Altered Liver Morphology After Portal Vein Thrombosis: Not Always Cirrhosis

Abstract

The macroscopic appearance of the liver after primary portal vein thrombosis often mimics cirrhosis, despite the absence of bridging fibrosis at histology. The purpose of this study was to describe unique morphologic changes of the liver after portal venous thrombosis. A retrospective review was performed to find patients with portal vein thrombosis and a corresponding noncirrhotic liver biopsy. The CT appearance of the liver was then evaluated, and the liver was categorized as having either peripheral or central hepatic atrophy. Of 15 patients included in this study, 12 had peripheral atrophy of the liver, while the remaining three had central atrophy. We concluded that maintenance of central portal venous blood flow and resultant relative peripheral atrophy of the liver may account for a distinctive rounded configuration of the liver after acute portal vein thrombosis. Awareness of this appearance after primary portal vein thrombosis may prevent an erroneous diagnosis of cirrhosis.

Focal nodular hyperplasia-like lesions in patients with cavernous transformation of the portal vein: prevalence, MR findings and natural history

“…Although rare, CTPV can profoundly alter liver morphology and vascular haemodynamics, mimicking other hepatic disorders (most notably cirrhosis) [2][3][4][5][6]. In addition, recent anecdotal observations suggest that CTPV might foster the growth of hypervascular liver nodules with histological features and pathogenesis similar to that of focal nodular hyperplasialike (FNH-like) lesions found in other vascular disorders of the liver (e.g., Budd-Chiari syndrome, hereditary hemorrhagic telangectasia, congenital portosystemic shunt, and congenital hepatic fibrosis [7][8][9][10][11][12][13][14]).…”

Does the right inferior phrenic artery has a supplying role in liver cirrhosis without HCC?: 64-slice CT evaluation

“…The decreased and reversed portal flow due to liver architectural derangement is the most important mechanism associated with non-malignant PVT. Thrombotic tendency is based on endothelial injury due to elevated portal pressure, coagulation abnormalities, and increased intrahepatic resistance to portal flow (14)(15)(16).…”

“…The central portion of the liver is preserved via collateral blood flow. However, collateral blood flow is insufficient to preserve the blood flow to the subcapsular regions of the liver (15).…”

Ultrasound of the liver, biliary tract, and pancreas

“…A B C segment and/or periphery of the liver (Vilgrain, 2001;Vilgrain et al, 2006;Tublin et al, 2008).…”