CASE 13659 Published on 24.05.2016

Focal confluent fibrosis in HCV-related liver cirrhosis

Section

Abdominal imaging

Case Type

Clinical Cases

Authors

Tonolini Massimo, M.D.; Adriana Vella, M.D.

"Luigi Sacco" University Hospital,
Radiology Department;
Via G.B. Grassi 74
20157 Milan, Italy;
Email:mtonolini@sirm.org
Patient

55 years, male

Categories
Area of Interest Liver ; Imaging Technique CT, MR
Clinical History
Middle-aged patient with compensated (Child-Pugh stage A) hepatitis C virus (HCV)-related liver cirrhosis, currently in good performance status and not receiving antiviral therapy. On regular clinical and ultrasound surveillance every six months. Recent laboratory finding of mildly increased serum alpha-fetoprotein (AFP, 12 ng/ml).
Imaging Findings
Hampered by liver inhomogeneity, ultrasound (not shown) did not disclose abnormal findings. Multidetector CT (Fig. 1) showed localised, smoothly marginated capsular retraction at the lateral aspect of right liver lobe. The parenchymal region underlying the retracted capsule showed linear parenchymal enhancement in arterial and portal-venous phases with non-interrupted, non-displaced arterial vessels, and a wedge-shaped homogeneous enhancement without mass effect in the delayed phase. Worrisome findings for hepatocellular carcinoma such as mass-forming, hypervascular lesions or contrast washout, diffuse parenchymal infiltration, portal thrombosis and lymphadenopathies were excluded.
Under presumptive diagnosis of benign change, follow-up was planned. Five months later, with stable clinical and laboratory features, MRI (Fig. 2) showed minimally increased capsular retraction overlying a wedge-shaped, demarcated T1-hypointense, faintly T2-hyperintense region compared to the remaining liver parenchyma, with unrestricted diffusion, apparently tapering towards the hepatic hilum. After gadolinium (non-liver specific) contrast (Fig. 3) the lesion still showed homogeneous delayed-phase enhancement, consistent with focal confluent fibrosis.
Discussion
Clinical and imaging surveillance is warranted for appropriate management of patients with chronic liver disease (CLD). Missing hepatocellular carcinoma (HCC) on imaging studies may preclude patients from potentially curative therapies; conversely misinterpretation of benign changes may lead to unnecessary procedures. However, the marked changes in liver architecture characteristic of cirrhosis often hamper detection and characterization of focal liver lesions (FLLs) [1-3].
Focal confluent fibrosis (FCF) is a not-unusual finding in long-standing cirrhosis, and is sometimes encountered also in patients with early-stage, compensated CLD. It results from progressive collapse and fibrotic replacement of hepatic parenchyma, and occurs in primary sclerosing cholangitis, alcohol-related and viral cirrhosis in descending order of frequency [3-5].
FCF is generally single and most usually located in the 4th, 7th and 8th liver segments. The characteristic appearance includes a wedge-shaped lesion with apex pointing towards the hilum and widest at the capsular surface, straight or slightly irregular margins, and either flattening of the normally convex liver contour or retraction of the overlying capsule: the latter is present at diagnosis in two-thirds of cases. FCF is hypoattenuating compared with the adjacent parenchyma on unenhanced CT scans, moderately T2-hyperintense and T1-hypointense at MRI. After intravenous contrast “trapped” vessels, often corded together from parenchymal collapse may occasionally be recognized within the FCF, which does not displace existing vessels differently from malignant lesions. Gradual enhancement is seen during dynamic CT and MRI studies, with persistence in the delayed phase corresponding to fibrosis. Conversely, when liver-specific contrast agents such as gaodxetic acid (Gd-EOB-DTPA) are used the FCF is hypointense compared to the enhanced hepatic parenchyma in the hepatobiliary phase of acquisition, reflecting the lack of hepatocyte function. The capsular retraction often increases slowly over time at serial cross-sectional follow-up [3-6].
In conclusion, FCF is generally suggested by its morphology, peripheral location and volume loss. Its attenuation, signal and enhancement features partly overlap with those of other disorders. Differentiation from HCC should consider the presence or absence of worrisome findings including capsular bulging or exophytic growth, satellite nodules, diffusion restriction, arterial hypervascularity, delayed phase washout and portal thrombosis, and may sometimes require biopsy. Capsular retraction may be observed in liver metastases (particularly from desmoplastic primary tumours and after chemotherapy), epithelioid haemangioendothelioma, and peripheral cholangiocarcinoma: the latter may also show delayed enhancement but is generally more mass-forming and containing dilated intrahepatic bile ducts [3-6].
Differential Diagnosis List
Focal confluent fibrosis in HCV-related liver cirrhosis
Uncomplicated cirrhosis
Perfusion abnormalities
Segmental / lobar hyperplasia
Hepatocellular carcinoma
Haemangioma
Hepatic epithelioid haemangioendothelioma
Intrahepatic cholangiocarcinoma
Final Diagnosis
Focal confluent fibrosis in HCV-related liver cirrhosis
Case information
URL: https://www.eurorad.org/case/13659
DOI: 10.1594/EURORAD/CASE.13659
ISSN: 1563-4086
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