Figure 1
Typical HCC in a patient with chronic hepatitis-C. Axial fat-suppressed SS-FSE T2-WI (A), axial in-phase precontrast (B) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (C) and interstitial (D,E) phases. A nodule with 2 cm is depicted on the right hepatic lobe (arrows, A–E), showing mild high signal intensity on T2-WI (A) and low-signal intensity on pre-contrast T1-WI (B). On the dynamic postcontrast images, the lesion shows arterial hyper-enhancement (C) and delayed washout with pseudocapsule enhancement (D,E). These features are diagnostic of HCC.
Figure 2
Fatty HCC in a patient with non-alcoholic fatty liver disease. Coronal SS-FSE T2-WI (A), axial fat-suppressed FSE T2-WI (B), axial in- (C) and out-of-phase (D) GRE T1-WI, axial pre- (E) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (F) and interstitial (G) phases, and coronal fat-suppressed 3D-GRE T1-WI in the interstitial phase (H). One nodule is depicted on the left hepatic lobe (arrows, A–G), showing mild high signal intensity on T2-WI (A,B), low-signal intensity on in-phase T1-WI (C), and heterogeneous drop of signal on out-of-phase T1-WI (D). On the dynamic postcontrast images, the nodule is hypervascular (F) and shows delayed washout and pseudocapsule enhancement (G,H). Note the fine fibrotic bands of the liver parenchyma, which are seen at the late interstitial phase (arrowheads, G).
Figure 3
HCC in a patient with chronic alcoholic liver disease. Axial fat-suppressed SS-FSE T2-WI (A), axial pre- (B) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (C) and interstitial (D) phases. There is a 2-cm lesion in the right hepatic lobe, showing mild high signal intensity on T2-WI (arrow, A), low signal on T1-WI, arterial hyper-enhancement with no washout on the delayed phase. Despite this lesion cannot be categorized as HCC by imaging criteria, the combination of mild high T2 signal intensity and hypervascular characteristics are very likely related to HCC in the setting of liver cirrhosis. Note the recanalization of the umbilical vein (arrows, D).
Figure 4
HCC in a patient with chronic hepatitis-C unable to fully cooperate with the recommended breath-holds on the dynamic GRE sequences. Axial DWI b = 50 s/m2 (A) and DWI b = 600 s/m2 (B), axial pre- (C) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (D) and interstitial (E) phases. One nodule on the right hepatic lobe is depicted (arrow, A–E), showing mild high-signal intensity on DWI (A,B). On the dynamic postcontrast images, the lesion shows arterial hyper-enhancement (D), and shows delayed washout and pseudocapsule enhancement (E). Note that the diagnosis of HCC is confident, despite the low quality images due to respiratory motion artifacts (arrowheads, C–E).
Figure 5
HCC evaluated using gadoxetate disodium (hepatobiliary contrast agent). Axial fat-suppressed (A) SS-FSE T2-WI, axial pre- (B) and postgadolinium (gadoxetate disodium) fat-suppressed 3D-GRE T1-WI in the arterial (C), interstitial (D) and hepatobiliary phases (E). An HCC is depicted in the right liver lobe, in a background cirrhotic parenchyma, showing mild high signal intensity on T2-WI, low signal intensity on T1-WI, hypervascular characteristics (C) and washout on the delayed phase (D). On the hepatobiliary phase, due to the presence of impaired hepatocytes, the HCC shows no enhancement (E). Note the enhancement of the biliary duct (arrowheads, E).
Figure 6
Small HCC diagnosed using gadoxetate disodium (hepatobiliary contrast agent). Axial fat-suppressed (A) SS-FSE T2-WI, axial pre- (B) and postgadolinium (gadoxetate disodium) fat-suppressed 3D-GRE T1-WI in the arterial (C), interstitial (D) and hepatobiliary phases (E). A small HCC is depicted in the right liver lobe, medial to the right hepatic vein, showing isointensity on T2-WI, mild low signal intensity on T1-WI, arterial hyper-enhancement (C) and no perceptible washout on the delayed phase (D). On the hepatobiliary phase, due to the presence of impaired hepatocytes, the HCC shows no enhancement (arrow, E). This case exemplifies the advantages of hepatobiliary contrast agents in the characterization of liver nodules in the setting of cirrhosis.
Figure 7
Diffuse HCC in a patient with chronic hepatitis C. Coronal SS-FSE T2-WI (A), axial fat-suppressed SS-FSE T2-WI (B), axial pre- (C) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (D) and interstitial (E) phases, and coronal postcontrast fat-suppressed 3D-GRE T1-WI in the interstitial phase (F). A diffuse area of mild high-signal intensity on T2-WI (asterisk, A,B) is depicted on the right liver lobe, showing low-signal intensity on pre-contrast T1-WI (C). On the dynamic postcontrast images, the lesion is hypervascular at the arterial phase (D) and shows delayed heterogeneous mottled washout (E,F). These features are diagnostic of diffuse HCC. Note the tumor thrombus filling and expanding the portal vein, typical of this type of HCC (arrows, A–F). The thrombus shows hypervascular characteristics and delayed washout comparable to the MRI dynamic features of the tumor.
Figure 8
Liver cirrhosis with confluent fibrosis. Coronal (A) and axial fat-suppressed (B) SS-FSE T2-WI, axial pre- (C) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (D) and interstitial (E) phases, and coronal postcontrast fat-suppressed 3D-GRE T1-WI in the interstitial phase (F). There is a linear pattern of fibrosis throughout the liver, with a focal region of confluent fibrosis in segments 7 and 8 peripherally (arrow, A,B), that is moderately high in signal on T2-WI (A,B) and mildly low in signal on T1-weighted image (C) and demonstrates negligible enhancement on early postcontrast image (D) and moderate enhancement on delayed image (E,F). The fine pattern of fibrosis is better depicted on late postgadolinium images as linear enhancing structures (E,F). Note the distorted anatomy and capsular retraction of segment 7, in relation to the more prominent region of fibrosis. The absence of portal vein thrombus, lack of arterial hyper-enhancement and delayed progressive enhancement allows the confident diagnosis of confluent fibrosis and excludes diffuse HCC.
Figure 9
Stereotypical simplified schematic representation, showing MRI features of cirrhotic nodules. In this schematic representation it is shown the appearance of common hepatocellular nodules in the cirrhotic liver, using a standard abdominal protocol. Abbreviations: HCC, hepatocellular carcinoma; HGDN, high grade dysplastic nodule; FS T2-WI, fat-suppressed T2-weighted image; T1-WI IP, T1-weighted in-phase image; T1-WI OP, T1-weighted out-of-phase image; T1-WI AP, post-contrast fat-suppressed T1-weighted image at the late arterial phase; T1-WI PVP, post-contrast fat-suppressed T1-weighted image at the portal-venous phase; T1-WI Inter P, post-contrast fat-suppressed T1-weighted image at the interstitial phase; T1-WI HBP, post-contrast fat-suppressed T1-weighted image at the hepatobiliary phase (with hepatobiliary contrast agent).
Figure 10
Post-microwave ablation of HCC in a patient with chronic hepatitis C. Axial fat-suppressed SS-FSE T2-WI (A), axial pre- (B) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (C) and interstitial (D) phases. The treated area is seen on the right hepatic lobe (arrow, A–D), showing low-signal intensity on T2-WI (A) and a rim of high-signal intensity on pre-contrast T1-WI (B). On dynamic postcontrast images, the treated lesion shows no enhancement along all postcontrast dynamic phases (C,D), i.e., the high-signal intensity rim is identical to that shown on unenhanced image (B), so it represents persistent high intrinsic T1 signal rather than enhancement. This feature is consistent with absence of residual viable neoplasm.
Figure 11
Recurrence of HCC treated by radiofrequency ablation. Axial fat-suppressed SS-FSE T2-WI (A), axial pre- (B) and post-contrast fat-suppressed 3D-GRE T1-WI in the arterial (C) and interstitial (D) phases. A treated area is seen at the right lobe (arrow, A,B), showing iso-signal intensity on T2-WI (A) and a partial/ interrupted rim of high-signal intensity on pre-contrast T1-WI (B). On the dynamic postcontrast images, progressive peripheral nodular enhancement is evident (arrows, C,D). These features are consistent with recurrence of disease.
Figure 12
Recurrence of HCC after chemoembolization. Axial fat-suppressed SS-FSE T2-WI (A), axial pre- (B) and postcontrast fat-suppressed 3D-GRE T1-WI in the arterial (C) and interstitial (D) phases, and coronal postcontrast fat-suppressed 3D-GRE T1-WI in the interstitial phase (E). A treated area post-TACE is seen in the right liver lobe (arrows, A–E), showing heterogeneous intensity on T2-WI, with areas of moderate high-signal (black arrow, A) and low-signal (white arrow, A) intensity. These same areas show low-signal (black arrow, B) and high-signal (white arrow, B) intensity on precontrast T1-WI, respectively. On the dynamic postcontrast images, the areas of high-signal T2-WI are hypervascular (black arrow, C) and show washout and pseudocapsule on interstitial phase (black arrow, D,E), consistent with residual/recurrent HCC. The medial aspect showed no signs of recurrence.
