Cirrhosis

Not a specific disease; it is an end stage of all progressive chronic liver diseases; which once fully developed is irreversible and may be associated clinically with symptoms and signs of liver failure and portal hypertension

IRREVERISBLE LIVER DAMAGE

Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration

Main Causes

Common

Others

Non-alcoholic fatty liver disease

Hepatitis B +/- D

Chronic alcohol abuse (most common in the West)

Hepatitis C

Hereditary haemochromatosis (iron overload)

Wilson's disease

Autoimmune hepatitis - presents as high ALT

Alpha-Antitrypsin deficiency

Primary biliary cirrhosis

Drugs e.g. amiodarone and methotrexate

Risk factors

Chronic alcohol abuse

Pathophysiology

Chronic liver injury results in inflammation, matrix deposition, necrosis and angiogenesis of all which lead to FIBROSIS

Liver injury causes necrosis and apoptosis, releasing cell contents and reactive oxygen species (ROS)

Activation of hepatic stellate cells and Kupffer cells

The characteristic features of cirrhosis are regenerating nodules separated by fibrous septa and loss of lobular architecture within the nodules

Two types

Micronodular cirrhosis

Macronodular cirrhosis

Regenerating nodules are usually < 3mm in size with uniform involvement of the liver

Often caused by alcohol or biliary tract disease

They are nodules of varying size and normal acini (functioning unit of the liver) may be seen within the larger nodules

Often caused by chronic viral hepatitis

Clinical Presentation

Xanthelasma - yellow fat deposits under skin usually around eyelids

Loss of body hair

Spider navei

Hepatomegaly

Dupuytren's contracture

Bruising

Palmar erythema

Ankle swelling and oedema

Clubbing

Abdominal pain due to ascites

Leuconychia - white discolouration on nails due to hypoalbuminaemia

Diagnosis

LFTs

Liver biopsy

Liver Biochemistry

Child-Pugh classification

Ascites, encephalopathy, bilirubin, albumin and prothrombin added up to give a score

GOLD STANDARD

Confirms diagnosis and type and severity of disease

Serum albumin and prothrombin time are best indicators of liver function

Low albumin and long prothrombin time (longer it is correlates to severity )

In most cases there us raised AST and ALT

May be normal depending on severity

Serum electrolytes: low Na - indicates severe liver disease

Raised serum creatine

Alpha-fetoprotein is highly suggestive of HEPATOCELLULAR CARCINOMA

Imaging

MRI

Endoscopy

Ultrasound

May be marginal modularity of the liver surface and distortion of the arterial vascular architecture

Good for detecting hepatocellular carcinoma

Shows change in size and shape of liver - hepatomegaly (small liver in severe disease)

Hepatosplenomegaly

Hepatocellular carcinoma

Detects tumours

Detection of varies and portal hypertensive gastropathy

Treatment

Complications

Encephalopathy - liver flap (asterisks - flapping tremor with wrist extended) & confusion/coma

Hypoalbuminaemia resulting in oedema

Coagulopathy; fall in clotting factors II, VII, IX & X

Portal hypertension

Ascites

Oesophageal varies

Treatment of the underlying causes may arrest or reverse the cirrhosis

Those at risk should have Hep A & B vaccination

Patients should undergo 6 mostly ultrasound screening for early development of hepatocellular carcinoma

Avoid NSAIDs and aspirin as these may precipitate GI bleeding or renal impairment

Alcohol abstinence

Reduced salt intake

Good nutrition is vital

If very advanced and no longer responsive to therapy then liver transplantation