Contrast-enhanced CT is widely used for the detection, characterization, and follow-up of hepatic metastases and a primary imaging tool for the management. Most of the hepatic metastases are supplied by hepatic arteries and do not have a significant supply from portal vein. Therefore, majority of the hepatic metastases are hypovascular than hepatic parenchyma in portal venous phase when hepatic parenchyma is maximally enhanced, and many institutions perform portal venous phase only for the patients of hepatic metastases. However, other phase images have some roles also. On non-contrast images, most of the metastases are low attenuated compared to hepatic parenchyma. Calcifications are clearly visible on non-contrast images. Size of the tumors is sometimes more accurate in non-contrast images because peritumoral shunts or hyperemia does not hinder the measurements. Hypervascular tumors are best seen on arterial phase, and some hypervascular tumors are not clearly visible on portal venous phase. Therefore, adding arterial phase to portal venous phase can increase detection rate of hypervascular metastases. Arterial phase images can be helpful to detect small tumors because they usually do not have central necrosis and hyperdense rim of metastases is well visualized on arterial phase. Hyperdense rim of arterial phase is caused by desmoplastic reaction, inflammation, or shunt due to high blood flow of hypervascular metastases. Common primary tumors with hypervascular metastases include renal cell carcinoma, neuroendocrine tumors, melanoma, pheochromocytoma, choriocarcinoma, and some cases of breast or lung cancer. Majority of hepatic metastases are hypovascular tumors seen as low attenuated lesion after contrast injection. These tumors are well visualized on portal venous phase. Gastrointestinal origin tumors, squamous cell carcinoma, urothelial cell carcinoma, lung, breast, and prostate cancer are common primary tumors for hypovascular metastases. Hypovascularity of these tumors is caused by dense cellularity, fibrosis, or necrosis. Peripheral area of these tumors consists of viable tumor cells and shows no or slight rim enhancement on arterial phase. This area is being thicker and showing slight washout on portal venous or delayed phase (“peripheral washout sign”). Central area of large hypovascular metastases consists of necrosis, hemorrhage, or desmoplastic reaction. Fibrosis due to desmoplastic reaction can show prolonged enhancement, and this finding is common in cases of metastatic adenocarcinoma, cholangiocarcinoma, lymphoma, and epithelioid hemangioendothelioma. As described early in Sect. 5.6.1, cystic metastases can be seen in patients with mucin-producing primary tumors or tumors with prominent necrosis. Some primary tumors are solid, but their hepatic metastases can be cystic because of the large size of metastatic lesions and poor vascularity. Diffuse and infiltrative metastases are very difficult to be differentiated from diffuse liver parenchymal disease such as cirrhosis. Heterogeneous parenchymal attenuation, deformity of hepatic contour, and narrowing of intrahepatic vasculatures are imaging findings of infiltrative metastases of the liver. However, direct invasion of hepatic vessels is uncommon. Lymphangitic metastases are tumor cell infiltration in periportal area, and imaging findings are widening of periportal space and low attenuated area along portal veins on contrast-enhanced images. However, this finding can be observed also in the cases of periportal edema due to various reasons. Pseudocirrhosis is the result of chronic liver injury after chemotherapy and almost exclusively reported in the patients of metastatic breast cancer. Retracted tumor tissue with scarring is the cause of pseudocirrhosis. Capsular retraction with coarse nodules is reported finding of pseudocirrhosis. Other features of liver failure including ascites, splenomegaly, and varices can be accompanied.

MRI was a problem-solving tool for hepatic metastases, and a role of MRI for hepatic metastases was characterization of focal hepatic lesions, mainly differentiating metastases from benign lesions such as cysts or hemangiomas. However, diagnostic performance of hemangiomas has been improved, and now MRI shows better sensitivity and specificity comparing to MDCT or PET. Especially, hepatocyte-specific contrast agents (Gd-EOB-DTPB, Gd-BOPTA) can enhance conspicuity and sensitivity of hepatic metastases on hepatobiliary phase images, and now sensitivity of liver MRI with these contrast agents is comparable or better than that of intraoperative US, which was the gold standard previously. Signal intensity of hepatic metastases on non-contrast T1- and T2-weighted images is variable according to the contents of the tumors such as hemorrhage, fibrosis, necrosis, and vascularity. However, in majority of cases, hepatic metastases are seen as iso- to low signal intensity compared to hepatic parenchyma on T1-weighted images and iso- to high signal intensity on T2-weighted images. T1 and T2 relaxation times of metastases are usually longer than normal hepatic parenchyma and shorter than common benign focal lesions such as cysts or hemangiomas. Still, one of the major strengths of MRI over CT is easy differentiation of hepatic metastases from such benign lesions. Heavily T2-weighted images are very helpful, and benign lesions such as cysts or hemangiomas look very bright. Therefore, signal intensities of metastases are lower than those of cysts or hemangiomas on T2-weighted images and higher on T1-weighted images. Peritumoral halo is seen as higher signal rim on T2-weighted images. Hypervascular tumors such as renal cell carcinoma and cystic metastases can be seen as very high signal intensity lesions, and differentiation from cysts or hemangiomas can be difficult in these cases. Intratumoral hemorrhage, coagulative necrosis, melanin, or mucin may be seen as mixed signal intensity on T1-weighted images. Also, T2-weighted images show coagulation necrosis, mucin, and fibrosis as low-signal area in the center of the tumors. Doughnut sign shows a low signal intensity rim surrounding the center of even lower signal intensity, and this pattern is usually observed in cases of large tumors prone to necrosis. Target sign is observed on T2-weighted image, and higher signal intensity due to necrosis is present in central area of large tumors. After contrast injection, vascularity of tumors is similar to that of CT scans, and peripheral washout sign can be observed (see 5.6.2). Lymphangitic metastases may be observed in high signal area along portal veins. On hepatobiliary phase images using hepatocyte-specific contrast agents (Gd-BOPTA or Gd-EOB-DTPA), hepatic metastases should appear low signal intensity (“defect”) comparing to the positive enhancement of hepatic parenchyma. However, there are some reports describing the slightly higher signal intensity in the central area of hepatic metastases at hepatobiliary phase using hepatocyte-specific contrast agents. The cause of this paradoxical phenomenon is unknown, but prominent desmoplastic reaction, large interstitial space, and coagulation necrosis of central area of metastases may retain gadolinium chelates. Diffusion-weighted images (DWI) also can be helpful for detecting and characterizing focal hepatic lesions. DWI has similar performance to hepatobiliary phase images for detecting hepatic metastases, and combining both techniques was reported to be best for the diagnostic performance. MRI can be helpful to differentiate lymphangitic metastasis from periportal edema. Delayed enhancement of periportal fibrosis can be delineated on delayed phase images after gadolinium-based contrast agent injection.