|
| Ultrasonography | Triphasic CT | MRI | 18F-FDG PET scan | CT angiography |
|
| Hemangioma (Figure 1) | More often: cavernous (high flow): heterogeneous, hypoechoic, sometimes calcifying
More rare: capillary (low flow): homogeneous, hyperechoic, sharp limited, no halo
Doppler: low flow, low index, absence of spectral broadening | Early phase: iridic diaphragm phenomenon with peripheral nodular enhancement
Late phase: CM- enhancement rise, determination of the size | Peripheral enhancement, centripetal progression,
T1: hypo intense
T2: hyperintense
Sensitivity >95%
Specificity 95%
10% atypically | No uptake or photopenic defect compared to liver baseline | Cotton wool pooling of contrast,
normal vessels without AV shunt, persistent enhancement |
|
FNH
(Figure 2) | Homogeneous, iso-, hypo- or hyperechoic,
Central hyper echoic area Central aterial signal (50–70%: central scar)
Doppler: high flow, spokes phenomenon, spectral broadening | Isodense with liver,
Central low density Scar
Arterial phase: homogeneous strongly enhance | Native: isodense
T1: isodense
T2: isodense hyper intense scar
sensitivity >95%
specificity >95% | No uptake | Hypervascular 70%;
centrifugal supply |
|
| Adenoma (Figure 3) | Unspecific,
Hypo- or hyper echoic
Hemorrhage or necrosis: heterogeneous, anechoic center
Doppler: variable flow, spectral broadening | Homogenous > heterogeneous
Peripheral feeders filling in from periphery | T1 Gd: hyperintense T2: hyperintense
(intralesional fat) capsule
necrosis:
T1: hypointense
T2: hyperintense
bleeding:
T1 + T2: hyperintense | No uptake
uptake
If transformation to HCC in 30% of the cases | Hypervascular;
large peripheral vessels; central scar if hemorrhage |
|
