Dysplastic Nodule, Early and Advanced hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy. Virus infections (B and particularly C), genetic hemochromatosis, primary biliary cirrhosis, environmental and dietary factors such as persistent organic pullulant substances, alcohol and aflotoxins are the most important causes. Regional distribution worldwide is related to the different etiologies. Chronic liver diseases correlated with C virus infection and alcohol abuse are becoming the most diffuse causes of HCC. Dysplastic nodules occupy an intermediate position between regenerative nodules and well-differentiated HCC. Dysplastic nodules are characterized by cellular atypia without the development of small arteries with a size ranging from 8 – 10 mm to 15 mm. Their pre-malignant nature has been well demonstrated. Hepatic carcinogenesis is described as a multi-step process where the progressive arterialization and gradual loss of portal vessels are the principal features (Ueda et al., 1992, Matsui et al., 1991). It is evident that the vascular enhancement behavior is related to the evolution of the lesion. Thus, during the arterial phase dysplastic nodules or early HCC appear usually hypo- iso-vascularized, while advanced HCCs are hyper-vascularized. On conventional US, findings are non-specific; usually small HCCs (< 3 cm) are hypo-echoic and homogeneous but may appear hyper-echoic due to fatty content (Kim et al., 2001; Ward and Robinson, 2002). Color Doppler or power Doppler may detect characteristic hyper-vascularity; the “basket” pattern of vessels surrounding and penetrating or “vessel-within the tumor” pattern may be visualized in HCC as has been reported (Tanaka et al., 1990). Contrast-enhanced ultrasound may show any selective enhancement in the arterial phase differentiating HCCs from regenerative nodules and dysplastic nodules (Migaleddu et al., 2004, Nicolau et al., 2006) (Fig. 1 a-d). The most common features are described below:
Arterial phase: hyper-enhancing, complete, non-enhancing areas (necrosis);
Portal Vein phase: iso-, hypo- enhancing, non-enhancing areas (necrosis);
Parenchymal phase: hypo- enhancing or wash-out.
Arterial phase: "chaotic" vessels, enhancing tumor thrombus in Portal Vein +HCC/portal vein: hypo- enhancing with intralesional vessels;
Portal Vein phase: hypo-iso- enhancing;
Parenchymal phase: hypo-iso- enhancing.
Focal liver lesion in segment 4, solid hypoechoic. It is found in arterial phase early but incomplete enhancement with intralesional areas of necrosis; progressive wash out in portal and parenchymal phases.
Focal liver lesion in segment 6, solid iso-hypoechoic, with hyper-vascularity. It is found in arterial phase early and complete hyper-enhancement with basket pattern; In progressive portal and parenchymal phases persist the enhancement with central lesion areas of necrosis.
Focal liver lesion in segment 7, solid hypoechoic. It is found in arterial phase early and complete hyper-enhancement with progressive wash out in portal and parenchymal phases.