The influence of endoscopic variceal ligation on the portal pressure gradient in cirrhotics

BACKGROUND/AIMS: After variceal eradication by endoscopic ligation, fundal varices and worsening of portal hypertensive gastropathy can occur. The aim of this study is to verify the impact of the eradication of esophageal varices by endoscopic ligation on the portal pressure gradient, worsening of portal hypertensive gastropathy and development of fundal varices. METHODOLOGY: Twenty-two (15M/7F, mean age: 54.5 years) cirrhotics with previous variceal bleeding were submitted to measurement of hepatic venous pressure gradient before and after variceal eradication by endoscopic ligation. RESULTS: The mean hepatic venous pressure gradient in the first measurement was 14.1 mmHg and after eradication, 13.5 mmHg (p = 0.403). After eradication, 12 patients experienced a reduction in portal pressure and 10, an elevation. Three patients developed fundal varices. Their mean gradient before treatment was 22 mmHg and 18.8 mmHg after therapy (p = 0.368). The gastropathy worsened in 9 patients (mean gradient before therapy of 15.2 mmHg; and 16.1 mmHg after treatment) (p = 0.303). The initial pressure gradient of these patients was not different from the other 13 cases (p = 0.463). CONCLUSIONS: The esophageal variceal eradication by endoscopic band ligation does not alter the hepatic venous pressure gradient. There is no significant variation in the portal pressure of patients in whom there was a worsening of portal hypertensive gastropathy or fundal varices development.     

The effects of endoscopic variceal ligation and propranolol on portal hypertensive gastropathy: a prospective, controlled trial

BACKGROUND: Endoscopic treatment of esophageal varices may accentuate portal hypertensive gastropathy. The impact of the combination of band ligation and propranolol on this condition remains unknown. METHODS: Patients with history of variceal bleeding were randomized to receive band ligation alone (control group, 40 patients) or a combination of band ligation and propranolol (propranolol group, 37 patients). Serial endoscopic evaluation of gastropathy was performed. Gastropathy was classified into 3 grades and scored as 0, 1, or 2. RESULTS: Before endoscopic treatment, 17% of the control group and 22% of the propranolol group had gastropathy (p = 0.78). The occurrence of gastropathy after endoscopic treatment was significantly higher in the control group than in the propranolol group (p = 0.002). Serial endoscopic follow-up revealed that the mean gastropathy score was significantly higher in the control group than in the propranolol group (p < 0.05). In patients with gastropathy the gastropathy score reached a peak at 6 months after endoscopic treatment in both the control and propranolol groups (85% vs. 48%, respectively). After variceal obliteration, accentuation of gastropathy was significant in the control group (p < 0.01) but not in the propranolol group. Gastropathy was less likely to develop in patients who developed gastric varices. Esophageal variceal recurrence was not related to the development of gastropathy after variceal obliteration with banding. Only one patient in the control group bled from gastropathy. CONCLUSION: Band ligation of esophageal varices may accentuate gastropathy, which in this study was partly relieved by propranolol.     

Argon plasma coagulation prevents variceal recurrence after band ligation of esophageal varices: preliminary results of a prospective randomized trial

BACKGROUND: Endoscopic variceal ligation is an established procedure for eradication of esophageal varices. However, varices frequently recur after endoscopic variceal ligation. Argon plasma coagulation has been used as supplemental treatment for eradication of varices and for prevention of variceal recurrence in small uncontrolled series. The aim of this study was to determine whether argon plasma coagulation is effective in reducing variceal recurrence after endoscopic variceal ligation. METHODS: Thirty patients with cirrhosis, a history of acute esophageal variceal bleeding, and eradication of varices by endoscopic variceal ligation were randomized to argon plasma coagulation (16 patients) or observation (14 patients). The 2 groups were similar with respect to all background variables including age, Child-Pugh score, presence of gastric varices, and degree of portal hypertensive gastropathy. In the argon plasma coagulation group, the entire esophageal mucosa 4 to 5 cm proximal to the esophagogastric junction was thermocoagulated circumferentially with argon plasma coagulation in 1 to 3 sessions performed at weekly intervals. Endoscopy was performed every 3 months to check for recurrence of varices in both groups. RESULTS: During the course of the study, no serious complication was noted. After argon plasma coagulation, transient fever occurred in 13 patients and 8 complained of dysphagia or retrosternal pain/discomfort. Mean follow-up for all patients was 16 months (range 9-28 months). No recurrence of varices or variceal hemorrhage was observed in the argon plasma coagulation group, whereas varices recurred in 42.8% (6/14) of the patients in the control group (p < 0.04) and bleeding recurred in 7.2% (1/14). CONCLUSIONS: Argon plasma coagulation of the distal esophageal mucosa after eradication of esophageal varices by endoscopic variceal ligation is safe and effective for reducing the rate of variceal recurrence.     

心得安联合内镜套扎术预防食管静脉曲张再出血的疗效分析

目的比较心得安联合内镜套扎治疗与单独内镜套扎治疗预防食管静脉曲张再出血的疗效。方法 65例食管静脉曲张破裂出血的患者随机分为心得安联合内镜套扎治疗组(33例),单独内镜套扎治疗组(32例),平均随访12个月,比较两组间再出血率,门脉高压性胃病,食管静脉曲张复发和胃底静脉曲张的发生率。结果两组治疗后随访第6,12个月显示,与单独内镜套扎治疗比较,心得安联合内镜套扎治疗显著降低再出血率(15.2%vs 37.5%,21.2%vs 46.9%,P<0.05),门脉高压性胃病(18.2%vs43.8%,30.3%vs 56.3%,P<0.05),食管静脉曲张复发(15.2%vs 37.5%,24.2%vs 50.0%,P<0.05)和胃底静脉曲张的发生率(12.1%vs 34.4%,21.2%vs 46.9%,P<0.05)。结论心得安联合内镜套扎治疗是二级预防食管静脉曲张出血的首选治疗方法。     

心得安单纯或联合使用在二级预防食管静脉曲张出血中的疗效比较

目的比较单纯心得安、套扎＋心得安、硬化剂＋心得安二级预防食管静脉曲张出血的疗效,探寻心得安二级预防食管静脉曲张出血的最佳组合。方法78例食管静脉曲张出血患者随机分成3组,每组26例,止血后分别给予心得安（心得安组）、套扎＋心得安（套扎组）、硬化剂＋心得安（硬化剂组）,比较各组12个月内再出血率、死亡率,以及各组门脉高压性胃病、胃底静脉曲张发生率、食管曲张静脉复发率。结果12个月内再出血率套扎组为30．77％,明显低于心得安组（53．85％）及硬化组（42．31％）（P均〈0．05）;套扎组和心得安组门脉高压性胃病及胃底静脉曲张发生率相似,都明显低于硬化组（P均〈0．05）;而食管静脉曲张再发率高于硬化组（P〈0．05）。结论在应用心得安的基础上进行套扎治疗可能是目前食管静脉曲张出血最有效的二级预防方法。     

The long-term outcome of patients with bleeding gastric varices after balloon-occluded retrograde transvenous obliteration

Background The purpose of our study was to evaluate the long-term outcome and complications of balloon-occluded retrograde transvenous obliteration (B-RTO) in patients with hemorrhage from gastric fundal varices. Methods Thirty-four consecutive patients with bleeding from gastric varices who were treated with B-RTO were enrolled in this study between December 1994 and September 2005 (urgent cases, n = 12; elective cases, n = 22). The long-term outcome, complications, and various liver functions were evaluated. Results Complete obliteration was achieved in 31 of 34 (91%) patients with an acute bleeding episode. In one of the remaining patients, there was a technical failure, and the other two had only partial obliteration. The two patients with partial obliteration did not obtain hemostasis. Thus, the rate of hemostasis was 94% (31/33). Gastric varices disappeared in all patients with complete obliteration during the treatment. The rate of gastric variceal eradication was 91%. Variceal rebleeding from esophageal varices occurred in three patients. The rate of rebleeding was 10% (3/31). Rebleeding from gastric varices was not observed after complete obliteration. None of the patients showed worsening of their Child-Pugh score. Although the 5-year cumulative worsening rate of esophageal varices was 52%, neither portal hypertensive gastropathy nor ectopic varices were observed. The patients with worsening esophageal varices were successfully treated with an endoscopic procedure. The 5-year survival rate was 68%. Conclusions B-RTO is useful for treatment of bleeding gastric varices, achieving high eradication of gastric varices, a low rebleeding rate, and a fairly good prognosis with improved hepatic function.     

密集多点结扎术治疗食管静脉曲张出血的临床疗效观察

目的探讨内镜下密集多点结扎术(DEVL)治疗食管静脉曲张出血的近远期疗效。方法对贲门口齿状线及以上5～6cm范围的曲张静脉密集多点结扎，每隔2～3周重复治疗，直至曲张静脉全部根治。术后3、6、12个月定期随访及胃镜复查，术后3个月结果作为近期疗效判断依据，6个月以后作为远期疗效判断依据。结果126例患者共完成403次、3641点结扎，平均每例结扎3．2次．28．9点。急诊止血率为100．0％；近期食管静脉曲张根治率为94．4％、总有效率为100．0％、复发出血率为3．9％；经过平均22．3个月随访，远期食管静脉曲张复发率为11．9％、复发出血率为3．2％、未见复发出血死亡。术后多数患者有一过性门静脉高压性胃病加重。结论DEVL治疗能有效急诊止血、根治食管静脉曲张和预防再出血，远期疗效较好。治疗不受肝功能状态的影响，并发症少。     

内镜治疗食管静脉曲张对门脉高压性胃病的影响

探讨内镜下硬化剂(EST)和套扎(EVL)治疗食管静脉曲张术后对门脉高压性胃病(PHG)和胃底静脉曲张(GV)的影响,对21例注射硬化剂治疗和27例套扎治疗的共48例患者进行了1年的内镜随访,观察PHG和GV的程度。结果在接受治疗3个月和1年后,PHG发生率较治疗前(35％,17/48)明显增加,分别为75％(36/48)和87％(42/48);GV较治疗前(17％,8/48)增多,分别为33％(16/48)和43％(21/48)。结论:食管静脉曲张的内镜下硬化剂和套扎治疗将加重PHG和GV且有可能增加PHG和GV的出血机会。     

The effects of chronic endoscopic variceal sclerotherapy on portal pressure in cirrhotics

The effect of obliterating esophageal varices by endoscopic sclerotherapy on portal pressure was prospectively studied in 11 cirrhotic patients with variceal hemorrhage. Portal venous pressure gradient, determined as the difference between transhepatic portal and hepatic vein pressure, increased by a mean of 31.1% +/- 14.5% in 8 (73%) and decreased by a mean of 30.1% +/- 11.7% in 3 (27%) patients, with no statistically significant change overall (P = 0.1). These changes in portal venous pressure gradient occurred despite an improvement in the laboratory and clinical parameters of hepatic function. Deep abdominal sonography with color flow imaging at variceal obliteration showed patent paraumbilical veins in 6 (55%) patients, 3 of whom had decreases in portal venous pressure gradient (29%, 19%, 42.5%) at variceal obliteration. In 5 (45%) patients without patent paraumbilical veins, a statistically significant increase in portal venous pressure gradient between initial endoscopic variceal sclerotherapy and variceal obliteration was noted (P = 0.008). Rebleeding (single episode in all 4 patients, before obliteration in 3 patients) occurred in those with an increase in portal venous pressure gradient; all patients with portal venous pressure gradient decreases were nonbleeders. No correlation between changes in portal venous pressure gradient and time to variceal obliteration, number of sclerotherapy treatments, or rebleeding episodes was observed. Thus, an increase in portal venous pressure gradient was noted in the majority of patients at variceal obliteration. Although the portal venous pressure gradient decrease may be explained by a patent paraumbilical vein, the mechanism of portal venous pressure gradient increase is not clear. It is speculated that this portal venous pressure gradient increase may be caused by an increase in collateral resistance or flow or a combination of both, resulting from obliteration of esophageal varices by endoscopic sclerotherapy.     

Endoscopic variceal ligation plus nadolol and sucralfate compared with ligation alone for the prevention of variceal rebleeding: a prospective, randomized trial

Both beta-blockers and endoscopic variceal ligation (EVL) have proven to be valuable alternatives to sclerotherapy in the prevention of variceal rebleeding. Sucralfate is a mucosal protector. The effects of combinations of beta-blocker, band ligation, and sucralfate (triple therapy) remain unknown. A total of 122 patients with a history of esophageal variceal bleeding were randomized to receive EVL only (group A, 62 patients) or triple therapy (group B, 60 patients). The procedure for the triple therapy included ligation with the addition of sucralfate granules until variceal obliteration. In addition, nadolol was administered during the course of the study or until death. After a median follow-up of 21 months, recurrent upper gastrointestinal bleeding developed in 29 patients (47%) in group A and 14 patients (23%) in group B (P =.005). Recurrent bleeding from esophagogastric varices occurred in 18 patients in group A and 7 patients in group B (P =.001). Twenty-one patients in group A (50%) and 12 patients (26%) in group B experienced variceal recurrence after variceal obliteration (P <.05). Treatment failure occurred in 11 patients (18%) in group A and in 4 patients (7%) in group B (P =.05). Twenty patients from group A and 10 patients from group B died (P =.08); 9 and 4 of these deaths, respectively, were attributed to variceal hemorrhage (P =.26). The combination of ligation, nadolol, and sucralfate (triple therapy) proved more effective than banding ligation alone in terms of prevention of variceal recurrence and upper gastrointestinal rebleeding as well as variceal rebleeding.     

The rebleeding course and long-term outcome of esophageal variceal hemorrhage after ligation: comparison with sclerotherapy

BACKGROUND: Endoscopic variceal ligation is widely accepted as the optimum endoscopic treatment for esophageal variceal hemorrhage. However, the rebleeding course and long-term outcome of patients with esophageal variceal hemorrhage after ligation have been poorly defined. Therefore, we conducted a long-term follow-up study to delineate the outcome of ligation and compare it with that after sclerotherapy. METHODS: One hundred and eighty-five liver cirrhotic patients with endoscopically proven esophageal variceal hemorrhage were randomized to undergo endoscopic variceal sclerotherapy or ligation. These patients received regular follow-up and detailed clinical assessment. RESULTS: Two patients developed hepatoma within 6 months of entry in each group and were excluded. Another six patients in the sclerotherapy group and seven patients in the ligation group were excluded because of poor compliance or lost to follow-up. Therefore, 84 patients in each group were analyzed. In this long-term follow-up (55.3 +/- 12.5 months) the rebleeding rate for ligation was lower than that for sclerotherapy, regardless of whether the rebleeding was analyzed by patient number or Kaplan-Meier analysis. With regard to the rebleeding risk of various periods, the sclerotherapy risk was higher than that of ligation within 4 weeks of the initial endoscopic treatment or before variceal eradication. Multifactorial analysis showed hematemesis, poor hepatic function, and sclerotherapy were the risk factors determining rebleeding. The annual hepatocellular carcinoma incidence was 4.9%. There was no difference in survival between sclerotherapy and ligation. Multifactorial analysis showed that poor hepatic function was the only factor determining survival. CONCLUSIONS: The rebleeding risk was higher in sclerotherapy than in ligation before variceal eradication, especially within 4 weeks of the initial endoscopic treatment. Long-term survival was dependent on hepatic reserve regardless of the treatment method.     

Effects of Esophageal Varice Eradication on Portal Hypertensive Gastropathy and Fundal Varices: A Retrospective and Comparative Study

Esophageal varice eradication results in gastric hemodynamic changes. The aim of this study was to detect the influence of variceal eradication on portal hypertensive gastropathy (PHG) and fundal varices and to compare the results of two therapeutic methods (endoscopic variceal ligation and endoscopic sclerotherapy). A total of 114 consecutive patients with cirrhosis and portal hypertension who underwent elective endoscopic variceal ligation (EVL) (85 patients) or endoscopic sclerotherapy (EST) (29 patients) for obliteration of esophageal varices were selected for this study. Both groups were compared for PHG and fundal varice formation before and after eradication. Fifty-eight (68.2%) patients in the EVL and 18 (62.1%) patients in the EST group had PHG before esophageal varice eradication (P > 0.05). PHG grade after eradication of esophageal varices by both EVL and EST was significantly higher compared to pre-eradication. PHG grade and aggregation were similar in both groups. Thirty-seven patients (34 F₁, 3 F₂) in the EVL group and 13 patients (10 F₁, 3 F₂) in the EST group had fundal varices before variceal eradication (P > 0.05). Fundal varices were detected in 46 (35 F₁, 11F₂) and 19 (11F₁, 8F₂) patients in the EVL and EST groups after eradication, respectively. There was a statistically significant increment in occurrence of fundal varices after eradication with EVL and EST groups. There was no significant difference regarding fundal varice development after esophageal variceal eradication in both groups. After varical eradication, PHG was found in 57 (87.7%) and 39 (79.6%) patients with and without fundal varices, respectively (P > 0.05). Esophageal eradication with EVL and EST increases both the incidence and the severity of PHG and fundal varice formation. Both methods have comparable influences on PHG and fundal 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。     

Improved survival in patients receiving medical therapy as compared with banding ligation for the prevention of esophageal variceal rebleeding

Both medical therapy and endoscopic variceal ligation (EVL) have proven to be comparable in the prevention of variceal rebleeding. However, the long-term results are still lacking. Our previous study enrolled 121 patients with history of esophageal variceal bleeding and randomized to receive EVL (EVL group, 60 patients) or drug therapy, nadolol plus isosorbide-5-mononitrate (N+I) (N+I group, 61 patients) to prevent variceal rebleeding. The EVL group received ligation regularly until variceal obliteration. The N+I group received N+I during the study period. Patients were followed for up to 8 years. After a median follow-up of 82 months, recurrent upper gastrointestinal bleeding developed in 28 patients (47%) in the EVL group and 49 patients (80%) in the N+I group (P = 0.001). Recurrent bleeding from esophageal varices occurred in 18 patients (30%) in the EVL group and 39 patients (64%) in the N+I group. The actuarial probability of rebleeding from esophageal varices was lower in the EVL group (P = 0.001). A total of 42 patients of the EVL group and 30 patients of the N+I group died (P = 0.013). The multivariate Cox analysis indicated that age, serum albumin, presence of encephalopathy, and treatment were the factors predictive of mortality. CONCLUSION: Our long-term follow-up study showed that combination of N+I therapy was inferior to banding ligation in the reduction of variceal rebleeding, but with enhanced survival.     

Factors predicting success of endoscopic variceal ligation for secondary prophylaxis of esophageal variceal bleeding

Introduction: Endoscopic obliteration of esophageal varices by endoscopic variceal ligation (EVL) is an effective form of secondary prophylaxis. However, there is no consensus regarding the technical aspects of EVL for secondary prophylaxis. The present study compares the technical aspects of EVL (frequency of sessions, number of sessions and number of bands used) in patients who rebled following secondary prophylaxis of esophageal varices by EVL compared to those who did not rebleed. Methods: All patients who underwent EVL for treatment of acute variceal bleeding followed by EVL for secondary prophylaxis and who subsequently developed recurrent variceal bleeding at Mayo Clinic, Rochester between January 1995 and May 2003 were identified. A control group of patients undergoing EVL for secondary prophylaxis who did not rebleed was identified. Results: During the study period, 216 patients with acute esophageal variceal hemorrhage underwent emergent EVL treatment with follow‐up EVL for secondary prophylaxis, of whom 20 (9.3%) subsequently rebled. Both rebleeding and non‐rebleeding patient groups were well‐matched with respect to liver function (Child–Pugh class), number and size of variceal trunks, endoscopic stigmata of hemorrhage and beta‐blocker usage. The median interval between EVL sessions in the rebleeding group (2 weeks, interquartile range 0–2 weeks) was significantly shorter compared to the non‐rebleeding group (5 weeks, interquartile range 3–7 weeks; P = 0.004). Adjusting for age, gender, and Child–Pugh class, interbanding interval ≥ 3 weeks was associated with increased likelihood of not rebleeding, hazard ratio 3.84 (95% confidence interval: 1.69–11.79; P = 0.0007). Conclusions: These findings demonstrate the importance of technical aspects of EVL on patient outcome, suggesting the benefit of longer interbanding intervals. Future prospective studies are required to define the optimal intersession interval. Standardizing procedural aspects of EVL will aid in objectively evaluating the benefit of this procedure when compared to other modalities such as medical treatment.     

Portal-hypertensive gastropathy develops less in patients with cirrhosis and fundal varices

Background/Aims: The aim of this prospective study was to examine the association of portal-hypertensive gastropathy and fundal varices in patients with cirrhosis.Methods: We carried out an endoscopic observation in 476 patients with cirrhosis (study 1), including 62 patients undergoing endoscopic obliteration of esophageal varices (study 2). In study 1, patients were classified into five subgroups: no esophagofundal varices (n=119), small esophagofundal varices (n=127), dominant esophageal varices (n=177), dominant fundal varices (n=27), and large esophagofundal varices (n=26). The severity of liver dysfunction was assessed by Pugh-Child classification: class A (n=222), class B (n=200), and class C (n=54). In study 2, two groups, poorly developed fundal varices (n=50) and well developed fundal (n=12), were distinguished and the follow-up endoscopic examinations were performed on the basis of 3-month intervals for 2 years. In each study, the severity of portal-hypertensive gastropathy was scored: 0 (absent), 1 (mild), 2 (severe), and 3 (bleeding).Results: Study 1: One-way ANOVA showed that both variceal pattern and Pugh-Child class significantly influenced portal-hypertensive gastropathy score. However, two-way ANOVA indicated that variceal pattern was the only significant variable. Portal-hypertensive gastropathy score was significantly higher in patients with dominant esophageal varices than in either patients with no esophagofundal varices or patients with small esophagofundal varices. In contrast, portal-hypertensive gastropathy score in patients with dominant fundal varices was similar to that in patients with no esophagofundal varices and was significantly lower compared with that in patients with dominant esophageal varices. Furthermore, portal-hypertensive gastropathy score was significantly lower in patients with large esophagofundal varices than in patients with dominant esophageal varices. Study 2: After the obliteration of esophageal varices, portal-hypertensive gastropathy score in patients with poorly developed fundal varices became significantly higher at 3-, 6-, 9-months while it was not modified in patients with well developed fundal varices during the follow-up period. Furthermore, the integrated incremental change in portal-hypertensive gastropathy score during the first 1-year follow-up period was significantly lower in patients with well developed fundal varices than in patients with poorly developed fundal varices.Conclusions: These results indicate that both spontaneous and obliteration-induced portal-hypertensive gastropathy lesions develop less in patients with cirrhosis and fundal varices.     

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.     

The critically ill liver patient: the variceal bleeder

Esophageal varices develop in patients with cirrhosis once portal pressure, measured by hepatic venous pressure gradient, and exceeds 10 mm Hg. At a portal pressure of 12 mm Hg, variceal bleeding may develop that is associated with a mortality of 30% to 50% per episode. In addition to an elevated portal pressure, other risk factors for the development of variceal hemorrhage include: variceal size, endoscopic features on the variceal wall (i.e., red wales), and Child-Pugh class. In patients with suspected variceal hemorrhage, the treatment of the acute episode includes intravascular volume expansion, hemostasis through the use of pharmacological agents and endoscopy, and the prevention and treatment of potential complications associated with variceal hemorrhage such as aspiration pneumonia, spontaneous bacterial peritonitis and hepatic encephalopathy. Given a high rate of rebleeding, long-term prevention through secondary prophylaxis should be instituted in all patients who have survived an episode of variceal bleeding. Current prophylactic options include: non-selective beta-blockers alone (first line) or in combination with long-acting nitrates (isosorbide mononitrate) and/or endoscopic variceal obliteration achieved through sclerotherapy or preferably, band ligation.     

Sclerotherapy versus banding in the treatment of variceal bleeding

Endoscopic sclerotherapy has been the mainstay in the management of esophageal variceal bleeding to control acute bleeding and decrease recurrent bleeding. Endoscopic variceal ligation is a new technique that is equally effective in the control of acute bleeding but achieves obliteration of varices in fewer treatment sessions with presumably less cost, results in a lower rebleeding rate, has fewer complications, and is associated with reduced mortality. Combination therapy with both endoscopic variceal ligation and endoscopic sclerotherapy appears to have no clear advantage over variceal ligation alone. On the basis of the results of a number of trials comparing sclerotherapy with band ligation, endoscopic variceal ligation has evolved to be the preferred first line modality for the endoscopic treatment of variceal bleeding.     

Endoscopic treatment of esophagogastric variceal bleeding in patients with noncirrhotic extrahepatic portal vein thrombosis: a long-term follow-up study

BACKGROUND: Esophagogastric variceal bleeding is the most important complication of extrahepatic portal vein thrombosis (EPVT) and is usually treated endoscopically. Little is known about the prognosis of these patients. OBJECTIVES: To investigate the long-term clinical outcome and efficacy of endoscopic treatment in patients with esophagogastric variceal bleeding secondary to EPVT. DESIGN: Retrospective observational study. SETTINGS: Single university center. PATIENTS: Twenty-seven consecutive patients with esophagogastric variceal bleeding, secondary to noncirrhotic, nonmalignant EPVT, who underwent endoscopic treatment between 1982 and 2005. INTERVENTIONS: Endoscopic band ligation and/or endoscopic sclerotherapy. MAIN OUTCOME MEASUREMENTS: The overall rebleeding risk, overall survival, complications of the endoscopic procedures, and predictive values of rebleeding. Analyses were performed by the Kaplan-Meier method and univariate Cox regression. RESULTS: All patients were followed-up after the first endoscopically treated variceal bleeding. A total of 241 endoscopic procedures were performed. In all patients, initial control of bleeding was obtained. The overall rebleeding risk was 23% (95% CI, 0%-24%) at 1 year and 37% (95% CI, 43%-83%) at 5 years. Extension of thrombosis into the splenic vein and the presence of fundal varices were significant predictors of rebleeding, with a nearly 5-fold increased risk for patients with EPVT and fundal varices at the time of the first variceal hemorrhage (hazard ratio 5.07, P = .01). A portosystemic shunt procedure was performed in 5 patients: 4 for variceal bleeding and in one patient for refractory ascites. Seven patients died, none from variceal bleeding. Overall 5-year and 10-year survivals were 100% and 62% (95% CI, 38%-96%), respectively. LIMITATIONS: Retrospective design. CONCLUSIONS: In patients with variceal bleeding secondary to EPVT endoscopic treatment, in particular, band ligation appears safe and effective. EPVT-related mortality is primarily determined by other causes than variceal bleeding.