脾切除贲门周围血管离断术治疗470例门静脉高压症疗效分析

目的总结脾切除贲门周围血管离断术治疗不合并肝癌及胆管癌的门静脉高压症患者的疗效。方法对不合并肝癌及胆管癌的门静脉高压症患者行脾切除贲门周围血管离断术并随访470例,其中肝炎后肝硬化436例,占92．8％。结果出血患者424例,手术止血率为993％（421／424）,围手术期病死率为1．4％（6／424）,主要死亡原因是上消化道出血、肝肾功能衰竭;急症及择期手术424例,预防手术46例,预防手术嗣手术期无死亡。平均随访时间4年,出血患者术后复发出血率为3．2％（15／470）,预防手术后无出血,肝性脑病发生率为1．9％（9／470）。结论脾切除贲门周围血管离断术防治门静脉高压症引起的上消化道出血效果好。合理选择手术适应证及手术时机、完全彻底断流、术后早期抗凝及近端脾静脉结扎预防术后肝外门静脉系统血栓形成是提高手术疗效的必要措施。     

肝硬化门脉高压症70例术前肝功能评估及术后并发症分析

门静脉高压症所致的上消化道出血是肝炎后肝硬化致死性并发症之一 ,本文对 70例肝炎后肝硬化门脉高压症手术治疗患者的术后存活率进行前瞻性分析 ,旨在探讨此类患者手术治疗的适应证及手术时机的选择问题 (外科术式及其它技术因素未列入本研究范畴 )。材料与方法一、对象70例手术治疗的患者为近 7年来本院肝病科诊治的乙型肝炎肝硬化合并门静脉高压症而在本院或外院行相关手术者 ,其中男性 5 4例 ,女性 16例。年龄最轻者 3 8岁 ,最高者 62岁。术式选择 :单纯脾切除 4例 ;断流术 (脾切除加贲门周围血管离断术 ) 5 4例 ;分流术 12例。术期选择…     

门静脉高压症的外科治疗 手术并发症及其处理

门静脉高压症的任何手术方式都有较高的术后并发症发生率和手术死亡率。手术并发症的发生主要与患者的肝脏功能、年龄以及手术时间有关。本文主要介绍分流术和断流术这两种手术后的并发症。1出血出血是门静脉高压症的主要并发症,发生率最高。可发生于术中,也可发生于术后。绝大部分门静脉高压症患者的原发病因为肝硬化,手术前有凝血因子合成障碍,凝血酶原时间(PT)延长,纤维蛋白原降低,如果同时合并有脾功能亢进,血小板数量也减少,较没有肝硬化的患者更容易发生出血。术中出血:断流手术需要切除脾脏,脾切除时有2%~3%的患者可能发生大出血。…     

胰源性门脉高压症诊治分析

对147例胰源性门静脉高压症(PPH)患者的临床资料进行回顾性分析和总结.结果 显示,122例PPH患者行手术治疗,其中合并上消化道出血76例中54例行脾切断流,无出血71例中62例行脾切除术,6例行脾切除 预防性断流术.经过长期随访,效果确切.认为PPH是一种可以治愈的疾病,手术治疗可获良好效果,诊断上有其自身特点,必须提高对本病的认识.     

门静脉高压症外科治疗进展

门静脉高压症合并食管胃底曲张静脉破裂出血是肝硬化患者死亡的主要原因，治疗上内科保守疗法效果较差，外科手术仍是治疗门静脉高压症的主要手段。目前的手术方式仍以断流术、分流术为主，这两种手术方式均取得了良好的临床疗效，但长期效果不够理想。是选择断流术还是分流术应该遵循个体化的原则。肝移植是治疗门静脉高压症一种标本兼治的方法，但目前还不能成为常规术式，只是对终末期肝病有其适应症。TIPS术作为肝移植前的准备已得到认可。     

肝硬化门静脉高压性脾肿大并发脾功能亢进的特点及临床意义

肝硬化门静脉高压性脾肿大患者并发脾亢本身包含了脾肿大,因而,评价肝硬化门静脉高压症患者是否有脾亢主要依据是外周血细胞减少.然而肝硬化门静脉高压性脾肿大患者不一定都有外周血细胞减少,他是肝硬化门静脉高压性脾肿大的并发症,而不是其必然表现.对于该病的治疗,外科手术一方面可以消除巨脾和/或重度外周血细胞减少,还可以止血,因而绝大多数患者均可采用手术治疗,但对肝硬化门静脉高压性脾肿大无外周血细胞减少、无巨脾、无出血史的患者可采用非手术治疗.     

三种术式治疗门静脉高压症疗效比较

近年来，针对门静脉高压症合并食管胃底曲张静脉破裂出血的合理术式的探索在不断进行。1986年1月至2001年12月，我院采用断流术、分流术、分流断流联合术治疗肝硬变门静脉高压症患者318例。现对治疗结果进行对比分析，以探讨治疗该病的良好手术方式。     

我国门静脉高压症外科治疗的现况和展望

门静脉高压症外科曾引领现代外科的发展。然而,在过去的10~20年里,筛查和控制食管胃曲张静脉破裂出血的药物、曲张静脉套扎和经颈静脉肝内门体分流术等非手术疗法获得广泛应用。手术治疗只适用于内镜疗法无效、肝功能Child-Pugh A级的患者。目前公认可取的3种手术是远端脾肾分流术、广泛的贲门周围离断术加脾切除术和二阶段经胸腹联合断流术。由于在中国供肝短缺,因此肝移植难以普及。腹腔镜脾切除以及腹腔镜脾切除联合贲门周围血管离断术对肝硬化门静脉高压症患者乃是重大挑战。认为外科治疗门静脉高压症应与非手术疗法合作,从而对肝硬化和非肝硬化门静脉高压症患者采取个体化治疗方案。     

肝细胞癌合并门静脉高压症的外科治疗

目的探讨肝细胞癌合并门静脉高压症的外科治疗方法。方法回顾性分析62例外科手术治疗的肝细胞癌合并门静脉高压症患者的临床资料。结果本组患者无手术死亡，术后并发症发生率为17．7％；术后1、3、5年生存率分别为85．6％、40．3％、20．9％。结论肝癌切除联合脾切除加断流术是治疗肝细胞癌合并门静脉高压症的一项安全的、有效的方法。     

胰源性区域性门脉高压症67例临床分析

回顾性分析67例胰源性门脉高压症（PSPH）患者的临床资料。发现67例患者的胰腺原发病以慢性胰腺炎和胰腺肿瘤居多，临床表现中脾大和胃底静脉曲张最为常见，手术及药物防治上消化道出血是主要的治疗手段。     

胰源性区域性门脉高压症合并上消化道出血的诊治分析

目的探讨胰源性区域性门脉高压症合并上消化道出血的诊断和治疗方法。方法回顾分析我院2000年1月至2011年2月收治的14例胰源性区域性门脉高压症合并上消化道出血患者的诊疗措施和随访资料。结果14例患者中胰体尾占位6例,胰腺假性囊肿4例,慢性胰腺炎4例。均有呕血或（和）黑便史,其中4例有失血性休克表现。所有患者均无肝硬化、腹水及肝功能异常等表现。胃镜和超声胃镜提示14例患者均有胃底静脉曲张,2例同时合并食管下段静脉曲张。8例患者有脾肿大和脾功能亢进的表现。14例患者均采用手术治疗。9例患者获得随访,曲张静脉明显改善或消失,随访5月～8年均无出血复发。结论孤立性胃底静脉曲张、脾肿大和脾功能亢进、无肝硬化和肝功能正常以及胰腺疾病病史是诊断胰源性区域性门脉高压症的基本要点。该疾病可通过脾切除术或联合胃底周围血管离断术治愈,应同时重视对胰腺原发疾病的治疗。     

Pattern of upper gastrointestinal haemorrhage in northern India—An endoscopic study of 316 patients

Three hundred and sixteen patients with acute upper gastrointestinal haemorrhage were studied prospectively and consecutively. The most frequent cause was variceal bleeding due to portal hypertension (36%), followed by peptic ulceration (24%) and gastric erosions (19%). Variceal haemorrhage tended to be severe and had a high individual mortality rate. Associated acute mucosal lesions with portal hypertension were strikingly less frequent when compared with the experience from the West. Seven per cent of patients died of bleeding alone and an equal number of an associated systemic disorder or complication. Splenomegaly was present in all patients with a variceal haemorrhage due to non-cirrhotic portal hypertension. However, in patients with portal hypertension due to cirrhosis splenomegaly was present in 63%. Endoscopy altered the clinical diagnosis in 13.2% of patients. Based on previous experience oesophago-gastro-duodenal endoscopy has been a useful tool in the management of acute upper gastrointestinal haemorrhage.     

门静脉高压症少见成因及其诊断

门静脉高压症是指由不同原因引起的门静脉血流受阻或者血流异常增多而导致门静脉系统压力增高和广泛侧支循环形成的临床综合征,最常见于肝硬化.而非硬化性门脉高压常见于特发性门静脉高压(idiopathic portal hypertension,IPH)、胰源性门脉高压(pancreatic sinistral portal hypertension,PSPH)、门静脉海绵样变性(cavernous transformation of the portalvein,CTPV)、先天性肝纤维化(congenital hepatic fibrosis,CHF)、Budd-Chiari综合征(Budd-Chiari syndrome,BCS)、肝窦阻塞综合征(hepatic sinusoidal obstruction syndrome,SOS)、门静脉血栓形成(portal vein thrombosis,PVT)、骨髓增生性疾病(myeloproli ferative disease,MLD)、肝淀粉样变(hepatic amyloidosis)、血色病(hemochromatosis,HC)等.本文就这几种门脉高压的...     

胰腺疾病相关性门脉高压症59例临床分析

目的探讨胰腺疾病相关性门脉高压症的临床特点及治疗。方法选择我院1986年1月至2005年4月收治的胰腺疾病相关性门脉高压症患者，回顾性分析其一般资料、受累静脉、临床表现、实验室和影像检查、治疗和结局。结果我院19年共收治本病59例，占同期门脉高压症的4．0％。常见基础胰腺疾病依次为慢性胰腺炎（21例，35．6％）、胰腺癌（20例，33．9％）、急性胰腺炎（8例，13．6％）和胰腺囊肿（3例，5．1％）。40例患者有明确的受累静脉，其中脾静脉阻塞27例（67．5％）、门静脉阻塞16例（40．0％）。脾脏肿大48例（81．4％），为轻、中度肿大，脾功能亢进31例（52．5％），程度较轻，以白细胞减少为主。45例患者（76．3％）有胃、食管静脉曲张（孤立性胃静脉曲张35例），19例有破裂出血（32．2％）。药物治疗可控制急性出血，但不能预防再出血。18例行脾切除术，主要指征是反复发生的消化道出血，术后患者均未再出血（随访8个月～9年）。结论胰腺疾病可累及门静脉主干及其属枝，导致广泛性或区域性门脉高压症。药物治疗可有效控制急性曲张静脉破裂出血，而手术可能是防止再出血的主要措施。     

Chronic oral anticoagulant therapy for extrahepatic visceral thrombosis is safe

Background Patients with hypercoagulability may thrombose visceral veins with resultant portal hypertension, esophagogastric varices, and hemorrhage. The role of chronic oral anticoagulant therapy in such patients is unclear. On the one hand, such patients are prone to significant hemorrhage and thus anticoagulant therapy may seem contraindicated. On the other hand, because the causal pathophysiology is typically hypercoagulability, it would seem rational to treat these patients with chronic anticoagulant therapy in order to both prevent other visceral and systemic thromboses and perhaps, over time, reduce the degree of portal hypertension. Experience and poor prognosis associated with the more common portal hypertension due to hepatic cirrhosis may bias judgment. Methods We retrospectively reviewed the course of chronic oral anticoagulant therapy regarding both the safety and effectiveness using our long-term follow-up of a cohort of seven patients with visceral thrombosis resulting in extrahepatic non-cirrhotic portal hypertension. Results Seven consecutive patients encountered over the past 19 years were observed for 78 patient-years, the first 14 patient-years prior to anticoagulant therapy and the latter 64 patient-years on oral anticoagulant therapy. No patients rethrombosed either visceral or systemic vessels while on oral anticoagulant therapy. There were no fatal or serious hemorrhagic events on oral anticoagulant therapy; in fact, upper gastrointestinal bleeding decreased from 1.2 to 0.2 bleeds/year. The endoscopic grade of esophageal varices decreased in four of five patients who underwent serial endoscopy, and platelet counts increased in all seven patients. Conclusions Chronic oral anticoagulant therapy is safe and not associated with an increase in upper gastrointestinal bleeding in such patients. Additionally, and by inference, perhaps in conjunction with the natural history of portal hypertension, such therapy is possibly effective in reducing portal hypertension in patients with hypercoagulability-induced extrahepatic portal hypertension. Condensed Abstract The safety and role of chronic oral anticoagulant therapy in the long-term management of extrahepatic esophageal varices is unclear. We followed seven patients with hypercoagulability-induced visceral thrombosis for a total of 78 patient-years. Our data show that this was safe, associated with an overall decrease in acute upper gastrointestinal hemorrhagic episodes, and perhaps, in a decrease in portal hypertension.     

胰源性门脉高压症44例临床分析

目的探讨胰源性门脉高压症(Pancreatogenicportalhypertension)的病因、临床特点及防治措施。方法回顾性分析我院1998年~2005年收治的44例胰源性门脉高压患者的临床资料,并结合1998~2006年中文科技期刊全文数据库累及报道的胰源性门脉高压症164例患者的临床资料进行综合分析。结果208例胰源性门脉高压症患者中脾大者占98.1%,胃底静脉曲张者占87.5%,伴上消化道出血者占80.2%,慢性胰腺炎、胰腺假性囊肿、胰腺肿瘤共占总数的93.1%。结论上述胰腺疾病容易并发胰源性门脉高压症,提高对本病的认识具有重要的临床意义;病变在胰尾的胰源性门脉高压,脾脏切除术是治愈本病的手段。     

The use of hemospray in portal hypertensive bleeding; a case series

Hemospray is a haemostatic agent licensed for endoscopic haemostasis of non-variceal upper gastrointestinal bleeding (NVUGIB) in Europe and Canada. Hemospray has been shown to be safe and effective in achieving haemostasis in bleeding peptic ulcers in a prospective clinical study and several further case series have described the use of hemospray in other non-variceal causes of gastrointestinal bleeding. Portal hypertensive gastropathy and colopathy are common in patients with portal hypertension. As hemospray is an easy to apply, non-contact method, which can cover large areas of mucosa, it may be of benefit in acute non-variceal portal hypertensive bleeding. We present data from the first four consecutive patients presenting to our institution with acute haemorrhage secondary to non-variceal diffuse portal hypertensive bleeding treated with hemospray.     

Distinctive aspects of peptic ulcer disease,Dieulafoy's lesion,and Mallory-Weiss syndrome in patients with advanced alcoholic liver disease or cirrhosis

AIM: To systematically review the data on distinctive aspects of peptic ulcer disease (PUD), Dieulafoy’s lesion (DL), and Mallory-Weiss syndrome (MWS) in patients with advanced alcoholic liver disease (aALD), including alcoholic hepatitis or alcoholic cirrhosis. METHODS: Computerized literature search performed via PubMed using the following medical subject heading terms and keywords: “alcoholic liver disease”, “alcoholic hepatitis”,“ alcoholic cirrhosis”, “cirrhosis”, “liver disease”, “upper gastrointestinal bleeding”, “non-variceal upper gastrointestinal bleeding”, “PUD”, ‘‘DL’’, ‘‘Mallory-Weiss tear”, and “MWS’’. RESULTS: While the majority of acute gastrointestinal (GI) bleeding with aALD is related to portal hypertension, about 30%-40% of acute GI bleeding in patients with aALD is unrelated to portal hypertension. Such bleeding constitutes an important complication of aALD because of its frequency, severity, and associated mortality. Patients with cirrhosis have a markedly increased risk of PUD, which further increases with the progression of cirrhosis. Patients with cirrhosis or aALD and peptic ulcer bleeding (PUB) have worse clinical outcomes than other patients with PUB, including uncontrolled bleeding, rebleeding, and mortality. Alcohol consumption, nonsteroidal anti-inflammatory drug use, and portal hypertension may have a pathogenic role in the development of PUD in patients with aALD. Limited data suggest that Helicobacter pylori does not play a significant role in the pathogenesis of PUD in most cirrhotic patients. The frequency of bleeding from DL appears to be increased in patients with aALD. DL may be associated with an especially high mortality in these patients. MWS is strongly associated with heavy alcohol consumption from binge drinking or chronic alcoholism, and is associated with aALD. Patients with aALD have more severe MWS bleeding and are more likely to rebleed when compared to non-cirrhotics. Pre-endoscopic management of acute GI bleeding in patients with aALD unrelated to portal hypertension is similar to the management of aALD patients with GI bleeding from portal hypertension, because clinical distinction before endoscopy is difficult. Most patients require intensive care unit admission and attention to avoid over-transfusion, to correct electrolyte abnormalities and coagulopathies, and to administer antibiotic prophylaxis. Alcoholics should receive thiamine and be closely monitored for symptoms of alcohol withdrawal. Prompt endoscopy, after initial resuscitation, is essential to diagnose and appropriately treat these patients. Generally, the same endoscopic hemostatic techniques are used in patients bleeding from PUD, DL, or MWS in patients with aALD as in the general population. CONCLUSION: Nonvariceal upper GI bleeding in patients with aALD has clinically important differences from that in the general population without aALD, including: more frequent and more severe bleeding from PUD, DL, or MWS.     

PATHOPHYSIOLOGY OF PORTAL HYPERTENSION AND IMPLICATIONS FOR ITS PHARMACOLOGICAL CONTROL

Bleeding from esophageal varices complicating portal hypertension is a major cause of morbidity and mortality in patients with chronic liver disease. Therapy has been directed towards obliteration of esophageal varices (endoscopic sclerotherapy, transhepatic sclerosis, or esophageal transection) or decompression of the portal vascular bed by the creation of surgical portasystemic shunts. The use of pharmacological agents to lower portal venous pressure (PVP) was for many years limited to intravenous or intraarterial vasopressin in the setting of acute variceal hemorrhage. However, since Lebrec et al.,¹ reported the favourable effect of propranolol on PVP and on the incidence of rebleeding from the upper gastrointestinal tract in patients with portal hypertension,² there has been an increasing interest in the potential use of a number of pharmacological agents in the short and long term management of patients with portal hypertension. The purpose of such therapy would be to reduce the incidence of complications of portal hypertension. These may include upper gastrointestinal bleeding, ascites via reduced ascitic fluid formation, and even portasystemic encephalopathy via improvement of hepatic perfusion and reduction of collateral shunting of blood.     

Unusual sites of upper gastrointestinal variceal bleeding

When patients with portal hypertension bleed from varices, these are most commonly located in the esophagus and gastric fundus. However, varices can develop anywhere in the upper or lower gastrointestinal tract. Oftentimes if an active upper gastrointestinal bleeding site is not evident at the time of endoscopy, bleeding is attributed to any esophageal or gastric varices that are present. This supposition may not always be true as illustrated in the two patients presented here. Likewise, the absence of esophagogastric varices in a patient with portal hypertension does not preclude the presence of varices elsewhere. Endoscopic examination of the second and third portion of the duodenum can sometimes be helpful in accurately locating the bleeding site.