PMC3350005_01
In T2-weighted HASTE sequence, (a) the reference lesion reveals hypointense (arrow). In precontrast T1-weighted FLASH 2D sequence, it is inhomogeneous hyperintense (arrow) (b). Arterial phase (c) and portal venous phase (d) T1-weighted VIBE show a progredient enhancement (arrows).
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fig1
On dynamic postcontrast examination, all lesions showed arterial enhancement which persisted in portal venous phase (Figure 1).
As the multiple lesions show a homogeneous enhancement in portal venous phase (a) (T1-weighted VIBE sequence), there is a central "washout" with a peripheral pooling of contrast agent (white arrow) in late phase (b) (T1-weighted FLASH sequence, 20 min p.i.). This is likely to be due to a missing washin of the more central parts. Additionally, there is an evidence of an inhomogeneous hilar pooling of the contrast agent, predominantly in the left liver lobe (green arrow). Contrast agent level in the ductus hepatocholedochus (yellow arrow).
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fig2
In the hepatobiliary liver-specific late phase, a central "washout" and a persistent rim enhancement (target sign), at least in larger lesions, was observed (Figure 2).
CEUS shows a more explicit centrifugal arterial (a) 16 s p.i.; (b) (17 s p.i.) and a liver like portal venous enhancement (c) (50 s p.i.) of the reference lesion (arrow).
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fig3
During the portal venous and the delayed liver phase, the lesions then appeared isoechoic compared with the surrounding liver parenchyma (Figure 3).
Histological preparation: (a) thickened arterial vascular wall (arrows), proliferation of bile ducts and of inflammatory cells (black), and normal hepatocytes/liver parenchyma (white) (b) dropout of hepatocytes as a sign of cirrhosis of the liver, liver vein (red), and normal liver parenchyma (light blue).
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fig4