由胃左静脉供血，大部分由前支经贲门进入曲张静脉，部分伴有食管旁静脉。胃底静脉曲张大部分由胃左静脉供血，但小部分则由胃短系统供血。     

多层螺旋CT门静脉成像评估肝硬化食管静脉曲张出血风险

目的 本文旨在评估多层螺旋CT（MSCT）门静脉重建对肝硬化门脉高压患者食管静脉曲张破裂出血风险的预测价值.方法 选取94例肝硬化可疑食管静脉曲张患者,1周内行MSCT和上消化道内镜检查.内镜排除合并胃底静脉曲张患者,共80例单纯食管静脉曲张患者入选本实验,对比分析MSCT及内镜资料.结果 食管曲张静脉评分、曲张静脉最大直径以及栅栏状静脉扩张均与内镜下曲张静脉形态、有无红色征及其严重程度明显相关.MSCT门静脉成像在判断红色征方面（≥4 mm）的灵敏度、特异度分别为71.3%、89.1%.结论 MSCT门静脉成像与内镜对食管静脉曲张程度的显示具有很好的一致性,可以作为预测曲张静脉出血的有效指标.     

多层螺旋CT门静脉血管成像在胰源性门脉高压症诊断中的应用

目的 研究多层螺旋CT门静脉血管成像在胰源性门静脉高压患者诊断中的应用.方法 应用16排多层螺旋CT门静脉血管成像,对47例临床怀疑胰腺体尾部病变的患者的门静脉系统形态改变与126例肝源性门脉高压患者和47例正常对照组进行形态学对比观察,并测量胃冠状静脉、门静脉、脾静脉、肠系膜上静脉内径、门静脉期肝实质和门静脉主干CT值,对比肝脏、脾脏体积.结果 在47例胰腺体尾部病变中发现有脾静脉狭窄、闭塞者38例,其中胰腺肿瘤患者27例(71.1%),急慢性胰腺炎患者11例(28.9%).38例胰源性门脉高压患者中,发现食管静脉曲张5例(13.2%),胃底静脉曲张25例(65.8%),胃体静脉曲张22例(57.9%),胃短-胃后静脉显示26例(68.4%),胃冠状静脉显示26例(68.4%),发现胃网膜静脉曲张24例(63.2%),肠系膜静脉曲张1例.脾静脉闭塞14例(36.8%),脾静脉狭窄23例(63.2%).结论 胰源性门脉高压在影像学上表现为脾静脉栓塞,脾脏增大,脾门处大量曲张静脉,胃后-胃短静脉及胃网膜静脉增粗迂曲,胃底和胃体静脉曲张,较少合并食管静脉曲张,肝脏形态大小亦无异常.多层螺旋CT门静脉血管成像检查可为胰源性门脉高压患者提供血管形态、病因诊断等多方面有价值信息,为临床诊断和治疗提供客观的影像学依据.     

多排螺旋CT门静脉成像对门静脉高压食管、胃底静脉曲张的评价

肝硬化失代偿期可引起门静脉高压,食管胃底静脉曲张是门静脉高压的一个严重并发症,其破裂可引起胃肠道大出血,对门静脉高压侧支循环的显示对患者的治疗方式的选择及预后的评估具有重要意义.多排螺旋CT门静脉成像(CTPV)可显示胃底静脉曲张的部位、形态及侧支循环血供的关系,在GEVI型,GV多为LGV或以LGV为主来供应,胃和(或)脾-肾分流较少见,GV的形态多为迂曲型.在GEV2型,GV大部分由PGV和(或)SGV供血,部分病例伴胃和(或)脾-肾分流.IGV型多以PGV和(或)SGV为主要血供,且较多合并胃和(或)脾-肾分流,GEV2和IGV型GV的形态以结节型和瘤型较多.CTPV可显示食管静脉曲张分型与其侧支循环的关系,EV以位于食管黏膜下、食管壁为主时,其血供多为胃左静脉前支优势型;EV为食管管旁静脉曲张为主时,其血供多为后支优势型;EV管壁、黏膜下静脉曲张程度与管旁静脉曲张接近时,其血供多为前后支均衡型.     

CT门静脉成像在肝硬化食管胃静脉曲张中的应用进展

食管胃静脉曲张是肝硬化门静脉高压常见的并发症,其引起的上消化道出血是肝硬化最常见的死亡原因。CT门静脉成像(CT povtal venography,CTPV)可清晰地显示门静脉及侧支循环的结构,对肝硬化食管胃静脉曲张的诊治具有重要意义。本文就CTPV在肝硬化食管胃静脉曲张诊治中的应用进展作一概述。     

Management of portal hypertension based on portal hemodynamics

Portal hypertension is most commonly caused by chronic liver disease. As liver damage progresses, portal pressure gradually elevates and hemodynamics of the portal system gradually change. In normal liver, venous returns from visceral organs join the portal trunk and flow into the liver (hepatopetal blood flow). As portal pressure increases due to liver damage, congestion of some veins of the visceral organ occurs (blood flow to and from). Finally, the direction of some veins (the left gastric vein in particular) of the visceral organ change (hepatofugal blood flow) and develop as collateral veins (portosystemic shunt) to reduce portal pressure. Therefore, esophagogastric varices serve as drainage veins for the portal venous system to reduce the portal pressure. In chronic liver disease, as intrahepatic vascular resistance is increased (backward flow theory) and collateral veins develop, adequate portal hypertension is required to maintain portal flow into the liver through an increase of blood flow into the portal venous system (forward flow theory). Splanchnic and systemic arterial vasodilatations increase the blood flow into the portal venous system (hyperdynamic state) and lead to portal hypertension and collateral formation. Hyperdynamic state, especially around the spleen, is detected in patients with portal hypertension. The spleen is a regulatory organ that maintains portal flow into the liver. In this review, surgical treatment, interventional radiology, endoscopic treatment, and pharmacotherapy for portal hypertension (esophagogastric varices in particular) are described based on the portal hemodynamics using schema.     

Non-cirrhotic portal hypertension versus idiopathic portal hypertension

Portal hypertension occurs in a number of disorders other than cirrhosis and they are collectively called non-cirrhotic portal hypertension (NCPH). The common causes of NCPH include idiopathic portal hypertension (IPH), non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous thrombosis (EHPVT). Other causes include schistosomiasis, hepatic venous outflow tract obstruction, veno-occlusive disease and congenital hepatic fibrosis. Patients with IPH and EHPVT present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation and jaundice due to portal biliopathy. The diagnosis is usually made by abdominal ultrasound, upper gastrointestinal endoscopy, normal liver function tests and normal liver histology. Variceal bleeding in NCPH has lower mortality as compared with cirrhosis because of better liver functions in NCPH. Treatment for NCPH includes primary prophylaxis for variceal bleeding and prevention of repeat bleeding using drugs like beta-blockers, endoscopic sclerotherapy and endoscopic band ligation of varices. In patients with uncontrolled variceal bleeding or symptomatic hypersplenism, porto-systemic shunt surgery or splenectomy are required.     

门静脉高压患者门静脉压力与血流动力学的相关性研究

目的 探讨门静脉高压患者门静脉血流动力学的变化特点及其与门静脉压力的相互关系。方法 采用彩色多普勒超声对４１例肝硬化门静脉高压患者（Ｃｈｉｌｄ Ａ、Ｂ级３１例、Ｃ级１０例）于手术前检测门静脉（ＰＶ）、脾静脉（ＳＶ）和肠系膜上静脉（ＳＭＶ）的内径和血流速度，再计算出相关的面积和血流量；于手术时对３１例ＣｈｉｌｄＡ十Ｂ级患者直接测量门静脉压力。３２例健康人和２６例慢性乙型肝炎患者（慢肝组）作为对照。结累 门静脉高压两组患者ＰＶ、ＳＶ和ＳＭＶ内径（ｃｍ）分别为１．５１和１．５２、１．３２和１．３４及１．１５和１．１５较慢肝组和正常组明显增宽，ｒ分别为１．３１和１．１６、０．９６和０．７９及０．９１和０．８２（Ｐ＜０．０１）；血流速度较正常组和慢肝组明显减慢（Ｐ＜０．０１）；门静脉高压Ｃ级组门静脉血流速度（ｃｍ／ｓ）为４．６５较门静脉高压Ａ十Ｂ级组（６．４２）明显减慢（Ｐ＜０．０１），而两组 ＳＶ和 ＳＭＶ的血流速度则差异无显著意义（Ｐ＞０．０５）；门静脉高压 Ａ＋Ｂ级组三条静脉的血流量明显大于正常组和慢肝组（Ｐ＜０．０１或Ｐ＜０．０５）；门静脉高压Ｃ级组门静脉血流量明显小于Ａ十Ｂ级组（Ｐ＜０．０１）；而ＳＶ和ＳＭＶ的血流     

Captopril reduces portal pressure effectively in portal hypertensive patients with low portal venous velocity

Background The effect of an angiotensin II blockade in lowering the portal pressure in patients with liver cirrhosis and portal hypertension is controversial. This prospective study was undertaken to evaluate the portal hypotensive effect of captopril compared to that of propranolol, and to determine the factors that contribute to a successful reduction in the portal pressure after longterm captopril administration in patients with liver cirrhosis.Methods The hepatic venous pressure gradient (HVPG) and portal venous velocity (PVV) were measured both before and 3 months after initiation of the administration of captopril (n = 29) or propranolol (n = 29) in cirrhotic patients with a variceal bleeding episode. Patients who showed a reduction in the HVPG of more than 20% of the baseline were defined as being responders.Results At 3 months, the mean reduction in the HVPG after captopril was less than that after propranolol (–3.0 ± 9.3% vs –28.5% ± 4.1%; P 0.05). However, of the 29 patients receiving captopril, 9 were classified as being responders. On multivariate analysis with parameters including age, cause, Child-Pugh score, HVPG, and PVV, only low PVV was found to be a significant independent factor for responders (PVV 12cm/s; odds ratio [OR], 12.2; 95% confidence interval [CI], 1.47–102.40) in the captopril group.Conclusions Longterm captopril administration reduces the portal pressure effectively in cirrhotic patients with a low PVV. This suggests that the reduction in portal pressure after captopril administration is a result of improved portal venous outflow brought about by a decrease in the intrahepatic vascular resistance. When the PVV is below 12cm/s, a captopril trial might be useful in preventing variceal bleeding in portal hypertensive patients.Part of this work has appeared in abstract form, in J Hepatol 2002;36 (Suppl 1):64     

胰源性与特发性门脉高压症的临床特点分析

目的探讨PPH与IPH的临床特点,加深对二者的认识,提高临床医师的诊治水平。方法对18例PPH与36例IPH患者的临床资料作一回顾分析。结果二者的肝脏形态、功能正常,病毒学指标阴性,超声检查脾静脉迂曲扩张,脾肿大;PPH患者超声检查门静脉正常,胰腺可见炎症、肿瘤、囊肿等表现;IPH患者门静脉及肠系膜上静脉迂曲扩张,但胰腺方面无异常。IPH患者汇管区纤维组织增生和炎性细胞浸润但无肝硬化改变而PPH患者肝脏组织学正常。结论临床中发现肝脏形态、功能正常,病毒学指标阴性,以门脉高压为主要表现而无肝硬化改变的患者,应考虑IPH与PPH的可能。进一步行超声检查门脉系统及胰腺情况,可进一步区分二者。     

Extrahepatic aneurysm of the portal venous system and portal hypertension

Portal venous aneurysm (PVA) is a rare condition characterized by dilatation of the portal venous system. PVA manifestation of symptoms is varied and depends on the aneurysm size, location and related-complications, such as thrombosis. While the majority of reported cases of PVA are attributed to portal hypertension, very little is known about the condition’s pathophysiology and clinical management remains a challenge. Here, we describe a 67-year-old woman who presented with complaint of dyspepsia and without a significant medical history, for whom PVA was incidentally diagnosed. The initial upper abdominal ultrasound revealed marked dilatation of the main portal vein, and subsequent contrast-enhanced computed tomography with angiography revealed a large aneurysm arising from the extrahepatic troncus portion of the portal vein, as well as gastroesophageal varices. A conservative approach using beta-blocker therapy was chosen. The patient was followed-up for 60 mo, during which time the asymptomatic status was unaltered and the PVA remained stable.