Biliary Tract Anatomy and its Relationship with Venous Drainage

Abstract

Portal cavernoma develops as a bunch of hepatopetal collaterals in response to portomesenteric venous obstruction and induces morphological changes in the biliary ducts, referred to as portal cavernoma cholangiopathy. This article briefly reviews the available literature on the vascular supply of the biliary tract in the light of biliary changes induced by portal cavernoma. Literature pertaining to venous drainage of the biliary tract is scanty whereas more attention was focused on the arterial supply probably because of its significant surgical implications in liver transplantation and development of ischemic changes and strictures in the bile duct due to vasculobiliary injuries. Since the general pattern of arterial supply and venous drainage of the bile ducts is quite similar, the arterial supply of the biliary tract is also reviewed. Fine branches from the posterior superior pancreaticoduodenal, retroportal, gastroduodenal, hepatic and cystic arteries form two plexuses to supply the bile ducts. The paracholedochal plexus, as right and left marginal arteries, run along the margins of the bile duct and the reticular epicholedochal plexus lie on the surface. The retropancreatic, hilar and intrahepatic parts of biliary tract has copious supply, but the supraduodenal bile duct has the poorest vascularization and hence susceptible to ischemic changes. Two venous plexuses drain the biliary tract. A fine reticular epicholedochal venous plexus on the wall of the bile duct drains into the paracholedochal venous plexus (also called as marginal veins or parabiliary venous system) which in turn is connected to the posterior superior pancreaticoduodenal vein, gastrocolic trunk, right gastric vein, superior mesenteric vein inferiorly and intrahepatic portal vein branches superiorly. These pericholedochal venous plexuses constitute the porto-portal collaterals and dilate in portomesenteric venous obstruction forming the portal cavernoma. ( J CLIN EXP HEPATOL 2014;4:S18-S26) P ortal cavernoma develops as a bunch of dilated and tortuous hepatopetal collateral venous channels in response to portomesenteric venous obstruction and induces morphological changes in the biliary ducts, referred to as portal biliopathy or portal cavernoma cholagiopathy. Available literature suggest that the venous plexuses draining the bile duct and veins around the head of pancreas act as preferential collateral venous pathways and dilate to form the portal cavernoma. It is believed that anatomically distinct collateral venous channels are available in cases of portal venous obstruction involving portal vein alone or superior mesenteric and splenic veins also. This article is an attempt to review the existing literature on the venous drainage of biliary tract to understand the mechanisms of development of portal cavernoma. Arterial supply of the biliary tract is more extensively studied than the venous drainage and since the general pattern of arterial supply and venous drainage is similar, this article includes the review of arterial supply also. A...

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

“…Detailed arterial supply and venous drainage of the biliary system has been described in an article in this issue of the Journal. 34 In EHPVO multiple porto-portal collateral veins with hepatopetal flow develop to bypass the obstructed segment of the portal vein. These collaterals involve the paracholedochal and epicholedochal venous plexuses and cholecystic veins.…”

Spectrum of biliary abnormalities in portal cavernoma cholangiopathy (PCC) secondary to idiopathic extrahepatic portal vein obstruction (EHPVO)—a prospective magnetic resonance cholangiopancreaticography (MRCP) based study

“…Collateral compression occurs secondary to dilatation of the venous plexuses around the common bile duct (CBD) in response to portal vein thrombosis, leading to fine irregularities due to dilatation of the intramural epicholedochal plexus of Saint and/or extrinsic compression due to dilatation of the extramural paracholedochal plexus of Petren. 6,7,8,9 Besides, it has been proposed that ischaemia occurs as a result of portal vein thrombosis, leading to fibrosis and strictures. [11][12][13][14][15] Ischaemic theory is supported by the observation that in several patients with EHPVO, the biliary abnormalities are not completely reversed following shunt surgery.…”

Biliary Anastomotic Stricture After Adult Living Donor Liver Transplantation With Duct-to-Duct Reconstruction

“…Variceal enlargement of the epicholedochal plexus causes ischemic changes and fibrosis of the CBD due to the reduction in the arterial supply of the CBD wall. 22 We suspected that decreased PV inflow caused by PVSinfluenced liver regeneration and BAS.…”