门静脉系统血流动力学与肝硬化门静脉高压的相关性

肝硬化门静脉高压导致的食管胃底静脉曲张出血是晚期肝硬化患者死亡的主要原因之一.目前仍缺乏简便易行的检测门静脉压力的方法和手段.本研究拟通过对89例肝病患者进行腹部彩色多普勒超声检查,了解门静脉系统血管直径和血流速度与肝硬化门静脉高压的相关性,为临床门静脉高压食管胃底静脉曲张出血的防治提供参考依据.     

肝硬变患者B超与内镜检查对预测门脉高压性上消化道出血的临床价值

目的为探讨B超与内镜检查对预测门脉高压性上消化道出血的临床价值.方法将入选的54例肝硬变患者均经B超与内镜检查,以了解门静脉的内径大小及食管胃底静脉曲张程度.结果门静脉内径大小及食管胃底静脉曲张程度呈正相关(相关系数R=0.411,P<0.05),门脉扩张程度及食管胃底静脉曲张程度与上消化道出血呈正相关(相关系数R=0.377,P<0.05).结论B超门静脉的内径大小与内镜检查食管胃底静脉曲张程度可作为门脉高压性上消化道出血的预测标志.     

门静脉高压无创性诊断研究进展

临床显著门静脉高压是食管胃静脉曲张破裂出血、腹水、肝肾综合征、肝性脑病等发病的始发点，了解肝病患者有无门静脉高压及其严重程度对于评估肝病患者病情、预后、选择和制定治疗方案、评估治疗后疗效意义重大。血清学检测、包括核素显像、超声、CT、MRI等在内影像学技术、内镜检查从门静脉高压形成机制和或门静脉高压相关并发症方面评估门静脉高压，有一定的诊断价值，但均无法量化门静脉压力。近年来提出的无创性诊断模型与HVPG 与较好的相关性，为无创性门静脉高压检测提供了新思路，有望成为有创HVPG的替代技术。     

超声内镜在食管胃底静脉曲张治疗及预后评估中的作用

超声内镜(EUS)通过全面评估门静脉高压侧支循环建立情况,既可预测评估食管胃底静脉曲张首次出血、治疗后复发及再出血的风险,又可引导并参与静脉曲张的治疗。介绍了EUS在食管胃底静脉曲张治疗及预后评估中的独特优势,为肝硬化合并食管胃底静脉曲张患者的个体化治疗提供了重要参考依据,并且提高了治疗的安全性和有效率,通过EUS系统诊治门静脉高压症已成为近几年的研究热点。     

肝硬化门静脉高压患者食管静脉曲张CT表现预测首次上消化道出血的价值

目的观察肝硬化门静脉高压患者食管静脉曲张的CT表现,并对首次上消化道出血的风险进行预测。方法选取延安大学附属医院肝硬化患者,根据是否存在门静脉高压,是否有门静脉高压并发食管静脉曲张破裂致上消化道出血进行分组,全部患者进行CT扫描,对静脉截面数量、门静脉主干、门静脉左支、门静脉右支、胃底静脉的直径进行测量。结果肝硬化门静脉高压患者中有63.1%患有食管静脉曲张,这些患者中有86.8%出现上消化道出血,无食管静脉曲张者仅9.7%出现上消化道出血。食管静脉曲张组较对照组静脉截面数多,门静脉主干、门静脉左支、门静脉右支和胃底静脉的直径均大于对照组(P0.05)。食管静脉曲张组出血者的静脉截面数多于未出血者,出血者门静脉主干、门静脉左支、门静脉右支和胃底静脉的直径均大于未出血者(P0.05)。结论门静脉高压是肝硬化发展的一个主要危险因子,可引发食管静脉曲张,导致上消化道出血。在临床中,可以用肝硬化门静脉高压食管静脉曲张患者的CT图来预测上消化道出血。     

肝硬化相关门静脉高压无创检测的研究进展

门静脉高压是肝硬化患者最常见也是最主要的并发症，其导致的食管胃底静脉曲张破裂出血是肝硬化患者最主要的死亡原因之一。肝静脉压力梯度(HVPG)是评价门静脉高压及其严重程度最准确的方法，胃镜检查是筛查和评估食管胃静脉曲张及其严重程度的金标准，但两项检查均为侵入性操作，限制了其临床适用性。CT、MR、弹性成像技术及新兴的无创检测方法被越来越广泛地应用于门静脉高压、食管胃底静脉曲张的诊断及分层，但能够媲美HVPG和胃镜检查的无创检测方法仍需进一步探索。     

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.     

内镜下套扎治疗胃底静脉曲张的临床应用

肝硬化门静脉高压常引发严重的食管胃底静脉曲张,对食管静脉曲张内镜下套扎治疗是常用治疗方法,而胃底静脉     

老年肝硬化门静脉高压并发上消化道出血的相关因素

目的探讨老年肝硬化门静脉高压并发上消化道出血的相关因素。方法肝硬化门静脉高压患者395例,研究其合并上消化道出血的发生情况。单因素和多因素Logistic回归分析影响老年肝硬化门静脉高压并发上消化道出血的危险因素。结果肝硬化门静脉高压合并上消化道出血214例,占54. 18%。单因素分析结果表明,性别、肝功能分级、肝硬化病因与是否合并上消化道出血无关(P>0. 05);上消化道出血患者食管胃底静脉曲张多于无上消化道出血患者、门静脉内径高于无上消化道出血患者、不良饮食习惯多于无上消化道出血患者,且有统计学差异(P<0. 05)。将单因素分析具有统计学差异的因素纳入多因素回归分析,食管胃底静脉曲张、门静脉内径和不良饮食习惯为影响肝硬化门静脉高压合并上消化道出血的独立危险因素。结论肝硬化门静脉高压合并上消化道出血相关影响因素中,食管胃底静脉曲张、门静脉内径和不良饮食习惯为其独立危险因素。     

经皮经肝食管胃底曲张静脉栓塞术联合部分脾栓塞术治疗肝硬化食管胃底静脉曲张破裂出血疗效观察

背景:食管胃底静脉曲张破裂出血是肝硬化门静脉高压常见且严重的并发症,再出血的预防是该病的治疗重点。目的:评价经皮经肝食管胃底曲张静脉栓塞术(PTVE)联合部分脾栓塞术(PSE)治疗肝硬化食管胃底静脉曲张破裂出血的疗效和安全性。方法:前瞻性选择10例肝硬化食管胃底静脉曲张破裂出血患者行PTVE联合PSE术,术前、术后行门静脉系统多普勒超声和血常规检查,记录超声血流变化和外周血细胞变化情况。术后随访1~2年,观察再出血和并发症发生情况。结果:PTVE联合PSE术后,患者门静脉主干较术前明显变细,门静脉主干和脾静脉血流速度减慢,术后3个月外周血白细胞和血小板计数仍高于术前,差异均有统计学意义(P0.05)。术后1年内2例患者发生再出血,再出血率为20.0%,其中1例复查见门静脉主干血栓形成,发生率为10.0%。该例患者术后胃底静脉曲张基本消失,予内镜下食管曲张静脉套扎治疗后未再复发。结论:PTVE联合PSE术能有效降低门静脉系统压力,是治疗肝硬化食管胃底静脉曲张破裂出血安全、有效的介入治疗方法。     

肝硬化和门脉高压症无创性诊断方法评价

肝硬化发主要生于慢性肝脏疾病的终末阶段,且常并发门静脉高压症。门脉高压症是引起肝硬化患者发病或死亡的重要因素。本文从实验室指标、瞬时弹性成像和多普勒超声技术等方面综述目前应用于临床的肝硬化和门脉高压症的无创性诊断及预后评估的方法。虽然这些方法尚不能替代侵入性的肝活检和肝静脉压力梯度测量以及胃食管静脉曲张的内镜检查,但是它们可以协助肝硬化和门脉高压症患者的治疗并提供有价值的预后评价。     

Noninvasive assessment of portal hypertension in patients with cirrhosis

Severe portal hypertension is responsible for complications and death. Although measurement of the hepatic venous pressure gradient is the most accurate method for evaluating the presence and severity of portal hypertension, this technique is considered invasive and is not routinely performed in all centers. Several noninvasive techniques have been proposed to measure portal hypertension. Certain methods evaluate elements related to the pathogenesis of portal hypertension through the measurement of hyperkinetic syndrome, for example, or they investigate the development of hepatic fibrosis through the measurement of increased intrahepatic vascular resistance. Other methods evaluate the clinical consequences of portal hypertension, such as the presence of esophageal varices or the development of portosystemic shunts. Methods evaluating increased hepatic vascular resistance are fairly accurate and mainly involve the detection of hepatic fibrosis by serum markers and transient elastography. The radiological assessment of hyperkinetic syndrome probably has value but is still under investigation. The assessment of severe portal hypertension by the presence of varices may be performed with simple tools such as biological assays, computed tomography, and esophageal capsules. More sophisticated procedures seem promising but are still under development. Screening tools for large populations must be simple, whereas more complicated procedures could help in the follow-up of already diagnosed patients. Although most of these noninvasive methods effectively identify severe portal hypertension, methods for diagnosing moderate portal hypertension need to be developed; this shows that further investigation is needed in this field.     

门静脉高压症患者食管静脉曲张多层螺旋CT与内镜分级的相关性

目的探讨门静脉高压症食管静脉曲张多层螺旋cT与内镜分级的相关性。方法选择2013年1至5月四川大学华西医院内镜诊断为食管静脉曲张的30例门静脉高压患者。对患者进行内镜分级和多层螺旋cT分级。采用Spearman等级相关分析检验食管静脉曲张多层螺旋CT分级结果与内镜分级结果的相关性。结果30例患者食管静脉曲张内镜分级结果：4例（13％）为轻度曲张,7例（23％）为中度曲张,19例（63％）为重度曲张。多层螺旋CT分级结果：5例（17％）为1级曲张,8例（27％）为2级曲张,17例（57％）为3级曲张。Spearman等级相关分析结果显示,食管静脉曲张多层螺旋CT和内镜分级结果不具有很好的相关性（r=0．339,P〉0．05）。结论食管静脉曲张多层螺旋CT与内镜分级不具有很好的相关性,使用多层螺旋CT对食管静脉曲张进行分级的相关标准有待探索。     

USEFULNESS OF EUS IN PORTAL HYPERTENSION WITH ESOPHAGEAL VARICES

We investigated the relationship between esophageal varices and the collaterals by endoscopy and endoscopic ultrasound (20 MHz ultrasonic miniprobe; UMP). Moreover, we investigated the correlation between the collaterals around the esophagus and recurrence of esophageal varices in patients with portal hypertension who had undergone EIS. The collaterals were divided into two groups: peri‐esophageal collateral veins (peri‐ECVs) and para‐esophageal collateral veins (para‐ECVs). These were scored as mild or severe according to the stage of development. According to endoscopy, the varix form was significantly larger in severe the peri‐ECVs group than in mild the peri‐ECVs group. The prevalence of perforating veins increased according to the varix form. With regard to variceal recurrence, in patients with variceal recurrences, UMP findings included a significantly higher incidence of severe peri‐ECVs, a significantly larger diameter of perforating veins compared with patients without recurrence. In conclusion, the presence of severe peri‐ECVs and large perforating veins in the esophageal wall strongly correlates with occurrence and recurrence of esophageal varices in patients with portal hypertension. An understanding of these UMP abnormalities on the basis of hemodynamics around the esophagus is thought to be important for management of esophageal varices in patients with portal hypertension.     

Management of gastroesophageal varices in cirrhotic patients: current status and future directions

Bleeding from gastroesophageal varices (GEV) is a serious event in cirrhotic patients and can cause death. According to the explosion theory, progressive portal hypertension is the primary mechanism underlying variceal bleeding. There are two approaches for treating GEV: primary prophylaxis to manage bleeding or emergency treatment for bleeding followed by secondary prophylaxis. Treatment methods can be classified into two categories: 1) Those used to decrease portal pressure, such as medication (i.e., nonselective β-blockers), radiological intervention [transjugular intrahepatic portosystemic shunt (TIPS)] or a surgical approach (i.e., portacaval shunt), and 2) Those used to obstruct GEV, such as endoscopy [endoscopic variceal ligation (EVL), endoscopic injection sclerotherapy (EIS), and tissue adhesive injection] or radiological intervention [balloon-occluded retrograde transvenous obliteration (BRTO)]. Clinicians should choose a treatment method based on an understanding of its efficacy and limitations. Furthermore, elastography techniques and serum biomarkers are noninvasive methods for estimating portal pressure and may be helpful in managing GEV. The impact of these advances in cirrhosis therapy should be evaluated for their effectiveness in treating GEV.     

Hallazgos endoscópicos no relacionados con hipertensión portal en pacientes con cirrosis hepática sometidos a un programa de cribado de varices

AimTo determine the prevalence of endoscopic lesions unrelated with portal hypertension in patients with cirrhosis.Patients and methodsCross-sectional study including a consecutive cohort of patients with liver cirrhosis enrolled in a screening program of oesophageal varices who underwent an upper gastrointestinal endoscopy from November, 2013, to November, 2018. Clinical predictors of endoscopic lesions unrelated to portal hypertension were analyzed by univariate and multivariate logistic regression.ResultsA total of 379 patients were included. The most frequent aetiology of liver disease was alcohol consumption (60.4%). The prevalence of endoscopic lesions unrelated with portal hypertension was 39.6% (n=150). Among 96 patients with peptic lesions, urease was obtained in 56.2% of patients (positive in 44.4% of them). The prevalence of endoscopic lesions unrelated to portal hypertension was not associated with age, gender, liver function or ultrasound findings of portal hypertension. The prevalence of endoscopic lesions unrelated to portal hypertension was not associated with age, gender, liver function or ultrasound findings of portal hypertension. Smokers had a trend to increased prevalence of endoscopic lesions unrelated to portal hypertension (43.2% vs. 34.6%; p=0.09), particularly peptic ulcer (6.4% vs. 0.6%; p=0.05) and peptic duodenitis (17.3% vs. 6.3%; p=0.002). Active smoking was the only independent predictor of peptic ulcer or duodenitis (OR=2.56; p=0.017).ConclusionActive smoking is a risk factor for endoscopic lesions unrelated to portal hypertension. This finding should be further investigated to reassess endoscopic screening programs in cirrhotic smokers.     

What's new in portal hypertension?

Portal hypertension is defined as increased pressure in the portal venous system. The most common cause of portal hypertension is cirrhosis. In this setting, there is an increase in intrahepatic resistance leading to an increase in portal pressure. By increasing portal blood flow, splanchnic vasodilation further aggravates portal hypertension. New pathogenic pathways are being established which might result in new therapeutic strategies. The presence of varices at endoscopy and/or other abdominal portosystemic collaterals confirms the diagnosis of portal hypertension. The role of non‐invasive and imaging tests in the diagnosis and prognosis of portal hypertension has been clarified. Non‐selective beta‐blockers decrease both the risk of variceal haemorrhage and hepatic decompensation. Terlipressin, somatostatin or octreotide, in combination with early endoscopic therapy, are recommended for the treatment of acute variceal haemorrhage. Early Transjugular intrahepatic portosystemic shunt (TIPS) is effective as salvage therapy in acute variceal bleeding in selected patients and prevents rebleeding more effectively than endoscopic and medical therapy resulting in an increased survival.     

The natural history of portal hypertensive gastropathy in patients with liver cirrhosis and mild portal hypertension

BACKGROUND: Portal hypertensive gastropathy is a potential cause of bleeding in patients with liver cirrhosis. Studies on its natural history have often included patients submitted to endoscopic or pharmacological treatment for portal hypertension. PATIENTS AND METHODS: A total of 222 cirrhotic patients with mild degree of portal hypertension (i.e., with no or small varices at entry, without previous gastrointestinal bleeding and medical, endoscopic, or angiographic treatment) were followed up with upper endoscopy every 12 months for 47 +/- 28 months. RESULTS: Upon enrollment 48 patients presented portal hypertensive gastropathy (43 mild and 5 severe) and the presence of esophageal varices was the only independent predictor of the presence of this gastric lesion at multivariate analysis. The incidence of portal hypertensive gastropathy was 3.0% (1.1-4.9%) at 1 yr and 24% (18.1-29.9%) at 3 yr, while the progression was 3% (1-6.9%) at 1 yr and 14% (4.2-23.8%) at 3 yr. The presence of esophageal varices and the Child-Pugh class B or C at enrollment were predictive of the incidence of portal hypertensive gastropathy, while only Child-Pugh class B or C was correlated with the progression from mild to severe, at multivariate analysis. During follow-up 16 patients bled from portal hypertensive gastropathy (9 acutely and 7 chronically) and one patient died of exsanguination from this lesion. CONCLUSIONS: The natural history of portal hypertensive gastropathy is significantly influenced by the severity of liver disease and severity of portal hypertension. Acute bleeding from portal hypertensive gastropathy is infrequent but may be severe.     

Ultrasonography in portal hypertension

High resolution real time ultrasound is a non-invasive method of evaluating patients with suspected portal hypertension. The portosystemic collateral most frequently identified is the dilated coronary vein and its associated gastro-oesophageal varices. Other collaterals that can be seen include: gastrorenal, splenorenal, paraduodenal, periportal, pelvic and retroperitoneal varices along with a recanalized umbilical vein and ductus venosus. Using duplex doppler ultrasound, the rate and direction of portal blood flow can be ascertained. Sonography is better than barium studies in assessing whether gastro-oesophageal varices are present, however, it is not as sensitive as endoscopy, laparoscopy or portography.     

Assessment of portal hypertension in humans

Patients suspected of having portal hypertension (either by clinical history, physical examination, or previous diagnosis) should undergo ultrasonography and upper gastrointestinal endoscopy. Ultrasonography, preferably using the duplex technique, can disclose the patency of the portal venous system, the presence of signs of portal hypertension (splenomegaly, portocollateral vessels, repermeabilization of the umbilical vein, and so forth) and provide additional information about liver, biliary, or pancreatic diseases that may be the cause of portal hypertension. Endoscopy can assess the presence and size of gastroesophageal varices, the appearance of the variceal wall, and the presence and severity of portal hypertensive gastropathy. Patients showing a patent portal vein should have hepatic vein catheterization to evaluate the presence of presinusoidal, sinusoidal, or postsinusoidal portal hypertension. Patients in whom presinusoidal portal hypertension is suspected (those having esophageal varices with an HVPG below 10 mm Hg) should have liver biopsy and percutaneous transhepatic measurement of portal pressure. In sinusoidal portal hypertension, the results of endoscopy and HVPG measurement are decisive for the therapeutic management of the patients. The authors' results indicate that, before starting prophylactic therapy with beta-blockers, all patients should undergo at least an hepatic vein catheterization to assess HVPG; it would be preferable to have a variceal pressure measurement also. These measurements must be repeated 3 to 4 weeks after the final dose of therapy has been reached to assess the risk of variceal bleeding or rebleeding.