2. An avidly enhancing mass is seen in the left lobe on arterial-phase imaging. It is slightly hyperintense on portal-venous-phase imaging but overall isointense relative to the liver on most sequences, including precontrast T1 imaging and T2 imaging. There is a slight contour abnormality on T2 imaging and obliteration of vessels in the expected location of this mass, but otherwise the mass is relatively "stealthy." Twenty-minute delayed hepatobiliary-phase imaging shows isointensity of this lesion to the adjacent liver.
FNH is a benign lesion composed of normal hepatocytes in a disorganized architecture with disorganized bile ducts and a predominantly arterial blood supply. This results in a nodular lesion with brisk arterial enhancement on arterial-phase dynamic contrast-enhanced imaging. Further, it is typically isointense on most other sequences and appears isointense or slightly hyperintense on portal-venous-phase imaging. Occasionally it appears slightly hyperintense on T2-weighted imaging. Two-thirds of FNHs demonstrate a central scar, which was not identified in this example. Isointense or even hyperintense appearance on delayed hepatobiliary imaging is typical of FNH, and in conjunction with the other imaging findings is entirely diagnostic. These overall findings are highly specific for FNH, and tissue sampling is not necessary. In this case, the lack of a central scar would lead to including hepatic adenoma in the differential diagnosis; however, the appearance on the delayed hepatobiliary-phase imaging leads us to make the diagnosis of FNH with confidence.

3. Significant signal dropout on opposed-phase imaging is consistent with diffuse hepatic steatosis (severe). Note 2 focal areas of relative sparing, but slight hypointensity on the in-phase T1 imaging (yellow arrows). These lesions also appear slightly hyperintense on precontrast T1-weighted imaging with fat suppression, and slightly hyperintense on T2-weighted imaging with fat saturation. Arterial-phase T1 imaging shows intense enhancement of these lesions as well as relative hypointensity of the background liver. Both lesions show persistent mild hyperintensity relative to the liver on portal-venous-phase imaging. Twenty-minute delayed hepatobiliary-phase T1 imaging shows hyperintensity of these lesions relative to the liver with internal architecture resembling central scars.
All imaging findings are compatible with 2 FNH lesions in a background of diffuse steatosis. FNHs do not typically accumulate significant fat, increasing their conspicuity in the setting of diffuse hepatic steatosis. For the same reason they appear slightly hyperintense on T2-weighted imaging and precontrast T1-weighted imaging, because fat saturation was used in these sequences. The use of fat saturation in the setting of diffuse steatosis also augments the relative hyperintensity of these lesions on arterial-phase and portal-venous-phase imaging, as well as delayed hepatobiliary-phase imaging. Finally, a slight hypointensity on T1-weighted in-phase imaging is also explained by the fact that the T1 fat is lower than that of normal liver parenchyma and FNH, and therefore the liver appears to have a higher signal intensity on the T1 in-phase image.

4. Significant signal dropout is seen on opposed-phase imaging, consistent with diffuse hepatic steatosis (severe). Note focal area of relative sparing that appears slightly hypointense on the in-phase T1 imaging. On T2 imaging with fat saturation, there is slight hyperintensity relative to the background liver with a bright central scar. Arterial-phase T1 imaging shows intense enhancement of the lesion, with a hypointense central scar and nodular configuration, particularly along its border. Portal-venous-phase imaging shows persistent enhancement with mild relative hyperintensity compared with the adjacent liver. Twenty-minute delayed hepatobiliary-phase T1 imaging shows the same architecture and relative hyperintensity of this lesion with a nodular, “popcorn-like” appearance. Accumulation of gadolinium is also noted within the common duct and gallbladder.
A central scar is seen in approximately two-thirds of FNH. It commonly appears hyperintense on T2 imaging. With conventional extracellular gadolinium-based contrast agents, the central scar often appears hyperintense relative to the lesion in the liver at approximately 5 to 10 minutes due to nonspecific uptake of contrast. However, with gadoxetic acid, the uptake into the functioning hepatocytes of the liver and focal nodular hyperplasia is relatively rapid, and enhancement of the central scar at 5 to 10 minutes will not be appreciated. In fact, the central scar does enhance relative to the precontrast imaging; however, this effect is not appreciated because the intense accumulation of gadolinium within the FNH and adjacent liver exceeds the nonspecific enhancement of the central scar. Therefore, 5- to 10-minute delayed imaging to observe the central scar is of limited utility when using gadoxetic acid. Finally, the uptake of gadolinium into this lesion in conjunction with all imaging findings is diagnostic of FNH. Please note that the presence of diffuse steatosis, which is spared within the FNH, alters the relative intensity of the lesion on sequences that use fat suppression, most notably the T2-weighted imaging, portal-venous-phase imaging, and delayed hepatobiliary-phase imaging.

5. Within segment 5, inferiorly there is a 6-cm lesion
Within segment 5, inferiorly there is a 6-cm lesion. It is relatively isointense on T2-weighted FSE with fat saturation but has a focal central scar that is hyperintense. The lesion is isointense on T1 imaging and the central scar is hypointense. Arterial-phase imaging shows brisk enhancement with a typical nodular “popcorn” appearance. It is isointense on portal-venous-phase T1-weighted imaging. Ninety-minute hepatobiliary-phase delayed images demonstrate isointensity of the lesion relative to the liver. Note the accumulation of gadolinium contrast within the gallbladder.
This example demonstrates typical imaging characteristics of FNH, including isointensity of the lesion on all sequences except the arterial-phase imaging, and the presence of a central scar that is hyperintense on T2-weighted imaging. Isointensity of the lesion on 90-minute delayed hepatobiliary-phase imaging using gadobenate dimeglumine, in combination with other imaging characteristics and the clinical history, is diagnostic of FNH.

6. In the 3 slices shown, 3 separate lesions are identified (arrows), 2 within the left lobe and 1 within the right lobe. The lesions are slightly hyperintense relative to liver on T2 imaging. All 3 lesions show relatively uniform and avid enhancement on arterial-phase imaging with slight hyperintensity on portal-venous-phase imaging (not shown). Delayed hepatobiliary-phase images show hyperintensity of these lesions relative to the adjacent liver. The largest lesion (middle row) in the left lobe shows a classic central scar appearance and approximately matches the hyperintense central scar seen on T2-weighted imaging. A relatively large area of hypointensity is seen in the second lesion (top row), a pattern that is also commonly observed on delayed-phase imaging. Finally, 1 small lesion (bottom row) demonstrates a hyperintense rim that is often seen in smaller FNH.
The constellation of imaging findings, including delayed hepatobiliary-phase imaging, is diagnostic for FNH, particularly in an asymptomatic patient. No other lesion should be considered in the differential diagnosis. The use of optimized delayed hepatobiliary-phase imaging with high flip angle (40o) to achieve optimized T1 contrast and use of free-breathing navigator-based sequences to obtain high-resolution images provides improved definition of the detailed structure of these lesions. Variability of the delayed hepatobiliary-phase appearance of FNH, particularly with some areas of central hypointensity, is commonly observed.

7. A 4 x 5-cm lesion is seen within the caudate lobe (segment 1), with mild to moderate mass effect on the inferior vena cava (yellow arrows). It is isointense on precontrast T1-weighted imaging and isointense or slightly hyperintense on T2-weighted imaging. On dynamic contrast-enhanced T1-weighted imaging, it enhances avidly on the arterial-phase imaging and is mildly hyperintense on portal-venous-phase imaging. On 20-minute delayed hepatobiliary-phase imaging, it is uniformly hyperintense relative to liver. A small central scar is noted on the arterial phase and portal venous phase and best appreciated on high-resolution delayed hepatobiliary-phase imaging.
All findings are highly typical of FNH, including the hyperintensity identified on the delayed hepatobiliary-phase images. In this patient, this benign lesion may have clinical relevance given its compression of the IVC. In general, FNH is a benign lesion that requires no surgical intervention.