Side-to-side lienorenal shunt without splenectomy in noncirrhotic portal hypertension in children

Mitra, Suvradeep; Rao, K. L. N.; Narasimhan, K. L.; Dilawari, J. B.; Batra, Yatindra Kumar; Chawla, Yogesh; Thapa, Babu Ram; Nagi, B; Walia, B. N. S.

doi:10.1016/0022-3468(93)90239-h

Cited by 71 publications

(71 citation statements)

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“…Whereas results of earlier reports had been disappointing, 28 the recent reports have shown rebleeding rates of 7% to 27%, operative mortality of 0% to 5%, and shunt thrombosis of 7% to 13%. [5][6][7][8][29][30][31] In some cases, shunt surgery may not be technically possible because of thrombosis of splenic and superior mesenteric veins or small-sized splenic vein. 1,8,30,31 Recently, a Rex shunt that involves insertion of venous jugular autograft between the left portal vein and superior mesenteric vein has been performed successfully in a small number of patients with EXPVO.…”

Section: Discussionmentioning

confidence: 99%

“…[5][6][7][8][29][30][31] In some cases, shunt surgery may not be technically possible because of thrombosis of splenic and superior mesenteric veins or small-sized splenic vein. 1,8,30,31 Recently, a Rex shunt that involves insertion of venous jugular autograft between the left portal vein and superior mesenteric vein has been performed successfully in a small number of patients with EXPVO. 32,33 Although a technically demanding procedure, it obviates technical problems associated with blocked splenic vein and restores the portal blood flow to the liver.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Bleeding from the esophageal varices is the most common presenting feature of EXPVO and is associated with significant morbidity. 1,3,4 Although optimal treatment for these patients is a matter of controversy, current therapeutic options include a variety of surgical procedures [5][6][7][8] or endoscopic injection sclerotherapy (EIS). 1,2,[9][10][11][12] Although EIS provides an effective treatment for esophageal varices, there is potential for improvement because sclerotherapy is associated with substantial complications, including rebleeding at a rate of 20% to 30% and sclerosant-induced esophageal injury that may cause ulceration, bleeding, perforation, or stricture formation.…”

Section: E Xtrahepatic Portal Venous Obstruction (Expvo) Ismentioning

confidence: 99%

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Endoscopic ligation compared with sclerotherapy for bleeding esophageal varices in children with extrahepatic portal venous obstruction

et al. 2002

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Endoscopic sclerotherapy is an effective treatment for bleeding esophageal varices, but it is associated with significant complications. Endoscopic ligation, a new form of endoscopic treatment for bleeding varices, has been shown to be superior to sclerotherapy in adult patients with cirrhosis. To determine the efficacy and safety of endoscopic sclerotherapy and ligation, the 2 methods were compared in a randomized control trial in 49 children with extrahepatic portal venous obstruction who had proven bleeding from esophageal varices. Twenty-four patients were treated with sclerotherapy and 25 with band ligation. No significant differences were found between the sclerotherapy and ligation groups in arresting active index bleeding (100% each) and achieving variceal eradication (91.7% vs. 96%, P ‫؍‬ .61). Band ligation eradicated varices in fewer endoscopic sessions than did sclerotherapy (3.9 ؎ 1.1 vs. 6.1 ؎ 1.7, respectively, P < .0001). The rebleeding rate was significantly higher in the sclerotherapy group (25% vs. 4%, P ‫؍‬ .049), as was the rate of major complications (25% vs. 4%, P ‫؍‬ .049). After eradication, esophageal variceal recurrence was not significantly different in patients treated by ligation than by sclerotherapy (17.4% vs. 10%, P ‫؍‬ .67). In conclusion, variceal band ligation in children is a safe and effective technique that achieves variceal eradication more quickly, with a lower rebleeding rate and fewer complications compared with sclerotherapy. (HEPATOLOGY 2002;36:666-672.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: E Xtrahepatic Portal Venous Obstruction (Expvo) Ismentioning

confidence: 99%

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Endoscopic ligation compared with sclerotherapy for bleeding esophageal varices in children with extrahepatic portal venous obstruction

et al. 2002

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“…60 The role of surgery is limited to those who fail to respond to endoscopic therapy. 61 Selective shunts, like distal splenorenal shunts, are preferred due to a low incidence of postshunt encephalopathy. If massive splenomegaly is present, splenectomy with a proximal shunt may be done.…”

Section: Managementmentioning

confidence: 99%

Noncirrhotic Portal Hypertension

Rajekar¹,

Vasishta²,

Chawla³

et al. 2011

Journal of Clinical and Experimental Hepatology

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Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained

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“…Proximal splenorenal shunt (PSRS) with splenectomy [9,26] iii. S-side splenorenal shunt without splenectomy (Mitra et al [27]) c. Selective or partial portosystemic shunts i. Distal splenorenal shunt (DSRS) [28] ii. Sarfeh's small diameter (8 mm) interposition (H graft) PCS [29] iii.…”

Section: Management Of Portal Hypertensionmentioning

confidence: 99%

Current Role of Surgery in Portal Hypertension

Pal

2011

Indian J Surg

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Treatment for portal hypertension (PHT) has evolved from surgery being the only option during the 1970s to the wide range of options currently available. Surgery has not vanished from the therapeutic armamentarium, but its role has changed and is constantly evolving. The present review primarily focuses on the role of surgery in tackling patients with PHT and varices with regard to the Indian scenario and also looks at its relevance, given the availability of a host of other therapeutic options.Keywords Portal hypertension . Portosystemic shunt . Surgery . Variceal haemorrhage Pathophysiology of PHTFor understanding how surgery can help modify the natural course in patients with PHT, it is necessary to understand its pathophysiology and the natural history of varices in such patients. PHT is usually the consequence of increased resistance to portal blood flow coupled with increased blood flow through the splanchnic circulation because of a hyperdynamic circulatory state that exists both in cirrhotics and to some extent in noncirrhotic etiologies (large congested splenomegaly) as well. Traditionally, at the ultrastructural level, PHT has been classified into presinusoidal, sinusoidal, and postsinusoidal. It is for the sinusoidal and postsinusoidal blocks that there is an accurate but invasive way of monitoring the portal pressure by using the method to estimate the hepatic venous pressure gradient (HVPG) in the vascular/hemodynamic lab [1][2][3]. In cirrhotic patients, as about a third to half of them will actually have PHT; HVPG >5 mmHg indicates PHT. PHT becomes clinically significant when the HVPG is ≥10 mmHg [1][2][3]. This is the pressure threshold when PHT leads to the formation of esophagogastric varices, retroperitoneal and periportal collaterals, hypersplenism, low serum albuminascitic albumin gradient ascites, spontaneous bacterial peritonitis, etc. Varices rupture and bleed only when the HVPG >12 mmHg [1][2][3]. Natural History of PHTIt has been estimated that varices are present in about 30-40% of compensated cirrhotics and nearly two-thirds of the decompensated patients. In cirrhotic patients without varices on the first endoscopy, the annual incidence of new varices is between 5% and 10% [1,4]. Once developed, the progression of varices from small to large depends on the deterioration of liver function and continued hepatic insult (virus-, alcohol-, metabolic-, drug-induced, etc.). The overall annual incidence of bleeding is about 4% and this increases to 15% per year in those with large varices, red signs, and poor Child's status [1,[4][5][6]. About a third of the cirrhotic patients with varices will bleed and the mortality following each episode of bleeding is about 20% (maybe higher) in experienced tertiary health centers. Early mortality (within 6 weeks) following an acute episode of variceal bleeding depends on the etiology of PHT, the severity of underlying liver disease (Child's C, model for end-stage liver disease [MELD] >18), actively bleeding varices, bleeding gastric varices (GV...

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Side-to-side lienorenal shunt without splenectomy in noncirrhotic portal hypertension in children

Cited by 71 publications

References 10 publications

Endoscopic ligation compared with sclerotherapy for bleeding esophageal varices in children with extrahepatic portal venous obstruction

Endoscopic ligation compared with sclerotherapy for bleeding esophageal varices in children with extrahepatic portal venous obstruction

Noncirrhotic Portal Hypertension

Current Role of Surgery in Portal Hypertension

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