Cirrhosis is a process associated with end-stage chronic liver disease and is not really a disease in itself. It can result from a wide range of pathological processes including chronic hepatitis and alcoholic disease. Ultrasound images appearances of cirrhosis In cirrhosis bands of fibrous tissue are laid down in the liver parenchyma between the hepatic lobules. This distorts and destroys the normal architecture of the liver, separating it into nodules. The process may be micronodular, which gives a generally coarse echotexture, or macronodular in which discrete nodules of 1 cm and above can be distinguished on ultrasound (Fig. below).
Ultrasound images Micronodular cirrhosis in a patient with alcoholic liver disease
ultrasound images Macronodular cirrhosis in a
patient with primary biliary cirrhosis. Cirrhotic nodules are demonstrated throughout the peripheral hepatic substance
with a lobulated liver outline. Ascites is also present.
Ultrasound images Monophasic ‘damped’ flow in the hepatic veins in a patient
with micronodular cirrhosis. This sign is not specific for cirrhosis and may be present under many other circumstances, including the presence of ascites.
The hepatocellular damage which causes cirrhosis gives rise to hepatic fibrosis, a precursor of cirrhosis. The fibrosis itself may have very little effect on the ultrasound appearances of the liver, but when advanced it is more highly reflective than normal liver tissue, giving the appearance of a ‘bright’ liver often with a coarse texture.10 Unlike fatty change, which is potentially reversible, fibrosis is the result of irreversible damage to the liver cells. The picture is further complicated by the association of fibrosis with fatty change, which also increases the echogenicity. The acoustic attenuation properties of fibrosis, however, are similar to normal liver, so the ultrasound beam can penetrate to the posterior areas using normal TGC settings. Fat, on the other hand, increases both the echogenicity and the attenuation, preventing penetration to the far field. The cirrhotic liver tends to shrink as the disease progresses. However, it may be normal in size, or may undergo disproportionate changes within different lobes. In some patients the right lobe shrinks, giving rise to relative hypertrophy of the caudate and/or left lobes. This is likely to be due to the venous drainage of the different areas of the liver. The rigid nature of the diseased liver also causes haemodynamic changes which can be demonstrated on spectral Doppler. The normally triphasic hepatic venous waveform can become flattened and monophasic (Fig. above ). This is not necessarily specific to cirrhosis but is also associated with numerous types of chronic liver disease or any condition, either intra- or extrahepatic, which compresses the venous flow, such as polycystic liver disease or the presence of ascites. The portal venous flow may also be compromised due to portal hypertension (see below) and is associated with numerous changes on ultrasound showing reduced velocity, reversed flow, partial or total thrombosis. A compensatory increase in hepatic arterial flow to the liver may also be seen as a result of portal venous compromise in portal hypertension. Patients with cirrhosis are at increased risk of developing HCC, the detection of which is particularly difficult in an already nodular liver. Both CT and ultrasound have a low sensitivity for detecting small focal lesions in cirrhotic livers.  The use of Doppler, contrast CT and contrast MRI continues to improve the detection rate of small lesions and many high-risk patients (i.e. those with cirrhosis) undergo regular ultrasound screening with tumour markers (AFP) as a precaution.14 Small lesions continue to present a diagnostic challenge, and the use of ultrasound contrast agents, and the development of MRI using iron oxide, are likely to improve both detection and characterization of HCCs. Cirrhosis has numerous aetiologies: Alcoholic cirrhosis The spectrum of alcoholic liver disease may take three forms: steatosis (alcoholic fatty liver), alcoholic hepatitis (often preceding cirrhosis) and finally cirrhosis. The later, chronic stages carry a worse prognosis, frequently associated with portal hypertension and an increased incidence of HCC (Fig.above). Alcoholic liver disease may be halted or reversed in the early stages in patients who discontinue alcohol intake, with subsequent nodular regeneration of hepatic tissue (Fig. above). Nodular regeneration is not easy to distinguish from frank cirrhosis or other focal liver lesions, such as HCC, and the use of ultrasound contrast agents, or other imaging such as MRI may be required. Regenerating nodules may cause the liver to enlarge, whereas end-stage cirrhosis causes shrinkage of the liver. Primary biliary cirrhosis (PBC) This is a progressive cholestatic liver disease of unknown aetiology which occurs predominantly in middle-aged females. The term ‘cirrhosis’ may be rather misleading for the early stages of this condition, which actually take the form of an inflammatory destruction of the intrahepatic bile ducts. These early stages of cholangitis are not, strictly speaking, cirrhotic. However as the destruction progresses, fibrotic bands form in a process of macronodular cirrhosis (Fig. above). Treatment of PBC involves control of the associated symptoms of portal hypertension and pruritus, but its progression is inevitable. Liver transplantation now offers a successful therapeutic option for these patients. Although the liver frequently looks normal on ultrasound in the early stages of the disease, gallstones,splenomegaly and lymphadenopathy can be demonstrated in many patients. Secondary biliary cirrhosis This occurs as a result of long-standing biliary obstruction. Causes usually include benign strictures or chronic stone impaction in the common bile duct causing progressive, gradual obstruction over a period of time. This causes ascending cholangitis and jaundice. The bile ducts may appear only mildly dilated on ultra- sound. It is also a recognized sequel of biliary atresia in children. Other causes of cirrhosis Cirrhosis may be drug-induced, particularly in patients on long-term treatment or therapy. It is also associated with many other diseases, such as hepatitis diabetes, ulcerative colitis, rheumatoid arthritis or any long-term conditions, acquired or congenital, which can affect the liver. Congenital forms of cirrhosis exist due to metabolic disorders: Wilson’s disease (deposition of copper in the liver and kidneys), glycogen storage disease (inability to break down glycogen to glucose), haemochromatosis (deposition of iron in the liver and pancreas) and others.
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