111 T2 Bright Central Scar

Evaluation of the T2-weighted sequence (Figs. 111.1A – 111.4A):

–All lesions have a bright central scar in non-cirrhotic liver. In the first example, the lesion is bright with a brighter central scar. The second example shows only the bright central scar within an almost isointense lesion. The third and fourth examples show large course central scars within large soli-

tary lesions.

Evaluation of the arterial enhancement pattern (Figs. 111.1B – 111.4B):

–In the first example, the lesion shows peripheral nodular enhancement. The second lesion shows very intense homogeneous enhancement with a central scar and septal sparing.

The third and fourth lesions show heterogeneous enhancement.

Evaluation of the portal enhancement pattern (Figs. 111.1C – 111.4C):

–In the first example, the lesion shows more prominent peripheral nodular enhancement. The following lesion becomes almost isointense. The third and fourth lesions show washout

with some capsular enhancement. Evaluation of the delayed enhancement pattern (Figs. 111.1D – 111.4D):

–In the first example, the lesion shows persistent enhancement with central scar sparing. The second lesion became isointense with central scar and septal enhancement.

Based on the following pertinent combination of findings the lesions can be characterized as:

1.Giant hemangioma (T2 bright lesion with a brighter central scar and peripheral nodular enhancement)

2.Focal nodular hyperplasia (isointense on T2; bright wellformed central scar; intense homogeneous arterial enhancement, and enhanced central scar and septa)

3.Hepatocellular carcinoma (large solitary lesion; large coarse central scar; heterogeneous enhancement with washout and capsular enhancement in a non-cirrhotic liver)

4.Hepatocellular carcinoma (idem)

Evaluation of the opposedand in-phase T1-weighted sequence (Figs. 112.1A, B – 112.4A, B):

–All livers become dark on opposed-phase images consistent with fatty liver. The lesions in the first example are isointense and surrounded by a rim of fatty sparing. In the third and fourth examples, the liver is severely fatty infiltrated and the

lesions appear bright on opposed-phase images.

Evaluation of the T2-weighted sequences (Figs. 112.1C – 112.4C):

–The lesions appear brighter than the liver. The third lesion contains a bright central scar.

Evaluation of the delayed enhancement pattern (Figs. 112.1D – 112.4D):

–In the first example, the lesions show some persistent perilesional enhancement. The lesions in the third example become almost isointense. The third lesion shows enhanced central scar and the lesion appears brighter within a strongly fatty liver after fat suppression. In the fourth example, the lesions appear brighter within a strongly fatty liver after fat suppression.

Based on the following pertinent combination of findings the lesions can be characterized as:

1.Colorectal carcinoma metastases (T2 bright lesions; persistent perifocal fatty sparing and enhancement)

2.Focal fatty sparing (isointense on in-phase T1; appear bright on fat-suppressed T2 and show faintly more enhancement)

3.Focal nodular hyperplasia (the appearance of this classical FNH is changed due to the severe fatty infiltration of the surrounding liver)

4.Hepatocellular adenoma (strong fatty infiltration of the liver is common in multiple adenomas)