Imaging Of Hepatocellular Carcinoma

Author

MD, Associate Professor of Radiology University of Palermo School of Medicine, Italy

Abstract

Hepatocarcinogenesis represents a progressive process in which regenerative hepatocytes give rise to hyperplastic hepatocyte nodules, and these progress to dysplastic nodules, which are thought to be the direct precursor of hepatocellular carcinoma. Distinction among regenerative nodules, dysplastic nodules, and hepatocellular carcinoma with varying degrees of differentiation requires an assessment of the hemodynamic nature of the mass. As with regenerative nodules, dysplastic nodules receive predominantly portal venous flow and do not usually demonstrate bright enhancement on arterial phase after rapid bolus injection of intravenous contrast at cross-sectional imaging. As the degree of (de-differentiation) malignancy increases, portal blood supply decreases, whereas nontriadal arteries (i.e., unaccompanied by portal venules and biliary ducts) and aberrant capillaries (a process known as “capillarization”) develop to feed the nodules. When trying to characterise nodules developing in cirrhosis at cross-sectional imaging, marked arterial phase enhancement with rapid washout during the portal venous and delayed phase should be regarded as highly suspicious for the presence of hepatocellular carcinoma. While the diagnosis of large hepatocellular carcinoma does not usually represent a diagnostic challenge, hepatocellular carcinoma smaller than 3 cm will show typical imaging features (i.e., enhancement in the hepatic arterial phase and washout in the venous phase) in approximately 50% of cases only at CT and approximately 65% of cases on MR Imaging, posing a problem of differential diagnosis with dysplastic nodules and other lesions and pseudolesions. In our and others experience, higher accuracy can be achieved with the use of combined MR contrast agents, compared with pure extracellular contrast agents, although the differential diagnosis between dysplastic nodules and hepatocellular carcinoma remains challenging. When the tumor is hypervascular in the hepatic arterial phase and isointense to the background parenchyma in the venous phase, the information obtained with the hepatobiliary phase is crucial. If the lesion will show hypointensity in the hepatobiliary phase, it will likely be a hepatocellular carcinoma that has not lost portal supply yet. Hypointensity on hepatobiliary phase will allow higher sensitivity, but unfortunately specificity will drop.  However, if the lesion is isointense in the hepatobiliary phase, differential diagnosis includes dysplastic nodules or pseudolesions. Finally, after combined agents injection, nodules might not be apparent at all in the extracellular portion of the study, being visible only in the hepatobiliary phase. These “invisible” nodules during the extracellular portion of the examination may show up in the hepatobiliary phase only as either hypointense or hyperintense, and are due to the altered ability of the hepatocytes to uptake the contrast medium through the vascular pole or excrete it through the biliary pole. While hypointense nodules have shown a high incidence of progression into hypervascular hepatocellular carcinoma, and should therefore be observed carefully, hyperintense nodules are usually benign (regenerative nodules), especially when multiple and below 1 cm. Hyperintensity in the hepatobiliary phase in larger nodules can however be observed in those hepatocellular carcinoma with a cholestatic components, the so called green hepatocellular carcinoma.

Volume 34, Issue 3
September 2018
Pages 65-65