Abdominal varices caused by chronic Budd-Chiari syndrome.

2 41-year-old man was diagnosed with Budd–Chiari syndrome 5 years previously after he developed bdominal pain and ascites. At that time, no underlying ypercoagulable state was detected. Liver biopsy examnation showed severe centrilobular congestion and nerosis, but no significant fibrosis. Stenting of the middle nd left hepatic veins successfully decompressed the ortal vasculature and his hepatic synthetic function emained intact during extended follow-up evaluation. he patient was instructed to remain on lifelong anticogulation, but he was adherent to this regimen only ntermittently. He recently returned to the hepatology clinic with rogressively enlarging subcutaneous abdominal wall rowths after stopping warfarin 3 months previously Figure A). On physical examination the growths were ainless and compressible. Laboratory data again howed normal liver function. No varices were detected n esophagogastroduodenoscopy. During the subseuent evaluation, computed tomography with coronal econstruction showed thrombus extending inferiorly rom the hepatic veins, through the stents, and into the nferior vena cava with associated serpiginous intrabdominal varices (Figure B, arrows); the mesenteric vasulature was patent. A transverse view shows the large bdominal wall collaterals that resulted from the hepatic ein and inferior vena cava obstruction and prompted the atient’s office visit (Figure C, arrows); there was no signifcant ascites. It was believed that his current anatomy recluded further endovascular treatment, and the patient as restarted on warfarin with plans for close follow-up valuation and for liver transplantation evaluation only in he setting of hepatic dysfunction. Although Budd–Chiari syndrome is a rare disorder ith a spectrum of presentations ranging from fulminant o chronic, the underlying cause of the hepatic outflow bstruction can be identified in up to three quarters of atients. If the obstruction is at the level of the inferior ena cava, the clinical presentation can include dilated eins in the flanks and over the back, and lower limb dema. If it occurs at the level of the hepatic veins, scites can be seen without dilated flank veins. In addiion, it is important to distinguish clinically between atients with cirrhosis (manifest by ascites with caput edusae) and Budd–Chiari (ascites with flank veins). In ppropriately selected Budd–Chiari patients without evdence of fibrosis on liver biopsy examination, placeent of portosystemic shunts, transjugular or surgical, an improve survival.