Diffuse Liver Disease: Cirrhosis, Focal Lesions in Cirrhosis, and Vascular Liver Disease

Excerpt

Nonalcoholic fatty liver disease (NAFLD) has become one of the most common causes of chronic liver disease. If NAFLD and chronic viral hepatitis remain untreated, patients gradually develop liver fibrosis further progressing to cirrhosis. Significant advances in magnetic resonance imaging (MRI) and MR elastography allow quantification of hepatic steatosis and fibrosis before end-stage liver disease and emerge as noninvasive screening and monitoring tools as an alternative to liver biopsy (Dulai et al. J Hepatol. 65(5):1006–1016, 2016). Cirrhosis is characterized by progressive fibrosis of the liver parenchyma with ongoing regeneration. However, at an early stage of cirrhosis, the liver may appear normal. Patients with cirrhosis are not only at risk of liver failure but also at risk to develop hepatocellular carcinoma (HCC) and intrahepatic cholangiocellular carcinoma.

HCC in cirrhosis either develops in a stepwise carcinogenesis from regenerative nodules to low-grade dysplastic nodule, high-grade dysplastic nodule, and HCC or develops de novo. To facilitate and standardize the categorization of these cirrhotic nodules seen in patients at risk for HCC along a spectrum from benign to malignant, the Liver Imaging Reporting and Data System (LI-RADS) provides a diagnostic algorithm for analysis of cross-sectional images (Santillan et al. Magn Reson Imaging Clin N Am. 22(3):337–352, 2014). HCC differs from most malignancies because it is commonly diagnosed on the basis of imaging features alone, without histological confirmation.

Vascular liver disease such as arterioportal shunts may be difficult to distinguish from HCC. Diffuse parenchymal alteration seen in Budd-Chiari syndrome with large hypervascular regenerative nodules can be mistaken for HCC. Portal vein thrombosis occurs in the setting of cirrhosis and HCC and either appears as bland thrombus or tumor thrombus.