Usually hepatitis is caused by a viral infection, mostly hepatitis virus type A and B; however, hepatitis C, D, E and other viruses such as CMV, Epstein Barr, herpes, and AIDS-HIV may also be involved. The clinical manifestations depend on the insult with jaundice, nausea, vomiting, and pyrexia commonly seen.
On US the liver will usually have a normal echo signal. However, in severe cases, the hepatocytes will swell and fatty infiltration will occur, and this may appear as a hyperechoic liver with increased echoes in the portal vein radicles. The gallbladder wall may be thickened and an increase in the size of the lymph nodes around the portal vein and around the cystic duct may be visualized.
Children with chronic hepatitis will initially have a hypoechoic liver that will advance to a heterogeneous liver and finally to a small liver with a hyper-echoic signal.
On CT, livers with acute hepatitis are usually heterogeneous in attenuation, with areas of low attenuation due to the presence of edema and lymphocytic portal infiltration. Areas of nodular regeneration will have high attenuation on unenhanced CT and low attenuation after contrast injection. Necrotic areas will be seen as low attenuation areas on unen-hanced CT, and will show higher attenuation than surrounding parenchyma on contrast CT. Enlarged lymph nodes close to the hilum or hepatogastric ligament may also be present.
In 80% of patients with acute hepatitis, MRI may demonstrate areas ofhigh signal intensity close to the periportal region on T2-weighted images. Necrotic tissue may be seen in fulminant hepatitis and will have high signal intensity on T2-weighted images and low signal intensity on T1-weighted images. After an episode of fulminant hepatitis, peripheral regeneration in the liver will be seen as nodular areas of high signal intensity on T1-weighted images and low signal on T2-weighted images.
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