Combined Upper and Lower Gastrointestinal Endoscopy: A Prospective Study in Alcoholic and Nonalcoholic Cirrhosis

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis. Most of the available data regarding the prevalence of upper and lower gastrointestinal sites of bleeding in cirrhotic patients have been obtained in individuals with alcoholic cirrhosis evaluated in the course of an acute gastrointestinal bleeding episode. Few data exist, however, as to the prevalence of either potential bleeding sites or of normal endoscopic findings in hemodynamically stable individuals with cirrhosis of any etiology. Five hundred ten cirrhotic subjects, who were evaluated for possible liver transplantation (OLTx) between January 1985 and June 1987, were included in this study. Seventy-five had alcoholic cirrhosis and 435 had nonalcoholic cirrhosis of various etiologies. Of these 510 patients, 412 underwent combined upper and lower gastrointestinal endoscopy and 98 underwent upper gastrointestinal endoscopy alone. Gastritis, gastric and duodenal ulcer disease were found significantly (each at least p less than 0.025) more often in patients with alcoholic liver disease than in those with nonalcoholic liver disease. The prevalence of the various lower gastrointestinal lesions in both groups was similar. Of particular interest is the fact that in alcoholic cirrhotics, the prevalence of gastritis, gastric ulcer and duodenal ulcer disease was unrelated to the degree of portal hypertension, whereas in the nonalcoholic cirrhotics the prevalence of gastritis and duodenal ulcer disease but not gastric ulcer disease was associated significantly with the degree of portal hypertension as assessed by the presence or absence of large esophageal varices, ascites, and hepatic encephalopathy.     

Portal hypertensive bleeding

Portal hypertension bleeding is a common and serious complication of cirrhosis. All patients with cirrhosis should undergo endoscopy and be evaluated for possible causes of current or future portal hypertensive bleeding. Possible causes of bleeding include esophageal varices, gastric varices, and PHG. Patients with esophageal varices at high risk of bleeding should be treated with nonselective beta-blockers for primary prevention of variceal hemorrhage. HVPG measurements represent the optimal way to monitor the success of pharmacologic therapy. EVL may be used in those with high-risk varices who do not tolerate beta-blockers. When active bleeding develops, simultaneous and coordinated attention must be given to hemodynamic resuscitation, prevention and treatment of complications, and active control of bleeding. In cases of acute esophageal variceal (Fig. 5) and PHG bleeding, terlipressin, somatostatin, or octreotide should be started. Endoscopic treatment is provided for those with bleeding esophageal varices. If first-line therapy fails, TIPS or surgery may need to be performed. Unlike esophageal variceal or PHG bleeding, there is no established optimal treatment for gastric variceal bleeding. Individual and specific treatment modalities for acute gastric variceal bleeding must be calculated carefully after considering side effects.     

Prognostic indicators in alcoholic cirrhotic men

The relationships between portal pressure, liver function and clinical variables on one hand and development of variceal hemorrhage and death on the other were investigated in 58 men with newly diagnosed alcoholic cirrhosis. Portal pressure was determined during hepatic vein catheterization as wedged minus free hepatic vein pressure, and median pressure was 14 mm Hg (range = 3 to 26 mm Hg). Fourteen of 31 patients (45%) had esophageal varices at upper gastrointestinal endoscopy (the size being considered large in nine patients). During follow-up (median = 31 months; range = 2 to 51 months), 12 patients (21%) developed variceal hemorrhage. Applying Cox's regression analysis, information about previous variceal bleeding (p = 0.0046), large varices at endoscopy (p = 0.012), hepatic vein pressure gradient (p = 0.0056) and indocyanine green clearance (p = 0.038) all contained significant prognostic information regarding development of variceal hemorrhage, even when easily obtained variables with known prognostic information were included [modified Child-Turcotte's criteria and incapacitation index (a weighted sum of days without normal health)]. During follow-up, 17 patients (29%) died. Applying Cox's regression analysis, large varices at endoscopy (p = 0.012) and hepatic vein pressure gradient (p = 0.019) contained significant prognostic information regarding death, in addition to the information contained in the modified Child-Turcotte's criteria and incapacitation index. In conclusion, prediction of prognosis in alcoholic cirrhotic men may be significantly improved by information about size of esophageal varices and level of portal pressure.     

肝衰竭并发消化道出血的诊断与治疗策略

严重的凝血功能障碍所导致的胃肠道黏膜弥漫性出血以及不同程度的食管胃静脉曲张、门脉高压性胃病以及下消化道异位静脉曲张是肝衰竭并发消化道出血的重要原因,其病情危重,预后极差,病死率高。本文对肝衰竭并发消化道出血与单纯的消化道出血的临床鉴别要点、肝衰竭并发消化道出血的疾病谱以及诊断进行了简要阐述,重点对其治疗的策略及相关进展进行了讨论,同时提出了以药物、内镜下治疗、TIPS 等多种治疗方法为依托的综合治疗策略的概念。     

Prevalence of endoscopic findings in 510 consecutive individuals with cirrhosis evaluated prospectively

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis and a major cause of death in such patients. The main sites of bleeding are esophageal varices, gastritis, and peptic ulcers. In order to determine the prevalence of either potential bleeding lesions or of other endoscopic findings in hemodynamically stable individuals with various etiologies of cirrhosis, 510 consecutive cirrhotic patients, evaluated for possible orthotopic liver transplantation (OLTx) underwent an upper gastrointestinal endoscopy for combined diagnostic and therapeutic purposes. The patients were divided into two main groups: 319 patients with parenchymal liver disease and 191 patients with cholestatic liver disease. Gastritis was found significantly more often in patients with parenchymal liver disease than in those with cholestatic liver disease (49.8% vs 30.9%; P <0.001). In contrast, the prevalence of esophagitis, esophageal and gastric varices, gastric ulcer, duodenal ulcer, and duodenitis was similar in both groups. Normal endoscopic findings were present in 5.0% of the parenchymal group and 11.5% of the cholestatic group (P <0.02). Ascites and encephalopathy were found significantly more often in subjects with parenchymal liver disease as compared to those with cholestatic liver disease. Portal hypertension and its degree, as assessed by the presence and size of esophageal varices, was similar in both groups, and in both groups there was a statistically significant qualitative trend of increasing prevalence of esophageal varices with increasing severity of disease as estimated using Pugh-Child's criteria.This work was supported in part by grant DK32556 from NIDDK, by grants AA06772 and AA06601 from NIAAA, and by a grant from the Gastroenterology Medical Research Foundation of Southwestern Pennsylvania.     

Does the measurement of portal flow velocity have any value in the identification of patients with cirrhosis at risk of digestive bleeding?

Abstract: Upper gastrointestinal bleeding is a leading cause of death in patients with liver cirrhosis. In most cases haemorrhage originates from oesophageal varices or from congestive gastropathy, and the evaluation of the bleeding risk is based on oesophagogastroduodenoscopic data. The aim of this prospective study was to determine whether the measurement of portal flow velocity by Duplex-Doppler, compared with endoscopic data, can help in detecting patients with cirrhosis at risk of bleeding. One hundred and seventy-three patients underwent endoscopy to ascertain the size of the varices and the severity of congestive gastropathy. For each patient maximal portal flow velocity measurements were obtained. No difference in portal flow velocity was observed between patients with or without oesophageal varices or congestive gastropathy. During a 2-year observation period, 27 patients (15.6%) had at least one episode of acute digestive bleeding. Stepwise multiple logistic regression analysis demonstrated a correlation between oesophageal varices and congestive gastropathy endoscopic grading and the incidence of bleeding; only the former was entered into the final regression equation (p>0.001). No relationship between the max portal flow velocity value and incidence of bleeding was found. This study shows that portal flow velocity is unrelated to the degree of the endoscopic abnormalities in patients with liver cirrhosis and that it has no value in the identification of patients with cirrhosis at risk of upper gastrointestinal bleeding.     

门脉高压患者内镜下胃静脉曲张分类及其发病分析

目的 对肝硬化患者内镜下胃静脉曲张进行分类，并分析其出血的好发因素。方法 确诊肝硬化门静脉高压患者139例，采用Soehendra和Sarin标准进行食管-胃静脉曲张分类，分析各类型的发生率、出血率、静脉曲张间的关系及出血与肝功能的关系。结果胃静脉曲张的发生率为35％，以GOV1发生率最高，多见于重度食管静脉曲张患者；胃静脉曲张出血率为12％，见于肝功能B级以上患者及GOV2和IOV1，显著低于食管静脉曲张出血率，食管静脉曲张出血见于中度以上静脉曲张、肝功能B级以上患者。结论胃静脉曲张在中国人群中有较高的发病率，出血多发生于胃底部位的曲张静脉，与肝功能差有关；食管静脉曲张出血发生率高于胃静脉曲张，与曲张静脉和肝功不良严重程度有关。     

Prospective evaluation of esophageal varices in primary biliary cirrhosis: development, natural history, and influence on survival

The aims of our prospective study were to determine the development and natural history of esophageal varices and variceal bleeding in patients with primary biliary cirrhosis. As part of a controlled clinical study, 265 patients with primary biliary cirrhosis who did not have esophageal varices at entry were followed for a median of 5.6 yr. The mean age was 49 yr (range 26-75 yr), 89% were women, and 69% had advanced histologic stage disease (stage 3-4) on liver biopsy at study entry. All patients were screened annually for esophageal varices by barium esophogram or endoscopy, or both; endoscopy was used to diagnose all episodes of esophageal variceal bleeding. Esophageal varices developed in 83 (31%) patients, and 40 (48%) of those with esophageal varices experienced one or more episodes of esophageal variceal bleeding. Cox regression analysis indicated that only serum bilirubin and histologic stage were associated independently with time to development of esophageal varices. In patients who developed esophageal varices, 33% and 41% developed esophageal variceal bleeding at 1 and 3 yr, respectively. After development of esophageal varices, 1- and 3-yr survival estimates were 83% and 59%, respectively. After the initial variceal bleeding episode, survival estimates were 65% and 46% at 1 and 3 yr and were dependent on Child's classification. These findings are important in considering indications for prophylactic therapy for esophageal varices in primary biliary cirrhosis and may influence timing of liver transplantation.     

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.     

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。     

Splenic artery ligature associated with endoscopic banding for schistosomal portal hypertension

AIM:To propose a less invasive surgical treatment for schistosomal portal hypertension.METHODS:Ten consecutive patients with hepatosplenic schistosomiasis and portal hypertension with a history of upper gastrointestinal hemorrhage from esophageal varices rupture were evaluated in this study.Patients were subjected to a small supraumbilical laparotomy with the ligature of the splenic artery and left gastric vein.During the procedure,direct portal vein pressure before and after the ligatures was measured.Upper gastrointestinal endoscopy was performed at the 30th postoperative day,when esophageal varices diameter were measured and band ligature performed.During follow-up,other endoscopic procedures were performed according to endoscopy findings.RESULTS:There was no intra-operative mortality and all patients had confirmed histologic diagnoses ofschistosomal portal hypertension.During the immediate postoperative period,two of the ten patients had complications,one characterized by a splenic infarction,and the other by an incision hematoma.Mean hospitalization time was 4.1 d(range:2-7 d).Pre-and post-operative liver function tests did not show any significant changes.During endoscopy thirty days after surgery,a decrease in variceal diameters was observed in seven patients.During the follow-up period(57-72mo),endoscopic therapy was performed and seven patients had their varices eradicated.Considering the late postoperative evaluation,nine patients had a decrease in variceal diameters.A mean of 3.9 endoscopic banding sessions were performed per patient.Two patients presented bleeding recurrence at the late postoperative period,which was controlled with endoscopic banding in one patient due to variceal rupture and presented as secondary to congestive gastropathy in the other patient.Both bleeding episodes were of minor degree with no hemodynamic consequences or need for blood transfusion.CONCLUSION:Ligature of the splenic artery and left gastric vein with supraumbilical laparotomy is a promising and less invasive method for treating presinusoidal schistosomiasis portal hypertension.     

ENDOSCOPIC AND CLINICAL STUDY ON HEMORRHAGIC GASTRITIS IN PATIENTS WITH LIVER CIRRHOSIS

Abstract: During a 5-year period from 1984 through 1988, an emergency endoscopy was performed for an upper digestive tract hemorrhage in 283 consecutive patients with 290 lesions. Of these, 54 patients were diagnosed as having hemorrhagic gastritis on the basis of the endoscopic findings and were employed as the subjects of the present study. They were classified on the basis of the presence/absence of liver cirrhosis into two groups, i. e. the cirrhosis group (C-group) and non-cirrhosis group (NC-group), and the two groups were comparatively studied. The incidence of hemorrhagic gastritis in hemorrhagic sources of the upper digestive tract was higher in the C-group than in the NC-group, and it was seen in the gastric body most frequently. In addition, no clear causes for hemorrhagic gastritis could be identified in many of the cases in the C-group. These clinical findings were thought to indicate that, in patients with liver cirrhosis, the gastric mucosa itself, especially of the gastric body, is in an impending state of mucosal hemorrhage. A hemorrhage was the major cause of death in the C-group. In patients with liver cirrhosis, the incidence of hemorrhagic gastritis had no correlation with the grade of esophageal varices, but was high in patients with severe liver cirrhosis. Thus, patients with severe liver cirrhosis were considered to be a high risk group of hemorrhagic gastritis.     

经皮穿脾食管胃底静脉栓塞术治疗血吸虫病上消化道出血

目的探讨经皮穿脾食管胃底静脉栓塞术(PTSVE)在治疗血吸虫病肝硬化上消化道出血中的应用价值。方法以血吸虫病肝硬化门脉高压合并食管胃底静脉曲张破裂出血患者16例(均为食管静脉套扎及硬化治疗术后再次出血患者)为研究对象,其中男12例,女4例。所有病例在X线透视引导下,实施PTSVE术。术后观察手术成功率、并发症发生率,术后1月复查CT,比较患者治疗前后静脉曲张程度。结果 14例(87.50%)患者PTSVE术取得成功,均获有效止血;2例(12.50%)失败;1例术后1周出现腹腔出血。术后1月复查CT,经评估显示患者食道静脉(P0.001)、食道旁静脉(P0.001)和胃底静脉(P0.001)曲张程度均较治疗前明显降低。结论 PTSVE治疗血吸虫病上消化道出血是安全有效的方法,该方法特别适合肝硬化严重,肝裂明显增宽,门静脉主干甚至分支裸露者。     

Predicting portal hypertension and variceal bleeding using non-invasive measurements of metabolic variables

Background & aim. This study assessed the involvement of metabolic factors (anthropometric indices, insulin resistance (IR) and adipocytokines) in the prediction of portal hypertension, esophageal varices and risk of variceal bleeding in cirrhotic patients.Material and methods. Two prospective and retrospective cohorts of cirrhotic patients were selected (n = 357). The first prospective cohort (n = 280) enrolled consecutively in three centers, underwent upper gastrointestinal endoscopy, seeking evidence of esophageal varices. Clinical, anthropometric, liver function tests, ultrasonographic, and metabolic features were recorded at the time of endoscopy, patients were followed-up every 6 months until death, liver transplantation or variceal bleeding. The second retrospective cohort (n = 48 patients) had measurements of the hepatic venous pressure gradient (HVPG). Statistical analyses of the data were with the SPSS package.Results. The presence of esophageal varices was independently associated with lower platelet count, raised HOMA index and adiponectin levels. This relationship extended to subset analysis in patients with Child A cirrhosis. HOMA index and adiponectin levels significantly correlated with HVPG. Beside Child-Pugh class, variceal size and glucagonemia, HOMA index but not adiponectin and leptin plasma levels were associated with higher risk of variceal bleeding.Conclusion. In patients with cirrhosis, HOMA score correlates with HVPG and independently predict clinical outcomes. Three simple markers i.e. platelet count, IR assessed by HOMA-IR and adiponectin significantly predict the presence of esophageal varices in cirrhotic patients.     

Endoscopic variceal ligation of patients with liver cirrhosis and cirrhosis accompanied by hepatocellular carcinoma

Background: Rupture of esophageal varices with severe gastrointestinal hemorrhage is one of the most serious complications of liver cirrhosis (LC) and hepatocellular carcinoma (HCC) complicating LC. The present study looks at the success of hemostasis in LC and LC accompanied by HCC, the success of breaking the varices cluster and the rate of rebleeding in patients of LC subject to emergency ligation and prophylactic ligation. Methods: Seventy‐five patients were divided into three groups. Group 1: 30 patients with LC accompanied by HCC with digestive bleeding; group 2: 30 patients with LC with digestive bleeding; and group 3: 15 patients with LC with high risk of digestive bleeding from esophageal varices (with no medical history of digestive bleeding). Success of hemostasis 72 h after endoscopic variceal ligation (EVL) was that patients did not vomit blood nor produce black feces. The effectiveness of EVL for iradication of the variceal cluster was classified into three levels: good, fairly good and poor. Results: The hemostasis success in group 1 (LC accompanied by HCC) and group 2 (LC with digestive bleeding due to esophageal varices) was 73.3% and 93.4%, respectively. The success of breaking the varix cluster in group 2 (LC) and group 3 (LC with high risk of digestive bleeding and treated by prophylactic ligation) was 73.3% and 80%, respectively. The rate of rebleeding in group 2 and group 3 after 1 year was 20% and 13.3%, respectively. Conclusion: Endoscopic variceal ligation is a good technique for variceal hemostasis and eradication of the esophageal varices cluster.     

Gastric antral vascular ectasia successfully treated by endoscopic electrocoagulation

We report two cirrhotic patients with gastric antral vascular ectasia (GAVE) in whom chronic blood loss presented a major problem. Case 1, a 69-year-old man, had alcoholic liver cirrhosis, and case 2, a 75-year-old woman, had liver cirrhosis associated with hepatitis C virus. The patients required repeated blood transfusions but still exhibited persistent anemia. On upper gastrointestinal endoscopy, both patients showed esophageal varices without stigmata of bleeding or red color signs and presented with a characteristic antral appearance so distinctive as to be diagnostic; diffuse erythemas consisting of ectatic and tortuous capillaries throughout the antrum. Endoscopic electrocoagulation treatment with a monopolar probe was effective for controlling blood loss from GAVE. The patients tolerated the procedure well and there were no resultant complications. Several sessions of the treatment resulted in eradication of almost all the vascular lesions, negative fecal occult blood test results, and marked alleviation of their anemia without further treatment. Endoscopic electrocoagulation is suggested to be a safe, non-invasive, and effective treatment for blood loss from GAVE, especially in patients with liver cirrhosis in whom surgery carries an increased risk. (Received Sept. 2, 1997; accepted Dec. 19, 1997)     

Natural history of portal hypertension in patients with cirrhosis

All patients with cirrhosis will eventually develop portal hypertension and esophagogastric varices. Bleeding from ruptured esophagogastric varices is the most severe complication of cirrhosis and is the cause of death in about one third of patients. The rate of development and growth of esophageal varices is poorly defined but in general seem to be related to the degree of liver dysfunction. Once varices have formed, they tend to increase in size and eventually to bleed. In unselected patients, the incidence of variceal bleeding is about 20% to 30% at 2 years. Variceal size is the single most important predictor of a first variceal bleeding episode. Several prognostic indexes based on endoscopic and clinical parameters have been developed to predict the risk of bleeding; however, their degree of accuracy is unsatisfactory. Death caused by uncontrolled bleeding occurs in about 6% to 8% of patients; the 6-week mortality rate after a variceal hemorrhage is 25% to 30%. There are no good prognostic indicators of death caused by uncontrolled bleeding or death within 6 weeks. Untreated patients surviving a variceal hemorrhage have a 1- to 2-year risk of rebleeding of about 60% and a risk of death of about 40% to 50%. The risk of bleeding is greatest in the first days after a bleeding episode and slowly declines thereafter. All patients surviving a variceal hemorrhage must be treated to prevent rebleeding. Varices can also be found in the stomach of cirrhotic patients, alone or in association with esophageal varices. Gastric varices bleed less frequently but more severely than esophageal varices. Portal hypertensive gastropathy is a common feature of cirrhosis, and its prevalence parallels the severity of portal hypertension and liver dysfunction. Portal hypertensive gastropathy can progress from mild to severe and vice-versa or even disappear completely. Acute bleeding from portal hypertensive gastropathy seems to be relatively uncommon, and less severe than bleeding from varices.     

胃冠状、胃短静脉栓塞术对胃底静脉曲张出血疗效评价

目的探讨胃冠状静脉、胃短静脉栓塞术对胃底静脉曲张出血治疗的价值。方法32例肝硬化并食管胃底静脉曲张出血经内镜下套扎、硬化治疗后仍有出血的患者，经皮经肝穿刺行胃冠状静脉、胃短静脉栓塞治疗。栓塞剂主要为无水乙醇、钢圈和明胶海绵。均行1次栓塞治疗，并经3～11个月随访，胃镜复查。结果29例复查胃镜，其中21例(72．4％)胃底曲张静脉完全消失，8例(27．6％)胃底曲张静脉明显减轻，无红色征及糜烂。随访期内有1例(3．1％)因门脉高压性胃炎致黏膜糜烂出血。未发现明显并发症。结论经皮经肝穿刺行胃冠状静脉、胃短静脉栓塞治疗具有消除胃底静脉曲张，并可预防出血的作用。     

肝硬变上消化道大出血病因的内镜诊断

肝硬变上消化道大出血患者６２例，出血后６小时～１周内行胃镜检查及硬化剂治疗。检查证实无食管胃底静脉曲张２例；胃及十二指肠球部明显糜烂１４例（２２．６％），胃和十二指肠球部溃疡６例（９．７％）。９例（１４．５％）为非静脉曲张性出血，７例（１１．３％）为双因素性出血，表明将肝硬变上消化道大出血一概推断为食管静脉曲张破裂出血是片面的。作者强调早期内镜检查和治疗的重要性。     

Selective splenorenal shunt and post-transfusional hepatitis. Short and medium-term follow-up

Eighteen patients with protal hypertension were studied. Portal hypertension was due to schistosomiasis (N = 9), cirrhosis (N = 7) and congenital hepatic fibrosis (N = 2) diagnosed by surgical biopsy during the decompressive surgery (selective splenorenal shunt). All the patients have had at least one episode of digestive hemorrhage due to rupture of esophageal varices and received blood transfusion before or during surgery. The incidence of post-transfusion hepatitis was 44% (eight cases). The short and medium-term follow-up was good regardless the etiology of portal hypertension. The authors attributed these results mainly to good hepatic function at the time of surgery, younger patient population and good surgical technical conditions.