Choledochal varices

Kim, S; Chew, F S

doi:10.2214/ajr.150.3.578

Cited by 32 publications

(13 citation statements)

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“…The veins of the epicholedochal plexus are not larger than 1 mm. 26 The paracholedochal venous plexus the right gastric vein. 23 In postmortem specimens Vellar 23 has demonstrated retrograde filling of the marginal veins and the venous plexus on the CBD after transecting the CBD and all communicating veins at the upper border of duodenum and suggested that this bidirectional pathway ensures good results seen in end-to-end anastomosis in liver transplantation.…”

Section: Venous Drainage Of Biliary Tractmentioning

confidence: 99%

Biliary Tract Anatomy and its Relationship with Venous Drainage

Babu¹,

Sharma

2014

Journal of Clinical and Experimental Hepatology

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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...

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Section: Venous Drainage Of Biliary Tractmentioning

confidence: 99%

Biliary Tract Anatomy and its Relationship with Venous Drainage

Babu¹,

Sharma

2014

Journal of Clinical and Experimental Hepatology

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“…Saint's anatomic studies suggest that dilatation of the PACD veins will occur first in portal hypertension, and ECD varices related to Saint venous plexus have not been described without accompanying PACD varices. 84 The varices have been labeled as intracholedochal varices and currently EUS appears to be the investigation of choice in tracing the origin, caliber, entry, and course of ICD varices throughout the CBD. 85 ICDV can temporarily disappear during controlled hypotension with nitroglycerin infusion and allow therapeutic completion of ERCP in PHB.…”

Section: Biliary Varicesmentioning

confidence: 99%

Collateral Pathways in Portal Hypertension

Sharma

Rameshbabu²

2012

Journal of Clinical and Experimental Hepatology

127

104

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Presence of portosystemic collateral veins (PSCV) is common in portal hypertension due to cirrhosis. Physiologically, normal portosystemic anastomoses exist which exhibit hepatofugal flow. With the development of portal hypertension, transmission of backpressure leads to increased flow in these patent normal portosystemic anastomoses. In extrahepatic portal vein obstruction collateral circulation develops in a hepatopetal direction and portoportal pathways are frequently found. The objective of this review is to illustrate the various PSCV and portoportal collateral vein pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. ( J CLIN EXP HEPATOL 2012;2:338-352) A lmost any vein in the abdomen may serve as a potential collateral channel to the systemic circulation. Presence of abnormal collateral vessels appears to be one of the most sensitive (70-83%) and specific sonographic signs for the diagnosis of portal hypertension. 1 When blood flow through a vessel or a vascular bed is obstructed due to occlusion, as in EHPVO, or distortion, as in liver cirrhosis, collateral pathways open up as blood bypasses the occlusion or obstruction, always flowing down a pressure gradient from a high pressure to a low-pressure vessel or bed. The formation of portosystemic pathways occurs due to reopening of collapsed embryonic channels or reversal of the flow within existing adult veins. 2,3 The number of collateral channels depends on the severity of portal hypertension i.e. the differential gradient driving the flow between the portal and the systemic circulations and the duration of portal hypertension. The more severe and more prolonged the portal hypertension, the higher are the number of portosystemic pathways. However, this traditional hypothesis has been challenged and it has been suggested that the formation of portosystemic collateral circulation may be due in part to angiogenesis driven by vascular endothelial growth factor. 4,5 Almost 50 years have passed since the first detailed description of portosystemic collateral veins (PSCV) in portal hypertension appeared. 6 Precise mapping of PSCV is essential to therapeutic decisions and multidetector computerized tomography (MDCT) is sometimes used for cartography of PSCV. 7 EUS is increasingly being used for evaluation of PSCV and additionally provides an option for performing therapeutic interventions. 8 In addition to PSCV, PPCV pathways are frequently found in extrahepatic portal vein obstruction (EHPVO). The objective of this review is to illustrate the various PSCV and PPCV pathways pertinent to portal hypertension in liver cirrhosis and EHPVO. NORMAL PORTOSYSTEMIC ANASTOMOSESThe left gastric vein (LGV) anastomoses with the esophageal veins, which in turn drain into the azygos vein (AV). The superior rectal vein (SRV) anastomoses with the middle and inferior rectal veins (IRV), which are, respectively, tributaries of the internal iliac and the pudendal veins. The paraumbilical vein (PUV) anastomoses with subcutaneous veins in the anterior abdominal...

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“…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.…”

Section: Introductionmentioning

confidence: 99%

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

Jabeen

Robbani

Choh

et al. 2016

BJR

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Objective: To characterize biliary abnormalities seen in portal cavernoma cholangiopathy (PCC) on MR cholangiopancreaticography (MRCP) and elucidate certain salient features of the disease by collaborating our findings with those of previous studies. Methods: We prospectively enrolled 52 patients with portal cavernoma secondary to idiopathic extrahepatic portal vein obstruction, who underwent a standard MRCP protocol. Images were analyzed for abnormalities involving the entire biliary tree. Terms used were those proposed by the Indian National Association for Study of the Liver. Angulation of the common bile duct (CBD) was measured in all patients with cholangiopathy.

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Choledochal varices

Cited by 32 publications

References 0 publications

Biliary Tract Anatomy and its Relationship with Venous Drainage

Biliary Tract Anatomy and its Relationship with Venous Drainage

Collateral Pathways in Portal Hypertension

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

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