Examine this patient's abdomen.



· Historyof fatigue, weight loss, jaundice.

· History of alcohol abuse.

· History of hepatitis B, intravenous blood products.

· History of intravenous drug abuse.

· Mental status changes (hepatic encephalopathy).

· History of drugs (methyldopa, amiodarone, methotrexate).

· History of Wilson's disease, alpha 1-antitrypsin deficiency.


· In the hands:

-Clubbing, leukonychia.

-Dupuytren's contracture (see Fig. 90), palmar erythema.

Spider nevi tattoos, hepatic flap, pallor.

Scratch marks, generalized pigmentation.

· Eyes and face: icterus, cyanosis, parotid enlargement.

· Chest: spider naevi, loss of axillary hair, gynaecomastia.

· Abdomen:

-Splenomegaly (seldom more than 5 cm below the costal margin).


- Hepatomegaly (particularly in alcoholic liver disease).

· Loss of hair on the shins.

· Leg oedema.

· Tell the examiner that you would like to look for testicular atrophy.


This patient has spider naevi, gynaecomastia, splenomegaly, parotid enlargement (lesions) due to cirrhosis of the liver caused by

alcohol abuse (aetiology). The patient has hepatic flap indicating liver cell failure (functional status).


What is cirrhosis ?

Cirrhosis is defined pathologically as a diffuse liver abnormality characterized by fibrosis and abnormal regenerating nodules.

Mention a few causes of cirrhosis of the liver.

· Alcohol dependence.

· Hepatitis B virus infection (look for tattoos).

· Lupoid hepatitis.

· Primary biliary cirrhosis.

· Haemochromatosis.

· Drugs - methyldopa, amiodarone, methotrexate.

· Metabolic: Wilson's disease, alpha 1-antitrypsin deficiency.

· Cryptogenic.

How would you investigate this patient?

· FBC including haemoglobin and platelet count.

· Liver function tests'including T-glutamyl transpeptidase (GGT).

· Prothrombin time.

· Hepatitis B markers.

· Serum autoantibodies.

· Serum iron and ferritin.

· Serum alpha -fetoprotein.

· Ascitic fluid analysis.

· Ultrasonography of the liver.

Why does this patient have a Iow serum albumin concentration?

Albumin is synthesized in the liver. In cirrhosis there is liver cell failure, causing impaired synthesis.

What are the major sequelae of cirrhosis?

· Portal hypertension.

· Variceal haemorrhages.

· Hepatic encephalopathy.

· Ascites and spontaneous bacterial peritonitis.

· Hepatorenal syndrome.

· Coagulopathy.

· Hepatocellular carcinoma.


What are the poor prognostic factors?

· Encephalopathy.

· Low serum sodium concentration, less than 120 mmol/l (not due to diuretic therapy).

· Low serum albumin level, less than 25 g/l.

· Prolonged prothrombin time.

What factors can precipitate hepatic encephalopathy in a patient with previously well-compensated hepatic cirrhosis?

· Infection.

· Diuretics, electrolyte imbalance.

· Diarrhoea and vomiting.

· Sedatives.

· Upper gastrointestinal haemorrhage.

· Abdominal paracentesis.

· Surgery.

How would you manage variceal bleeding in cirrhosis?

· Blood transfusion to replace falling haematocrit. · Early endoscopy to confirm the bleeding site.

· Endoscopic sclerotherapy with octreotide (N Engl J Med 1995; 333: 555-60). · Intravenous vasopressin is less effective than

sclerotherapy. · Endoscopic ligation (N Engl J Med 1999; 340: 988-93).

· Balloon tamponade is effective in temporarily stopping bleeding while awaiting more definitive therapy.

· Combination of vapreotide (a somatostatin analogue) and endoscopic treatment (N Engl J Med 2001; 344: 23-8).

· Transjugular intrahepatic portosystemic stent-shunt (N Engl J Med 1994; 330: 165-71).

· Combination of nadolol and isosorbide mononitrate (N Engl J Med 1996; 334: 1624-9).