MRI Evaluation of Masses in the Noncirrhotic Liver

Kiran Gangahdar, MD; Deepa Santhosh, MD; Kedar N. Chintapalli, MD


Appl Radiol. 2014;43(12):20-28. 

In This Article

Malignant Lesions

Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy worldwide.[32] Although the prevalence is highest in Africa and Asia, the incidence of HCC in Western countries is increasing.[32] HCC usually occurs in patients with cirrhosis due either to infection with hepatitis C/B or to chronic alcohol abuse HCC may also arise de novo, without known insult, in an otherwise normal liver.[33]

A large HCC may have a number of characteristic features, such as a mosaic pattern, a tumor capsule, extracapsular extension with formation of satellite nodules, vascular invasion, and extrahepatic dissemination, including lymph node and distant metastases.[34] On T1- and T2-weighted images, the mosaic pattern appears as areas of variable signal intensities (Figures 6A-6D), whereas on gadolinium-enhanced images (Figures 6E-6G), the lesions enhance in a heterogeneous fashion during the arterial and later phases. These lesions show diffusion restriction (Figure 6F) The tumor capsule is hypointense on both T1- and T2-weighted images in most cases.[35]

Figure 6.

(A) Axial in-phase and (B) Axial out-of-phase images showing a well-defined encapsulated hypointense lesion within segment VI/VII with foci of signal drop on OP sequence suggesting fatty degeneration. (C and D) Axial T2-weighted and axial TI-weighted THRIVE noncontrast study displays T2 hyperintense and T1 hypointense heterogenous lesion. (E) Axial postcontrast arterial phase T1 THRIVE sequence shows heterogenous enhancement of the lesion. (F) Axial post-contrast T1 THRIVE sequences portal phase showing heterogenous washout and pseudocapsule formation. (G) Coronal postcontrast 10 min delayed postcontrast T1 THRIVE sequences demonstrates heterogenous washout and progressive capsular enhancement of the lesion. (H) ADC map hypointensity suggests diffusion restriction.


Cholangiocarcinoma is more common in men than women, occurring most frequently between the 6th and 7th decades.[4,36] Most patients have no predisposing risk factors, but the presence of the following risk factors may lead to development of the tumor at a younger age:[37–38] primary sclerosing cholangitis (5–15% lifetime risk); choledochal cysts (5% will transform and risk increases with age); Caroli disease (7% lifetime risk); hepatolithiasis; chronic intraductal stones; bile duct adenoma; biliary papillomatosis; Clonorchis sinensis infection; and Thorotrast (thorium dioxide) exposure.[38–39] The occurrence of cholangiocarcinoma in association with chronic inflammatory conditions suggests that inflammation and glandular regeneration may be the precursors to carcinoma.[40]

The classification scheme for primary liver cancer proposed by the Liver Cancer Study Group of Japan.[41] divides intrahepatic cholangiocarcinomas into three types based on macroscopic appearance: 1) mass-forming, 2) periductal infiltrating, and 3) intraductal.

Imaging plays a role in (a) noninvasive diagnosis and characterization of cholangiocarcinomas, (b) confirmation of diagnosis, (c) pre-therapeutic staging and assessment of respectability and (d) screening of high-risk patients (eg, those with primary sclerosing cholangitis) for early detection. By virtue of its superior contrast resolution, MR imaging with MR cholangiography has been found to be superior to CT for the assessment of intraductal lesions. Relative to the liver parenchyma, intraductal lesions appear hypo- to isointense on T1-weighted images (Figures 7A, 7B). Their T2 signal intensity is variable, but they usually appear slightly hyperintense (Figure 7C). At dynamic imaging with gadolinium-based contrast material, they usually show heterogeneous enhancement (Figure 7D) on early-phase images that gradually peaks on delayed phase images. These lesions usually show diffusion restriction (Figs. 7E, 7F). Concurrently performed high-quality T2-weighted MR cholangiography can further depicting the site of ductal obstruction and associated upstream biliary dilatation.[42]

Figure 7.

(A) Axial in-phase and (B) axial out-of-phase images showing an ill-defined hypointense geographic mass lesion involving both hepatic lobes without foci of signal drop on OP sequence. (C) and (D) Axial T2 fat-saturated and axial T1-weighted THRIVE postcontrast imaging reveal T2 hyperintense and heterogeneously enhancing lesion with capsular retraction. (E) and (F) DWI and ADC maps showing diffusion restriction.


Hepatic metastases have variable appearances (Figures 8A-8C) depending on the primary tumor and are characterized as hypervascular or hypovascular, enhancing more or less than surrounding parenchyma. Hypervascular metastases are seen with neuroendocrine tumors, renal cell carcinoma, thyroid carcinoma, melanoma, and sarcoma. Metastases from other primaries tend to be hypovascular (Figure 8D). Internal hemorrhage may occur with metastases from renal cell carcinoma, melanoma, and lung cancer, often demonstrating T1 hyperintensity. Hepatobiliary imaging with Eovist and DWI (Figure 8E) can be useful for detection of small hepatic metastases, demonstrating improved sensitivity over traditional MRI and CT.[43–45]

Figure 8.

(A) Axial in-phase and (B) axial out-of-phase images showing an ill-defined hypointense lesion within the right hepatic lobe. (C) Axial T2WI showing T2 hyperintense heterogenous mass lesion. (D) Axial postcontrast arterial phase T1 THRIVE sequences heterogenous shows enhancement of the lesion. (E) and (F) DWI and ADC map demonstrate diffusion restriction.

Although the ADC (Figure 8F) values in hepatic metastasis foci are slightly greater than those in hepatocellular carcinoma foci, the ADC values in liver parenchyma with hepatic metastasis are lower than those in hepatocellular carcinoma. Patients with hepatic metastasis have a higher ratio of ADC values of lesion/liver than those with hepatocellular carcinoma.[46–48]

Biliary Cystadenocarcinoma

Benign biliary cystadenomas and cystadenocarcinomas are rare cystic neoplasms which usually arise in the liver or, less frequently, in the extra hepatic bile ducts or the gall bladder.[49] Erdogan, et al hypothesized that epithelial cells covering the embryonic gonads in early fetal life might be the common origin for cystadenoma and ovarian stroma.[50] Moreover, bilary cystadenocarcinoma has been demonstrated to develop from biliary cystadenoma based on the existence of a transitional zone between normal cells and atypical cells in the cystic wall.[51] Devaney et al, divided hepatobiliary cystadenocarcinoma into two types, one is usually accompanied by an ovarian-like stroma, which develops exclusively in women with an indolent course and he other which lacks stroma and occurs in men taking a more aggressive course.[52]

MRI demonstrates T1 hypointense (Figure 9A) and T2 hyperintense (Figure 9B) lesions with septations and T2 intermediate signal intensity areas showing enhancement (Figures 9B, 9C) that represent cyst wall fibrosis and papillary projections suspicious for malignancy. MRI may also provide further information concerning the nature of the fluid in the cyst, blood versus mucin.[53] Image guided biopsies will help obtain a tissue diagnosis (Figure 9D).

Figure 9.

(A) Axial T1-weighted image and (B) axial T2-weighted image showing multiple large cystic lesions with a cyst showing heterogeneous T1 dark and T2 intermediate signal intensity focus. (C) Axial post-gadolinium sequence reveals heterogenous enhancement of solid portion and (D) US-guided biopsy of the same focus revealed biliary cyst adenocarcinoma in a background of biliary cystadenomas.

The differential diagnosis of patients with complex cystic lesions of the liver includes biliary cystadenoma, as well as hydatid cyst, post-traumatic cyst, liver abscess, polycystic disease, hemorrhagic cyst, embryonal sarcoma, primary or metastatic necrotic neoplasm, atypical simple cyst, and biliary intraductal papillary mucinous neoplasm.