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Objective: The authors report a 15-year experience with injection sclerotherapy in the management of adult and teenage patients with esophageal varices due to extrahepatic portal venous obstruction (EHPVO)., Summary Background Data: Extrahepatic portal venous obstruction is an uncommon cause of esophageal varices and is associated with normal liver function. Effective control of variceal bleeding is the major factor influencing survival. The results of surgery have been unsatisfactory, and therefore, more conservative management policies have been adopted., Methods: Fifty-five patients with proven EHPVO underwent repeated injection sclerotherapy via either a modified rigid esophagoscope under general anaesthesia or a fiber-optic endoscope under light sedation, using ethanolamine oleate as the sclerosant., Results: Esophageal varices were eradicated in 44 patients after a median number 6 injections (range 1-17) over a mean of 12.5 months (range 1-48). The mean follow-up was 6.8 years (range 1.1-14.6 years). Eleven patients were admitted on eighteen occasions with bleeding from esophageal varices before eradication and there were seven bleeding episodes in six patients from recurrent varices after initial eradication. Complications related to sclerotherapy included injection site leak (6), stenosis (11) and mucosal ulceration (32) during 362 injection sclerotherapy episodes. Four patients died during the study period., Conclusions: Injection scelotherapy is the treatment of choice in most patients with EHPVO.

This report describes the long-term results of one-stage total gastrectomy and distal two-thirds esophagectomy, with reconstruction by esophagojejunostomy (16 Roux-en-Y; 2 interposition), in 18 adult patients with recurrent variceal hemorrhage due to unshuntable extrahepatic portal hypertension (EHPH) from occlusion of all major tributaries of the portal venous system. The etiology of portal venous occlusion was unknown in 11 patients, abdominal trauma in 3, peritonitis in 3, and thrombotic coagulopathy in 1. Almost half of the patients had their first episode of bleeding in childhood, and 83% experienced bleeding before 40 years of age. The severity of the problem was reflected by frequent previous bleeding episodes (mean: 12.8, range: 4 to 21), a large cumulative requirement for blood transfusions (mean: 129 units, range: 28 to 247 units), repeated, costly hospital admissions (mean: 15, range: 4 to 24), and numerous previous unsuccessful operations (mean: 4.4, range: 1 to 14). Blood transfusions transmitted serum hepatitis to three patients and AIDS to one, for an incidence of 22%. Bleeding recurred after repetitive endoscopic sclerotherapy in 10 patients and after various operations in 16 (failed portal-systemic shunts in 9, splenectomy in 16, devascularization procedures in 13). All patients had large esophageal and gastric varices on endoscopy, normal liver function, and widespread portal venous occlusion on visceral angiography. Radical esophagogastrectomy was usually a long and arduous operation because of dense adhesions, extensive collateral veins, and a scarred, contracted bowel mesentery due to previous operations. All patients survived the operation and are currently alive. No patient has had recurrent bleeding during 1 to 26 years of follow-up (mean: 13.9 years, 7 or more years in 14 patients). Quality of life has been good. It is concluded that radical esophagogastrectomy is the only effective treatment of unshuntable EHPH and that the operation should be performed promptly when this disease, which is associated with high mortality, high morbidity, and high costs, is diagnosed.

We propose a computerized mathematical model of the natural history of patients with liver cirrhosis in order to investigate the relationships between the various events that characterize the clinical course of the disease. By means of a rigorously probabilistic approach, the stimulation exposes each hypothetical patient to a series of risks of significant clinical events; whether or not these events occur is determined by preestablished probabilities. Analysis of the effects of arbitrary modifications of these theoretical risks provides useful information on the prospective relevance of the clinical events examined. For example, we compared the simulated follow-up of a population of control cirrhotic subjects with follow-ups of patient groups in whom different degrees of reduction of the risk for gastroesophageal bleeding were postulated on the basis of hypothetical primary or secondary prophylaxis. Our data confirm that the size of the investigated population strongly influences the threshold level of the bleeding-risk reduction able to determine a significant improvement in overall survival. In fact, in large populations (a 6 year follow-up of 3000 cirrhotic subjects), the threshold level was 25% (primary risk) and 45% (secondary risk) with respect to control subjects, while in more limited populations (300 subjects) even a 100% risk-reduction does not seem sufficient to bring about significant improvement in overall survival. Our data may help to explain the different results of controlled trials found in the literature; in fact, only the conclusions arrived at through meta-analysis procedures in large populations have been confirmed.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to define the risk factors linked to the rupture of esophageal varices following endoscopic injection sclerotherapy. A total of 197 patients with esophageal varices who had been treated by endoscopic injection sclerotherapy between 1985 and 1991 were observed for post-therapeutic bleeding from esophageal varices. Among 197 patients, 96 had esophageal varices and concomitant hepatocellular carcinoma. Analysis by the multivariate Cox's proportional hazard model disclosed that incomplete eradication of esophageal varices, the presence of hepatocellular carcinoma, and Child-Pugh classes were statistically significant predictors for rupture of esophageal varices after sclerotherapy. We conclude that complete eradication of esophageal varices is essential for sustained effectiveness of endoscopic injection sclerotherapy. The presence of hepatocellular carcinoma and a lack of hepatic functional reserve, as indicated by Child's classification, are also major determinants of post-therapeutic bleeding.

In order to determine the incidence of infection following sclerotherapy and the role of antimicrobial prophylaxis, a prospective randomized control study was performed comparing i.v. imipenem/cilastatin, with an infusion of dextrose-saline as a control group. One hundred patients with bleeding esophageal varices were included. All episodes of infection were documented during admission to the unit. Ninety-seven patients were evaluable. Post-sclerotherapy bacteremia developed in six (5.6%) of 107 sclerotherapy sessions in the control group and one (1.1%) of the 88 sclerotherapy sessions in the imipenem/cilastatin group (P < or = 0.1, NS): six of these seven post-sclerotherapy bacteremias occurred after emergency sclerotherapy. Infection within 7 days of the procedure was documented after 43 (22.1%) of the 195 sclerotherapy sessions, 18 (20.5%) in the imipenem/cilastatin group and 25 (23.4%) in the control group (P = NS). These infections were significantly more common after emergency sclerotherapy, 40 (34.8%) of 115 sessions, than after elective sclerotherapy, three (3.8%) of 80 sessions (P < or = 0.0001). A short prophylactic antibiotic regime does not reduce the risk of early bacteremia or the frequency of infection after sclerotherapy. The higher risk of infection after emergency sclerotherapy may be therefore related more to the gastrointestinal hemorrhage and its associated effects than to sclerotherapy.

Endoscopic variceal ligation was performed in 20 patients with portal hypertension of varied etiology. Variceal obliteration was achieved in 18 patients (90%) while recurrence of bleeding occurred in two patients (10%). The average number of bands required was four per patient and average number of sessions required for variceal obliteration was two. We found the procedure to be cheap, safe and effective in achieving early variceal obliteration.

Background: Small esophageal varices are difficult to inject intravariceally and complete eradication of varices may not be therapeutically necessary., Methods: A prospective study designed to compare the use of different end points of sclerotherapy ie (i) total eradication (grade 0) (ii) grade I varices or (iii) grade II white (IIw) varices, by stopping variceal injection when one of these was reached. The patients were followed endoscopically and clinically at 3-4 mo intervals., Outcome Measures: Variceal recurrence and rebleeding rates., Results: Of 266 patients with portal hypertension (147 cirrhosis, 51 non-cirrhotic portal fibrosis, 68 extra-hepatic portal venous obstruction), 232 (87.2%) reached one of the three end points--six to grade 0, 96 to grade I and 130 to grade IIw. Among 212 patients followed up for a mean post-sclerotherapy period of 12.2 mo (range 3-48 mo), variceal recurrence rates, time intervals to recurrence and rebleed rates were comparable in patients with endpoints of grade I and grade II (white) varices (28.5% vs 38.9%, 10.8 mo vs 9.2 mo, and 7.7% vs 7.8%, respectively; all p = ns). Overall, 51 patients had interval bleed before reaching the end point--50 (98%) of them bled from grade III and IV varices while only one patient (2%) bled with grade IIw varices., Conclusion: Grade I or grade IIw varices should be acceptable as the end points for endoscopic sclerotherapy of esophageal varices.

The contribution of the intrahepatic portal branch to the gastroesophageal varices is rare. This anomalous pathway (a large left intrahepatic portal branch) was proved by portographic study and by imaging techniques in a 54-year-old man with cirrhosis. The overall prevalence of this type of collateral in the literature is only 1.9% in 908 patients with portal hypertension. In addition, all are via the left portal venous branch. It may be speculated that the mechanism of this variation is due to dilatation of the rest of the intrahepatic portal system via a small anastomosis due to portal hypertension.

In a long-term survival study, we compared the prognostic significance of the hepatic venous pressure gradient and of the aminopyrine breath test (ABT) in 99 alcoholic cirrhotic patients. Thirty patients survived and had a complete follow-up for at least 4 yr. Mean hepatic venous pressure gradient was 19.1 +/- 5.8 mm Hg (range 8-35 mm Hg). Variceal rupture occurred only when the gradient was > or = 12 mm Hg. Variceal bleeding was observed exclusively in patients with large varices. Survival was not influenced by the level of gradient. We used the ABT to classify patients into three groups (group I, ABT > or = 2%; group II, 1% < or = ABT < 2%; and group III, ABT < 1%). Survival was significantly higher in group I than in group II (p < 0.05) or III (p < 0.01), indicating a better prognosis at a residual functional hepatic cellular mass of about 50% of the lower limit of normal value.

This study reports the final results of a randomized multicenter trial on prophylactic endoscopic sclerotherapy of large esophageal varices in patients with liver cirrhosis. Forty-one patients received prophylactic treatment and 41 patients were in the control group. A first analysis 3 years after beginning the study revealed no significant difference in the distribution of the bleeding free intervals between both groups, but indicated a tendency towards longer survival of patients with prophylactic sclerotherapy. The follow-up of patients was continued for an additional 3 years. After this time, 53.7% of patients in the sclerotherapy group and 39.1% of patients in the control group were still alive. During the study period of 6 years, variceal bleeding was observed in 31.7% of patients in the sclerotherapy group and in 36.6% of patients in the control group. Neither survival nor incidence of bleeding were statistically different between the two groups. The etiology of cirrhosis did not influence the survival.

In order to identify the predictive factors of hospital mortality in cirrhotics with spontaneous bacterial peritonitis (SBP), we studied 64 patients who fulfilled the accepted diagnostic criteria. All cases were treated with cefotaxime up to 2 days after the infection was considered cured (7.7 +/- 2.9 days). Eleven patients (17%) died while in hospital, six of them before SBP was cured. After uni- and multivariate analyses, only seven routine clinical, biological, and bacteriological variables studied were independently associated with hospital mortality. These were: the presence of upper gastrointestinal bleeding at admission (beta = 2.01), the absence of abdominal pain as presenting symptom (beta = -1.29), the polymorphonuclear count (%) in the ascites (beta = 0.48), prothrombin rate (beta = -0.22), and serum Na (beta = -0.64), creatinine (beta = 0.50), and cholesterol (beta = -0.68). When the equation obtained was computed in a randomly selected sample of the patients studied, it correctly predicted the outcome in 92.3% of the cases. We conclude that short-term outcome of SBP patients depends on the existence of recent gastrointestinal bleeding, the severity of SBP, and the degree of liver and renal failure. The prognostic value of this model needs prospective validation in a new series of patients.

Fibreoptic endoscopy was performed on 5,086 consecutive patients with upper gastrointestinal tract disease (UGITD) symptoms, at two endoscopy centres in Khartoum over five years. Oesophageal disease was diagnosed in 559 patients (11%) comprising (20.5%) of all the positive findings. In 46% of all the endoscopies no abnormality was detected. The commonest oesophageal disease was varices occurring in 186 patients (3.7%) of the 5,086 endoscopies with a mean age of 33.5 +/- 12 and a male/female ratio of 3.4:1. Hiatus hernia occurred in 124 patients (2.4%) with a male/female ratio of 1.6:1, oesophagitis in 115 patients (2.3%) with a male/female ratio of 2:1. Carcinoma of the oesophagus was diagnosed in 108 patients (2.1%), with a mean age of 56 +/- 14 years and a male/female ratio of 1.4:1. Achalasia of the oesophagus occurred in 20 patients (0.4%), Mallory Weiss syndrome in 4 patients (0.08%) and benign strictures in 2 patients (0.04%).

The influence of alcohol on portal vein haemodynamics was assessed prospectively in 30 patients (20 men, 10 women; mean age 54.3 [34-70] years) with nutritional-toxic cirrhosis of the liver (Child-Pugh stages A-C) and portal vein hypertension. During the period of observation hepatic vein occlusion pressure as an indirect measure of portal vein pressure was repeatedly determined. In addition, the size of oesophageal varices and the Child-Pugh stage were monitored. After complete alcohol abstinence of one year, portal vein pressure fell from 23.11 to 12.43 mm Hg (-46%, P < 0.001), the Child-Pugh score from 8.08 to 7.2 (-10.9%, not significant), and the size of oesophageal varices was reduced from grade 1.33 to grade 0.79 (-40%, P < 0.02). On resuming alcohol abuse, portal vein pressure increased by an average of 10 mm Hg (+60%, P < 0.001) to its previous level of 25 mm Hg. The portal vein pressure has thus proved to be a sensitive gauge of alcohol abstinence or abuse. Lasting, absolute alcohol abstinence is essential in nutritional-toxic liver cirrhosis.

Bleeding gastroesophageal varices is associated with a high morbidity and mortality. Forty-four cases of bleeding gastroesophageal varices were treated at the Department of Surgery, Universiti Kebangsaan Malaysia, General Hospital, Kuala Lumpur over four and a half years. Thirty-two of them had liver cirrhosis. Hepatitis B infection was noted in 13 and alcoholic abuse was present in 14 patients. Five patients had associated hepatoma. Thirty-four percent had gastric fundal varices and a third of these bled from them. A total of 179 endoscopic injection sclerotherapy sessions were performed averaging 4 per person. Rebleeding rate was 4% and mortality was high (50%) in these cases. It was concluded that injection sclerotherapy is a safe and effective means of controlling bleeding oesophageal varices. Operative surgery was employed in those who rebled after injection and would be considered in those in Child's A.

To determine the prevalence and natural history of gastric varices, we prospectively studied 568 patients (393 bleeders and 175 nonbleeders) with portal hypertension (cirrhosis in 301 patients, noncirrhotic portal fibrosis in 115 patients, extrahepatic portal vein obstruction in 117 patients and hepatic venous outflow obstruction in 35 patients). Primary (present at initial examination) gastric varices were seen in 114 (20%) patients; more were present in bleeders than in non-bleeders (27% vs. 4%, respectively; p < 0.001). Secondary (occurring after obliteration of esophageal varices) gastric varices developed in 33 (9%) patients during follow-up of 24.6 +/- 5.3 mo. Gastric varices (compared with esophageal varices) bled in significantly fewer patients (25% vs. 64%, respectively). Gastric varices had a lower bleeding risk factor than did esophageal varices (2.0 +/- 0.5 vs. 4.3 +/- 0.4, respectively) but bled more severely (4.8 +/- 0.6 vs. 2.9 +/- 0.3 transfusion units per patient, respectively). Once a varix bled, mortality was more likely (45%) in gastric varix patients. Gastric varices were classified as gastroesophageal or isolated gastric varices. Type 1 gastroesophageal varices (lesser curve varices) were the most common (75%). After obliteration of esophageal varices, type 1 gastroesophageal varices disappeared in 59% of patients and persisted in the remainder; bleeding from persistent gastroesophageal varices was more common than it was from gastroesophageal varices that were obliterated (28% vs. 2%, respectively; p < 0.001). Type 2 gastroesophageal varices, which extend to greater curvature, bled often (55%) and were associated with high mortality. Type 1 isolated gastric varices patients had only fundal varices, with a high (78%) incidence of bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

The authors have performed 28 sessions of endoscopic sclerotherapy of dilated esophagus veins in children. The 70% ethyl alcohol was used. Six sessions were carried out in patients with gastroesophageal hemorrhage. In 22 patients the sclerotherapy was carried on according to plan. The fiber gastroscope with a standard injector was used. A conclusion is made of expediency of using endoscopic sclerotherapy in complex treatment of portal hypertension in children.

Hemorrhage from esophageal varices in cirrhotics is a frequent event with high mortality in spite of therapy. Preventive sclerotherapy seems to be beneficial only if the patient's bleeding risk is higher than 40 to 50% a year. A series of 320 patients with esophageal varices without previous bleeding was studied prospectively; the varices were classified according to three widely used endoscopic classifications. During follow-up (6 to 36 months, average 14 months), hemorrhage occurred in 49 patients (15.3%) of whom 30 (61.2%) bled from varices (8.2 and 11.0% at 12 and 24 months, respectively). At the same time intervals, mortality of the entire population studied was 18.0 and 23.8%, respectively, of which one third was directly due to hemorrhage. With all three classifications, the higher the degree of bleeding risk, the greater the actual percentage of hemorrhages recorded; however, it never reached 40% a year. In predicting the bleeding event, Dagradi's classification proved more sensitive than JRSPH or NIEC, but the latter classifications were more specific and assessed a higher predictive value for a positive test. Endoscopic observation probably needs integration with other methods if a reliable bleeding prediction is to be made.

Background: Controversies exist on the prevalence of peptic ulcer and on the relationship between the presence of portal hypertension associated lesions in the upper gastrointestinal tract and the histological and functional stages of primary biliary cirrhosis, Aim: To evaluate the prevalence of peptic ulcer and endoscopic signs of portal hypertension in subjects with primary biliary cirrhosis., Patients and Methods: A retrospective study based on upper gastrointestinal endoscopies in 36 patients with primary biliary cirrhosis and 45 subjects with chronic active hepatitis., Setting: Gastroenterology Center, Hospital Clínico, University of Chile, Santiago., Main Results: No differences were demonstrated between the two groups for the prevalence of peptic ulcer (11% in primary biliary cirrhosis vs 13% in chronic active hepatitis). Esophageal varices were found in 5 of 16 patients (31%) in prefibrotic stages of primary biliary cirrhosis compared with 10 of 20 (50%) in whom fibrosis or cirrhosis were noted; NS. Endoscopic signs suggesting hypertensive gastropathy were present in 2 patients with early primary biliary cirrhosis (13%) and in 5 (25%) in advanced stages., Conclusions: Peptic ulcer is not more prevalent in patients with primary biliary cirrhosis than in those suffering from chronic active hepatitis. Esophageal varices and endoscopic stigmata of portal hypertension induced changes in gastric mucosa can be observed in early stages of primary biliary cirrhosis.

The sonographic parameters in portal hypertension (PHT) were examined in a consecutive population of 118 patients who had PHT diagnosed using specific endoscopic, sonographic and Doppler signs. A patent or enlarged paraumbilical vein was found in 85.6% of patients overall and 82.5% of patients with varices indicating a relatively high sensitivity. A portal vein diameter greater than or equal to 13mm was found in only 41.1% and greater than or equal to 15mm in only 20% of patients. A thrombosed portal vein and reversed portal vein flow were present in 3.4% and 5.3% of patients respectively. These signs have only been reported in the context of PHT and are felt to be specific for PHT, but both have a very low sensitivity. Portal vein velocities were highly variable suggesting that this is not a useful predictor of PHT. Splenomegaly was found in only 53.5% of patients demonstrating its poor sensitivity as a sign of PHT. Varices were found in 73.3% of patients overall, and in 100% of patients with a patent or enlarged paraumbilical vein combined with ascites. No other statistically significant correlation between varices and sonographic findings was demonstrated. We conclude that the presence of a patent or enlarged paraumbilical vein is a practical, useful and sensitive ultrasound sign to look for in the diagnosis of PHT.

About one third of cirrhotic patients with esophageal varices eventually bleed from ruptured varices. The incidence of rebleeding is extremely high during the first 6 weeks after the initial bleeding but declines gradually thereafter. Later, the rebleeding risk returns to baseline levels, i.e., equals that of patients who have never bled. The size of varices and the presence of red color signs on the variceal wall are recognized by most investigators as important in assessing the risk of variceal hemorrhage. Prognostic indexes such as the NIEC index, which incorporate the endoscopic signs with clinical data such as the Child-Pugh score, have been shown to predict the probability of first variceal hemorrhage of individual patients reliably. Other important parameters are the presence of ascites and, in alcoholic cirrhotics, the lack of abstinence from alcohol. The presence of endoscopic signs of bleeding or of stigmata of recent bleeding, of large varices, or of liver failure at the time of first bleeding are risk factors for early rebleeding. The most important risk factors for late rebleeding are the presence of large varices, overt signs of hepatic decompensation, the development of hepatocellular carcinoma, and lack of alcohol abstinence.

Clinical and anamnestic data, Pugh score, and size of esophageal varices were obtained in 129 cirrhotics. Hepatic vein catheterization was performed to measure hepatic venous pressure gradient (HVPG), indocyanine green (ICG) intrinsic hepatic clearance, and hepatic plasma flow. During a follow-up period of up to 60 months, 44 patients experienced gastrointestinal bleeding and 54 died. Applying Cox regression analysis, ICG intrinsic hepatic clearance, Pugh score, previous variceal bleeding, and HVPG were the only significant prognostic determinants of survival. In addition, Cox's regression analysis showed that HVPG, Pugh score, size of varices, and previous variceal bleeding all contained significant prognostic information regarding risk of gastrointestinal bleeding. The models were validated using a split-sample technique, and prognostic indexes for death and gastrointestinal bleeding were calculated. The prognostic index predicting death had significantly improved prognostic accuracy over a prognostic index calculated excluding the data obtained from hepatic vein catheterization (P less than 0.05). In conclusion, prognostic accuracy in cirrhosis with portal hypertension is significantly improved by information obtained from hepatic vein catheterization.

There are different opinions in respect to the main sources in upper gastrointestinal bleeding in hepatic cirrhosis. Some authors claim that ruptured esophageal varices are the cause of most of the hemorrhages. Recently, characteristic lesions have been showed in the gastric mucosa in portal hypertension (congestive gastropathy), and many believe that they are frequently the origin of the bleeding. We reviewed the records of 195 episodes of upper gastrointestinal bleeding in cirrhosis, with endoscopy performed within 12 hours of entry, and report here the endoscopic findings and the bleeding sites. We also investigated the relation between the etiology and functional class of the hepatic disease and the bleeding source. We observed variceal hemorrhage in 52.2% of cases; by gastroduodenal mucosal lesions in 13.8%; by gastric and duodenal ulcers in 13.8%; undetermined origin in 14.8% (due to coexistence of two or more lesions, without active bleeding). We found no differences between alcoholic and nonalcoholic cirrhotics in the bleeding sources. Furthermore, the bleeding sites were not different either in child A, B and C patients. In contrast, in major hemorrhages, esophageal varices were more frequently the origin (73.5%) than in minor ones (40.4%) (p < 0.002). The mortality was significantly higher in CHild C group (25%), than in groups B (14.3%) and A (2.3%) (p < 0.05 and p < 0.002, respectively). We recommend to carry out early endoscopy in every cirrhotic patient suffering from gastrointestinal bleeding, by skilled performers who are able to recognize the gastric red signs, before making a decision about potentially dangerous therapeutic measures, such as surgery, balloon tamponade, etc.

In 27 variceal patients completely treated by ethanolamine oleate and polidocanol and followed for more than one year, the recurrence of varices was studied by measuring portal vein pressure and oxygen tension in the portal vein and peripheral arteries and veins before and after EIS. Frequent recurrence was observed in patients with increased PVP after EIS and lower or inverse PVO2-VO2 tension after EIS. The recurrence of varices after EIS may thus possibly be predicted based on portal vein pressure and PVO2-VO2 tension differences.

In a field study of two villages in the Gezira, an area of the Sudan endemic for Schistosoma mansoni, liver ultrasonography was used to detect subjects with Symmers' hepatic periportal fibrosis, some of whom underwent oesophagoscopy to detect oesophageal varices. The prevalence of oesophageal varices in subjects undergoing oesophagoscopy was 54 per cent and 67 per cent respectively, occurring mainly in males aged about 30 years. The varices were usually asymptomatic. Symptomatic varices (with a positive history of haematemesis) occurred in 4 per cent and 3 per cent respectively of subjects with sonographic evidence of liver periportal fibrosis. By detecting oesophageal varices in an asymptomatic phase, hepatic ultrasonography and fibreoptic oesophagoscopy may elucidate the natural history of the varices and their response to periodic anti-schistosomal chemotherapy.

Controlled trials of sclerotherapy for the prevention of the first variceal hemorrhage in cirrhotics have given conflicting results. In the present study, 106 cirrhotics were randomized to sclerotherapy (55 patients) or control group (51 patients). Admission criteria were no history of previous variceal bleeding and the presence of high-risk varices, i.e., a variceal score less than or equal to 0 according to Beppu et al. Sclerotherapy sessions were performed at time zero, 7 days, 30 days, and then monthly until eradication. Follow-up endoscopies were performed at 6-month intervals thereafter. Control patients underwent repeat endoscopy at 6-month intervals. Bleeding episodes were treated by sclerotherapy in both groups, whenever possible. Mean follow-up was 24 months. Analysis of the results was performed by the intention-to-treat method. Variceal bleeding occurred in 19 sclerotherapy patients (34.5%) and in 17 controls (35.4%, P = NS). Overall mortality was 34.5% in sclerotherapy patients and 50% in controls (P = NS). Seven of the 19 sclerotherapy patients (36.8%) and 11 of the 17 controls (64.7%) who bled died of hemorrhage (P less than 0.05, log-linear model). It is concluded that prophylactic sclerotherapy does not reduce the incidence of first variceal bleeding in cirrhotics. However, there seems to be a trend toward a lower bleeding-related mortality in sclerotherapy patients than in controls.

The aim of this study was to compare the efficacy of: (i) somatostatin infusion, (ii) balloon tamponade with the Sengstaken-Blakemore tube and (iii) the combination of both methods, in the management of acute variceal haemorrhage. Ninety-two consecutive patients with liver cirrhosis who proved to have active variceal bleeding on emergency endoscopy were studied. Thirty-one patients were randomly assigned to an intravenous infusion of 250 micrograms/h of somatostatin (Group I), 30 to the Sengstaken-Blakemore tube (Group II) and 31 to the combination of both methods (Group III). Somatostatin was administered for 24 h, while the gastric and esophageal balloons remained inflated for 48 and 24 h, respectively, then deflated. Patients were under observation for a further 24-h period after withdrawal of treatment. If bleeding recurred, the same treatment was repeated in each group. Following treatment the bleeding was controlled initially in 22 patients (71%) in Group I, in 24 (80%) in Group II and in 25 (80.6%) in Group III. In Group II a significantly (p less than 0.05) higher proportion of patients (14/24) rebled as compared to Groups I (5/22) and III (6/25). Bleeding was controlled following retreatment in four, ten and five patients of the three respective groups. There were marked differences, in the number of complications noticed with each form of therapy. Only three patients (9.7%) in Group I developed complications (p less than 0.05) as compared to ten (33%) in Group II and ten (32%) in Group III. Hospital mortality in all three treatment groups was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Because several studies have suggested that beta blockers are effective in the prophylaxis of first variceal bleeding in cirrhosis, screening for oesophageal varices might be appropriate. We prospectively studied 84 cirrhotic patients without obvious evidence of large oesophageal varices and previous bleeding during a mean follow up of 16 months. At entry to the study 41 patients had no oesophageal varices and in 43 these were grade 1. The subsequent percentages of patients without large oesophageal varices were 74% at one year and 52% at two years. Univariate analysis showed that a longer duration of cirrhosis (p less than 0.05) and grade 1 oesophageal varices at entry (p less than 0.001) were predictive factors for the occurrence of large oesophageal varices, whereas, multivariate analysis showed that the initial size of the oesophageal varices (p less than 0.001), a high initial Child-Pugh score, and a smaller improvement in Child-Pugh score during the study were independent risk factors. Among patients with grades 0 and 1 oesophageal varices at the start of the study the proportions with large oesophageal varices at two years were 31% and 70% respectively. We have calculated that, accepting a maximum risk of first bleeding of 10% without prophylactic treatment, a patient without oesophageal varices should be screened endoscopically every other year, while a patient with grade 1 disease should benefit from one annual upper gastrointestinal endoscopy.

A significant increase in associated liver disease has been confirmed in duodenal ulcer cases, with various studies showing a 5-14% incidence of the ulcers in patients with cirrhosis. The present study was undertaken to discover the incidence of peptic ulcer in such patients, to investigate a series of epidemiological data in a group cirrhosis patients with ulcers and to establish an adequate protocol for the treatment of the ulcer in both its acute and post-healing stage. The incidence of peptic ulcers in cirrhosis patients was calculated in a retrospective study of 377 hospitalised patients in two consecutive years (1986, 1987). The epidemiological data are based on 99 of them. Acute ulcer treatment was given in 31, while 41 with healed ulcers were put on maintenance therapy. Ulcers were found in 16-17% of the cirrhosis patients; the cirrhosis was caused by alcohol abuse in 61.53% and was post-necrotic in 21.79%. Endoscopy revealed duodenal ulcers in 60.6%, gastric ulcers in 32.3%. In this sample, 39.39% were non-smokers, while 23.23% smoked over 20 cigarettes a day.

Nowadays, gastroesophageal endoscopic features of portal hypertension are the recognized predictive factors for bleeding and consequently allow the selection of patients for prophylactic therapies. The aim of this prospective study was to investigate the interobserver agreement, the interassociations between these features, and the relationship between these signs and the degree of hepatic dysfunction. In 100 consecutive cirrhotic patients (84% with alcoholism) without history of digestive bleeding, gastroesophageal endoscopic examination was performed and recorded using a videoendoscope. Four independent observers evaluated the following endoscopic features: the size, extent, color, and red signs of esophageal varices, the mosaic pattern, congestive gastropathy, fundic varices, and associated lesions of the stomach. Agreement was assessed using kappa statistics (kappa) and a quantitative score. The size of esophageal varices was significantly associated with their extent and the presence of red signs, whereas no relation was found either between gastropathy or mosaic pattern and fundic varices, or between esophageal and gastric features. Agreement between observers was good for the size of esophageal varices (kappa = 0.59), the presence of red signs (kappa = 0.60), and of gastric-associated lesions (kappa = 0.68) and gastropathy (kappa = 0.50), while it was poor for the extent (kappa = 0.37) and the color (kappa = 0.28) of esophageal varices as well as for the mosaic pattern (kappa = 0.38). The Child-Pugh score significantly increased along with the presence or the size of esophageal varices as well as with the presence of red signs; no relationship could be shown between this score and the presence of gastric features. We conclude that (1) interobserver agreement was good for the main endoscopic features, especially for the size and the red signs of esophageal varices; (2) esophageal patterns were significantly associated between themselves and related to hepatic dysfunction; and (3) gastric patterns were related neither to esophageal features nor to hepatic dysfunction and were not associated between themselves.

We analyzed the endoscopic findings in 788 patients with esophageal and gastric varices who underwent upper gastrointestinal endoscopy between 1 January 1979 and 31 December 1988. Of these, 154 patients (19.6%) had gastric varices associated in various patterns with esophageal varices. Congestive gastropathy, occurring with esophageal and gastric varices (43.4%), was the most frequent pathology detected in our patients. Esophagitis was present in 15.8% of patients, but did not correlate with variceal bleeding. Endoscopy performed at 1 day to 1 week post-hemorrhage in 313 patients accurately identified the source of bleeding in only 57.2% of patients. This figure increased to 98.2% when we performed the examination within the first 24 h of hemorrhage. In this group varices were the source of hemorrhage in 72.3% of patients while the hemorrhage came from other sources, such as erosive gastritis, duodenal and gastric ulcer in 27.6% of patients.

Up to 80% of patients with liver cirrhosis develop esophageal variceal bleeding which is lethal in up to 30% after the first bleeding episode. Parameters suitable to identify patients being on risk to bleed from their varices are severe liver disease (Child's C), large varices with red color sign and red wall markings and high intra-variceal pressure above 12 mmHg.

Of 245 patients undergoing corrective operations for biliary atresia, jaundice was cleared in 113. In January 1988, 84 of them were living and free of jaundice and the other 19 were alive with jaundice. A vast majority of long-term survivors showed normal growth and development, and were leading normal lives for their respective ages. Portal hypertension, a common late complication, improved spontaneously or after sclerotherapy in jaundice-free patients. Therefore, liver transplantation is not recommended for jaundice-free patients even with esophageal varices. Patients with persistent severe jaundice (serum bilirubin over 10 mg/dL) and those with moderate jaundice (serum bilirubin 5 to 10 mg/dL) and severe esophageal varices require liver transplantation. Patients with moderate jaundice having no or slight varices should be carefully followed. When varices become worse or serum bilirubin rises, liver transplantation is indicated. Patients with mild jaundice (serum bilirubin lower than 5 mg/dL) have a possibility of improvement in their condition before the age of 15 years, and are not recommended for liver transplantation. The high value of the lowest postoperative bilirubin level suggests the necessity of liver transplantation in early childhood. Liver transplantation as the primary treatment for biliary atresia may be indicated only for patients over 120 days of age with an enlarged and hard liver.

Incidentally detected "downhill" varices of the entire esophagus in a 26-year-old man were found to be due to a benign giant lymphoma in the posterior mediastinum. The superior vena cava was not obstructed. Following resection of the tumor the varices disappeared. Substantial blood drainage to the esophageal veins was assumed to be the causal mechanism.

Because of the diagnostic and prognostic value of gastroesophageal endoscopic signs in cirrhosis, we studied their interobserver and intercenter agreement. Fifty cirrhotic patients without previous digestive bleeding were included in this study. The gastroesophageal endoscopic examinations of these patients, recorded on video tape, were independently viewed by 12 observers belonging to different hospitals. Agreement was evaluated by the kappa index (k), the values of which were given with p less than 0.001. Agreement was good for the presence (k = 0.40) or the size (k = 0.51) of esophageal varices as well as for red signs on the mucosa overlying esophageal varices, but it was poor for the color (k = 0.10) or the extent (k = 0.20) of esophageal varices. Agreement was poor for all gastric signs: fundic varices (k = 0.35), red spots (k = 0.28), associated lesions (k = 0.27), mosaic pattern (k = 0.27), gastropathy (k = 0.11). The mean diameter of esophageal varices, evaluated without any scale, varied from 3.5 +/- 1.4 to 7.5 +/- 4.0 mm between the 12 observers (p less than 0.001). Agreement was maximum for the more developed grade of a sign and minimum for the intermediate grade. The value of kappa indexes in this intercenter study was compared to that obtained in a previous study from one institution: interobserver agreement was significantly better within one center than between different centers. In conclusion, intercenter agreement is good for the size of esophageal varices and the presence of red signs, and poor for all the other signs. The millemetric measurement of esophageal varices diameter, without any scale, appears to be unreliable.(ABSTRACT TRUNCATED AT 250 WORDS)

This presentation describes a further survey conducted under the auspices of the OMGE Research Committee: an international survey of over 4000 patients presenting to 205 clinicians in 44 centres in 21 countries. This multinational survey has been the first in this area of medicine to use specifically designed proformata and pre-agreed definitions of terminology, alongside automated data analysis. A total of 4506 patients' data were forwarded from 44 centres, the vast majority (4431; 98.3%) containing acceptable data fro subsequent analysis. The commonest cause of bleeding was peptic ulceration (36.7% of the total group), followed by oesophageal varices (13.3%) and gastric erosions (6.7%). Over 600 cases exhibited dual pathology. As regards outcome, in 1137 patients bleeding failed to settle (25.5%), whilst 409 patients died (9.2% of the total group, and 36.0% of those whose bleeding failed to settle). Detailed computer-aided studies show it is currently impossible to determine the source of bleeding without recourse to high technology such as radiologic or endoscopic intervention. If identification of the source of the bleeding is desirable clinically, then these high-technology investigations must be employed. As regard prognosis, a computer program has enabled categorisation of patients into risk categories as regards further or continued bleeding or death. This program has been tested on 2623 patients with considerable accuracy. In the computer's 'high-risk' category, 60% of patients re-bled, and 32% died. Conversely in the 'very low' risk category, only 4% re-bled, and no patient died. These findings have enabled the construction of a simple prognostic system for use in remote areas.(ABSTRACT TRUNCATED AT 250 WORDS)

This paper analyzes experience with 106 patients treated primarily with DSRS during a ten year period. Operative mortality was 5% of cases. Shunt patency was evaluated by postoperative angiography in 70 patients. A shunt thrombosis and a recanalization of the splenic vein were noted in a patient who had a Britton's operation resulting in a side-to-side shunt. In the other 31 cases, shunt patency was indirectly confirmed by the absence of varices at postoperative or long-term endoscopic examination. At postoperative check, esophageal varices had disappeared in only 19% of patients. However, this rose to 60% at long-term check-up. Ten patients bled from varices in the postoperative period (9%). During the follow-up period, no patient bled from varices, while five patients bled from gastroduodenal lesions (5%). During the postoperative period, 52% of cases had ascites. In the long-term, ascites developed in only 15% of cases and was well controlled by standard medical treatment. Analysis of the actuarial curve showed a 5-year survival rate of 63%. During the follow-up period, 17% of patients experienced at least one episode of acute encephalopathy. Chronic encephalopathy appeared in 14% of cases: ten patients suffered a mild form (10%) and four (4%) a moderate form. No patient had severe chronic encephalopathy. DSRS is effective as treatment of portal hypertension with a low long-term morbidity despite a more troublesome early postoperative period.

Eleven patients with angiographically demonstrated splenic vein thrombosis associated with chronic pancreatitis were followed for an average of 6.5 yr to determine the natural history of this condition. Repeat angiography was performed in five patients. Significant gastric or gastroesophageal varices were noted in six cases. In another patient, peri-colonic varices and spleno-portal collaterals were demonstrated. Two patients bled massively during follow-up; one from gastric varices and one from colonic varices. Another patient, with known gastric varices, intermittent hematochezia and iron deficiency anemia, underwent surgery. All three patients responded well to splenectomy. Since three of the seven patients with splenic vein thrombosis and significant varices eventually required surgical correction, it may be that the long-term risk of gastrointestinal bleeding exceeds the risks of elective splenectomy in these patients.