布加氏综合征超声诊断临床分析

布加氏综合征(Budd-Chiari)是由于各种原因引起的肝静脉和其开口以及肝段下腔静脉阻塞病变所引起的门静脉高压症,有或不伴有下腔静脉高压,属肝后门静脉高压症,临床表现为肝脾肿大、腹水、食管静脉曲张、下肢水肿或色素沉着等一系列门静脉高压征的临床体征。     

经颈内静脉肝内门腔分流术治疗肝硬化门脉高压症临床观察

目的探讨经颈内静脉肝内门腔分流术治疗肝硬化门脉高压症的临床疗效及并发症。方法肝硬化并发门脉高压症患者29例行经颈内静脉肝内门腔分流术,支架置入前后测量门静脉主干压力,术前术后分别测定门静脉内径及门静脉、分流道血流速度。结果分流术成功率100%,门脉主干压、门静脉内径、门脉主干血流速度较术前明显下降(P<0.01),分流道血流速度(139.0±48.8)cm/s。食道胃底静脉曲张、腹水等临床症状明显好转。常见并发症有肝性脑病、支架狭窄及闭塞。结论经颈内静脉肝内门腔分流术是治疗肝硬化门脉高压症的有效方法,它能有效地降低门脉压,控制食道、胃底静脉曲张破裂出血。     

肝硬化门静脉高压食管胃静脉曲张出血的防治共识(2008,杭州)

门静脉高压症是指由各种原因导致的门静脉系统压力升高所引起的一组临床综合征．其最常见病因为各种原因所致的肝硬化。其基本病理生理特征是门静脉系统血流受阻和（或）血流量增加，门静脉及其属支血管内静力压升高并伴侧支循环形成．临床主要表现为腹水、肝性脑病、食管胃静脉曲张出血等。其中食管胃静脉曲张出血病死率最高，是最常见的消化系统急症之一。中华医学会消化病学分会、肝病学分会、内镜学分会及从事该项工作的外科和放射介入科专家，参照国内外有关资料．结合我国具体情况，就其基本概念、诊断治疗原则等，     

儿童门静脉高压症研究进展

儿童门静脉高压症是指在多种病因作用下,门静脉系统的血流受阻和（或）血流量增加、血管舒缩功能障碍,引起门静脉及其属支的压力持续增高,门静脉压力＞5 mmHg（1 mmHg=0.133 kPa）,或门静脉、肝静脉压力梯度＞10 mmHg,最终导致脾大、门腔侧支循环形成和开放、腹水等临床表现,是一种血流动力学异常综合征。儿童门静脉高压症根据病因不同分为肝硬化性门静脉高压症和非肝硬化性门静脉高压症;根据压力来源的解剖部位,可将门静脉高压症分为肝前性、肝内性（窦前性、窦性、窦后性）及肝后性。治疗方法有药物治疗、曲张静脉套扎或硬化、手术治疗等。虽然儿童门静脉高压症发病率较低,但可以引起胃食管静脉曲张破裂出血、肝性脑病等严重并发症。为加强对本病的认识,减少并发症,提高治愈率,现将其病因分类、发病机制、诊断和治疗方面的研究进展作一综述。     

彩色超声诊断肝硬化门脉高压征250例分析

目的 通过对内镜下证实肝硬化门脉高压征患者250例进行彩色超声检测分析,为彩色超声检测肝硬化门脉高压征提供更可靠的依据.方法 根据内镜结果将肝硬化门脉高压征患者250例按食管静脉曲张程度分为轻、中、重度3组,检测门静脉主干宽度、脾静脉宽度、脾脏厚度及胃左静脉宽度,研究其与食管静脉曲张程度的关系.结果 随食管静脉曲张程度的不同,门静脉主干内径、脾静脉内径、脾脏厚度、胃左静脉内径之间存在显著性差异,脾脏厚度与脾静脉内径之间存在显著差异.结论 门静脉系统的主要分支扩张的检测值及门静脉侧支循环的检测可为判断门静脉高压提供参考依据.     

肝硬化合并上消化道出血421例临床分析

目的 观察肝硬化合并上消化道出血(UGH)的临床表现及胃镜检查结果并寻找原因.方法 对421例UGH患者急诊胃镜检查,分析静脉曲张破裂出血与非静脉曲张破裂出血的临床与胃镜表现.结果 421例中,静脉曲张破裂所致为200例,其中食管静脉曲张破裂为99例,贲门区、胃底静脉曲张破裂分别为74例、27例;非静脉曲张破裂为221例,其中门脉高压性胃病为98例,然后依次为急性胃黏膜病变、肝源性溃疡等.结论 静脉曲张破裂出血仍是UGH的主要原因,而非静脉曲张破裂出血也是重要原因,以门静脉高压性胃病最常见.及时的胃镜检查有助于鉴别不同病因并及时采取防治措施.     

腹部超声在诊断肝硬化门脉高压中的临床应用

目的:研究腹部超声诊断方案应用在肝硬化门静脉高压诊断中的效果。方法:本文选择的研究对象为2017年8月~2018年11月本院收治的门静脉高压患者100例作为研究对象,对所有研究对象均进行腹部超声检验,并对所有患者的临床检验结果与胃镜检验结果进行比较采集,选择同期进行腹部超声检查的100例健康体检者的临床资料作为对照组,比较对照组和门静脉高压患者门静脉主干内径和脾静脉内径等相关状况。结果:经过食管胃底静脉曲张分级,可将患者分为0级、轻度、中度和重度等4个等级,其中0级患者14例,轻度患者31例,中度患者24例,重度患者31例,患者食管胃底静脉曲张的发生率为86.00%;本文结果显示肝硬化门静脉高压患者门静脉主干内径和脾静脉内径通过腹部超声检验得出相关值均比对照组高,P<0.05,差异存在统计学意义;对胃镜和腹部超声检验结果进行比较能够得出,随着食管胃底静脉曲张程度的增加,脾脏会有增厚的表现,脾静脉也会出现内径增宽,门静脉主干内径增宽,腹部超声检验结果和胃镜检验结果之间具有较好的相符性,P>0.05,差异不存在统计学意义。结论:临床可以通过腹部超声对患者的肝硬化门静脉高压病症加以诊断和评估,对指导患者临床治疗工作具有显著的价值。     

门脉高压症上消化道出血的治疗

门静脉高压,食道、胃底静脉曲张破裂是上消化道出血的常见原因之一,约占18.4～25％,仅次于溃疡病出血,居第二位。由于大多数(85～90％)门静脉高压症是肝硬化所致,故其预后不如溃疡病出血。除了出血更为凶险之外,和肝功能代偿情况有着密切的关系。据统计肝外型门静脉高压症出血的死亡率仅1～2.5％,而肝内型门静脉高压症肝功能欠佳者的死亡率可高达50％。因此,对其治疗措施的选择应结合出血对病员的威胁和患者的肝功能     

肝硬化患者眼底血管改变的临床观察

目的观察肝硬化患者眼底血管改变,探讨肝硬化门脉高压与眼底血管分级的关系。方法肝硬化有、无食道静脉曲张破裂出血病人各52例,分别检查B超、肝纤维化指标和眼底血管等,并与正常人组进行对照,对检查结果进行统计分析。结果肝硬化患者眼底血管异常率明显高于正常人组,而并发食道静脉曲张破裂出血组眼底血管扩张Ⅱ级、Ⅲ级例数较无出血组显著增多。眼底血管扩张分级与门静脉及脾静脉内径、脾厚度、肝纤维化指标呈正相关。结论观察眼底血管扩张分级可作为了解肝硬化程度、门脉高压和预测胃底食道静脉曲张出血的一种指标。     

食管静脉曲张出血的药物治疗进展

食管静脉曲张是门脉高压症的主要表现,其破裂出血为致死的重要原因。门脉高压６０％由肝硬化引起,大约７０％肝硬化病人出现门脉高压和食管静脉曲张,其中３０％发生静脉曲张破裂出血。急性静脉曲张出血是门脉高压症最常见并发症之一,病死率高达３０％～５０％。静脉曲...     

肝硬化合并上消化道出血的相关因素分析及预后评估

目的 探讨肝硬化合并上消化道出血的相关因素及预后评估。方法 对1990-01～2004-09 502例住院病人临床资料进行统计分析。结果 肝硬化合并上消化道出血以男性及中老年人多发，食道胃底静脉曲张破裂、门脉高压性胃病、消化性溃疡为主要病因，易合并失血性休克、肝性脑病、肝肾综合征等并发症，饮酒及及非甾体类药物为主要诱因，内科治疗有效率(2周)为89、84％，死亡率为10．16％，主要死亡原因为失血性休克、肝肾综合征、肝性脑病。结论 肝硬化合并上消化道出血与性别、年龄、季节等多因素相关，病因、肝功、合并症、年龄等因素影响预后。     

门脉高压食管胃底静脉曲张大出血患者心理特点及护理干预

目的：探讨门脉高压食管胃底静脉曲张破裂大出血病人的心理特点,为指导临床治疗工作提供依据。方法：选择抢救成功后肝硬化失代偿期门脉高压食管胃底静脉曲张破裂大出血（EGVB）患者和消化性溃疡（PU）并发出血患者各40例。进行基本信息、汉密尔顿焦虑量表（他评）、抑郁自评量表的调查,分析两组各项指标间差异有无统计学意义。结果：EGVB组和PU组之间紧张、恐惧型和悲观、失望型发生率比较均有显著的统计学差异,而焦虑、抑郁型发生率差异无统计学意义。结论：门脉高压食管胃底静脉曲张大出血患者的心理状况和生存质量状况不容乐观,在对其积极进行综合治疗的同时加大心理护理干预的力度,对改善其心理问题从而提高其生存质量具有重要意义。     

Gastroesophageal variceal haemorrhage--new advances in pathophysiology

Ruptured gastroesophageal varices are the most severe and frequent causes of upper gastrointestinal bleeding in patients suffering from liver cirrhosis, accounting for 80% of all bleeding episodes. Despite recent progress in treatment strategies, variceal bleeding is still considered the most severe type of gastrointestinal bleeding associated with a mortality of 20% at 6 weeks. The most widely accepted explanation for the rupture is the "explosion hypothesis": bleeding is a result of the elevated intravariceal pressure and increased wall-straining due to a rapid increase in the portal pressure gradient. The rupture of the varices and the early rebleeding cannot be attributed solely to mechanical changes. Furthermore, the factors involved in the sudden increase of portal pressure gradient are yet to be discovered. Recently it was postulated that various humoral factors may also play an important role in the pathomechanism of the rupture. The pivotal role of bacterial infection and consequent endotoxaemia must be emphasized. Passage of both viable microbes and microbial products, such as endotoxins from the intestinal lumen to peripheral and portal circulation in cirrhotic patients can be explained by the intestinal bacterial overgrowth, the intestinal dysmotility and the increased intestinal permeability. Endotoxaemia can be a critical factor that triggers a cascade of humoral events, resulting in a further increase of portal pressure, impairment of liver function and worsening of haemostasis, and eventually leads to variceal bleeding. Early administration of prophylactic antibiotics to variceal bleeders recently became an integral and important part of therapeutic strategy. Antibiotics are not only useful in the prevention of early rebleeding but also they are proven to significantly decrease the rate of mortality. The improvement in mortality is equivalent to that seen with terlipressine.     

Surgical implications of chronic liver diseases]

Complications of chronic liver diseases requiring surgical interventions are the following: esophageal varices and bleeding, ascites hypersplenism, some forms of liver insufficiency. The most widely accepted method for treatment of esophageal varices is endoscopic sclerotherapy. Portal systemic shunts are indicated in some cases. Intractable ascites is to be treated by peritoneovenous shunt insertion. "Ressissance" of paracentesis is not confirmed by late results. Splenectomy is proposed if clinical signs are prominent. If portal hypertension exists, shunt should be performed simultaneously. Liver transplantation is indicated in cases of irreversible liver damage. Optimal selection of patients and timing of transplantation remains of critical importance. As a consequence of numerous technical modifications liver transplantation becomes more popular. Statistical data on liver diseases in Hungary call for urgent development of hepatology. Cooperation of physicians is of outmost importance to realize it.     

Splenectomy as therapy for esophageal varices in a myeloproliferative syndrome

We describe the history of a man aged 73 with a myeloproliferative syndrome and massive splenomegaly, who was admitted with bleeding oesophageal varices. After sclerotherapy and other conservative measures had failed to stop the bleeding, splenectomy was performed. Liver biopsy obtained at the time of splenectomy showed extramedullary haematopoiesis and no signs of cirrhosis. Six weeks after the operation no varices were present any more. Studies of the pathogenesis of portal hypertension in splenomegaly of different causes show the importance of the increased splenic blood flow as one of the main contributory causes to this specific type of portal hypertension. Therefore this type of portal hypertension can probably be cured by splenectomy, as we saw in our patient and as has been described in several case reports.     

Duplex ultrasonography of the portal circulation before and after sclerotherapy of esophageal varices

Authors examined 40 patients suffered from portal hypertension before and after sclerotherapy of esophageal varices with duplex ultrasonography. The patients were divided into four groups: the first and recurrently bleeding patients and those who were treated with propranolol. The average velocity of the main portal vein before the treatment was significantly lower in the patient group, than in the normal control group. There were no significant changes observed after treatment. The portal blood flow increased in the first bleeding patients who did not take propranolol. The diameter of the main portal vein increased in the recurrently bleeding patients. The conclusion is, that the duplex ultrasonography of the portal circulation is a valuable noninvasive method. One has to take into consideration the limits of this technique and further data are needed for the diagnostic and prognostic accuracy.     

Prevention and treatment of esophageal variceal bleeding

Portal hypertension leads to special complications, which tend to progression. Increase in the size of varices, and variceal-wall tension may cause life-threatening bleeding, which affects mortality. Therefore the reduction of portal hypertension is essential. For prevention of the first bleeding (primary prevention) beta-blockers must be given. For estimation of the effectiveness of this drug, patients should be followed. In case of inefficiency or intolerability variceal ligation or sclerotherapy can prevent bleeding. In case of acute variceal hemorrhage, hemodynamic stabilization of the patient is the first step. Transfusion if necessary, somatostatin or terlipressin should be given for reduction of portal hypertension and also endoscopic treatment of varices is mandatory. Early antibiotic administration for prophylaxis or treatment of infections is associated with a significant reduction in mortality. Up to now in absence of exact data, correction of haemostasis is suggested by the administration of fresh frozen plasma. For secondary prevention i. e. to prevent repeated bleeding beta-blockers (probably with nitrates) can be used. If necessary, drug administration should be complemented with varix ligation or sclerotherapy. In case of inefficiency TIPS implantation or liver transplantation must be considered.     

Pathogenesis of portal hypertension

It is now well established that portal hypertension is not a purely mechanical phenomenon. Primary hemodynamic alterations develop in the hepatic and systemic circulatory systems; these alterations in combination with mechanical factors contribute to the development of portal hypertension. In the hepatic circulation, these hemodynamic alterations are characterized by vasoconstriction and impaired hepatic vasodilatory responses, whereas in the systemic circulation, particularly in the splanchnic bed, vessels are hyperemic with increased flow. Thus, an increase in intrahepatic resistance in conjunction with increased portal venous inflow, mediated through splanchnic dilation, contributes to the development of portal hypertension. The ensuing development of elevated flow and transmural pressure through collateral vessels from the hypertensive portal vasculature into the lower pressure systemic venous circulation accounts for many of the complications, such as bleeding esophageal varices, observed with portal hypertension. The importance of the primary vascular origin of portal hypertension is emphasized by the utility of current therapies aimed at reversing these hemodynamic alterations, such as nitrates, which reduce portal pressure through direct intrahepatic vasodilatation, and ,B blockers and octreotide, which reduce splanchnic vasodilatation and portal venous inflow. New evidence concerning relevant molecular mechanisms of contractile signaling pathways in hepatic stellate cells and the complex regulatory pathways of vasoactive molecules in liver endothelial cells makes a better understanding of these processes essential for developing further experimental therapies for portal hypertension. This article examines the current concepts relating to cellular mechanism that underlie the hemodynamic alterations that characterize and account for the development of portal hypertension.     

内镜套扎-部分脾栓塞联合术治疗肝硬化门脉高压症的疗效观察

[目的]探讨内镜套扎—部分脾栓塞联合术治疗肝硬化门脉高压症的临床应用价值。[方法]对28例肝硬化门脉高压患者进行内镜套扎—部分脾栓塞联合术,对其术前后的外周血象、门静脉及脾静脉内径的变化进行对比研究。[结果]联合术后患者食管静脉曲张得到根治,脾功能亢进明显缓解,脾脏缩小,门静脉及脾静脉内径缩小。[结论]内镜套扎—部分脾栓塞联合术治疗肝硬化门脉高压症具有简便安全、效果显著、创伤小、并发症少等优点,因此是治疗的一种新的途径。