Hemangioma is the most frequent solid focal lesion in the liver from 1% to 20% in the general population (Ros et al., 2001). These can be divided into two different types: capillary and cavernous hemangioma. The first are relatively small networks of vascular spaces (< 3 cm). Some of them can show an early hypervascular pattern in the arterial phase due to concentrated arterial micro-vessels - high-flow hemangioma (Jang et al., 1998). These are generally characterized by the presence of small arterial branches, venous lakes and fibrous areas, and absence of capsule. The latter, cavernous hemangiomas (> 3 cm) and giant hemangiomas (> 10 cm) may show an inhomogeneous structure composed of venous lakes, dense connective tissue and thrombosed areas (Unal et al., 2002).
Arterial portal micro-fistulas can be identified with CEUS. On conventional US hemangiomas are often incidental findings since they are asymptomatic except for the relatively rare giant type. Conventional US capillary hemangiomas have a typical homogeneous hyper-echoic appearance in comparison with surrounding hepatic parenchyma with well defined margins; in a fatty liver it may be found as a hypo-echoic lesion. Cavernous hemangiomas can present an inhomogeneous aspect with hyper-echoic and hypo-echoic areas (Moody and Wilson, 1993). In all cases conventional US findings cannot be considered specific particularly in oncologic and cirrhotic patients. Intralesional blood flow Doppler signals may be identified in high-flow capillary hemangioma (Tanaka et al., 1990).
Contrast-enhanced ultrasound can show several appearances (Bleuzen and Tranquart 2004, Catalano et al., 2005). In fact contrast material uptake may be fast or slow depending on intralesional circulation speed. Typical and atypical features are summarized as follows:
Arterial phase: peripheral-nodular enhancement, no central enhancement, rim enhancement;
arterial-portal fistula and arterial inflow vessel;
Parenchymal phase: non enhanced central areas (partial thrombosis, fibrosis)
In early arterial phase a peripheral rim of enhancement. In portal phase it begins centripetal enhancement of globular type, it continues in early and late parenchymal phase. In this phase a total homogenization of enh of the lesion similar to the rest of parenchyma, with centripetal course.
Focal liver lesion between 6-7 segment, solid hypoechoic, show center-nodular enhancement departure from central vessel with graduates filling of all the lesion; to 2-3 min it is not found wash out.
C.R: angioma to high flow and/or INF.
Focal liver lesion in segment 6, solid iso-hyperechoic. In arterial phase late gradual periferical enhancement; In progressive portal and parenchymal phases incomplete globular periferical enhancement with central lesion area of necrosis.