肝硬化性腹水治疗进展

肝硬化(LC)并门静脉高压(PVH)引起的腹水就其发生机理和治疗进展,国外报道很多,笔者愿对近几年内国外发表的文献进行综述。供同道参考。 LC并PVH引起的两大主要合并症:食管-胃静脉曲张出血和腹水,其共同的的发病机理是LC所致的肝纤维瘢痕和再生结节所造成的肝结构扭曲,它使门静脉血流(PBF)受阻,导致门静脉血管阻力(PVR)增高,这是LC发生PVH的病理生理学基础。PBF受阻可发生于肝内血管床的所有水平部位,如门静脉小分支、血窦和肝静脉流出道,以血窦受阻为重要.结果引起肝内血窦压升高并门静脉压(PVP)升高。临床上测     

肝硬化门静脉高压食管胃静脉曲张出血的防治指南

正1概述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。门静脉高压症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、食管胃静脉曲张(gastroesophageal varices,GOV)、食管胃静脉曲张破裂出血(esophagogastric variceal bleeding,EVB)和肝性脑病等,其中     

应重视门静脉高压症的病因诊断及规范治疗

门静脉高压症是由门静脉系统阻力/血流增加或肝静脉系统回流受阻所导致的门静脉压力异常升高,常表现为脾大、脾功能亢进、食管胃静脉曲张及破裂出血、腹水及肝性脑病等。肝硬化所引起的窦性门静脉高压症临床最为常见,通常伴有肝脏合成功能障碍。而肝外、肝内门静脉系统异常所致的肝(窦)前门静脉高压,以及肝内、肝外肝静脉系统回流受阻所致的肝(窦)后性门静脉高压,多无明显肝脏合成功能障碍。可首先根据临床症状、体征及血液学指标判断有无门静脉高压症,再通过影像学、肝静脉压力梯度及组织病理学检查明确其类型和病因。应在积极治疗原发病的基础上,采取非选择性β受体阻断剂、内镜、介入或手术治疗,以防治门静脉高压症的并发症。     

长期控制肝硬化门静脉高压症的策略

一、肝硬化门静脉高压症的自然史 门静脉高压症是指各种原因引起门静脉系统血流受阻和(或)血流量增加,导致门静脉及其属支血管内压力升高,伴侧支循环形成的一组临床综合征,包括腹水、食管胃底静脉曲张出血(EVB)、肝性脑病、肝肾综合征、肝肺综合征、门静脉高压性胃病等[1].     

肝硬化门静脉高压食管胃静脉曲张出血的防治指南

正1概述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。门静脉高压症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、食管胃静脉曲张     

肝硬化腹水形成机制及利尿剂的应用

肝硬化腹水的形成机制尚未完全明 ,门脉高压是腹水形成的基础 ,血液动力学的改变促进腹水的形成 ,许多介质参与腹水的发生。限制钠的摄入、卧床休息及利尿剂的应用仍是肝硬化腹水治疗最基本手段 ,多数患者对利尿剂反应良好。一、腹水形成机制(一 )局部因素　正常情况下 ,肝脏血流由肝动脉和门静脉双重支配 ,经肝静脉回流至腔静脉。肝静脉与门静脉压差仅为 5ｍｍＨｇ ,因此肝血管具有良好的顺应性。肝血窦周围具有孔径较大的小窗 ,径孔约 10 0 0～ 5 0 0 0Ａ° ,能使血中的大分子物质包括白蛋白自由出入Ｄｉｓｓｅ间隙 ,营养肝细胞 ,因此肝…     

肝硬化门静脉高压食管胃静脉曲张出血防治指南(2015)

<正>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。门静脉高压症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、食管胃静脉曲张(gastro-oesophageal varices,GOV)、食管胃静脉曲张破裂出血(esophag-ogastric variceal bleeding,EVB)和     

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。门静脉高压症的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（gastroesophageal varices, GOV）出血等,其中GOV出血病死率最高,是最常见的消化系统急症之一。     

原发性肝癌患者肝静脉压力梯度与门静脉压力梯度相关性研究

目的 探讨原发性肝癌患者肝静脉压力梯度（hepatic vein pressure gradient, HVPG）与门静脉压力梯度（portal pressure gradient, PPG）相关性。方法 161例原发性肝癌患者在TIPS术中测量下腔静脉压力（inferior vena cava pressure,ICVP）、肝静脉自由压（free hepatic vein pressure, FHVP）、肝静脉楔压（wedged hepatic vein pressure, WHVP）和门静脉压力（portal vein pressure, PVP），计算HVPG(HVPG=WHVP-FHVP)和PPG(PPG=PVP-IVCP)。结果 161例患者HVPG为（20.18±9.22）mmHg,PPG为（26.44±6.82）mmHg,2者无相关性（r=0.112）;PPG明显高于HVPG (P <0.05)。HVPG与PPG相差在5 mmHg以上者90例，占55.9%,HVPG与PPG相差在5 mmHg以内者71例，占44.1%。球囊阻断肝静脉造影有肝内静脉-静脉侧支分流（in...     

门静脉高压症的病因与病因分类

门静脉高压症(PHT)系由各种原因引起的门静脉系统血流受阻和(或)血流量增加导致压力增高的一组综合征群。由于门静脉系统缺乏瓣膜,其引流范围内的小静脉与心脏之间任何部位血流受阻,均可以导致阻塞部位远端血管内的压力升高,出现门静脉高压或局限性门静脉高压。1　病因1.1　门静脉血流增加　1非肝病性脾肿大:如Gaucher病、热带性脾肿大、淋巴瘤等;2动静脉瘘:肝内或肝外的动静脉瘘均可以引起门静脉血流增加,导致门静脉高压,如腹外伤或肿瘤继发肝-门动静脉瘘。1.2　门脾静脉血栓形成或阻塞　此类病因可引起肝外窦前门静脉高压。脾静脉栓塞原…     

ERCP and MRCP--when and why

Since the introduction of endoscopic retrograde cholangiopancreatography (ERCP) in the 1970s, gastroenterologists have a wide spectrum of diagnostic and therapeutic options in the biliopancreatic ductal system at their disposal. With its arrival in the 1990s, magnetic resonance cholangiopancreatography (MRCP) developed as a potent diagnostic tool in biliopancreatic pathology. Currently, MRCP is widely replacing diagnostic ERCP and thereby avoiding complications related to endoscopic technique.We summarize evidence-based data and demonstrate indications and differential indications for MRCP and ERCP in pancreatic disease. Complications related to the procedures and possible medical prevention are discussed. The feasibility of interventional endoscopy in pancreatic disease is reported in detail. The role of gastroenterologists in performing MRCP is outlined on the basis of practical examples.     

Micronutrients and infection: interactions and implications with enteric and other infections and future priorities

Symposium presentations have focused on the elegant molecular science and the biologic mechanisms by which micronutrients play critical roles in cellular and humoral immune responses, cellular signaling and function, and even in the evolution of microbial virulence. The concluding session examined the practical issues of how best to evaluate the nutritionally at-risk host, especially in the areas of greatest need-an analytical model of nutrient-immune interactions, implications of nutritional modulation of the immune response for disease, and the implications for international research and child health. This overview illustrated how malnutrition may be a major consequence of early childhood diarrhea and enteric infections, as enteric infections may critically impair intestinal absorptive function with potential long-term consequences for growth and development. The potentially huge, largely undefined DALY (disability-adjusted life years) impact of early childhood diarrheal illnesses demonstrates the importance of quantifying the long-term functional impact of largely preventable nutritional and infectious diseases, especially in children in developing areas.