Cirrhosis

common chronic disease of the liver characterized by parenchymal necrosis, scarring and extensive fibrosis associated with parenchymal nodular regeneration leading to lobular and vascular disorganization. The main complications are liver failure and portal hypertension with intestinal bleeding from oesophageal varices (see varices oesophageal). There is an increased incidence of hepatocellular carcinoma in patients with cirrhosis secondary to viral hepatitis. The aetiology of liver cirrhosis is multiple as the end process of many diffuse parenchymal hepatic processes is cirrhosis. The most frequent cause of cirrhosis in the Western world is excessive chronic alcohol consumption whereas viral hepatitis is the usual cause in Asia and Africa. Other less common causes include: toxic agents; nutritional and metabolic disturbances; chronic cholestasis; congestive heart failure or hepatic vein obstruction (Budd Chiari syndrome). In the micronodular type of cirrhosis the fibrous septa are thin while the regenerative nodules are small and measure between 1 and 3 mm in diameter. This form is seen mostly in cirrhosis caused by alcohol abuse, haemochromatosis, biliary obstruction and venous outflow obstruction.

In macronodular cirrhosis the septa are of variable thickness while the nodules vary in size between 3 mm and several cm. This form has also been referred to as postnecrotic necrosis and is frequently secondary to viral hepatitis. The two other forms are mixed micro- and macronodular and incomplete septal.

Gross changes in size and shape of individual liver hepatic segments are frequently noted. Typically there is increase in size of the quadrate lobe and of the left segment of the left lobe, whereas the right lobe and the medial segment of the left lobe tend to become atrophic with an outer concave contour. The caudate lobe is spared in cirrhosis and in other hepatic diseases.

In advanced cirrhosis the gallbladder is frequently in an abnormal position and may occupy an intrahepatic position or may be situated in a more lateral superficial position. In addition the gallbladder wall is frequently thickened due to oedema and the galbladder may contain small pigment stones.

Liver cirrhosis may be asymptomatic in 3049% of patients and may remain so for many years. Patients with decompensated cirrhosis may present with a large variety of symptoms such as general fatigue, loss of appetite, dyspepsia, diarrhoea or weight loss. In more advanced disease state jaundice, ascites and enlarged liver are observed.

Radiological diagnosis

Radiological imaging may provide a correct diagnosis if regenerating nodules can be demonstrated. Furthermore imaging will contribute to the clinical management by providing objective information about the size, the form and contours of the liver, as well as about the state of the parenchyma and by detecting complications such as portal hypertension, ascites and HCC.

Radiographic features

Cirrhosis may cause several abnormalities on the standard chest roentgenogram. The right diaphragm may be elevated and its movements restricted by the hepatomegaly. In addition, if portal hypertension is present, one may notice azygous vein dilatation and lateral displacement of the paravertebral line secondary to hemiazygous vein hypertrophy. On barium studies of the gastrointestinal system displacement of the stomach, duodenum and colon secondary to the changes in liver volume and morphology will be noted. Cirrhosis and ascites predisposes to interposition of the colon between the liver and the right diaphragm (Chilaiditis syndrome).

Ultrasound

The sonographic features suggesting liver cirrhosis are re indicative for cirrhosis. The relative size of the diameter of the right and the left portal vein branches can also be used as a criterium to detect liver cirrhosis. Due to the relative increase in size of the left liver lobe the diameter of the left portal vein branch tends to become equal to or greater than the diameter of the right portal vein.

In patients with cirrhosis duplex Doppler ultrasound examination of the hepatic veins may reveal loss of the normal triphasic wave pattern with flattening of the wave form. Sonography can also be helpful to detect secondary and indirect signs of liver cirrhosis in patients with an advanced stage of cirrhosis. These findings include splenomegaly, varices and ascites.

Computed tomography

During the early stage of liver cirrhosis the liver parenchyma may appear normal on CT or hepatomegaly with or without inhomogeneous attenuation of the liver parenchyma may be noted. This inhomogeneous aspect is due to focal steatosis or fibrosis.

In the later stages there is overall loss of volume as well as volume redistribution. The increase in the caudate lobe/right liver lobe ratio is a striking finding in liver cirrhosis and can usually be better evaluated on CT than on ultrasound. CT is also well suited to display the topographical changes in the right upper abdominal quadrant affecting the position of the gallbladder, colon, stomach and duodenum as a consequence of the loss in volume of the liver.

The increased nodularity of the liver borders in advanced stages of liver cirrhosis is well displayed on CT. In many instances the change in liver architecture caused by regenerative nodules that are located not in the periphery but in more central areas of the liver is not demonstrated well on CT. Exceptions are those regenerative nodules that are hyperattenuating relative to the normal liver parenchyma due to their abnormal concentration of haemosiderin or regenerative nodules occurring in livers with marked steatosis.

Following contrast enhancement an inhomogeneous degree of enhancement of the liver parenchyma is observed in the cirrhotic liver. Intrahepatic arterioportal fistulas in patients with liver cirrhosis may be suggested on CE CT by an abnormally early and elevated degree of enhancement of the lobe in which the fistula is located and by abnormally early opacification of segmental portal vein. "Confluent" hepatic fibrosis is a form of cirrhosis characterized on CT as a triangular hypoattenuating area extending from the liver hilum to the periphery, or as peripheral band-like hypoattenuating areas. Capsular retraction is usually present. On postcontrast scans these lesions appear either isoattenuating relative to the liver parenchyma or remain hypoattenuating.

Extrahepatic CT findings in patients with cirrhosis, similarly to ultrasound are mostly related to portal hypertension and include varices, ascites and splenomegaly.

Magnetic Resonance Imaging

Cirrhosis does not significantly alter the T1 nor the T2 relaxations times but if supermagnetic iron oxide is administered as a contrast agent there is a reduced uptake because of the reduced number of Kupffer cells. This results in a signal intensity decrease of only 52% as compared to 75% in normal liver. Regenerative nodules are mostly hypointense on both the T1-weighted and T2-weighted images. If superparamagnetic iron oxide is administered these nodules may appear hyperintense relative to the liver parenchyma because they contain less Kupffer cells. The fibrous septa are hypointense on T1-weighted images and have an intermediate signal intensity on T2-weighted images. On MRI confluent hepatic fibrosis presents features characterized by hypointense aspects on T1-weighted images and raised signal intensity on T2-weighted images.