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Bleeding from gastric varices (GVs) is generally more severe than bleeding from esophageal varices (EVs), but is thought to occur less frequently. Although several recent developments in the agents and the techniques have improved the outcome of GV bleeds no consensus has been reached on the optimum treatment. Because the blood flow in the GVs is relatively large and the bleeding is rapid and often profuse endoscopic means of treating bleeding GVs are the treatments of choice. Endoscopic injection of cyanoacrylate glue is the treatment of choice for the control of active bleeding of gastric avarices and to prevent rebleeding. This article reviews the current endoscopic treatment modalities used in gastric variceal bleeding, and the primary and secondary prophylaxis of gastric variceal bleeding., (2010 Elsevier Inc. All rights reserved.)

Background: A beta-blocker is recommended for primary prophylaxis of variceal bleeding; however, only one-third have hepatic venous pressure gradient (HVPG) response. The role of addition of isosorbide-5-mononitrate (ISMN) to beta-blocker and benefits of HVPG-guided 'a la carte' approach remain unclear., Aim: To determine the benefits of HVPG-guided pharmacotherapy in primary prophylaxis of variceal bleeding using beta-blocker and ISMN., Patients and Methods: Consecutive patients of cirrhosis, with high-risk varices, with no previous variceal bleeding were included. After baseline HVPG, patients received incremental propranolol to achieve HR of 55/min. After one-month, HVPG was repeated to determine response (<12 mmHg or >or=20% reduction). ISMN was added in nonresponders and HVPG repeated. Patients were followed up for 24 months., Results: Of 56 patients (age 47 +/- 13, males 79%) from 89 eligible patients, 21 (38%) responded to beta-blocker alone. Six additional patients responded to combination. Thus, overall 48% (27/56) patients responded. Variceal bleeding occurred in seven of 56 (13%) patients [one of 27 (4%) responder, five of 23 (22%) nonresponders and one of six (17%) with unknown response; P = N.S.]. The actuarial probability of variceal bleeding at median 24 months was 4% in responders and 22% in nonresponders (P < 0.05). Ten (18%) patients developed adverse effects to propranolol and six of 35 (17%) to nitrates requiring dose reduction. Risk factors of variceal bleed were grade IV varices and haemodynamic nonresponse., Conclusions: For primary prophylaxis, a beta-blocker is effective in 38% and addition of ISMN raises the response rate to about half of patients. The HVPG-guided 'a la carte' approach may be considered for these patients.

Objective: The natural history and likelihood of bleeding from portal hypertensive gastropathy (PHG) present in patients with portal hypertension before endoscopic variceal obliteration may differ from that in patients who develop PHG during or after variceal eradication., Methods: A total of 967 variceal bleeders who had achieved variceal eradication by endoscopic sclerotherapy in the recent past were prospectively studied. In all, 88 (9.1%) patients (cirrhosis in 54, noncirrhotic portal fibrosis in 18, and extrahepatic portal vein obstruction in 16) had distinct mucosal lesions. PHG alone was present in 78, PHG with gastric antral vascular ectasia (GAVE) in eight, and GAVE alone in two patients. PHG was graded as mild or severe and according to whether present before (group A) or after endoscopic intervention (group B). Patients underwent regular endoscopy at follow-up to see if the PHG was transitory (disappearing within 3 months), persistent (no change), or progressive. Bleeding from PHG lesions was defined as acute or chronic., Results: Twenty-two (26%) patients had PHG before (group A) and 64 (74%) developed PHG after variceal eradication (group B). During a mean follow-up of 25.1 +/- 14.2 months, PHG lesions disappeared in group A in only two patients (9%), but in group B in 28 (44%) patients (p < 0.05). PHG lesions more often progressed in the former as compared to the latter (18% vs 9.4%, p = NS). The incidence of bleeding was higher in group A than group B (32% vs 4.7%, p < 0.02). Bleeding from PHG occurred in 10 patients (11.6%); seven of them were from group A, and all had either progressive (n = 3) or persistent (n = 4) lesions., Conclusions: PHG developing after variceal eradication is often transitory and less severe. If PHG is pre-existing, endoscopic therapy for varices could worsen the PHG, with a likelihood of bleeding. Such patients may be benefited by concomitant beta-blocker therapy.

Background and Methods: We compared propranolol therapy and endoscopic ligation for the primary prevention of bleeding from esophageal varices. This prospective, controlled trial included consecutive eligible patients who had large varices (>5 mm in diameter) that were at high risk for bleeding. The patients were assigned to either propranolol therapy, at a dose sufficient to decrease the base-line heart rate by 25 percent, or variceal ligation, to be performed weekly until the varices were obliterated or so reduced in size that it was not possible to continue treatment., Results: Of the 89 patients, 82 of whom had cirrhosis of the liver, 44 received propranolol and 45 underwent variceal ligation. The mean (+/-SD) duration of follow-up in each group was 14+/-9 and 13+/-10 months, respectively. The mean time required to achieve an adequate reduction in the heart rate was 2.5+/-1.7 days; the mean number of sessions needed to complete variceal ligation was 3.2+/-1.1. After 18 months, the actuarial probability of bleeding was 43 percent in the propranolol group and 15 percent in the ligation group (P=0.04). Twelve patients in the propranolol group and four in the ligation group had bleeding. Three of the four in the ligation group had bleeding before their varices had been obliterated. Nine patients in the ligation group had recurrent varices, a mean of 3.7 months after the initial treatment. Five patients in each group died; bleeding from the varices was the cause of death of four patients in the propranolol group and of three in the ligation group. There were no serious complications of variceal ligation; in the propranolol group, treatment was stopped in two patients because of side effects., Conclusions: In patients with high-risk esophageal varices, endoscopic ligation of the varices is safe and more effective than propranolol for the primary prevention of variceal bleeding.

Background: Bleeding from gastric varices is often a serious medical emergency. The role of endoscopy in the management of gastric variceal bleeding is still controversial. The types of gastric varices and their respective management strategies have not been identified., Methods: Gastric varices were observed in 209 patients with portal hypertension. Seventy-one patients (with cirrhosis 33, noncirrhotic 38) underwent gastric variceal sclerotherapy, 53 of these (75%) for gastric variceal bleeding. By use of a previously described classification, gastric varices were divided into gastroesophageal varices, type 1 (GOV1) and type 2 (GOV2), and isolated gastric varices, type 1 (IGV 1). Gastric variceal sclerotherapy was done every week using a combination technique of paravariceal and intravariceal injections with absolute alcohol., Results: Emergency gastric variceal sclerotherapy arrested acute bleeding in 12 (66.7%) of 18 patients. Variceal obliteration was achieved in 43 of the 60 (71.6%) patients who underwent repeated elective sclerotherapy. Variceal obliteration was higher in patients with GOV1 (94.4%) than in those with GOV2 (70.4%) and IGV1 (41%). Rebleeding after elective gastric variceal sclerotherapy was seen in 5.5%, 19%, and 53%, respectively, in the three types of gastric varices. Gastric variceal recurrence was not seen during a mean follow-up of 24.2 +/- 22.9 months. Seventeen (24%) patients died, nearly equally from rebleeding and liver failure., Conclusions: (1) Sclerotherapy can effectively arrest acute gastric variceal bleeding and achieve gastric variceal obliteration, (2) it is more effective in patients with gastroesophageal varices, and (3) alternative therapies need to be evaluated for patients with IGV1.

Objective: To assess the efficacy and safety of endoscopic variceal band ligation (EVL) for primary prophylaxis of variceal bleeding in patients with high-risk varices., Design: A randomized, controlled trial., Setting: Hospital based., Subjects: Sixty-eight patients with portal hypertension with high-risk varices were randomized to undergo either EVL (n = 35) or no treatment (n = 33)., Interventions: Endoscopic variceal band ligation or no therapy., Main Outcome Measures: Probability of first variceal bleeding, probability of survival, variceal obliteration, complications of EVL., Results: Oesophageal varices could be obliterated by EVL in 3.2 +/- 1.2 sessions within 4.9 +/- 2.2 weeks. Three (8.6%) patients in the EVL group and 13 (39.4%) in the control group bled during a mean follow-up of 14.1 +/- 5.0 months (range 2-22) (P < 0.01). The cumulative probability of the patients remaining free of bleeding was higher (P < 0.01) in the EVL group than the control. Variceal recurrence was seen in 10 (28.6%) patients and was managed by repeated EVL. None of the patients developed oesophageal stricture. Four (11.4%) patients in the EVL and eight (24.2%) in the control group died (P = NS). Bleed-related mortality was lower in the EVL than the control group (2.9% vs. 15.2%, P = 0.08)., Conclusion: EVL significantly decreases the frequency of first variceal bleed. It should be evaluated further to see if bleeding-related mortality could be reduced in cirrhotics with high-risk varices who have not bled.

Gastric varices (GV) are a common (20%) accompaniment of portal hypertension; they are more often seen in those patients who bleed than in those who do not (27% versus 4%, p < 0.01). They can develop in both segmental and generalized portal hypertension. Depending on their location and relation with oesophageal varices, GVs can be classified as gastrooesophageal varices (GOV) and isolated gastric varices (IGV); each of these can be further subdivided as follows: GOV1 (extension of oesophageal varices along lesser curve) and GOV2 (extension of oesophageal varices towards fundus); and IGV1 (varices in the fundus) and IGV2 (isolated varices anywhere in the stomach). The common presentation of GVs is variceal bleeding and encephalopathy. In comparison with oesophageal varices, GVs bleed significantly less often (64% versus 25%, p < 0.01) but more severely (2.9 +/- 0.3 versus 4.8 +/- 0.6 transfusion units, p < 0.01). Patients with GOV2 and IGV1 bleed more often than patients with other types of GVs. Sclerotherapy for oesophageal varices can significantly influence the natural history of GVs. GOV1, or lesser curve varices, disappear in the majority of cases (59%) after obliteration of oesophageal varices. In those with persisting GOV1, the incidence of bleeding and mortality is high and these patients require gastric variceal sclerotherapy (GVS). During oesophageal variceal sclerotherapy, bleeding can occasionally be induced from GVs. After obliteration of oesophageal varices, recurrence as GVs (secondary GVs) can occur in about 9% of patients. Emergency GVS is quite effective in controlling acute bleeding from GVs, more so than balloon tamponade. Potent sclerosants like tetradecyl sulphate and alcohol and a glue, bucrylate, have been quite effective. Elective GVS can achieve obliteration of GVs in nearly 70% of patients. Rebleeding and ulceration are common complications of GVS; probably related to incomplete obliteration and mucosal injury respectively. Splenectomy is quite effective in treating GVs due to segmental protal hypertension. For GV bleeding due to generalized portal hypertension, a shunt operation is often effective. TIPS procedure appear to be a very promising therapy for GV bleeding. Liver transplantation may be a superior alternative to sclerotherapy and shunt surgery for gastric varices.

Effective control of variceal rebleeding (secondary prophylaxis) or prevention of the initial bleeding (primary prophylaxis) are the main objectives of the treatment of portal hypertension. Endoscopic sclerotherapy is the treatment of choice for secondary prophylaxis, since it significantly decreases rebleeding and, to some extent, mortality. A combination of propranolol and sclerotherapy may be of benefit by decreasing postsclerotherapy rebleeding. Endoscopic variceal band ligation and transjugular intrahepatic shunt are emerging as useful alternative techniques. Devascularisation and preferably selective shunts should be reserved for use as salvage of sclerotherapy failures. Liver transplantation, if feasible, could become the ultimate therapy by controlling variceal bleeding and improving hepatic function. Pharmacotherapy, while not very successful for secondary prophylaxis, has shown promise for primary prophylaxis of variceal bleeding. Nonselective beta-blockers significantly decrease the rebleeding rates but are associated with only marginal survival benefits. beta-Blockers alone cannot decrease the hepatic venous pressure gradient adequately (to less than 12mm Hg). Combination with nitrates and other drugs may prove beneficial and requires clinical evaluation. Endoscopic sclerotherapy and surgery have little role in primary prevention of variceal bleeding in patients with cirrhosis but need evaluation in noncirrhotic patients.

Endoscopic sclerotherapy is a well-accepted technique for the treatment of variceal bleeding. It is carried out by injecting a sclerosant into or around a varix. Sclerosants are oily or aqueous chemicals which produce sclerosis, depending on their necroinflammatory and thrombotic properties. The safety and efficacy of various sclerosants has been evaluated in experimental and human studies. However, due to the presence of a large number of variables, conflicting results have been reported. Based primarily on anecdotal experiences, sodium tetradecyl sulfate, ethanolamine oleate, polidocanol, and alcohol appear to be potent and safe sclerosants. There is great need to perform double-blind trials to identify ideal sclerosant(s) with optimum thrombogenic and minimum necroinflammatory properties.

To investigate whether alcohol used as variceal sclerosant has any effect on pulmonary hemodynamics, 14 patients with portal hypertension received intravariceal injections of absolute alcohol. Six additional patients were injected with equivalent volumes of saline and they served as controls. After intravariceal injection of absolute alcohol (8 ml in 12 patients and 12 ml in 2 patients), mean +/- SD pulmonary artery pressure was seen to increase significantly (p less than 0.01) at 1 and 5 min and return to basal level by 15 min. Similar changes in pulmonary arterial pressure were seen after intravariceal injection of saline; the difference in the rise in pulmonary arterial pressure between the two groups was not significant. The pulmonary capillary-wedged pressure and systemic blood pressure did not change significantly after intravariceal injection of alcohol. Absolute alcohol in the amount usually used for sclerotherapy has minimal and transient effects on pulmonary hemodynamics and, in this respect, it appears to be a relatively safe sclerosant.

Mosaic pattern of gastric mucosa has been reported to be a sensitive and specific criterion for the diagnosis of portal hypertension and an important marker of nonvariceal upper gastrointestinal bleeding. So that the validity of this endoscopic sign could be assessed, 136 patients with portal hypertension, 25 chronic alcoholics without portal hypertension, and 366 controls were carefully endoscoped. Mosaic pattern was significantly (p less than 0.01) more common in portal hypertension patients (7.4%) than in controls (1.4%). It was not seen in chronic alcoholics. The incidence of mosaic pattern was 10.9% in cirrhotics, 2.9% in noncirrhotic portal fibrosis, and 5.4% in extrahepatic portal obstruction patients; the differences were not significant. Mosaic pattern was significantly (p less than 0.01) more often seen in postsclerotherapy (13.8%) than in presclerotherapy patients (2.6%). Bleeding from nonvariceal causes was uncommon, and was seen in only one patient (0.8%) showing mosaic pattern. Endoscopic gastric biopsies from areas showing mosaic pattern did not reveal any vascular abnormalities. In conclusion, gastric mucosal lesions are not very common in Indian patients with portal hypertension. In our experience, "mosaic pattern" is not a useful diagnostic feature in portal hypertension patients.

Emergency endoscopic sclerotherapy (EEST) during continued moderate to severe bleeding was carried out using a flexible endoscope and absolute alcohol as a sclerosant in 38 patients with variceal bleeding. Portal hypertension was due to cirrhosis in 27, noncirrhotic portal fibrosis in eight, extrahepatic obstruction in two, and Budd-Chiari Syndrome in one patient. A technically adequate EEST could be carried out in 36 (95%) patients, with successful control of variceal bleeding in 35 (92%). Thirty-one episodes of rebleeding occurred in 12 (31.6%) patients. Twenty-nine (93.5%) of these episodes could be controlled with repeated EEST, giving an overall success of 87%. The new approach of repeating sclerotherapy on every rebleeding episode up to a maximum of three course within 24 hours, use of a wide bore injector, and certain other technical innovations were found safe and effective. The mean (+/- SD) amount of alcohol injected per patient was 9.23 +/- 3.3 ml and the mean (+/- SD) number of injections needed per patient were 6.0 +/- 3.07. Complications were minor, transient, and similar to conventional sclerotherapy. There were three deaths, two due to massive rebleeding and one due to hepatic encephalopathy. It can be concluded that EEST is technically feasible during active variceal bleeding and is an effective and relatively safe procedure. It can serve as the first line treatment in this group of patients.

Absolute alcohol and 50% alcohol were compared as sclerosants in 79 patients who underwent sclerotherapy for esophageal varices every 3 weeks with either of the solutions. Active variceal bleeding could be controlled more often (p less than 0.05) with absolute alcohol (93.3%) compared with 50% alcohol (53.8%). Variceal eradication could be achieved with absolute alcohol in a significantly shorter time with smaller amounts and fewer sclerotherapy sessions than with 50% alcohol. Except for a higher incidence of retrosternal pain and fever noted with the use of absolute alcohol, there was no significant difference in the incidence of various complications, rebleeding rate, or mortality between the two sclerosants. Absolute alcohol is a more effective and equally safe sclerosant compared with 50% alcohol.

Fifty four consecutive patients with oesophageal variceal bleeding were randomised to undergo intravariceal (28 patients) or paravariceal (26 patients) sclerotherapy, every three weeks. Intravariceal technique was found significantly (p less than 0.01) more effective in controlling active variceal bleeding than the paravariceal technique (91% v 18.7% respectively). The mean (+/- SD) time taken for variceal eradication by intravariceal sclerotherapy (15.4 +/- 5.3 weeks) was significantly (p less than 0.001) less than paravariceal (26.8 +/- 6.6 weeks) technique. The number of sclerotherapy sessions needed with intravariceal technique were also significantly less. Rebleeding was seen in 38.5% patients after para and 14.3% after intravariceal injections (NS). Except for retrosternal pain, which occurred more often (p less than 0.01) with paravariceal technique, there was no difference in the incidence of other complications or mortality between the two groups. Variceal recurrence was seen in seven patients (25%) in the intra and one (3.9%) patient in the paravariceal group (p less than 0.01) after a mean follow up of 29.4 +/- 9.1 weeks. Intravariceal sclerotherapy was superior to paravariceal in the control of active variceal bleeding and for total variceal obliteration, but was associated with a higher variceal recurrence.

To assist in the prediction of variceal bleeding we examined 12 clinical, endoscopic and haemodynamic variables in 126 patients with portal hypertension (72 bleeders and 54 non-bleeders). Multiple regression and discriminant analysis were utilised for 101 patients. Stepwise regression among the 12 variables explained only 54% of the variability existing between bleeders and non-bleeders. Six of the 12 variables accounted for 51% of the total bleeder/non-bleeder variability. A predicting equation was evolved [Yp = -0.60 + 0.19 X1 (colour of varices) + 0.16 X2 (cherry red spots) + 0.03 X3 (red wale, markings) + 0.01 X4 (haematocystic spots) + 0.15 X5 (Conn's grading of variceal size) + 0.03 X6 (intravariceal pressure)]. Of the six variables used, variceal size indicated 35%, and intravariceal pressure accounted for 12%, of the explained variability between bleeders and non-bleeders. The presence of the three red colour signs and the colour of the varices accounted for only 3% and 1% respectively of the total explained variation. Using the discriminant function analysis, we were able to correctly identify 85% of the bleeders and 81% of the non-bleeders. Additional studies are required to detect the variables responsible for the unexplained variability (46%) between bleeders and non-bleeders.

The effect of noradrenaline (8 mg in 100 ml cold saline) gastric lavage was compared with that of cold saline alone in 42 patients with upper gastrointestinal haemorrhage in a prospective, randomized, double blind study. Fifty three per cent (11/21) of the patients given noradrenaline stopped bleeding within two hours of treatment compared with 14% (3/21) of those given saline alone. We suggest that noradrenaline gastric lavage is a simple, safe and effective method for controlling upper gastrointestinal haemorrhage and could be used with advantage in peripheral hospitals in tropical countries.

To assess the efficacy of absolute alcohol as a sclerosant, endoscopic sclerotherapy was carried out using a conventional endoscope and an indigenously designed injector. Forty three patients with portal hypertension who had presented with history of variceal bleeding were included in the study. Portal hypertension was caused by cirrhosis in 30 (69.8%), non-cirrhotic portal fibrosis in eight (18.6%) and extra-hepatic obstruction in five (11.8%). Acute bleeding was successfully controlled in all 11 patients, seven with a fresh bleed and four who rebled while on endoscopic sclerotherapy regimen. All patients with fresh, recent, or old bleeding were treated with a weekly endoscopic sclerotherapy schedule. Reduction in variceal size of two or more grades was achieved in all 20 patients who had completed at least four endoscopic sclerotherapy courses with total eradication of varices in 16 (80%). The mean (+/- SD) number of endoscopic sclerotherapy courses and time required for variceal eradication was 6.06 (+/- 1.87) and 9.1 (+/- 4.69) weeks respectively. None of these patients has shown appearance of fresh varices in a follow up of 18.47 +/- 8.50 weeks (range six to 38 weeks). Six patients died; all deaths were caused by progressive hepatic encephalopathy. Complications usually seen were dysphagia, retrosternal pain and fever; these were mild and easily tolerated by the patients. Rebleeding occurred in four patients who had received less than four endoscopic sclerotherapy courses. Absolute alcohol appears to be an effective, safe, economical, and freely available sclerosant. advocate endoscopic sclerotherapy as the first line of treatment for acute variceal bleeding and recommend a weekly schedule for the early eradication of varices.

Thirty-one children with variceal bleeding due to portal hypertension (extrahepatic obstruction 19, non-cirrhotic portal fibrosis five, and cirrhosis of liver seven patients) were treated with endoscopic sclerotherapy with absolute alcohol. Acute variceal bleeding was successfully controlled in 10 patients by emergency sclerotherapy. A 3 weekly schedule of sclerotherapy could achieve obliteration of varices in all the patients. The mean (+/- SD) number of sclerotherapy courses and the time required for variceal eradication was 4.5 +/- 1.7 and 14.4 +/- 3.9 weeks, respectively. During a mean follow-up of 23.3 +/- 11.4 months, variceal recurrence was seen in three (9.7%) patients, two with cirrhosis and one with noncirrhotic portal fibrosis. Recurrence was not seen in any patient with extrahepatic obstruction. Five (16.1%) patients had a rebleed that could be controlled with emergency sclerotherapy. Esophageal stricture developed in four (12.9%) patients and could be dilated easily in all of them. The other complications of sclerotherapy included retrosternal pain, dysphagia, and fever; these were mild and short lasting. Survival in patients with extrahepatic obstruction and noncirrhotic portal fibrosis was 100%. The only death was in a cirrhotic, who died due to terminal hepatic failure. In conclusion, endoscopic sclerotherapy can be recommended as a safe and effective treatment in children for the control of acute variceal bleeding and for variceal obliteration.

To compare the efficacy and safety of one week versus three weeks interval treatment schedules of endoscopic sclerotherapy, injections were carried out in a prospective manner in 96 patients with variceal bleeding; 47 on a one week and 49 on a three weeks treatment schedule. Weekly endoscopic sclerotherapy eradicated oesophageal varices significantly (p less than 0.01) earlier (mean +/- SD 7.1 +/- 2.43 weeks) as compared with the three weeks regimen (mean +/- SD 14.86 +/- 4.86 weeks). The rebleeding rate was also significantly less (p less than 0.05) with weekly endoscopic sclerotherapy (8.5%) as compared with three weeks endoscopic sclerotherapy treatment (26.5%). The amount of alcohol and the number of endoscopic sclerotherapy courses required for complete variceal eradication did not differ significantly between the two groups. Patients undergoing weekly injections were seen to have significantly more oesophageal ulcers (p less than 0.01) as compared with the three weeks group, necessitating at times (23%) postponement of the procedure. There was, however, no difference between the two groups in the frequency of oesophageal stricture formation, dysphagia, retrosternal pain, and fever. Mortality was also similar in the two groups. It can be concluded that a weekly schedule of endoscopic sclerotherapy appears superior to a three weeks schedule.

Amongst the many non-surgical techniques for the treatment of variceal bleeding, endoscopic sclerotherapy (EST) has shown great promise. EST can successfully obliterate esophageal varices and prevent variceal rebleeding. It is also very effective in the control of active bleeding from esophageal varices. The technique of EST is simple and can be carried out with a conventional, forward viewing, flexible endoscope and a teflon injector. Weekly intravariceal injections of an aqueous sclerosant are preferable. Though complications of EST in experienced hands are low, prophylactic EST at present should be advocated only to patients at high risk of bleeding. While controversy exists, most reports indicate that EST improves survival of patients with portal hypertension who have bled from esophageal varices. With regular follow-up endoscopies, recurrence of varices and bleeding from them can be substantially reduced. Sclerotherapy may successfully obliterate gastric varices in some patients either following EST for esophageal varices or by direct gastric variceal injections. For the long-term management of portal hypertension, combination of pharmacotherapy before as well as after eradication of esophageal varices, needs proper evaluation.