HCC lesions have a variable appearance on T1-weighted images. Lesions can be hypo, iso-, or hyper-intense compared to surrounding liver parenchyma [55–57]. Many well-differentiated HCCs and high grade DNs can have high signal intensity on T1-weighted images which can be related to copper, iron, glycogen deposition, high protein/lipid content, and possibly the degree of differentiation [58, 59]. T1-weighted in-phase and opposed-phase gradient echo sequences provide the opportunity to detect signal drop on opposed phase images, representing microscopic fat components that may be present in HCC lesions [60] (Fig. 4). On T2-weighted images, HCCs are classically hyperintense (Fig. 5). There is, however a great deal of variability as DNs are typically T2 hypointense and well-differentiated HCCs can be iso- or rarely even T2 hypointense compared to liver parenchyma [58, 59]. A focus of high T2 signal intensity within a hypo- or isointense nodule (“nodule within a nodule” sign) has been described as suggestive of HCC developing within a DN [61]. In the end, however, given the variability present, studies have shown a limited utility of T2-weighted imaging for HCC detection/characterization [62, 63].

Using DWI, benign lesions (cysts and hemangiomas) show generally higher ADCs than HCC, secondary to free water motion in benign lesions and restricted water motion in tumors. A mass in the cirrhotic liver with restricted diffusion (remaining hyperintense on high b-value diffusion images with low ADC) is highly suggestive of HCC when associated with other typical MRI features [64–66] (Fig. 6).

Most HCCs obtain their blood supply almost exclusively from the hepatic artery and 80–90 % of HCCs are thus hypervascular during the arterial dominant phase [67, 68]. This feature allows differentiation from regenerative nodules as well as from focal fibrosis, which generally demonstrate delayed enhancement.

On portal venous and late venous phases, arterial phase enhancing HCCs become typically hypo-intense relative to background liver parenchyma (“wash-in and wash-out pattern”). When arterially enhancing lesions larger than 2 cm are present with delayed washout, HCC is confirmed without the necessity of further evaluation [69, 70] (Figs. 2, 4, 5). In addition, delayed post-contrast T1-weighted imaging sequences can show late enhancement of a fibrous capsule/pseudocapsule which is a typical feature of HCCs larger than 2 cm, but not regenerative or dysplastic nodules. Approximately 10–20 % of HCCs can be hypovascular [44]. These tumors are typically smaller in size or well differentiated HCCs, with lack of sufficient neovascularization and hepatic arterialization. On the contrary, extremely large and/or infiltrative HCCs may appear hypovascular on arterial phase with more delayed, heterogeneous enhancement.

Extracapsular invasion in HCC is associated with poor prognosis and can be detected on MRI as projection of the tumor through the capsule with associated small satellite lesions [71].

Macrovascular invasion can be present in large, non-encapsulated HCCs, affecting the main and segmental portal and hepatic veins, with either absence of portal venous branches or an intraluminal space occupying mass with typically arterial enhancement and a filling defect on portal venous phase images (Figs. 3, 7). With the current imaging technology, there are no clear predictive findings of microvascular invasion in HCC [72].

Hepatobiliary contrast agents are taken up by hepatocytes and excreted into the biliary system [73]. Gadobenate dimeglumine (Gd-BOPTA, MultiHance, Bracco Diagnostics) and Gadoxetate disodium (Gd-EOB-DTPA, Eovist/Primovist, Bayer Healthcare) are the agents that are currently FDA approved in the United States, and used to evaluate hepatocellular function within hepatic lesions. Less than 5 % of administered dose of Gd-BOPTA and approximately 50 % of dose of Gd-EOB-DTPA are excreted in bile [73]. Each function as extracellular agents on the early post-contrast images, however are hepatocyte specific on delayed images (60–120 min for Gd-BOPTA and 10–20 min for Gd-EOB-DTPA) [74]. While further studies are necessary, preliminary results demonstrate that well differentiated HCCs often react similarly to normal hepatic parenchyma and are iso- to hyper- intense to liver on delayed hepatobiliary phases. This is in contrast to moderately and poorly differentiated HCC’s which do not retain hepatobiliary agents and are hypointense on delayed phases [73, 75] (Fig. 8). One study demonstrated that gadobenate dimeglumine–enhanced MRI had a sensitivity of 80–85% and a positive predictive value of 65–66 % for HCC detection [76]. The technique, however, is of limited value for detecting and characterizing lesions smaller than 1 cm in diameter [76]. Contrarily, a second study, utilizing Gd-EOB-DTPA in comparison to MDCT for preoperative detection of HCC, demonstrated that Gadoxetic acid-enhanced MRI and triple-phase MDCT have similar diagnostic performance in the preoperative detection of HCC, but MRI may be better than MDCT in the detection of HCCs smaller of equal to 1 cm in diameter [75]. Further studies are necessary and in progress.

TACE involves selective embolization with chemotherapeutic agents mixed with Lipiodol. The Lipiodol is radiodense on CT and its distribution usually indicates foci of uptake within the tumor. Since viable tumor tissue is superimposed by Lipiodol artifacts in MDCT, MRI is mandatory for reliable decision making during follow-up after TACE procedures [80]. Lipiodol can cause transient T1 hyperintense signal intensity within the first 3 months after therapy as well as drop of signal on opposed phase sequences in regions of Lipiodol deposition [81]. Positive treatment response findings include increased T1 signal, decreased T2 signal, and lack of enhancement [82]. Post-contrast processed subtraction sequences are essential in the presence of T1 hyperintensity [83]. Even without decreased tumor size, presence of necrosis is a positive indicator of treatment response. Although definitive data have yet to be accumulated, a significant increase in ADC values with decreased diffusion restriction secondary to necrosis may be an early indicator of treatment response [84–86].

The goal of RFA is to create an area of thermocoagulation with a diameter larger than that of the tumor. US is limited as the echogenicity of necrotic and viable tumor tissue may have a similar appearance on post-treatment images. As accessibility and usage becomes more widespread, contrast-enhanced US may be useful to differentiate tumor from necrosis [87]. Contrast-enhanced CT and MRI are considered standard modalities for evaluation post RFA. Findings from preliminary reports show that the size of the nonenhancing region depicted on CT and MR images corresponds to within 2 mm of the size of the coagulated necrosis measured histologically [88]. Optimal time for initial follow-up after therapy varies from 1–3 months where expected findings include uniform hypointensity on T2-weighted images and lack of enhancement on post-contrast T1-weighted images. Most RFA treated areas are hyperintense on T1-weighted images, likely due to hemorrhage and image subtraction is essential to assess for residual enhancement. Local regrowth tends to be detected at the periphery of the treated area either as irregular thickening of one margin or a new tumor nodule [89]. Hyperintense appearance on T2-weighted images with associated nodular enhancement is characteristic of tumor regrowth (Fig. 9). Care should be taken not to diagnose peripheral regrowth when a thin/regular (<1 mm) rim of progressive enhancement is present, a sign of simple vascularized inflammation [90].

While in 30–40 % of patients HCC is diagnosed at early stages and is amenable to potentially curative treatments, such as surgery/locoregional therapy, disease that is diagnosed at an advanced stage or with progression after locoregional therapy has a dismal prognosis, owing to the underlying liver disease and lack of effective treatment options. Sorafenib (Nexavar, Bayer HealthCare Pharmaceuticals–Onyx Pharmaceuticals) is a small molecule that inhibits tumor-cell proliferation and tumor angiogenesis and increases the rate of apoptosis in a wide range of tumor models. Imaging of advanced HCC post systemic treatment with Sorafenib has been performed with both CT and MRI [91].