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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.

Background: Isolated ectopic gastric varices (IGV2) are present either in the body or antrum of the stomach or upper duodenum. The prevalence, natural history and clinical significance of these varices has not been adequately described., Materials and Methods: Consecutive patients with portal hypertension, prospectively studied and diagnosed to have IGV2, were assessed for their time of appearance - primary (at first presentation) or secondary (after obliteration of oesophageal varices), association with other varices, portal hypertensive gastropathy and any overt bleeding., Results: Fifty-three of the 1128 (4.7%) patients had IGV2. The IGV2 were commonly seen in the antrum (53%), duodenum (32%), or at both sites (11%) and rarely in body and fundus (4%). IGV2 were predominantly (84.9%) secondary in origin, developing after oesophageal variceal obliteration. The median time for emergence of secondary IGV2 was 8.2 months for patients with cirrhosis, 12.8 months for non-cirrhotic portal fibrosis and 10.8 months for extra-hepatic portal vein obstruction. Eight (15%) patients had primary IGV2, 6 of them had underlying portal vein obstruction. Portal gastropathy (p < 0.05) and UGI bleeding were more common in the secondary than in primary IGV2. Bleeding due to IGV2 was seen only in 3 (5.7%) patients during a mean follow-up of 36.3 +/- 12.1 months, and could be successfully managed with endoscopic ligation or obliteration., Conclusions: Isolated ectopic gastric varices are not uncommon and generally develop following obliteration of main variceal columns. They rarely bleed and often can be managed with endoscopic interventions., (Copyright 2003 S. Karger AG, Basel)

Gastric varices and portal hypertensive gastropathy (PHG) are an important complication of both generalized and segmental portal hypertension. The natural history and risk factors for bleed from GV are not extensively studied as that for esophageal varices. Recently, effective therapy for gastric variceal bleed in form of tissue adhesives, balloon-occluded retrograde transvenous obliteration of gastric varices (BRTO) has been developed. Further advances are still needed regarding natural history, risk factors, bleeding, and mechanism of GV rupture.

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.

Background/aims: Endoscopic variceal ligation and endoscopic sclerotherapy are both recommended for the prevention of variceal rebleeding. To compare their efficacy, their influence on gastric varices and the development of portal gastropathy, 95 patients with variceal bleeding were studied., Methods: The patients were randomized to receive weekly endoscopic sclerotherapy using alcohol (n=48) or endoscopic variceal ligation (n=47). The endoscopic sclerotherapy and endoscopic variceal ligation groups were comparable in etiology, severity of liver disease and grade of varices., Results: In the arrest of acute bleed, endoscopic sclerotherapy and endoscopic variceal ligation were comparable (86% vs. 80%, p=ns). Endoscopic variceal ligation as compared to endoscopic sclerotherapy, obliterated esophageal varices in fewer sessions (4.1+/-1.2 vs. 5.2+/-1.8, p<0.01) and a shorter time (4.4+/-1.3 vs. 6.9+/-3.4 wk, p<0.01). Three (6.4%) patients bled after endoscopic variceal ligation and 10 (20.8%) after endoscopic sclerotherapy (p<0.05). The actuarial percentage of variceal recurrence during a follow-up of 8.5+/-4.4 months, was higher after endoscopic variceal ligation than endoscopic sclerotherapy (28.7% vs 7.5%, p<0.05). Esophageal stricture formation after endoscopic sclerotherapy occurred in five (10.4%) patients, but in none after endoscopic variceal ligation. Significantly more patients developed gastropathy after endoscopic sclerotherapy than ligation (20.5% vs. 2.3%; p=0.02). Endoscopic sclerotherapy (52%) and endoscopic variceal ligation (59%) were equally effective in obliterating the lesser curve gastric varices. Six patients died: three in each group., Conclusions: (i) Endoscopic sclerotherapy and endoscopic variceal ligation were equally effective in controlling acute bleed; (ii) endoscopic ligation achieved variceal obliteration faster and in fewer treatment sessions; (iii) endoscopic variceal ligation had a significantly lower rate of development of portal gastropathy and rebleeding, (iv) while both techniques influenced gastric varices equally, there was significantly higher esophageal variceal recurrence after endoscopic variceal ligation than sclerotherapy.

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.

Objective: Effective and safe reduction of variceal pressure by pharmacological means., Methods: Twenty patients with portal hypertension and large esophageal varices. Ten patients received i.v. nitroglycerin (300 micrograms-bolus) and an equal number received a combination of i.v. nitroglycerin (150 micrograms) and metoclopramide (20-mg bolus). Continuous measurement of variceal pressure and systemic hemodynamics was carried out., Results: Compared with the baseline, the variceal pressure was reduced at 10 min after injection of 300 micrograms nitroglycerin (22.3 +/- 7.9 vs. 17.3 +/- 7 mm Hg, p, not significant); the percentage reduction was 23.5 +/- 15.8%. With the combination of low dose (150 micrograms) nitroglycerin and metoclopramide, variceal pressure significantly decreased from 23.1 +/- 4.7 to 15.9 +/- 5.9 mm Hg (p < 0.01) (a reduction of 29.5 +/- 24.1%). There was no significant alteration in the heart rate or mean arterial pressure with either regimen., Conclusions: Our results suggest that a combination of i.v. metoclopramide and low-dose nitroglycerin reduces variceal pressure more effectively than high-dose nitroglycerin used alone. This combination should be further evaluated in the control of acute variceal bleeding.

In search of an effective agent for decreasing intravariceal pressure, 27 patients with portal hypertension and large esophageal varices were studied. Thirteen patients received iv nitroglycerin (150-micrograms bolus), and 14 received iv metoclopramide (20-mg bolus). Continuous measurement of variceal pressure and systemic hemodynamics was carried out. Compared with the baseline, the variceal pressure was significantly reduced 10 min after nitroglycerin injection (20.23 +/- 3.1 vs. 14.6 +/- 4.8 mm Hg, p < 0.05): the percentage reduction was 27 +/- 25.4%. With metoclopramide, variceal pressure decreased by 12.7 +/- 22%; from 21.9 +/- 5.6 to 19.1 +/- 7.7 mmHg (p = NS). There was no significant alteration in the heart rate and mean arterial pressure with either drug. Our results thus suggest that in the dosages used, intravenous nitroglycerin effectively and safely reduces the variceal pressure. Further studies using a combination of nitroglycerin and metoclopramide need to be considered.

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)

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.

Esophageal variceal ulcers have been held responsible for most postsclerotherapy complaints. To investigate a possible relation between these ulcers and symptoms, we followed for 4 weeks 40 patients with portal hypertension who had received a single course of intravariceal sclerotherapy. All 40 patients were found to have mucosal variceal ulcers on the day after sclerotherapy. One or more symptoms were given by 26 (65%) patients; dysphagia by 53% (mean duration 4.6 +/- 2.2 days), retrosternal pain by 28% (mean duration 3.0 +/- 2.5 days), and fever by 15% (mean duration 2.1 +/- 0.4 days). A gastric variceal ulcer was responsible for bleeding in one (2.2%) patient. We found no correlation between the occurrence and duration of symptoms and the presence of variceal ulcers. While symptoms were transient, ulcers persisted for several days to weeks in most patients. Patients who had received a higher amount of sclerosant developed larger ulcers (greater than 1 cm) with more symptoms and healing was more delayed than in those who had received lesser amounts and developed smaller ulcers (less than 1 cm). In patients with a serum albumin level greater than 3.0 g/dl, ulcers healed more often than in those with a less than 3.0 g/dl albumin (72 versus 18%, p less than 0.05). Development of mucosal ulcers is a natural consequence of intravariceal sclerotherapy and it appears unrelated to symptoms. The chemical nature and the volume of the injected sclerosant are probably responsible for the symptoms after sclerotherapy. Further, postsclerotherapy ulcers heal spontaneously, more often in patients with good nutritional status.

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.

One hundred one patients, 54 with cirrhosis of liver, 31 with noncirrhotic portal fibrosis (NCPF), and 16 with extrahepatic obstruction (EHO), were followed up at monthly intervals for a mean (+/- SD) period of 17.9 +/- 4.8 months after achieving total variceal eradication with endoscopic sclerotherapy. Recurrence of esophageal varices was seen in 19 (18.8%) patients, 12 with cirrhosis and seven with NCPF, within a mean (+/- SD) period of 5.7 +/- 1.6 months. No patient with EHO showed recurrence. Three (2.9%) patients rebled from the recurred varices. Mean (+/- SD) number of sclerotherapy sessions and the amount of absolute alcohol required for eradication of recurred varices were 1.6 +/- 0.8 and 3.6 +/- 1.8 ml, respectively. Dysphagia and esophageal stricture were present in 15 (14.9%) patients with nearly similar frequency in patients with cirrhosis, NCPF, and EHO. Dysphagia in four patients with stricture improved without dilatation. While there were no deaths in patients with NCPF and EHO, 11 patients with cirrhosis died. There was significant (p less than 0.01) improvement in the liver status of surviving patients with cirrhosis after variceal eradication. It can be concluded that variceal recurrence and rebleeding are not major problems after sclerotherapy. Sclerotherapy probably helps in spontaneous improvement of the liver status of surviving cirrhotics and reduces long-term morbidity and mortality of patients with NCPF and EHO.

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.

Of 309 patients with portal hypertension, gastric varices were found in 48 (16 per cent). While the majority (88 per cent) of the patients had gastric varices in association with oesophageal varices, 6 (12 per cent) patients had 'isolated' gastric varices. Gastric varices were seen significantly (P less than 0.01) more often with grade 4 than with grade 3 varices. In 11 (28 per cent) of the 40 patients who completed sclerotherapy for oesophageal varices, gastric varices disappeared concurrently on eradication of oesophageal varices or during the following 6 months. Of the initial five patients with gastric varices who received direct intravariceal injections, four rebled; this technique was therefore replaced by combination (paravariceal + intravariceal) gastric variceal sclerotherapy. Emergency combination sclerotherapy successfully controlled bleeding from gastric varices in six of the eight treated patients. Thirty-two patients entered a programme of elective combination gastric variceal sclerotherapy. Variceal obliteration was achieved in 12 cases (38 per cent) and reduction in size was noted in another 7 patients (22 per cent) after a minimum of four courses. There were 11 (23 per cent) deaths, 8 due to uncontrolled bleeding from gastric varices and 3 due to hepatic coma. The other complications of gastric variceal sclerotherapy were minor and included retrosternal pain, fever and dysphagia. It is concluded that gastric varices often coexist with large oesophageal varices. If they persist for 6 months after eradication of oesophageal varices, a combination of paravariceal and intravariceal sclerotherapy should be attempted for their obliteration.

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

Forty-five consecutive patients underwent sclerotherapy with absolute alcohol. Post-sclerotherapy ulcers were detected in all of them (100%) on the following day. In order to evaluate its influence on ulcer healing, 20 patients were given sucralfate (1 g QID before meals), while 25 patients received identical-looking placebo, in a double-blind randomised manner. Endoscopy done at weekly intervals revealed healing of ulcers in 25%, 55%, 95% and 100% in the sucralfate, and 24%, 40%, 72% and 84% in the placebo group at 1, 2, 3, and 4 weeks, respectively. Differences between the two groups were not significant. Gastric variceal ulcers healed better with sucralfate (7 out of 7) than placebo (0 out of 2). Healing was influenced by the size of the ulcer. At two weeks, 63% of ulcers less than 1 cm, 43% of ulcers 1-2 cm, and only 16.6% of ulcers greater than 2 cm had healed. The size of the ulcer also correlated with the amount of the sclerosant injected. Our results show that (a) mucosal ulcers universally develop after adequate sclerotherapy, (b) most ulcers heal spontaneously, (c) sucralfate does not hasten ulcer healing, with the exception of gastric variceal ulcers, (d) a larger amount of sclerosant produces larger ulcers that take longer to heal.

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.

Forty eight patients with oesophageal varices were serially endoscoped over a period of 3 weeks for the presence of oesophageal ulcers after the first course of sclerotherapy with absolute alcohol. Post-sclerotherapy oesophageal ulcers were seen in 94% patients on day 1, in 69% patients at 1 week and in only 12.5% patients at the end of 3 weeks. A strong correlation (r = + 0.88) was observed between the incidence of ulceration and the amount of sclerosant injected. In fact, all patients who received 3 ml or more of the sclerosant showed development of oesophageal ulcers. It can be concluded that oesophageal ulcers are probably a necessary accompaniment of sclerotherapy and should not be considered an avoidable complication.

Sixty-three patients with acute variceal haemorrhage were treated with the Sengstaken-Blakemore tube (SBT). Bleeding was initially controlled with the gastric balloon in 37 patients (60%) and with both gastric and oesophageal balloons in another 17 (27%), giving overall primary success in 54 patients (87%). Sixteen (26%) patients re-bled within 24 hours of deflation of the tube. Repeat balloon tamponade helped in controlling bleeding in 9 of these. Thus, a total of 47 (75%) patients stopped bleeding with SBT. There was no mortality. The only major complication was pulmonary infection (15%), which improved with antibiotics. Use of the SBT was found to be simple, quick, low cost and attended with few complications. Its use is recommended in patients with acute variceal bleeding, especially in developing countries with limited resources.

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.

Forty-seven patients with esophageal variceal bleeding were randomly allocated to undergo sclerotherapy on a 3 weekly schedule with either 5% ethanolamine oleate (23 patients) or absolute alcohol (24 patients), in an attempt to compare the efficacy and safety of the two sclerosants. Sclerotherapy with absolute alcohol eradicated esophageal varices significantly earlier compared with ethanolamine oleate (12.9 +/- 5.2 vs 22.3 +/- 8.2 wk, respectively, p less than 0.001). The mean number of injection courses and the mean amount of sclerosant required for variceal obliteration was also significantly (p less than 0.001) less in the alcohol-injected group. Although the total number of rebleeding episodes were significantly (p less than 0.05) less in the alcohol-injected group, the frequency of rebleeding was not significantly different between the two groups (20.8% vs 30.4%, respectively, p greater than 0.05). Two (8.1%) patients died due to rebleeding in the ethanolamine-injected group, whereas in the alcohol group, none died. There was no significant difference in the frequency of complications with the two sclerosants. Besides the relative ease of rapid injection due to its aqueous nature, alcohol is readily available and relatively economical (total cost of sclerosant per patient; alcohol US $0.50, ethanolamine US $60). In conclusion, absolute alcohol appears to be a useful alternative to 5% ethanolamine oleate as a variceal sclerosant.

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.