Figure 1
Small HCC. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast 3D-GRE T1-weighted image, with fat suppression (B), and axial postcontrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). A 10-mm subcapsular nodule is depicted with minimal high signal intensity on the T2-weighted image (arrow, A), low signal intensity on a T1-weighted image (arrow, B), arterial hyperenhancement (arrow, C) and wash-out on the delayed phase (arrow, D), consistent with HCC.
Figure 2
Siderotic nodules. Axial SSFSE T2-weighted image, with fat suppression (A) and axial in-phase 3D-GRE T1-weighted image (B). Multiple siderotic nodules, showing low signal intensity on T2- and T1-weighted images, can be seen throughout the hepatic parenchyma. Note that the low signal intensity of the iron-containing nodules is better depicted on the T1-weighted scans with longer echo times.
Figure 3
Low-grade dysplastic nodule in a patient with chronic hepatitis C virus infection. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast 3DGRE T1-weighted image, with fat suppression (B), and axial post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). A 3.5-cm nodule is depicted with low-signal intensity on T2-weighted images (arrow, A) and mild high-signal intensity on pre-contrast T1-weighted image (arrow, B). On the dynamic post-contrast images, the lesion shows the same pattern of enhancement as the background liver parenchyma (arrow, C and D). Although unusual, this nodule was prospectively considered a large regenerative nodule or a lowgrade dysplastic nodule. The histopathological correlation was consistent with a lowgrade dysplastic nodule.
Figure 4
High-grade dysplastic nodule vs. perfusion abnormality. Axial FSE T2-weighted image, with fat suppression (A), axial pre-contrast 3D-GRE T1-weighted image, with fat suppression (B), and axial post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). In the context of a patient with cirrhosis, one hepatic nodule is depicted only on the arterial phase (arrow, c), showing hypervascularity with no wash-out on the delayed phase (D). This nodule is not well depicted in the pre-contrast images, due to the isointense signal, comparable to that of the background liver parenchyma, on T1- and T2-weighted images (B and A, respectively). This abnormality is peripheral, not well-defined, and seen only in the arterial phase, raising the suspicion of perfusion abnormality. The differential diagnosis includes high-grade dysplastic nodule and this abnormality should therefor be followed closely, preferentially with hepatobiliary contrast-enhanced scans.
Figure 5
Progression from high-grade dysplastic nodule to HCC in a patient with a history of chemoembolization for HCC. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast 3D-GRE T1-weighted image, with fat suppression (B), and axial post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). In the right hepatic lobe, a small high-grade dysplastic nodule is depicted, showing an isointense signal on the T2-weighted image (arrow, A), mild low signal intensity on a T1-weighted image (arrow, B), slight arterial hyperenhancement (arrow, C) and no perceived wash-out in the delayed phase (D). Axial SSFSE T2-weighted image, with fat suppression (E), pre-contrast 3D-GRE T1-weighted images, with fat suppression (F), and post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (G and H, respectively) in the same patient 2 months later. The follow-up MRI shows the same nodule with mildly high signal intensity on the T2-weighted image (arrow, E), peripherally arterial hyperenhancement (arrow, G) and clear wash-out in the late phase (arrow, H). This case illustrates the importance of short follow-up studies for arterially enhanced nodules without typical characteristics of HCC.
Figure 6
Small HCC arising from a high-grade dysplastic nodule - nodule-within-a-nodule appearance. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast 3D-GRE T1-weighted image, with fat suppression (B), and axial post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). A heterogeneous 15-mm nodule is depicted in the left hepatic lobe (arrows, A-D). Within the lesion (medial aspect), there can be seen a small nodule (< 10 mm) with mildly high signal intensity on the T2-weighted image (small arrow, A) and low signal intensity on the pre-contrast T1-weighted image (small arrow, B), with hyperenhancement in the arterial phase (small arrow, C) and wash-out in the interstitial phase (small arrow, D). The remaining part of the main nodule (lateral aspect; 15 mm) shows signal intensity similar to that of the background liver parenchyma on T2- and T1-weighted images (arrows, A and B, respectively), hyperenhancement in the arterial phase (arrow, C), and no delayed wash-out, features consistent with a high-grade dysplastic nodule or early HCC (arrow, D). These features are also consistent with a small HCC arising within a high-grade dysplastic nodule (small arrow, A), as well as with early HCC (arrows, A-D), giving the lesion a typical and highly specific nodule-within-a-nodule appearance.
Figure 7
Typical HCC in a patient with chronic hepatitis C. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast in-phase 3D-GRE T1-weighted image, with fat suppression (B), and axial post-contrast in-phase 3DGRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). A 6-cm nodule is depicted in the right hepatic lobe (arrow, A), showing mild high signal intensity on T2-weighted image (A) and low-signal intensity on pre-contrast T1-weighted image (B). On the dynamic post-contrast images, the lesion shows arterial hyperenhancement (C) and delayed wash-out with pseudocapsule enhancement (D).
Figure 8
Isovascular HCC in a patient with chronic hepatitis C. Axial SSFSE T2-weighted image, with fat suppression (A), axial pre-contrast 3D-GRE T1-weighted image, with fat suppression (B), axial post-contrast 3D-GRE T1-weighted images, with fat suppression, in the arterial and interstitial phases (C and D, respectively). One small nodule is depicted in the right hepatic lobe (arrows, A-D). The nodule shows an isointense signal on T2-weighted images (A), and minimally high signal intensity on the pre-contrast T1-weighted image (arrow, B). On the dynamic postcontrast images, this lesion shows isovascular properties in the arterial phase (C), together with delayed washout and partial pseudocapsule enhancement (D). These characteristics are consistent with an isovascular HCC. The patient was treated with thermal ablation.