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。     

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。     

胰源性门脉高压症的诊断和治疗

胰腺疾病是区域性门脉高压症最常见的病因。孤立性胃底静脉曲张、肝功能正常、脾肿大是胰源性门脉高压最典型的临床表现。胰源性门脉高压症并发胃底静脉曲张破裂出血最有效的治疗是脾切除术,但预后主要取决于胰腺原发疾病。     

肝积合剂对肝硬化门静脉高压的影响

目的：探讨肝积合剂对肝硬化门脉高压的影响。方法：将60例肝硬化门脉高压症患者随机分为两组，治疗组患者口服中药肝积合剂，对照组患者口服心得安，共3个月。用彩色双功能多普勒超声诊断仪测量门静脉内径、脾静脉内径、门静脉血流速度、脾静脉血流速度。采用胃镜观察食管静脉曲张部位、条数、形态、颜色及胃底有无静脉曲张。结果：肝积合剂可显著缩小肝硬化患者门静脉及脾静脉内径、加快血流速度、减少血流量。尤其在加快门静脉、脾静脉血流速度及减少血流量上与心得安比较，差异有显著性意义（P〈0．05）。结论：肝积合剂对肝硬化门脉高压症有一定的防治作用。     

多层螺旋CT门静脉血管成像在胰源性门脉高压症诊断中的应用

目的 研究多层螺旋CT门静脉血管成像在胰源性门静脉高压患者诊断中的应用.方法 应用16排多层螺旋CT门静脉血管成像,对47例临床怀疑胰腺体尾部病变的患者的门静脉系统形态改变与126例肝源性门脉高压患者和47例正常对照组进行形态学对比观察,并测量胃冠状静脉、门静脉、脾静脉、肠系膜上静脉内径、门静脉期肝实质和门静脉主干CT值,对比肝脏、脾脏体积.结果 在47例胰腺体尾部病变中发现有脾静脉狭窄、闭塞者38例,其中胰腺肿瘤患者27例(71.1%),急慢性胰腺炎患者11例(28.9%).38例胰源性门脉高压患者中,发现食管静脉曲张5例(13.2%),胃底静脉曲张25例(65.8%),胃体静脉曲张22例(57.9%),胃短-胃后静脉显示26例(68.4%),胃冠状静脉显示26例(68.4%),发现胃网膜静脉曲张24例(63.2%),肠系膜静脉曲张1例.脾静脉闭塞14例(36.8%),脾静脉狭窄23例(63.2%).结论 胰源性门脉高压在影像学上表现为脾静脉栓塞,脾脏增大,脾门处大量曲张静脉,胃后-胃短静脉及胃网膜静脉增粗迂曲,胃底和胃体静脉曲张,较少合并食管静脉曲张,肝脏形态大小亦无异常.多层螺旋CT门静脉血管成像检查可为胰源性门脉高压患者提供血管形态、病因诊断等多方面有价值信息,为临床诊断和治疗提供客观的影像学依据.     

区域性门静脉高压症的诊治

目的总结区域性门静脉高压症的诊治经验.方法回顾性分析16例区域性门静脉高压症的临床表现、诊断方法、治疗措施和疗效.结果16例区域性门静脉高压症中,合并胰腺疾病12例,未发现明确胰腺疾病4例.临床表现主要为脾肿大16例(100%)、腹痛10例(63%)、消化道出血7例(44%)、腹部肿块3例(19%).肝功能检查均正常.诊断方法主要为超声、CT和内镜.7例行彩色多普勒检查均提示脾静脉主干栓塞(7/7).增强CT可明确脾门周围及胃短静脉、胃网膜静脉扩张、迂曲(16/16).胃镜检查示孤立性胃底静脉曲张(4/5).脾脏切除对治疗消化道出血效果确切,发生门静脉栓塞1例.结论超声、CT和内镜检查联合特殊的临床特点,诊断区域性门静脉高压症并不困难.治疗上提倡个体化原则,但对有消化道出血者,应行脾脏切除术.     

门静脉高压脾切除门奇静脉离断术后再出血的食管胃静脉曲张分类研究

目的：探讨门静脉（门脉）高压患者脾切除门奇静脉离断术（脾切断流术）后再发上消化道出血的平均时间、内镜下食管和胃静脉曲张的分类特点及门脉高压性胃病的发病率。方法：190例肝硬化门脉高压出血患者分为脾切断流术后再出血组（40例）和未行手术组（150例）,统计手术患者术后至首次出血的平均时间间隔,每组患者分别行内镜检查,观察并对比其曲张静脉的分型特点及门脉高压性胃病发生率。结果：脾切断流术后再发出血时间平均为24个月,再出血患者内镜皆提示存有食管和（或）胃静脉曲张,2组患者内镜下的曲张静脉分型构成比有明显差异,脾切断流术者以单纯食管静脉曲张及食管胃静脉曲张（GOV）1型为主,未发现孤立性胃静脉曲张（IGV）1型及IGV2型,60．0％患者存在门脉高压性胃病,其发病率及严重程度均高于未行手术组患者。结论：脾切断流术治疗门脉高压近期止血疗效确切,但术后曲张静脉并未有效消退,须强调手术的规范性,并在再出血高发时段定期内镜随访．及时掌握食管胃曲张静脉及门脉高压性胃病的发展情况,早期干预治疗,从而改善患者预后。     

部分脾动脉栓塞治疗慢性胰腺炎相关脾静脉血栓致区域性门静脉高压1例报告

区域性门静脉高压为门静脉某一分支障碍,导致血流异常及侧枝循环开放的临床较少见的疾病,据报道有多达37种原因可导致该类疾病,其中脾静脉血栓是最常见原因之一［1］。而胰腺炎是导致脾静脉血栓的主要原因之一［2］。早在1920年报道了第1例胰腺炎相关脾静脉血栓形成导致的区域性门静脉高压患者,如不及时诊治,患者会出现难治性胃底静脉曲张及出血。本文将报告因反复胰腺疾病所致脾静脉血栓形成,导致脾静脉部分堵塞,引发难治性胃底静脉曲张经部分脾动脉栓塞治疗患者1例。     

门脉高压食管静脉曲张破裂出血的治疗

门静脉由肠系膜上静脉与脾静脉汇合而成，是肝脏供血的主要来源。由于门静脉系统血流受阻或血流量增加所致的以门脉压力升高、脾大、食管胃底静脉曲张和腹水为特点的临床症候群称为门脉高压症。而食管静脉曲张（EV）是门脉高压症的特征性表现，EV破裂出血是门脉高压症最凶险的并发症，首次出血病死率为40％以上，再次出血病死率达60％以上。因此，对EV病人的处理尤为重要。现就门脉高压症合并食管静脉曲张的药物、三腔双囊管、内镜介入以及手术等治疗做一回顾及瞻望。     

肝硬化患者食管静脉曲张及曲张程度的早期诊断方法分析

目的 对乙肝后肝硬化门脉高压症患者胃镜、B超、血液检验等进行分析，探讨这些检查在肝硬化门脉高压症患者食管静脉曲张诊断中的意义。方法 148例乙肝后肝硬化患者（合并或无门脉高压者）进行电子胃镜、腹部B超、血液检验，观察食管胃底静脉曲张的情况，测量门静脉主干内径、脾静脉内径及脾脏长径之间的差异，并分析这些指标与食管静脉曲张的关系。结果 食管静脉曲张发生率为61％，食管静脉曲张程度越重，伴胃底静脉曲张比例越高；随食管静脉曲张程度不同，门静脉主干内径、脾静脉主干内径及脾脏长径之间存在差异。血小板记数、脾脏长径、血小板记数／脾脏长径、Child—Pugh分级在合并有食管静脉曲张与未合并食管静脉曲张两组中存在明显差异。多因素分析发现，血小板记数／脾脏长径指数与食管静脉曲张的发生密切相关，独立性强。结论 门静脉主十内径、脾静脉内径、脾脏厚度可为判断门静脉高压提供参考，综合上述3点并结合胃镜检查结果可较准确判断有无食管静脉曲张及程度；血小板记数／脾脏长径指数能够较为准确地预测肝硬化门脉高压症食管静脉曲张的发生。     

Extrahepatic portal venous obstruction of different pathogenesis in pancreatic diseases: reports of 4 autopsy cases with chronic pancreatitis and pancreatic carcinoma

Four autopsy cases of extrahepatic portal venous obstruction associated with pancreatic diseases, 1 case of pancreatitis and 3 cases of pancreatic carcinoma, are presented. The pathogenesis of portal obstruction was different in each case; old thrombosis with recanalization due to chronic pancreatitis with pseudocysts formation in 1 case, fresh thrombosis due to intraportal venous catheterization for pancreatic carcinoma in 1 case, fresh thrombosis probably due to pancreatitis accompanying pancreatic carcinoma in 1 case, and direct invasion of pancreatic carcinoma into the portal vein in the remaining 1 case. Morphologic evidence for portal hypertension was present in each case. In the pancreatitis case and one pancreatic carcinoma case with portal tumor invasion, both of which had chronic portal obstruction, there were many thin-walled vascular channels (cavernous transformation) around the occluded portal vein. Their endothelia were positive for factor VIII-related antigen and Ulex europaeus lectin I, implying that these vessels were hepatopetal blood vascular collaterals. It was shown that pancreatic diseases resulted in portal venous obstruction by several different mechanisms and chronic portal obstruction in pancreatic diseases led to the formation of hepatoperal blood vascular collaterals.     

Splenic and portal venous obstruction in chronic pancreatitis

The aim of this study was a prospective search for splenoportal venous obstruction (SPVO) in a medical-surgical series of 266 patients with chronic pancreatitis who were followed up a mean time of 8.2 years. SPVO was systematically searched for using ultrasonography and then confirmed by angiography or computed tomography. SPVO was found in 35 patients (13.2%) but was symptomatic in only two. Initial obstruction involved the splenic vein in 22 patients, the portal vein in 10, and the superior mesenteric vein in three. Since venous obstruction extended from the splenic to the portal vein in five patients, the prevalence of portal obstruction was 5.6% (15/266). Acute pancreatitis and pseudocysts were the probable cause of SPVO in 91.4% of our cases. Half the cases of splenic venous obstruction were related to pseudocysts of the caudal pancreas. Esophageal varices were found in two patients and gastric varices in four at the time of diagnosis and during follow-up. At the end of follow-up, 12 patients had undergone splenopancreatectomy (N = 11) or splenectomy (N = 1). Only one patient was operated on for massive esophageal variceal bleeding, and another patient died due to intractable colic variceal bleeding. In four of six patients operated on with portal vein obstruction, surgery was difficult due to venous collaterals. Ten patients were not operated on and 13 patients operated on were not treated for SPVO. The mean follow-up after diagnosis of SPVO for these final 23 patients was 28.9 months. None of these patients bled.(ABSTRACT TRUNCATED AT 250 WORDS)     

Retrospective evaluation of risk factors of postoperative varices after pancreaticoduodenectomy with combined portal vein resection

BackgroundCombined portal vein (PV) resection is performed for pancreatic head cancer to achieve clear resection margins. This can be complicated by the formation of varices due to sinistral portal hypertension after pancreaticoduodenectomy (PD) with combined PV resection. However, clinical strategies to prevent varices formation due to sinistral portal hypertension remain controversial. Moreover, the critical vein among splenic vein (SPV), inferior mesenteric vein, left gastric vein, or middle colonic vein requiring preservation to prevent the development of varices remains unclear.MethodsWe retrospectively analyzed patients with pancreatic cancer who underwent PD with combined PV resection over 18 years at our institution. Varices were evaluated using enhanced computed tomography (CT) and endoscopy. Preoperative types of porto-mesenterico-splenic confluence, venous drainage, and venous resection types were determined by operative records and CT findings.ResultsOf the 108 subjects, the incidence of postoperative varices was observed in 24.1% of cases over 5.6 months. These varices were classified into five types based on location, as pancreaticojejunostomy anastomotic (11.5%), gastrojejunostomy anastomotic (11.5%), esophageal (11.5%), splenic hilar-gastric (23.1%), and right colonic (65.4%) varices. No case of variceal bleeding occurred. Multivariate analysis showed SPV ligation as the greatest risk factor of varices (P < 0.001), with a higher incidence of left-sided varices in patients with all the SPV venous drainage sacrificed (60%) than in the others (16.7%). Therefore, sacrificing all the SPV venous drainage was the only independent risk factor of varices (P = 0.049).ConclusionsPreservation of SPV venous drainage should be considered during SPV ligation to prevent post-PD varices.     

Long-term follow-up study of adult patients with non-cirrhotic obstruction of the portal system: comparison with cirrhotic patients.

Thirty-two patients with non-cirrhotic portal system obstruction and oesophageal varices of non-malignant etiology were recruited over 13 years. Diagnosis was based on the presence of oesophageal varices at endoscopy, minor alterations in liver function tests and liver histology, a low hepatic venous pressure gradient, and pertinent angiographic patterns. Twenty-three had portal vein thrombosis, nine had splenic vein thrombosis. Twenty-one had idiopathic portal vein obstruction, 11 had secondary obstruction. The outcome was compared with a group of 32 patients with cirrhosis and portal hypertension, matched for age, Child-Pugh class, previous history of gastrointestinal bleeding, and size of oesophageal varices. Patients with non-cirrhotic obstruction of the portal system were followed for up to 171 months (mean 94 months). During follow-up ten patients had gastrointestinal bleeding, and eight died (five of gastrointestinal bleeding). After 6 years of follow-up, the cumulative risk of gastrointestinal bleeding was 24%, the cumulative risk of death was 17%, and the cumulative risk of death from gastrointestinal bleeding was 14%. Cumulative probability of death by any cause and the probability of gastrointestinal bleeding were significantly lower in patients with non-cirrhotic obstruction of the portal system than in patients with cirrhosis comparable for liver function and portal hypertension (p = 0.04 for both). The cumulative probability of death by gastrointestinal bleeding was not significantly different. In conclusion, the prognosis for non-cirrhotic obstruction of the portal system is significantly better than for patients with cirrhosis with comparable levels of liver function impairment and severity of portal hypertension.     

Sinistral portal hypertension. A case report

Sinistral portal hypertension is a clinical syndrome of gastric variceal hemorrhage in the setting of splenic vein thrombosis due to a primary pancreatic pathology. The distinguishing features from other forms of portal hypertension are preserved liver function and a patent extrahepatic portal vein. The important causes include acute and chronic pancreatitis, pancreatic pseudocysts and pancreatic carcinomas. Benign pancreatic neoplasms only rarely cause sinistral portal hypertension. Splenic vein thrombosis complicates 7-20% of patients having pancreatitis or a pancreatic pseudocyst; however, bleeding occurs in only approximately 5% of patients. The diagnosis of sinistral portal hypertension is achieved by a combination of gastroscopy, liver function tests, ultrasound examination (with Doppler) and/or contrast-enhanced CT scan of the abdomen. A mere demonstration of sinistral portal hypertension does not warrant intervention. An expectant management is justifiable in asymptomatic patients with pancreatitis. However, concomitant splenectomy may be considered in patients undergoing operative treatment of symptomatic chronic pancreatitis if sinistral portal hypertension and gastroesophageal varices are present. In patients presenting with gastric variceal hemorrhage, splenectomy (with treatment for the primary pancreatic pathology, e.g. distal pancreatectomy) is curative with excellent long term results.     

Rectosigmoid Varices and Other Mucosal Changes in Patients with Portal Hypertension

A prospective study was performed to evaluate the prevalence of anorectal varices and their clinical significance as well as to study other proctosigmoidoscopic changes in 75 patients with portal hypertension of diverse etiology. Sixty-seven patients (89.3%) had lower gastrointestinal varices with no significant difference (p greater than 0.05) in prevalence between cirrhosis (92.1%), noncirrhotic portal fibrosis (87%), and extrahepatic portal venous obstruction (85.7%). The rectum was the most common site of lower gastrointestinal varices. External anal and sigmoid colonic varices almost always occurred in the presence of rectal and/or internal anal varices. There was no correlation between the presence of rectosigmoid varices and the severity of esophagogastric mucosal changes or portal hypertension. There was no suggestion that esophageal variceal sclerotherapy influenced the presence of anorectal varices. Seven patients (9.3%) had recent hematochezia, including three patients in whom it occurred in the absence of any upper gastrointestinal hemorrhage. Varices were the cause of bleeding in at least five patients. An abnormal mucosal vascular pattern in the form of telangiectasias or spiders was seen, irrespective of etiology of portal hypertension, in nine patients (12%). Hemorrhoids were present in 31 patients (41.3%) with an age-related difference (p less than 0.05) between patients with cirrhosis (55.3%) and extrahepatic portal venous obstruction (21.4%).     

Sonographic demonstration of portal venous system thromboses secondary to inflammatory diseases of the pancreas

Sonographic demonstration of abdominal venous thromboses subsequent to pancreatic benign inflammatory diseases has been seldom reported up to now. Seven cases of thromboses of the portal venous system associated with acute or chronic pancreatitis are reported. All cases were detected by sonography in patients without clinical manifestations of portal hypertension. Echogenic thrombus within the lumen of the vein was observed only in the short-term follow-up of acute pancreatitis. Cavernomatous transformation was observed in 6 patients with long-term calcifying pancreatitis. Extrinsic compression by pseudocyst of the pancreas was observed in only 1 case. In all the other cases, thromboses seems to be secondary to local inflammatory phenomena during previous episodes of acute pancreatitis.     

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。