Cavernous transformation of the portal vein SreyRam Kuy, MD, MHS,a Anahita Dua, MD,b,c Joseph Rieland, BS,d and David C. Cronin II, MD, PhD,e Shreveport, La; Milwaukee, Wisc; and Houston, Tex
A male patient with an unknown medical history sustained injuries that were deemed incompatible with life. He became an organ donor. At the time of donor liver harvest, periportal collaterals were seen around the liver (A), with webs visualized inside the portal vein (B) consistent with cavernous transformation of the portal vein (CTPV). This made the liver unsuitable for transplantation, and the procedure was aborted. DISCUSSION Since Balfour and Stewart1 first reported CTPV in 1869, it remains a disease with the potential for insidious clinical sequel. CTPV, also known as portal cavernoma, is the result of portal vein thrombosis that causes the formation of periportal or intrahepatic venous collaterals. CTPV is also referred to as a portal cavernoma, due to the spongelike appearance of the portal vein. In CTPV, a partial recanalization of the thrombosed portal vein occurs with the formation of venous collaterals in the hepatocolic and hepatoduodenal ligaments, along the gallbladder, and on the peritoneal surface of the liver, either from pre-existing venous collaterals or, among liver transplant recipients, these collateral communications can arise de novo.2 The onset of CTPV usually occurs 6 to 20 days after the portal obstruction occurs.3 These venous collaterals can be categorized into hepatopetal (portal-portal shunts) and hepatofugal (portal-systemic shunts). Sequelae of CTPV can include portal hypertension, splenomegaly, ascites, gastrointestinal varices, obstructive jaundice, mesenteric venous congestion and ischemia, ascending cholangitis, and biliary cirrhosis. REFERENCES 1. Balfour GW, Stewart TG. Case of enlarged spleen complicated with ascites, both depending upon varicose dilation and thrombosis of the portal vein. Edinb Med J 1869;14:589-99. 2. Gaetano A, Lafortune M, Patriquin H, De Franco A, Aubin A, Paradis K. Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected with Doppler sonography. AJR Am J Roentgenol 1995;165:1151-5. 3. Hajdu CH, Murakami T, Diflo T, Taouli B, Laser J, Teperman L, et al. Intrahepatic portal cavernoma as an indication for liver transplantation. Liver Transpl 2007;13:1312-6. Submitted Jun 21, 2013; accepted May 5, 2014. From the Department of Surgery, Louisiana State University Health Sciences Center at Shreveport and the Department of Surgery, Overton Brooks Veterans Affairs Hospital, Shreveporta; the Department of Surgery, Medical College of Wisconsin, Milwaukee, Wiscb; the Center for Translational Injury Research, Department of Surgery, University of Texas-Houston, Houstonc; the Blood Center of WisconsineWisconsin Donor Network, Milwaukeed; and the Division of Transplantation, Department of Surgery, Medical College of Wisconsin, Milwaukee.e Author conflict of interest: none. E-mail: [email protected]. The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. J Vasc Surg 2016;63:529 0741-5214 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2014.05.013
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A male patient with an unknown medical history sustained injuries that were deemed incompatible with life. He became an organ donor. At the time of donor liver harvest, periportal collaterals were seen around the liver (A), with webs visualized inside the portal vein (B) consistent with cavernous transformation of the portal vein (CTPV). This made the liver unsuitable for transplantation, and the procedure was aborted. DISCUSSION Since Balfour and Stewart1 first reported CTPV in 1869, it remains a disease with the potential for insidious clinical sequel. CTPV, also known as portal cavernoma, is the result of portal vein thrombosis that causes the formation of periportal or intrahepatic venous collaterals. CTPV is also referred to as a portal cavernoma, due to the spongelike appearance of the portal vein. In CTPV, a partial recanalization of the thrombosed portal vein occurs with the formation of venous collaterals in the hepatocolic and hepatoduodenal ligaments, along the gallbladder, and on the peritoneal surface of the liver, either from pre-existing venous collaterals or, among liver transplant recipients, these collateral communications can arise de novo.2 The onset of CTPV usually occurs 6 to 20 days after the portal obstruction occurs.3 These venous collaterals can be categorized into hepatopetal (portal-portal shunts) and hepatofugal (portal-systemic shunts). Sequelae of CTPV can include portal hypertension, splenomegaly, ascites, gastrointestinal varices, obstructive jaundice, mesenteric venous congestion and ischemia, ascending cholangitis, and biliary cirrhosis. REFERENCES 1. Balfour GW, Stewart TG. Case of enlarged spleen complicated with ascites, both depending upon varicose dilation and thrombosis of the portal vein. Edinb Med J 1869;14:589-99. 2. Gaetano A, Lafortune M, Patriquin H, De Franco A, Aubin A, Paradis K. Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected with Doppler sonography. AJR Am J Roentgenol 1995;165:1151-5. 3. Hajdu CH, Murakami T, Diflo T, Taouli B, Laser J, Teperman L, et al. Intrahepatic portal cavernoma as an indication for liver transplantation. Liver Transpl 2007;13:1312-6. Submitted Jun 21, 2013; accepted May 5, 2014. From the Department of Surgery, Louisiana State University Health Sciences Center at Shreveport and the Department of Surgery, Overton Brooks Veterans Affairs Hospital, Shreveporta; the Department of Surgery, Medical College of Wisconsin, Milwaukee, Wiscb; the Center for Translational Injury Research, Department of Surgery, University of Texas-Houston, Houstonc; the Blood Center of WisconsineWisconsin Donor Network, Milwaukeed; and the Division of Transplantation, Department of Surgery, Medical College of Wisconsin, Milwaukee.e Author conflict of interest: none. E-mail: [email protected]. The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. J Vasc Surg 2016;63:529 0741-5214 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2014.05.013
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