A Controlled Study of the Prophylactic Portacaval Shunt

Resnick, Robert H.; Chalmers, Thomas C.; Ishihara, Albert M.; Garceau, Arthur J.; Callow, Allan D.; Schimmel, Elihu M.; O'Hara, Edward T.

doi:10.7326/0003-4819-70-4-675

Cited by 226 publications

(41 citation statements)

References 14 publications

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“…These older studies suggested that, in patients with alcoholic and nonalcoholic causes of cirrhosis, the risk of variceal hemorrhage is highest in the first year after diagnosis of varices, and decreases with time afterward. [11][12][13][14][15]20 (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

Propranolol for the prevention of first esophageal variceal hemorrhage: A lifetime commitment?

Abraczinskas

2001

Hepatology

117

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Although ␤ blockers have had significant impact in the treatment of portal hypertension, the question of how long they should be continued for prevention of variceal hemorrhage remains unknown. Prospective studies on ␤ blockers to prevent variceal hemorrhage lack long-term follow-up, and indefinite administration of ␤ blockers for primary prevention of variceal bleeding has become standard practice. The aim of this study was to determine the outcomes of patients in whom ␤ blocker therapy was discontinued. Patients completing a prospective, randomized, double-blind, placebo-controlled trial of propranolol for the primary prevention of variceal hemorrhage were tapered off of propranolol and placebo and followed prospectively for subsequent events. Of the 49 patients in the follow-up study (25 former propranolol, 24 former placebo), 9 experienced variceal hemorrhage (6 former propranolol, 3 former placebo). Following withdrawal of propranolol, the freedom from variceal bleeding was not significantly different between these 2 groups of patients, suggesting that the protective effect of propranolol against variceal hemorrhage, noted previously, was no longer present. Seventeen patients died (12 former propranolol, 5 former placebo) during the follow-up study. Cumulative survival was longer in the placebo group. These trends for EVH and survival were opposite to those observed in the original study population while patients were taking medication. When propranolol is withdrawn, the risk of variceal hemorrhage returns to what would be expected in an untreated population. Patients who discontinue ␤ blockers experience increased mortality compared with an untreated population. These observations support the current practice of indefinite prophylactic therapy. (HEPATOLOGY 2001;34:1096-1102.)

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Section: Discussionmentioning

confidence: 99%

Propranolol for the prevention of first esophageal variceal hemorrhage: A lifetime commitment?

Abraczinskas

2001

Hepatology

117

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“…4 Reduced portal pressure also decreases intestinal venous congestion and could increase blood flow through the hepatic parenchyma and hence increase liver function. 5 In 1991, Habib et al 6 first introduced the concept of mechanical pumping of portal blood to enhance hepatic portal inflow. Since then, we have seen a number of publications in this field.…”

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confidence: 99%

The effect of mechanically enhancing portal venous inflow on hepatic oxygenation, microcirculation, and function in a rabbit model with extensive hepatic fibrosis

et al. 1999

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Enhancing the portal venous blood flow (PVBF) has been shown to reduce portal pressure and intrahepatic vascular resistance and to improve liver function in isolated cirrhotic rodent livers in vitro. The aim of this study was to assess the short-term effect of mechanically pumping the portal inflow on hepatic microcirculation (HM), oxygenation, and function in an animal model of extensive hepatic fibrosis. New Zealand white rabbits underwent laparotomy and exposure of the liver: group 1 (n ‫؍‬ 7) were normal controls; group 2 (n ‫؍‬ 7) had hepatic fibrosis. Total hepatic blood flow (THBF) and HM was measured along with continuous monitoring of intrahepatic tissue oxygenation using near infrared spectroscopy (NIRS). Baseline hepatic hemodynamics and liver function were measured in both groups. PVBF was then increased by 50% over a 3-hour period in the hepatic fibrosis group using a miniature portal pump designed for human implantation, and the hemodynamics were monitored continuously. Liver function tests were repeated after portal pumping. In comparison with normal controls, animals with hepatic fibrosis had a higher portal pressure (13.0 ؎ 3.6 vs. 3.7 ؎ 1.4 mm Hg, P F .001, mean ؎ SD vs. controls), reduced PVBF (52.4 ؎ 24.6 vs. 96.9 ؎ 21.1 mL/min, P ‫؍‬ .003), and increased portal vascular resistance (P ‫؍‬ .001). THBF and flow in the HM was lower than in controls, and liver function tests were abnormal. After a 3-hour period of enhanced portal flow in animals with hepatic fibrosis, the portal pressure greatly reduced (13.0 ؎ 3.6 to 2.5 ؎ 1.1 mm Hg, P F .001) as did the intrahepatic portal resistance ( Current aims in the management of portal hypertension are to reduce portal venous pressure (PVP), to increase blood flow through hepatic parenchyma, 1 and to decompress esophageal and gastric varices. 2,3 Reduction of PVP minimizes the risk of bleeding from varices, the likelihood of hepatic encephalopathy and problems relating to first pass uptake of drugs. 4 Reduced portal pressure also decreases intestinal venous congestion and could increase blood flow through the hepatic parenchyma and hence increase liver function. 5 In 1991, Habib et al. 6 first introduced the concept of mechanical pumping of portal blood to enhance hepatic portal inflow. Since then, we have seen a number of publications in this field. 7-10 Cardoso et al. [7][8][9] showed that augmenting portal inflow to isolated perfused cirrhotic rat and human livers decreased intrahepatic resistance without a change in intrahepatic shunting and resulted in liver function improvement. Bernadich et al. 10 found that in rats with portal hypertension owing to portal vein stenosis, mechanical portal pumping decreased portal pressure and portal-systemic shunting without having a significant effect on systemic hemodynamics. In cirrhosis, several early studies provided evidence that it was vasoactive mediators coupled with the extensive destruction of hepatocytes and nodular regeneration that contributed to the pathogenesis of portal hypertension. [11][12][13]...

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“…By and large, β-blockers and EVL are preferred in this setting [2][3][4]. Also, there is evidence from controlled trials that prophylactic shunt surgery in cirrhotics is associated with faster decompensation and higher rate of liver failure despite protection from variceal bleeding [34][35][36]. But the results are different when Sugiura devascularization technique is used for prophylactic indications.…”

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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A Controlled Study of the Prophylactic Portacaval Shunt

Cited by 226 publications

References 14 publications

Propranolol for the prevention of first esophageal variceal hemorrhage: A lifetime commitment?

Propranolol for the prevention of first esophageal variceal hemorrhage: A lifetime commitment?

The effect of mechanically enhancing portal venous inflow on hepatic oxygenation, microcirculation, and function in a rabbit model with extensive hepatic fibrosis

Current Role of Surgery in Portal Hypertension

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