LIVER CIRRHOSIS BILIARY CIRRHOSIS
Category: Diagnostic Radiology
Abstract : 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
appearances of cirrhosis In cirrhosis bands of fibrous tissue are laid down
in the liver parenchyma between the hepatic lobules.This distorts and destro
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
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.
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. 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 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. 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. 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. 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. 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
ultrasound. 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.
Clinical features and management of cirrhosis :
Clinical
presentation depends upon the aetiology, and may involve either chronic symptoms
or an acute episode. Pruritus, fatigue and jaundice, with steatorrhoea and
deranged LFTs (raised alkaline phosphatase and serum bilirubin in PBC, raised
alanine aminotransferase [ALT] and aspartate aminotransferase [AST] in alcoholic
disease) are generally present by the later stages. This is followed by the
symptoms of portal hypertension, which is a poor prognostic feature associated
with late-stage cirrhosis.
The process may be reversed in alcoholics who
stop drinking. However the prognosis of any cirrhotic condition is extremely
poor if malignancy is present. In severe cases, the management revolves around
trying to treat the symptoms of portal hypertension rather than the disease
itself. Liver transplant is now an established and highly successful treatment
option for PBC when the symptoms can no longer be controlled with drugs. It is
also an option for alcoholic cirrhosis, although there is currently a
significant incidence of posttransplant return to alcoholism.
Hit: 263 times
Related Articles in Diagnostic Radiology :
|
Advertise with Health Information Encyclopedia