Table 3: Morphology of the most common benign lesions in imaging techniques [1, 3, 10, 11, 18, 3335].

UltrasonographyTriphasic CTMRI18F-FDG PET scanCT 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 baselineCotton 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 uptakeHypervascular 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

CT: computed tomography, MRI: magnetic resonance imaging, FNH: focal-nodular hyperplasia CM: contrast medium, HCC: hepatocellular carcinoma.