Isolated gastric varices: splenic vein obstruction or portal hypertension?

The presence of isolated gastric varices without esophageal varices is thought to be highly suggestive of splenic vein obstruction. A review of our radiologic files revealed 14 patients with isolated gastric varices on barium studies performed during the past 10 years. Eight of the 14 patients had adequate clinical and/or radiologic follow-up to suggest the pathophysiology of the varices. Seven had evidence of portal hypertension, and the remaining patient had evidence of splenic vein obstruction. Six patients had signs of upper gastrointestinal (GI) bleeding. Double-contrast upper GI examinations revealed thickened, tortuous fundal folds in 6 patients and a lobulated fundal mass in 2. Thus, most patients with isolated gastric varices have portal hypertension rather than splenic vein obstruction as the underlying cause.     

Gastric Varices: Profile, Classification, and Management

Development of gastric varices is an important manifestation of portal hypertension. In segmental portal hypertension, gastric varices originate from short gastric and gastroepiploic veins. In generalized portal hypertension, intrinsic veins at cardia participate in the formation of gastric varices. Endoscopy and/or splenoportovenography and a high index of suspicion are required for the diagnosis of gastric varices. The incidence of gastric varices in patients with portal hypertension has been variably reported (2-70%), probably due to difficulties in diagnosis. In a small proportion of patients with gastric varices, chronic portal-systemic encephalopathy or significant variceal bleeding develops. Gastric varices can be classified, depending on their anatomical location, into gastroesophageal varices (a continuation of esophageal varices) or "isolated" gastric varices (fundal or ectopic varices). This distinction is necessary for management. Whereas surgery is recommended for bleeding fundal varices, in acute bleeding from gastroesophageal varices, sclerotherapy could be attempted successfully. In more than a quarter of patients, gastric varices disappear after obliteration of esophageal varices. Prophylactic sclerotherapy of gastric varices is not recommended.     

Upper gastrointestinal bleeding in patients with portal hypertension: a reappraisal

The current medical literature states that upper gastrointestinal bleeding in patients with cirrhosis and portal hypertension originates from a variety of sources. Although variceal bleeding has been recognized as the principal source, acute erosive gastritis and peptic ulcer are said to be the bleeding site in a large percentage of cases. In 140 consecutive patients with endoscopically documented esophageal varices who came to our service with upper gastrointestinal hemorrhage, varices were the source of bleeding in approximately 90%, regardless of whether the underlying liver disease was due to alcoholism or not. We conclude that: 1) patients with varices almost always bleed from varices, and 2) the incidence of erosive gastritis and peptic ulcer as a cause of bleeding in this group has been overemphasized.     

Evaluation of esophageal varices in liver disease by splenic-pulp manometry,splenoportography, and esophagogastroscopy

Summary and Conclusion Esophagogastroscopy, splenic-pulp manometry, and splenoportography were combined in a prospective study of 60 patients with documented liver disease and suspected portal hypertension. All three procedures were performed on each of the patients within a 6-day period. Twenty patients were actively bleeding at the time of endoscopic examination.Esophagogastroscopy demonstrated varices in 90% of the patients studied. Splenoportography, however, demonstrated collateral circulation in only 50% of the patients with endoscopically demonstrated varices. In no instance did splenoportography demonstrate collateral circulation not previously seen on endoscopy. Splenoportography failed to demonstrate collateral circulation in all patients whose splenic-pulp pressure was less than 270 mm. water.In 20 patients with upper gastrointestinal bleeding, the height of the splenic-pulp pressure was a poor index of the site of bleeding. Eight patients with portal hypertension and esophageal varices were found to be bleeding from nonvariceal sites. Conversely, 5 patients with active bleeding from endoscopically demonstrated varices had no collateral circulation revealed by splenoportography.It is evident from this study that splenic-pulp manometry, splenoportography, and esophagogastroscopy will frequently yield divergent results in the evaluation of portal hypertension and portosystemic collateral circulation in patients with liver disease. While splenoportography may be useful in determining the patency of the portal vein and demonstrating large spontaneous or surgical portosystemic shunts, esophagogastroscopy is a better method for detecting esophageal varices and determining whether they are bleeding. The height of the splenic-pulp pressure is of little value in indicating the site of upper gastrointestinal bleeding.Supported in part by Graduate Training Grant TI-AM-5237 and Clinical Research Center Grant AM-05576-02 from the National Institute of Arthritis and Metabolic Diseases, N.I.H., U. S. Public Health Service, and Contract U 1373 of the Health Research Council of the City of New York.     

门脉高压性小肠病

小肠改变是门脉高压门静脉高压症是一组由门静脉压力持续增高引起的症候群,最常见表现是消化道出血,特别是食管胃静脉曲张破裂出血.随着小肠检查手段的发展,特别是胶囊内镜和双气囊小肠镜,发现门脉高压下小肠发生了病变,被定义为门脉高压性小肠病(PHE),这种改变也是消化道出血的重要原因.消化道出血的患者,胃或食管没有静脉曲张情况...     

门-体分流程度评估血吸虫病肝硬化上消化道出血的应用

目的探讨门-体静脉分流程度在评估血吸虫病肝硬化上消化道出血中的应用。方法以金山医院经临床证实的33例血吸虫病肝硬化上消化道出血患者,及29例血吸虫病肝硬化非出血患者为研究对象,对其进行上腹部128层螺旋CT扫描。采用薄层块最大强度投影(TSMIP)、多平面重建(MPR)对门静脉系进行血管重建,对两组患者门-体静脉分流程度进行评分和比较,分析各侧支血管分流程度与血吸虫病肝硬化上消化道出血的关系。结果 33例上消化道出血患者中,侧支血管发生率如下:胃左静脉曲张86.4%、胃短静脉曲张68.2%、食管静脉曲张50.0%、食管旁静脉曲张50.0%、胃底静脉曲张37.9%、胃肾静脉69.7%、脾肾静脉51.5%、腹壁静脉曲张25.8%、网膜静脉曲张15.2%、脾周静脉曲张63.6%、附脐静脉曲张34.8%、腹膜后-椎旁静脉40.9%、肠系膜静脉曲张36.4%。出血组食管静脉、食管旁静脉、胃左静脉和胃底静脉的发生率和分流程度均明显大于非出血组(P值均0.05)。结论 CT门静脉系成像可精确显示各类侧支血管的部位、程度及走向。食管静脉、食管旁静脉、胃左静脉和胃底静脉能较准确地预测血吸虫病肝硬化上消化道出血的风险情况,上述侧支血管分流程度越高,上消化道出血危险性就越大。     

Nodular regenerative hyperplasia related portal hypertension in a patient with hypogammaglobulinaemia

Nodular regenerative hyperplasia (NRH) of liver is a relatively rare liver disorder, but a frequent cause of noncirrhotic portal hypertension. We present a lady with common variable immune deficiency who presented with upper gastrointestinal bleeding and deranged liver function tests but preserved synthetic function. Upper gastrointestinal endoscope showed bleeding gastric varices and non-bleeding oesophageal varices. Although her oesophageal varices were eradicated by repeated endoscopic band ligation, the gastric varices failed to resolve after repeated endoscopic histocryl injection and she eventually needed transjugular intrahepatic portosystemic shunt placement. Liver biopsy showed NRH. We review the association of hypogammaglobinaemia and NRH and discuss the appropriate management of portal hypertension in NRH.     

Transjugular intrahepatic portasystemic stent shunting for control of acute and recurrent upper gastrointestinal haemorrhage related to portal hypertension.

The insertion of a transjugular intrahepatic portasystemic stent shunt (TIPSS) was evaluated in 22 patients with recurrent upper gastrointestinal haemorrhage related to portal hypertension (bleeding from oesophageal varices 10, gastric varices six, portal hypertensive gastropathy six). TIPSS was successfully performed electively in 15 patients and as an emergency in three patients. Twelve patients have had no further admissions with bleeding after TIPSS. Single episodes of bleeding were noted in six patients after TIPSS associated with shunt thrombosis (two), intimal hyperplasia within the shunt (two), and shunt migration (one). Another patient presented with reaccumulated ascites suggesting poor shunt function but died from massive variceal haemorrhage before further assessment could be performed. There was one death related to the procedure. Two patients developed encephalopathy after TIPSS, in one patient this was controlled by the insertion of a smaller diameter stent within the existing TIPSS. Several complications arose in earlier patients that have not recurred after modification of the initial technique. TIPSS can be life saving and is effective in controlling variceal haemorrhage and rebleeding from oesophageal or gastric varices and portal hypertensive gastropathy. Larger and longer term studies are required, however, to define the role of TIPSS in the overall management of such patients.     

Fundal varices: problem and management.

BACKGROUND/AIMS: The pathophysiology of gastric varices may be due to generalized or segmental portal hypertension. A considerable debate has arisen regarding the role of injection sclerotherapy in the pathogenesis of gastric varices. METHODOLOGY: During the period from 1987 to 1997, a total of 1686 cases with bleeding varices were presented to our center and 225 cases (13.3%) with bleeding gastric varices were diagnosed. There were 198 males and 27 females with a total mean age of 45.7 years (+/- 7.6). Primary fundal varices (FV) were found in 121 (54%) cases and secondary FV were found in 104 (46%) cases. All patients with isolated FV presented with repeated attacks of upper gastrointestinal bleeding. RESULTS: The pathological diagnosis was studied in 120 cases; it was schistosomal in 8.3% of cases, non-schistosomal in 33.3% of cases, and mixed (Schistosomal with post viral cirrhosis) in 58.3% of cases. Seventy-five cases were subjected to splenectomy and gastroesophageal decongestion (SGED), 64 cases were subjected to distal splenorenal shunt (DSRS), and 86 cases were subjected to sclerotherapy. Mortality after DSRS was 7.8%, after SGED it was 12%, and after sclerotherapy it was 21%. Rebleeding was the major complication and occurred in 3% after DSRS, in 13% after SGED, and in 18% of cases after sclerotherapy. CONCLUSIONS: Gastric varices are not an uncommon condition as a cause of upper gastrointestinal bleeding. Our findings support the hypothesis that gastric varices may be considered a late sequel of injection sclerotherapy, though they may also be considered as one of the pathophysiologies of generalized portal hypertension. Finally, DSRS was found to be the treatment of choice in the management of fundal varices.     

Peripapillary duodenal varices as a rare cause of severe bleeding in a patient with no other signs of portal hypertension--successful endoscopic treatment with cyanoacrylate injection

Duodenal varices (DVs) are a rare cause of upper gastrointestinal bleeding and rather suspected in patients with portal hypertension. Bleeding DVs are difficult to manage and often fatal due to delayed diagnosis. We report on a 71-year-old patient with massive upper gastrointestinal haemorrhage, who did not show any clinical signs of portal hypertension; however, he had a history of duodenal segmental resection 8 years before. The source of bleeding could not be detected with different imaging methods such as angiography and computed tomography. Upper gastrointestinal endoscopy finally revealed DVs, which were located just adjacent to the papilla. After endoscopic injection therapy with n-butyl 2-cyanoacrylate the bleeding stopped immediately and the patient soon stabilised. Despite the peripapillar localisation no signs of pancreatitis or cholestasis occurred; during 10-month follow-up a marked regression of the varices without further signs of variceal bleeding was observed.     

门静脉高压患者胃静脉曲张的内镜识别和分类

背景：肝硬化门静脉高压的出血原因中，食管和（或）胃静脉曲张破裂出血最为常见。胃静脉曲张的发生率较食管静脉曲张低，但再出血率高，出血量大，死亡率亦较高。尽管如此，胃静脉曲张在临床诊治过程中未受到应有的重视。目的：根据内镜下对食管和胃静脉曲张的识别和分类，了解食管和胃静脉曲张的比例。方法：根据Sarin分类，在内镜直视下将114例门静脉高压患者分为单纯食管静脉曲张、胃食管静脉曲张1型（GOV1型）、胃食管静脉曲张2型（GOV2型）、孤立性胃静脉曲张1型（IGV1型）和孤立性胃静脉曲张2型（IGV2型）五种类型。结果：本组患者中单纯食管静脉曲张42例（36．8％），GOV1型40例（35．1％），GOV2型20例（17．5％），IGV1型12例（10．5％），未见IGV2型。结论：半数门静脉高压患者存在胃静脉曲张，临床工作中仅处理食管静脉曲张是很片面的。须努力开展组织黏合剂、球囊闭塞下逆行经静脉栓塞术（B．RTO）或外科分流等治疗：对有条件的患者应鼓励开展肝移植治疗。     

Upper gastrointestinal bleeding in patients with esophageal varices. What is the most common source?

The course of portal hypertension often is complicated by variceal bleeding, which tends to be massive and has a poor prognosis. In contrast to previous reports, this study of 299 episodes of gastrointestinal bleeding found that among patients with upper gastrointestinal bleeding in whom varices are seen endoscopically, the varices are the cause of bleeding in the great majority.     

多排螺旋CT门静脉成像对门静脉高压食管、胃底静脉曲张的评价

肝硬化失代偿期可引起门静脉高压,食管胃底静脉曲张是门静脉高压的一个严重并发症,其破裂可引起胃肠道大出血,对门静脉高压侧支循环的显示对患者的治疗方式的选择及预后的评估具有重要意义.多排螺旋CT门静脉成像(CTPV)可显示胃底静脉曲张的部位、形态及侧支循环血供的关系,在GEVI型,GV多为LGV或以LGV为主来供应,胃和(或)脾-肾分流较少见,GV的形态多为迂曲型.在GEV2型,GV大部分由PGV和(或)SGV供血,部分病例伴胃和(或)脾-肾分流.IGV型多以PGV和(或)SGV为主要血供,且较多合并胃和(或)脾-肾分流,GEV2和IGV型GV的形态以结节型和瘤型较多.CTPV可显示食管静脉曲张分型与其侧支循环的关系,EV以位于食管黏膜下、食管壁为主时,其血供多为胃左静脉前支优势型;EV为食管管旁静脉曲张为主时,其血供多为后支优势型;EV管壁、黏膜下静脉曲张程度与管旁静脉曲张接近时,其血供多为前后支均衡型.     

Diagnosis and management of ectopic varices

Abstract   Ectopic varices are dilated portosystemic venous collateral vessels that may occur anywhere in the gastrointestinal tract. Ectopic varices account for approximately 5% of all hemorrhages from varices. Ectopic varices may occur as a result of portal hypertension from any cause but are more common (particularly duodenal and biliary varices) in patients with extrahepatic portal vein thrombosis. Ectopic varices may also develop following successful endoscopic obliteration of gastroesophageal varices. With the exception of isolated gastric fundal varices, ectopic varices have relatively low risk for bleeding. Diagnosis is often made by endoscopy; however, computed tomography, magnetic resonance imaging and portal venography may be needed in some cases. Endoscopic treatment is successful in many cases and is the safest option provided bleeding is definitively controlled. Surgical options are now reserved for treatment of life-threatening bleeding or for shunt insertion in patients who are not candidates for transjugular intrahepatic portosystemic shunt (TIPS) as a result of portal vein thrombosis. Portal decompression using TIPS, in spite of the risk for encephalopathy, is the treatment of choice for bleeding from ectopic varices that cannot be successfully managed endoscopically.     

Formation, hemodynamics and new management options for gastric varices

Abstract   Gastric varices develop in patients with portal hypertension, including liver cirrhosis, idiopathic portal hypertension as well as left sided-local portal hypertension such as splenic vein thrombosis or splenic AV malformation. The inflow vein is the left gastric vein, posterior vein, or short gastric vein, while the outflow vein is the gastro-renal shunt in most of the patients with gastric varices. The form of the gastric varices is classified into three types of venous dilatation; tortuous type, notched type and tumor type according to the shape and size of the varices. The location is classified into five sites; the posterior site, anterior site, greater curvature site and lesser curvature site of the cardiac area, and the fundic area. The risk of the rupture depends on the mucosal factor of the varices as well as the location and the form. The hemostasis rate has been improved to 94–97% with the usage of the endoscopic occlusive agent such as Histoacryl. It is absolutely necessary to eradicate the gastric varices within a few weeks after rupture of the gastric varices. There are new management options such as laparoscopic Hassab's operation or balloon-occluded retrograde transvenous obliteration of the varices (B-RTO). The 5-year cumulative rate of the non-variceal bleeding is more than 90% after the B-RTO as well as after surgery. Further prospective clinical trials are to be investigated for an evidence-based medicine.     

The prevalence and spectrum of colonic lesions in patients with cirrhotic and noncirrhotic portal hypertension

Portal hypertension diffusely affects the gastrointestinal tract. The frequency and profile of distinct colonic mucosal lesions (portal colopathy) and rectal varices (RV; veins >4 cm above the anal verge) is not well studied. Fifty consecutive patients with portal hypertension (25 with cirrhosis, 10 with noncirrhotic portal fibrosis [NCpf], and 15 with extrahepatic portal vein obstruction [EHPVO]) were assessed clinically and by upper and lower gastrointestinal (GI) endoscopy. Colorectal lesions were seen in 35 (70%) patients, significantly more often in bleeders than in nonbleeders. Rectal varices were detected in 22 (44%) patients; larger and more often seen in EHPVO (80%) than in cirrhosis (28%) and NCPF (30%) (P < .01) patients. Portal colopathy was seen in 26 (52%) patients, with nearly similar frequency in cirrhotics, NCPF, and EHPVO patients. Previous sclerotherapy or presence of gastric varices had little influence on the development of these lesions. An association (P < .01) was, however, seen between the presence of colopathy and portal gastropathy. Overt bleeding was seen in 8% and 4% of patients with RV and colopathy, respectively. In conclusion, our results demonstrate that colorectal lesions are present in about two thirds of patients with portal hypertension. Patients with portal hypertension and lower GI bleeding should be colonoscoped. Patients with extrahepatic portal vein obstruction may in turn benefit from baseline sigmoidoscopic examination to define the presence and size of rectal varices.     

Endoscopic sclerotherapy of gastric variceal bleeding with N-butyl-2-cyanoacrylate

BACKGROUND: bleeding from gastric varices is a life-threatening complication of portal hypertension. Fundal and isolated gastric varices are at high risk for variceal bleeding. In this study, we report our experience with n-butyl-2-cyanoacrylate (BC) in patients with large gastric varices. STUDY: twenty-nine patients (15 male, 14 female) with large fundal varices (active bleed, 5; passive bleed after eradication of esophageal varices, 13; unbled fundal varices with red color sign, 11) underwent endoscopic sclerotherapy with BC. Cirrhosis was present in 13 patients; extrahepatic portal venous obstruction, in 13; and noncirrhotic portal fibrosis, in 3. N-Butyl-2-cyanoacrylate after mixing with lipiodol (1:1) was given to the initial 10 patients and was given in undiluted form to the remaining patients, followed by injection of 0.7 mL of distilled water to rinse the injection catheter. One to three injections (0.5-1 mL) were given until all gastric varices became hard. All patients were on long-term endoscopic sclerotherapy or variceal ligation programs for eradication of esophageal varices. RESULTS: acute variceal bleeding was controlled in all five patients with BC injections. Eradication of gastric varices was achieved in 27 (93.1%) patients (20 patients in 1 session, 4 patients in 2, and 3 patients in 3-6). Rebleeding occurred in three (10.3%) patients who responded to repeat BC injections. Complications related to the procedure occurred in two (6.9%) patients. In one patient, the needle became impacted into the tissue adhesive. This patient died 5 days later because of massive upper gastrointestinal bleeding. In the other patient, there was distal embolization. CONCLUSIONS: sclerotherapy of gastric varices with BC is a safe and an effective treatment for control of bleeding and eradication. The needle should be withdrawn immediately after the BC injection to prevent its impaction into the tissue adhesive.     

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%).     

Clinical significance and prediction factors of gastric varices in patients with hepatocellular carcinoma

BACKGROUND/AIMS: Hepatocellular carcinoma is part of the natural history of liver cirrhosis. Gastrointestinal bleeding and hepatic failure are the leading causes of death in hepatocellular carcinoma patients. With gastrointestinal bleeding, variceal bleeding is the most prominent, and most variceal bleeding is of esophageal origin. Gastric varices bleeding is often a massive and severe bleeding episode. The role of gastric varices among patients with hepatocellular carcinoma remains to be clarified. In this study, we aimed to evaluate the prevalence, clinical significance and prediction of gastric varices in patients with hepatocellular carcinoma. METHODOLOGY: From 1998 to 2000, we reviewed 304 patients with hepatocellular carcinoma receiving upper gastrointestinal endoscopic examinations. Patients' clinical characteristics, physical findings, laboratory data, image studies, endoscopic examinations and treatment were reviewed. RESULTS: Among 304 patients with HCC, twenty-one (6.9%) had gastric varices among 304 patients with hepatocellular carcinoma. The location of gastric varices were the posterior wall in 12 (57%), the lesser curvature in 1 (5%), the greater curvature in 4 (19%) and the fundus in 4 (19%). Three (14%) of these 21 patients with hepatocellular carcinoma and gastric varices had clinical evidence of bleeding. One of them died due to uncontrollable bleeding. Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count were significantly different between hepatocellular carcinoma patients with gastric varices and without gastric varices under the univariate analysis. Ascites (Odds ratio: 5.45; 95% confidence interval: 2.12-14.01) and portal vein or splenic vein dilatation (Odds ratio: 4.38; 95% confidence interval: 1.77-10.86) were the two most important predictors under the stepwise logistic regression analysis. CONCLUSIONS: The prevalence of gastric varices in patients with hepatocellular carcinoma is 6.9% and the risk of bleeding is low in this study. The Predictors of gastric varices among hepatocellular carcinoma are related to liver cirrhosis, Child-Pugh classification, hepatic encephalopathy, portal vein or splenic vein dilatation, ascites, splenomegaly, albumin level, prothrombin time and platelet count.