Teaching Case

A 55-year-old female with long-standing history of chronic hepatitis C virus (HCV)-related liver disease previously treated with interferon+ribavirin, human immunodeficiency virus (HIV) coinfection in good immunologic conditions (>500 CD4+ cells/mm) on antiretroviral therapy presented with back pain, dyspnoea, non-tender abdominal distension. Mild increase of liver transaminases was the only abnormal laboratory test.

Ultrasound (Fig.1) showed echogenic thrombosis of the main portal vein and lobar branches, without focal liver masses. Days later, despite diuretics and low-molecular-weight heparin, CT (Figs.2&3) showed increased ascites, massive vascularised portal thrombosis, plus an ill-defined region of faint hyperperfusion involving the 7th liver segment with subtle inhomogeneous hypoattenuation in venous and equilibrium phases.
Increased (930 ng/mL) serum alpha-fetoprotein and MRI (Figs.4&5) confirmed suspicion of malignant portal thrombosis with solid, inhomogeneous signal with internal vascular flow voids. Compared to subtle T2-hypersignal, faint hypervascularisation and washout, the true intraparenchymal extent of the infiltrative-growing hepatocellular carcinoma was demonstrated by "geographic" regions of the right lobe with T1-hypointense signal, restricted diffusion and hypointensity on hepatocyte-specific phase after Gd-EOB-DTPA compared to areas without neoplastic infiltration.
Transplantation and chemoembolisation were unfeasible, antiangiogenic (sorafenib) therapy was soon stopped because of toxicity. MRI follow-up (Fig.6) showed abundant ascites, progression of malignant thrombosis, parenchymal infiltration of the entire right liver and most of caudate lobe.

Infiltrative-type hepatocellular carcinoma (I-HCC) represents the less common (7-20%) of the three classical histopathological growth patterns, and is characterised by tumour spread throughout large regions of the liver occupying multiple segments, a lobe or even the entire liver. Despite its name, I-HCC does not show irregular or ill-defined margins, but includes distinct tumour nodules or masses with demarcated borders. Whereas I-HCC is generally believed to result from rapid, widespread intrahepatic dissemination from a primary focus via the portal system, other Authors postulated a multiclonal nature of I-HCC corresponding to independently growing tumours without a dominant mass [1, 2].
From the radiologist’s perspective, differently from the usual mass-forming HCCs, I-HCC is often poorly perceptible within the underlying cirrhotic background, but awareness of its peculiar features is crucial for proper diagnosis. Sonographically, I-HCC appears as an ill-defined region of markedly heterogeneous echotexture. Despite large size, at CT I-HCC is often inconspicuous relative to the cirrhotic parenchyma due to the combined effect of permeative growth, perfusion changes, and inconsistent arterial enhancement which may be minimal, “patchy” or miliary. The most reliable sign (50% of I-HCCs) is “reticular” or “mosaic” washout appearance in the portal and equilibrium phases. As this case exemplifies, MR better depicts the true extent of I-HCC on precontrast and diffusion-weighted imaging (DWI) rather than on dynamic contrast-enhanced sequences, with hypointense T1-weighted signal, moderate heterogeneous T2-hyperintensity, and restricted diffusion at high b-values. In the delayed hepatobiliary phase I-HCC should not be confused with focal confluent fibrosis, since both entities are poorly vascularised and don’t take up liver-specific MR contrast agents [1-4].
I-HCC has associated neoplastic portal thrombosis (NPT) in 68-100% of cases, which usually involves the main portal vein and also intrahepatic branches. Characterization of thrombus malignancy is crucial since it determines the therapeutic strategy: NPT contraindicates surgical resection and liver transplantation, and indicates dismal prognosis. The usual features of NPT include proximity or direct extension from intrahepatic tumour, portal vein expansion, neovascularisation and washout on dynamic contrast-enhanced cross-sectional studies. As in this case, at MRI NPT shows analogous signal features to the primary HCC with heterogeneous T2-hyperintensity, restricted diffusion. Albeit some controversy exists about low apparent diffusion coefficient (ADC) cutoff values, DWI may easily enable differentiation from bland portal thrombosis which doesn’t have diffusion restriction [3-10].