Current Role of Surgery in Portal Hypertension

Abstract

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...

Extra Hepatic Portal Vein Obstruction with Solitary Left Kidney: A Case Report

“…Surgical management includes esophagogastric devascularisation with or without splenectomy and porto-systemic shunt surgeries. 4 Outcome of splenectomy and esophagogastric devascularisation in case of EHPVO is found to be good. Esophageal varices has been found to be resolved in 62% cases, gastric varices in 100% cases after splenectomy and esophagogastric devascularisation.…”

Surgical management of noncirrhotic portal hypertension

“…PSSs can be classified as nonselective (decompress the entire portal system by diverting all portal flow), selective (decompress only the variceal‐bearing compartment of the portal venous system and preserve some portal flow to the liver), and partial (incompletely decompress the portal system and maintain some portal flow) . Nonselective PSS include end‐to‐side and side‐to‐side portocaval shunts (Fig.…”

“…As a bridge to transplant, a side‐to‐side PSS (either mesocaval or portocaval) can be performed if the retrohepatic vena cava is patent, but cases where caudate hypertrophy results in caval occlusion require a long mesoatrial shunt. Mesocaval shunts are often preferred because of not needing hilar dissection and being technically simpler to construct, but late graft occlusion is common when a prosthetic graft is employed because of the underlying hypercoagulability . Mesenterico‐left portal vein bypass is, at present, the treatment of choice in EPVO because it restores the normal portal flow to the liver, although PSS (especially distal splenorenal shunt) can be used in cases of unfavorable anatomy …”

“…PSSs can be classified as nonselective (decompress the entire portal system by diverting all portal flow), selective (decompress only the variceal-bearing compartment of the portal venous system and preserve some portal flow to the liver), and partial (incompletely decompress the portal system and maintain some portal flow). 4,5 Nonselective PSS include end-to-side and side-to-side portocaval shunts ( shunt. The only portoportal shunt is the mesenterico-left portal vein bypass (Rex shunt), which restores the splanchnic flow to the liver, and thus its physiology and function, through the connection between the superior mesenteric vein and the portal system at the level of the recessus of Rex (Fig.…”

“…Mesocaval shunts are often preferred because of not needing hilar dissection and being technically simpler to construct, but late graft occlusion is common when a prosthetic graft is employed because of the underlying hypercoagulability. 5 Mesenterico-left portal vein bypass is, at present, the treatment of choice in EPVO because it restores the normal portal flow to the liver, although PSS (especially distal splenorenal shunt) can be used in cases of unfavorable anatomy. 6 Outcomes After Surgery for NCPH Shunt surgery effectively prevents rebleeding from esophageal varices and also improves portal gastropathy, portal biliopathy, and growth retardation.…”