Pathologic gross inspection of cirrhotic livers generally shows two types of patterns:
- micronodular in which parenchymal nodules are small (< 3 mm diameter) and separated by thin fibrous septa;
- macronodular in which parenchymal nodules are large (>3 mm) and separated by fibrous septa sometimes reaching the proportions of large scars.
Cirrhotic nodules may be characterized based on the histological features into three major categories, namely:
- regenerative, representing a benign proliferation of hepatocytes surrounded by fibrous septa;
- dysplastic, representing regenerative nodules (RNs) with cellular atypia, an intermediate step in the pathogenesis of HCC;
- malignant or HCC.
On MRI a variety of morphological findings are observed. Atrophy of the right lobe and the medial segment of the left lobe are common in cirrhotic livers. The caudate lobe and lateral segment of the left lobe may undergo hypertrophy. In cirrhotic livers, enlargement of the hilar periportal space is commonly observed in patients with atrophy of the medial segment of the left lobe (Ito et al. 2002).
Expansion of the major interlobar fissure may be seen in the late stage of disease, causing extrahepatic fat to fill the space between the left medial and lateral segments (Ito et al. 2002). These findings are accompanied by enlargement of the pericholecystic space (gallbladder fossa), which is subsequently filled with fat, in what is known as the “expanded gallbladder fossa sign.” The presence of regenerative nodules and confluent or diffuse parenchymal fibrosis causes irregularities and distortion in the liver surface and parenchyma (Ito et al. 2002).
The most consistent morphological feature of cirrhosis is the demonstration of focal or diffuse fibrous tissue, that have low signal intensity on T1-weighted images and high or low signal intensity on T2-weighted images, depending on chronicity, with acute fibrous tissue having a higher fluid content and therefore higher signal intensity. Fibrous tissue enhances negligibly on hepatic arterial dominant- phase images and demonstrates late enhancement on hepatic venous phase images.
On MRI, the majority of RNs are isointense on T2- and T1-weighted images. Occasionally, RNs may appear low in signal intensity on T2-weighted images relative to high-signal-intensity inflammatory fibrous septa or damaged liver (Ito et al. 2002). RNs containing iron have low signal intensity on T2-weighted and T2*-weighted gradient- echo images. Approximately 16% of RNs are hyperintense on T1-weighted images. RNs demonstrate negligible enhancement on both hepatic arterial dominant phase and interstitial phase images.
Dysplastic nodules (DNs) are defined as neoplastic, clonal lesions that represent an intermediate step in the pathway of carcinogenesis of hepatocytes in cirrhotic livers. On MR imaging, DNs are most commonly recognized as isointense or hypointense on T2-weighted images and hyperintense on T1-weighted images. Like RNs, DNs may also contain iron, which then results in low signal intensity on both T2- and T1-weighted images. Unlike RNs, DNs have been found to contain isolated arteries unaccompanied by bile ducts. Correlations exist between extent of enhancement on arterial dominant images and the grade of DNs.
Malignant nodules (HCC)
Increase in arterial blood supply and decrease of portal blood supply of hepatic nodules is closely related to the process of malignant transformation to HCC. On MR imaging, low-grade DNs show negligible enhancement, or similar enhancement to the background parenchyma (i.e., isointense) on arterial dominant-phase images; and high-grade DNs may demonstrate enhancement ranging from mild to intense on arterial dominant-phase images. DNs tend to fade toward background signal of the liver in the interstitial phase of enhancement; whereas small HCCs are more likely to exhibit lesion washout with late capsule enhancement. A focus of small HCC that develops in a high-grade DN appears as a high signal intensity focus within a low signal intensity nodule on T2 — a nodule within a nodule. This reflects the development of a high T2 signal malignancy within a low T2 signal dysplastic nodule. On T1-weighted images, the high-grade DN exhibits low signal intensity, and the foci of small HCC may appear isointense with the liver parenchyma.
Portal hypertension results from obstruction at presinusoidal (e.g., portal vein), sinusoidal (e.g., cirrhosis), postsinusoidal (e.g., hepatic vein), or multiple levels. The most common cause of portal hypertension is cirrhosis. Portal hypertension causes or exacerbates complications of cirrhosis such as variceal bleeding, ascites, and splenomegaly. Portosystemic shunts may be identified with gadolinium- enhanced imaging. In the early stages of portal hypertension, the portal venous system dilates, but flow is maintained.
Later, substantial portosystemic shunting develops, reducing the volume of flow to the liver and decreasing the size of the portal vein. With advanced portal hypertension, portal flow may reverse and become hepatofugal. Thrombosis of the portal veins may develop with development of collaterals referred to as cavernous transformation. Other associated findings of portal hypertension includes: mesenteric, omental and retroperitoneal edema, gastrointestinal wall thickening.
Portal varices arise from increased portal pressure, and portal blood is shunted into systemic veins, bypassing hepatic parenchyma. This may play a role in the development of hepatic atrophy in advanced cirrhosis. Major sites of portosystemic collateralization include gastroesophageal junction, paraumbilical veins, retroperitoneal regions, perigastric, splenorenal, omentum, peritoneum, and hemorrhoidal veins. Esophageal varices are a serious complication because they may rupture and produce lifethreatening hemorrhage.
Varices are particularly conspicuous using fat suppression or water excitation with gadolinium enhancement on gradient-echo images (Ito et al. 2002).