Expertise Details



Aetiology of cirrhosis

• Alcoholic cirrhosis

• Post-necrotic cirrhosis or post-viral cirrhosis

   • Hepatitis B • Hepatitis C • Delta hepatitis (hepatitis D) + hepatitis B Chronic autoimmune hepatitis

• Drug-induced cirrhosis

  • Methotrexate • Methyldopa, isoniazid • Sulphonamides

• Biliary cirrhosis

  • Primary • Secondary

• Non-alcoholic fatty liver disease (NAFLD) • Cardiac cirrhosis • Haemochromatosis

• Wilson's disease • alpha 1 -antitrypsin deficiency • Glycogen storage diseases

• Galactosaemia • Intestinal bypass surgery • Hepatic outflow tract obstruction

• Veno-occlusive disease • Cryptogenic (Idiopathic) cirrhosis


Pathology and Pathogenesis

• Cirrhotic changes affect the whole liver, but not necessarily every lobule.

• Widespread necrosis of liver cells.

• Extensive fibrosis that distorts the hepatic architecture.

• Regenerative, nodular hyperplasia of the remaining surviving liver cells leads to regenerating nodules.

• Destruction and distortion of hepatic vasculature by fibrosis lead to obstruction of blood flow, which eventually leads to portal hypertension and its sequelae.

• Ascites and hepatic encephalopathy result from both hepatocellular insufficiency and portal hypertension.

• Hepatocellular damage leads to jaundice, oedema, coagulopathy and a variety of metabolic abnormalities.

• Alcoholic cirrhosis:

• Safe limits of alcohol are 200 g and 140 g of alcohol per week in males and females, respectively.

• 10 g of alcohol equals 30 mL of whisky, 100 mL of wine and 250 mL of beer.

• Occurrence of cirrhosis six times when alcohol intake is double the safety limit.

• Ingestion of 180 g of alcohol/day for 25 years increases the risk of developing cirrhosis 25 times.

• Hepatitis C infection is an important contributor for progression to cirrhosis.


Clinical Features


• Low-grade fever. • Weakness, fatigue and weight loss. • Anorexia, nausea, vomiting and upper abdominal discomfort. • Abdominal distension due to ascites and gas. • Loss of libido. • Menstrual irregularities like amenorrhoea and irregular menses. • Haemorrhagic tendencies like easy bruising, purpura, epistaxis, menorrhagia and gastrointestinal bleeding. • Haemorrhagic tendencies are due to underproduction of coagulation factors by the liver and thrombocytopenia resulting from hypersplenism. • Symptoms of hepatic insufficiency • Symptoms of portal hypertension and its sequelae


Signs of hepatocellular failure

• Jaundice • Palmar erythema • Parotid enlargement • Dupuytren's contracture

• Diminished body hair • Clubbing • Spider naevi • White nails • Flapping tremors

• Gynaecomastia • Testicular atrophy • Ascites

Features dominant in alcoholic cirrhosis

• Parotid enlargement • Gynaecomastia • Spider naevi • Dupuytren's contractures (related to alcoholism) • Liver enlarged, normal or small in size

End Stage

• End stage of cirrhosis is characterised by:

• Chronic jaundice.

• Progressive, refractory ascites. Worsening of signs of portal hypertension.

• Progressive renal dysfunction.

• Most of them die in hepatic encephalopathy.



• Complete blood picture • Liver function tests

•Prothrombin time • Hepatitis B and C markers • Blood ammonia estimation

• Respiratory alkalosis • Metabolic abnormalities • Ultrasonographic examination

• Fibroscan to determine amount of fibrosis • Liver biopsy confirms the diagnosis of cirrhosis

• Relevant investigations related to the specific aetiologies of cirrhosis in individual patients

• Ascitic fluid examination, barium swallow for demonstration of varices, upper gastrointestinal scopy for delineation of varices



• Treatment of underlying causes

• Removal of causative agents like drugs, alcohol, etc.

• High-protein diet-minimum 1 g/kg/day.

• 2000--3000 kcal/day.

• Diets enriched in branched-chain amino acids, in patients predisposed to hepatic encephalopathy.

• Multivitamin supplementation daily.

• Vaccination against hepatitis A and B viruses, influenza virus, and pneumococcus.

• Specific treatment of complications-e.g. variceal bleeding, hepatic encephalopathy and ascites



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