内镜治疗食管静脉曲张对门脉高压性胃病的影响

探讨内镜下硬化剂(EST)和套扎(EVL)治疗食管静脉曲张术后对门脉高压性胃病(PHG)和胃底静脉曲张(GV)的影响,对21例注射硬化剂治疗和27例套扎治疗的共48例患者进行了1年的内镜随访,观察PHG和GV的程度。结果在接受治疗3个月和1年后,PHG发生率较治疗前(35％,17/48)明显增加,分别为75％(36/48)和87％(42/48);GV较治疗前(17％,8/48)增多,分别为33％(16/48)和43％(21/48)。结论:食管静脉曲张的内镜下硬化剂和套扎治疗将加重PHG和GV且有可能增加PHG和GV的出血机会。     

内镜下注射硬化剂聚桂醇治疗胃血管畸形出血14例分析

目的探讨内镜下注射硬化剂聚桂醇治疗胃血管畸形的疗效。方法对14例胃血管畸形患者行急诊内镜下注射硬化剂聚桂醇(1%乙氧硬化醇)。结果急诊内镜治疗14例,止血成功12例,2例直接由内镜室转外科手术治疗,1例术后1d再出血亦转外科手术。术后4例出现上腹痛、发热等症状。止血成功的11例随访1～3月均无再出血。结论内镜下注射硬化剂聚桂醇治疗胃血管畸形有较好的疗效,但存在一定的并发症和再出血风险。     

经内镜结扎和硬化剂治疗食管静脉曲张和门脉高压性胃病的疗效及预后

目的：观察经内镜结扎和硬化剂治疗食管静脉曲张的疗效及对门脉高压性胃病（PHG）的影响。方法;对92例患者随机分为套扎组（n=43)和硬化剂（n=49),分别在治疗后1－3月和1－3年内复查。观察静脉曲张及PHG的转归情况。结果：1－3月内复查套扎组完成26例,其中食管静脉曲张根除12例,曲张减轻12例,无效2例,PHG加重17例。硬化剂组完成29例,其中静脉曲张根除4例,曲张减轻22例,无效3例,PHG加重11例。1－3年内复查套扎组和硬化剂组的再曲张率及再出血率分别为61．5％、46．7％和44．4％．33．3％。结论：近期套扎治疗在根治静脉曲张方面优于硬化剂注射,但更易诱发和加重PHG。而套扎组和硬化剂组远期均可出现再曲张和再出血。两组比较无差异。     

内镜下圈套结扎治疗食管静脉曲张的体会

在我国食管胃底静脉曲张(EGV)破裂出血是肝硬化门脉高压症(PHG)患者常见的死亡原因，其病死率达30％-40％以上，20％-30％的肝硬化食管静脉曲张(EV)患者迟早会发生出血(EVB)。内镜下食管静脉套扎术(EVL)是近年来治疗食管静脉曲张的一种新方法。我院自1997-2003年对21例食管静脉曲张患者行内镜下圈套结扎治疗，现报告如下。     

门脉高压性胃病86例与食管静脉曲张的关系

目的分析门脉高压性胃病（PHG）与食管静脉曲张的关系。方法回顾性分析86例患者胃镜检查结果，总结门脉高压性胃病与食管静脉曲张的相关性。结果均可见食管静脉曲张，其中轻度32例，中度23例，重度31例。合并胃底静脉曲张16例，PHG轻度31例，重度55例。结论门脉高压性胃病与食管静脉曲张呈正相关，两者均与门脉高压程度相关，在预防治疗上具有共同点。     

内镜外套管在辅助急诊内镜治疗食管胃静脉曲张出血中的作用研究

目的 探讨内镜外套管在辅助急诊内镜治疗食管胃静脉曲张破裂出血中的作用.方法 选择临床诊断为肝硬化门静脉高压食管胃静脉曲张破裂出血患者62例作为治疗组,采用外套管辅助急诊内镜注射硬化剂治疗.另选择同期行常规急诊内镜治疗的62例食管胃静脉曲张破裂出血患者作对照组,比较两组治疗效果.结果 治疗组62例患者在行急诊内镜止血中先用外套管压迫止血均获成功,止血效率为100%,显著高于对照组的80.65%（P＜0.05） 治疗组食管胃静脉曲张注射后消失率为59.32%显著高于对照组7.27%（P＜0.05）.胸痛和食管溃疡、总住院天数、总医疗费用,治疗组显著低于对照组（P＜0.05）.结论 应用外套管辅助急诊内镜注射硬化剂治疗食管胃静脉曲张出血可提高治疗效率,减少患者负担.     

食管静脉曲张套扎对痔疮、肛门直肠静脉曲张及门脉高压性结肠病的影响

近几年,内镜下曲张静脉套扎术(EVL)已基本取代了硬化剂注射(EST)而成为食管静脉曲张的治疗性手术。已知EVL后,食管静脉曲张的消退会导致门脉高压性胃病(PHG)的发病率增高,但是并未明确食管静脉曲张套扎对痔疮、肛门直肠/结肠静脉曲张以及门脉高压性结肠病的影响情况。本项实验的目的是研究内镜下食管静脉曲张套扎术对痔疮、肛门直肠/结肠静脉曲张以及门脉高压性结肠病的影响。 病人和方法:60例肝硬化门静脉高压病患者参加了这项前瞻性研究。患者均至少有一次食管曲张静脉破裂出血史,而那些已经接受过EST/EVL治疗以及做过门静脉高压手术的病人被排除在外。将病人随机分组,每周一次或隔周一次     

内镜套扎联合硬化剂夹心法治疗食管静脉曲张破裂出血的远期疗效观察

[目的]探讨内镜下静脉曲张套扎同时应用硬化剂夹心法(套扎-硬化-套扎即EVL-EVS-EVL)治疗食管静脉曲张破裂出血的疗效。[方法]对23例肝硬化食管静脉曲张破裂出血的患者采用夹心法治疗,每条曲张静脉结扎皮圈不超过3个,并在2个结扎点之间的曲张静脉内注射l~3ml硬化剂。其中10例在首次内镜治疗时接受食管静脉造影检查。于治疗后2周、1个月、3个月、6个月、12个月胃镜随访,了解静脉曲张变化情况,记录患者不良反应及并发症。[结果]10例行静脉造影检查中7例硬化剂在曲张静脉内滞留时间超过40min。夹心法控制活动性食管静脉曲张出血的止血成功率为100%,静脉曲张消除率为86.9%(20/23),再出血发生率为8.6%(2/23),随访期内静脉曲张复发率为13.0%(3/23)。[结论]夹心法能使硬化剂在曲张静脉内滞留较长时间,在一次治疗后能有效提高静脉曲张消除率,降低再出血率及静脉曲张复发率,是内镜下治疗食管静脉曲张破裂出血的较理想选择。     

胃静脉曲张黏合剂治疗对门脉高压性胃病的影响

目的:探讨黏合剂治疗胃底静脉曲张对门脉高压性胃病(portal hypertensive gastropathy,PHG)的影响。方法:收集2013年1月至2015年8月乙型肝炎(乙肝)后肝硬化失代偿具有食管胃静脉曲张(GOV)或孤立性胃静脉曲张(IGV)的患者171例,应用硬化剂+黏合剂+硬化剂的改良"三明治"注射治疗法治疗。在治疗后3个月、6个月及1年随访,观察内镜治疗效果以及PHG的发生率变化。结果:171例患者进行内镜下硬化治疗共242例次。术后6个月治疗的有效率为98.8%(169例),术后12个月的有效率为88.9%(152例),存活率为98.2%(168例)。治疗前PHG的总发生率为35.5%,治疗3个月后,发生率为38.1%,与治疗前比较无显著性差异(P0.05);治疗6个月及1年后,发生率分别为48.0%及84.2%,与治疗前相比,有显著性差异(P0.05)。结论:胃底静脉曲张硬化治疗明显减少急性出血的死亡率,延长生存时间。PHG的发生率在黏合剂治疗后会有明显上升,需要采取多种联合治疗的方法减少PHG的发生,提高PHG患者的生活质量及生存率。     

门脉高压性胃病的进展

门脉高压性胃病（ponalhypertensivegastropathy，PHG）是指门脉高压症伴发的胃黏膜病变，主要发生于肝硬化门脉高压症病人，也见于非肝硬化门脉高压症病人，临床主要表现为消化道出血等症状，严重时危急生命。1984年Sarfeh等提出PHG与非PHG在形态、功能、治疗上都有不同，因其病理组织学上炎性改变依据不足，可称其为门脉高压性胃病。PHG常与食管静脉曲张同时存在，而PHG出血可占门脉高压消化道出血的10％～60％。食管胃底静脉曲张、肝功能损害越重，则门脉高压性胃病并发消化道出血的发生率越高。在上消化道出血患者，食管静脉曲张程度较轻者以PHG合并出血为主，食管静脉曲张程度较重者则以曲张静脉破裂出血为主。     

Effects of Esophageal Varice Eradication on Portal Hypertensive Gastropathy and Fundal Varices: A Retrospective and Comparative Study

Esophageal varice eradication results in gastric hemodynamic changes. The aim of this study was to detect the influence of variceal eradication on portal hypertensive gastropathy (PHG) and fundal varices and to compare the results of two therapeutic methods (endoscopic variceal ligation and endoscopic sclerotherapy). A total of 114 consecutive patients with cirrhosis and portal hypertension who underwent elective endoscopic variceal ligation (EVL) (85 patients) or endoscopic sclerotherapy (EST) (29 patients) for obliteration of esophageal varices were selected for this study. Both groups were compared for PHG and fundal varice formation before and after eradication. Fifty-eight (68.2%) patients in the EVL and 18 (62.1%) patients in the EST group had PHG before esophageal varice eradication (P > 0.05). PHG grade after eradication of esophageal varices by both EVL and EST was significantly higher compared to pre-eradication. PHG grade and aggregation were similar in both groups. Thirty-seven patients (34 F₁, 3 F₂) in the EVL group and 13 patients (10 F₁, 3 F₂) in the EST group had fundal varices before variceal eradication (P > 0.05). Fundal varices were detected in 46 (35 F₁, 11F₂) and 19 (11F₁, 8F₂) patients in the EVL and EST groups after eradication, respectively. There was a statistically significant increment in occurrence of fundal varices after eradication with EVL and EST groups. There was no significant difference regarding fundal varice development after esophageal variceal eradication in both groups. After varical eradication, PHG was found in 57 (87.7%) and 39 (79.6%) patients with and without fundal varices, respectively (P > 0.05). Esophageal eradication with EVL and EST increases both the incidence and the severity of PHG and fundal varice formation. Both methods have comparable influences on PHG and fundal varices.     

An endoscopic injection with N-butyl-2-cyanoacrylate used for colonic variceal bleeding: a case report and review of the literature

We report a 64-yr-old patient with liver cirrhosis and bleeding esophageal varices that were obliterated by repeated endoscopic sclerotherapy. Eleven years later, he developed a massive, life-threatening rectosigmoid variceal hemorrhage. An endoscopic injection with N-butyl-2-cyanoacrylate (Histoacryl), performed over the rectosigmoid varices, achieved temporary hemostasis. The etiology, prevalence, relationship with portal hypertension, diagnosis, and treatment of colorectal varices are discussed.     

The natural history of portal hypertensive gastropathy: influence of variceal eradication

OBJECTIVE: The natural history and likelihood of bleeding from portal hypertensive gastropathy (PHG) present in patients with portal hypertension before endoscopic variceal obliteration may differ from that in patients who develop PHG during or after variceal eradication. METHODS: A total of 967 variceal bleeders who had achieved variceal eradication by endoscopic sclerotherapy in the recent past were prospectively studied. In all, 88 (9.1%) patients (cirrhosis in 54, noncirrhotic portal fibrosis in 18, and extrahepatic portal vein obstruction in 16) had distinct mucosal lesions. PHG alone was present in 78, PHG with gastric antral vascular ectasia (GAVE) in eight, and GAVE alone in two patients. PHG was graded as mild or severe and according to whether present before (group A) or after endoscopic intervention (group B). Patients underwent regular endoscopy at follow-up to see if the PHG was transitory (disappearing within 3 months), persistent (no change), or progressive. Bleeding from PHG lesions was defined as acute or chronic. RESULTS: Twenty-two (26%) patients had PHG before (group A) and 64 (74%) developed PHG after variceal eradication (group B). During a mean follow-up of 25.1 +/- 14.2 months, PHG lesions disappeared in group A in only two patients (9%), but in group B in 28 (44%) patients (p < 0.05). PHG lesions more often progressed in the former as compared to the latter (18% vs 9.4%, p = NS). The incidence of bleeding was higher in group A than group B (32% vs 4.7%, p < 0.02). Bleeding from PHG occurred in 10 patients (11.6%); seven of them were from group A, and all had either progressive (n = 3) or persistent (n = 4) lesions. CONCLUSIONS: PHG developing after variceal eradication is often transitory and less severe. If PHG is pre-existing, endoscopic therapy for varices could worsen the PHG, with a likelihood of bleeding. Such patients may be benefited by concomitant beta-blocker therapy.     

Endoscopic sclerotherapy for bleeding esophageal varices secondary to extrahepatic portal vein obstruction

Portal hypertension and variceal bleeding secondary to extrahepatic portal vein obstruction continue to present a therapeutic challenge. We performed endoscopic injection sclerotherapy in eight patients with extrahepatic portal vein obstruction and bleeding esophageal varices. In contrast to other reported series, all but one of our patients were adults at the time sclerotherapy was initiated. Six had episodes of continued bleeding after a variety of surgical procedures. After sclerotherapy, five had no further bleeding with a mean follow-up of 26 months. Three patients had episodes of bleeding prior to variceal obliteration; two of these patients underwent surgical intervention after emergency sclerosis to stabilize their condition. Transfusion requirements were less after sclerosis (p = 0.035), although the follow-up has been relatively short (mean, 24 months) compared to the duration of bleeding. Our results suggest that endoscopic sclerotherapy is an effective therapeutic alternative, and perhaps the initial treatment of choice, in patients with extrahepatic portal vein obstruction and bleeding esophageal varices.     

Longterm outcome after injection sclerotherapy for oesophageal varices in children with extrahepatic portal hypertension.

A consecutive series of 36 children with bleeding from oesophageal varices secondary to extrahepatic portal hypertension was successfully treated by endoscopic injection sclerotherapy and followed up over a mean period of 8.7 years after variceal obliteration. There were no deaths from portal hypertension or its treatment and morbidity related to oesophageal sclerotherapy was minimal. Endoscopic injection sclerotherapy alone proved safe and effective in controlling variceal bleeding from portal hypertension in over 80% of the children. Recurrent variceal bleeding developed in 10 (31%) patients but half of these were effectively treated by further sclerotherapy. Gastric variceal bleeding unresponsive to sclerotherapy necessitated successful portosystemic shunt surgery in four (13%) patients. Two children required splenectomy for painful splenomegaly. In most children injection sclerotherapy is the best treatment for the primary management of bleeding oesophageal varices, reserving portosystemic shunting or other surgical procedures for those with bleeding from gastrointestinal varices.     

心得安单纯或联合使用在二级预防食管静脉曲张出血中的疗效比较

目的比较单纯心得安、套扎＋心得安、硬化剂＋心得安二级预防食管静脉曲张出血的疗效,探寻心得安二级预防食管静脉曲张出血的最佳组合。方法78例食管静脉曲张出血患者随机分成3组,每组26例,止血后分别给予心得安（心得安组）、套扎＋心得安（套扎组）、硬化剂＋心得安（硬化剂组）,比较各组12个月内再出血率、死亡率,以及各组门脉高压性胃病、胃底静脉曲张发生率、食管曲张静脉复发率。结果12个月内再出血率套扎组为30．77％,明显低于心得安组（53．85％）及硬化组（42．31％）（P均〈0．05）;套扎组和心得安组门脉高压性胃病及胃底静脉曲张发生率相似,都明显低于硬化组（P均〈0．05）;而食管静脉曲张再发率高于硬化组（P〈0．05）。结论在应用心得安的基础上进行套扎治疗可能是目前食管静脉曲张出血最有效的二级预防方法。     

Effects of endoscopic injection sclerotherapy on portal hypertensive gastropathy: a prospective study.

The effect of endoscopic injection sclerotherapy (EIS) for esophageal varices on portal hypertensive gastropathy (PHG) was investigated in 137 patients who underwent EIS from July 1987 to March 1990. Two groups, PHG(+) (N = 35) and PHG(-) (N = 102) were distinguished by endoscopic findings obtained before EIS. PHG was classified into four grades by endoscopy scored as 0, 1, 2, or 3. The PHG score significantly worsened after EIS (p < 0.01), and PHG became worse 6 to 9 months after the eradication of varices followed by gradual improvement. Recurrent small veins, which required additional EIS, appeared more frequently in the PHG(+) group (p < 0.05). New gastric varices appeared or gastric varices enlarged after EIS more frequently in the PHG(+) group (7 patients, 20.0%) than in the PHG(-) group (12 patients, 11.8%), but this was not statistically significant. Thus, frequent endoscopy after EIS is needed with special attention directed to development of PHG and gastric varices, especially for patients with PHG prior to treatment.     

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.     

Endoscopic injection sclerotherapy for esophageal variceal hemorrhage in a patient with idiopathic myelofibrosis

A 74-year-old female with idiopathic myelofibrosis (IMF) was admitted to our hospital because of massive hematemesis and melena. Immediate upper gastrointestinal endoscopy revealed an intermittent spurting hemorrhage from extensive esophageal varices. Endoscopic injection sclerotherapy (EIS) was carried out and the bleeding ceased. After five courses of EIS, all the esophageal varices were eradicated. About 15 months later, the patient died,due to a cerebral hemorrhage, without further variceal bleeding. A postmortem examination was carried out and the portal hypertension was considered to be due not only to extramedullary hematopoiesis in the sinusoids, but also to increased splenic blood flow. We are confident that EIS is an effective therapeutic procedure for patients with IMF showing esophageal variceal hemorrhage. EIS should be the preferred choice of treatment for esophageal varices in patients with IMF, since it is less invasive than splenectomy.