Diffuse Liver Disease

Fatty liver (hepatic steatosis) may be associated with a variety of clinical disorders. US shows a diffuse or focal increase in the echogenicity of the liver. Increased fat content produces a decrease in mean hepatic CT attenuation value [26]. Milder degrees of diffuse fatty change can be diagnosed when the attenuation value of the liver is less than that of the spleen on plain study. Fatty liver may be more difficult to diagnose on scans obtained after administration of iv contrast material. Focal fatty infiltration frequently has a segmental or wedge-shaped configuration and characteristically produces no mass effect or bulging of the hepatic contour. In addition, it is simpler to diagnose when it occurs in typical locations such as adjacent to the gallbladder fossa. Normal coursing of hepatic vessels can often be seen in the affected area. MRI is extremely useful in providing definite diagnosis when the CT scan is equivocal. Proton chemical shift imaging tech niques (in- and out-of-phase imaging) can readily diagnose focal and diffuse fatty infiltration [27].

The role of imaging in cirrhosis is to identify effects of portal hypertension and to detect HCC. The liver in early cirrhosis often has a normal appearance on CT. Early CT features include hepatomegaly and heterogeneity of hepatic parenchymal attenuation. Advanced cirrhosis is characterized by decreased hepatic volume with prominence of the porta hepatis and intrahepatic fissures, decreased size of the right hepatic lobe and medial segment of the left lobe, with a corresponding relative increase in the size of the caudate lobe and left lateral segment [28]. Regenerative nodules are seen on CT in those patients with siderotic nodules (dense on unenhanced CT, and signal void on MRI) and are better appreciated on MRI than on CT due to greater MR susceptibility to iron [29]. Dysplastic nodules (DN) represent a continuum and transition between regenerative nodules and HCC, and therefore is an important imaging diagnosis. When large, they are characteristically hyperintense on Tl-weighted images and hypointense on T2-weighted images. On the contrary, HCCs generally appear iso- or hyperintense on T2-weighted images. Unfortunately, all small DNs and many large DNs have no characteristic appearance and are often not visualized. Although early enhancement on dynamic enhanced MRI may help in reliably distinguishing HCC from DN, some DN will exhibit marked contrast enhancement.

In patients being screened for cirrhosis and possible transplantation, 10-20% of patients harbor a HCC (higher rates for patients with hepatitis B and C), and arterial phase imaging is the only methodology that with high sensitivity (70-80%) can detect these patients [30]. Caution is recommended, however, as it is now known that many small benign lesions can enhance and simulate HCC, most prominently in patients with hepatic vascular disorders, particularly Budd-Chiari [31, 32]. Probably the best approach to a patient with just one or a few small enhancing nodules is to take the same approach as upon visualizing a lung nodule in a cancer patient - suspicious but not definitive.

Of the myriad of lesions simulating HCC in cirrhosis (arteriovenous [AV] malformation, small hemangiomas, infracted regenerative nodules among the less common), the most common and problematic lesions, that can enhance are enhancing benign or dysplastic regenerating nodules (usually small, but not always) and focal confluent fibrosis [32]. Key to the latter diagnosis is the characteristic finding of associated overlying capsular retraction, and characteristic locations and shape (wedge shaped, radiating to porta hepatic).

Extrahepatic imaging features of cirrhosis are ascites, splenomegaly and portosystemic collateral vessels.

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