Hepatobiliary and pancreatic: Commentary

Abstract

Journal of Gastroenterology and HepatologyVolume 15, Issue 8 p. 960-961 Free Access Hepatobiliary and pancreatic: Commentary First published: 25 December 2001 https://doi.org/10.1046/j.1440-1746.2000.2300b.x Contributed by Prof. K Okuda, Chiba University Hospital, Chiba, Japan. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat INTERPRETATION OF FIG. 1 The liver is enhanced irregularly with unenhanced areas in the posterior aspect of the liver. There is a small amount of ascites. The arrowed mass-like lesion is continuous with the liver indicating that this is the caudate lobe, but it does not enhance with contrast. The caudate lobe enlarges in various liver diseases such as cirrhosis, but the magnitude of the enlargement is much more pronounced in the Budd–Chiari syndrome in the presence of a patent inferior right hepatic vein. The lack of enhancement indicates poor perfusion. The diagnosis is readily made from the symptoms the patient had at presentation. The real question is why this caudate lobe is so large without blood flow. One possibility is that the once functioning inferior right hepatic vein has now thrombosed. DIAGNOSIS: CLASSICAL BUDD–CHIARI SYNDROME (HEPATIC VEIN THROMBOSIS) Figure 2 is a dynamic computed tomography (CT) scan performed 1 year earlier, shortly after the onset of symptoms. The markedly enlarged caudate lobe (arrow) did enhance, indicating that the inferior right hepatic vein which drains this lobe 1 had enlarged, compensating for the lack of outflow channels in other lobes through multiple venous anastomoses that had developed within the liver. This vein subsequently thrombosed, impairing caudate lobe perfusion. The clearly demarcated areas without enhancement (asterisk) represent ischaemic infarcts. Figure 2Open in figure viewerPowerPoint Enhanced computed tomography 1 year prior to the present investigation. The caudate lobe (arrow) was enhanced. Asterisk indicates the infarcted area. Figure 3 shows a CT scan made half a year after Fig. 1. The caudate lobe (arrow) has atrophied due to absorption of the infarcted tissue. The spleen size has increased in 1.5 years suggesting evolving portal hypertension. In this patient, Doppler sonography demonstrated a communication between the right portal vein and the right hepatic vein caused by repeated therapeutic catheterizations of the right hepatic vein for dissolving recurrent mural thrombosis. The infe-rior vena cava (IVC) was narrowed but patent. In Western countries, most patients have a hypercoagulable state, and this patient was positive for cardiolipin antibodies. Outside the Western countries, hepatic vein outflow block is mostly caused by primary IVC thrombosis which produces a membranous obstruction of the IVC. 2 Figure 3Open in figure viewerPowerPoint Computed tomography scan taken half a year after Fig. 1. The caudate lobe (arrow) has shrunk. REFERENCES 1 Takayasu K, Moriyama N, Muramatsu Y et al. Intrahepatic venous collaterals forming via the inferior right hepatic vein in three patients with obstruction of the inferior vena cava. Radiology 1985; 154: 323 8. 2 Okuda K, Kage M, Shrestha SM. Proposal of a new nomenclature for Budd–Chiari syndrome: Hepatic vein thrombosis versus thrombosis of the inferior vena cava at its hepatic portion. Hepatology 1998; 28: 1191 8. Volume15, Issue8August 2000Pages 960-961 FiguresReferencesRelatedInformation