How to Approach Patient of Liver Disease

Approach Patient of Liver Disease

  • Liver is the largest organ of the body weighing about 1 Kg.
  • It is present in the right upper quadrant of the abdo­men under the right lower rib cage and projects into the left upper quadrant.
  • 20% of the blood flow is from hepatic artery and rich in oxygen.
  • 80% of its blood is rich in nutrients from the portal vein from stomach, intestine, pancreas, and spleen.
  • Cells of liver are called hepatocytes.
  • Other cells are cells of reticulo-endothelial system of liver called Kupffer cells, fat cells, endothelial cells, blood vessels, bile ductular cells and supporting structures. .
Patient of Liver Disease

How to Approach Patient of Liver Disease

  • Liver cells are organized in lobules with central veins in the centre of lobule and portal areas at the bor­ders.
  • Portal areas of the liver consist of small veins, arter­ies, bile ducts and Iymphatics. Blood flows from por­tal areas through sinusoids to the hepatic veins (cen­tral veins). Bile flows from central vein to portal area.
  • The hepatocytes synthesize serum proteins like albu­min, coagulation factors, hormonal and growth fac­tors, produce bile acids, cholesterol, and regulate nutrients like glucose, glycogen, lipids, cholestero.L.­amino acids, and excrete bilirubin, anions and cat­ions in the bile or urine.
  • Therefore, function of the liver is tested by mea­surement of serum bilirubin, albumin, prothrom­bin time.


  • 1. Hepatocellular – viral hepatitis, alcoholic liver disease.
  • 2. Cholestatic – gall stones, malignancy, biliary cir­rhosis, drug-induced.
  • 3. In viral hepatitis, hepatocellular damage as well
  • as cholestatic disease is seen.

Presenting features are:

  • 1. Jaundice
  • 2. Itching
  • 3. Fatigue and weakness
  • 4. Right upper quadrant pain
  • 5. Abdominal distention
  • 6. Intestinal bleeding.

Evaluation of patients of liver disease

  • 1. For etiology
  • 2. For severity
  • 3.For staging. Diagnosis is :
  • 4. Category – Hepatocellular or cholestatic or both.
  • 5. Grading – Active, Inactive, Mild, Moderate, Se­vere.
  • 6. Staging – Acute or chronic, early or late, cir­rhotic or precirrhotic, or end-stage.

CLINICAL HISTORY of liver disease

  • A complete medical history is the single most important part of the evaluation of the patient with elevated LFTs.
  • Important considerations include: The use of or exposure to any chemical or medication (including prescription and over-the-counter medications as well as herbal therapies) which may be temporally related to the onset of LFT abnormalities
  • The duration of LFT abnormalities
  • The presence of any accompanying symptoms such as jaundice, arthralgias, myalgias, rash, anorexia, weight loss, abdominal pain, fever, pruritus, and changes in the urine and stoo
  • Fatigue, weakness, nausea, loss of appetite, malaise, jaundice, dark urine, light stools, itch­ing, pain in abdomen, bloating of abdomen.
  • · Fatigue occurs during the afternoon. Nausea oc­curs by the site of food.
  • · Jaundice is not detectable when serum bilirubin is less than 2.5 mg/dl.
  • · Jaundice without dark urine indicates indirect or unconjugated bilirubinemia as in hemolytic ‘ anaemia and Gilbert’s syndrome and Crigler ­Najjar syndrome.
  • History: Alcohol use, herbal drugs, birth control pills, sexual activity, travel, exposure, surgery, blood trans­fusion, exposure to blood or needle, family history of liver disease.
  • Sexual exposure is important for hepatitis B but not for hepatitis C.
  • Mother to child transmission occurs in hepatitis Band C.


  • The physical examination should focus upon findings suggesting the presence of liver disease.
  • Specific findings may provide clues toward diagnosis of an underlying cause.
  • Temporal and proximal muscle wasting suggest longstanding diseases
  • Stigmata of chronic liver disease include spider nevi, palmar erythema, gynecomastia, caput medusae
  • Dupuytren’s contractures, parotid gland enlargement, and testicular atrophy are commonly seen in advanced Laennec’s cirrhosis and occasionally in other types of cirrhosis
  • An enlarged left supraclavicular node (Virchow’s node) or periumbilical nodule (Sister Mary Joseph’s nodule) suggest an abdominal malignancy
  • Jugular venous distension, a sign of right sided heart failure, suggests hepatic congestion
  • A right pleural effusion, in the absence of clinically apparent ascites, may be seen in advanced cirrhosis
  • Familial causes of liver disease are:
  • 1. Wilson’s disease.
  • 2. Hemachromatosis – suggested by cirrhosis, dia­betes and liver disease in adult.
  • 3. Alpha 1 antitrypsin deficiency
  • 4. Benign intrahepatic cholestasis.


  • 1. Icterus or jaundice
  • 2. Hepatomegaly
  • 3. Hepatic tenderness
  • 4. Splenomegaly
  • 5. Spider angiomata
  • 6. Palmar erythema
  • 7. Excoriations
  • 8. Muscle wasting
  • 9. Ascites, edema
  • 10. Dilated abdominal veins
  • 11. Hepatic fetor (foul breaths)
  • 12. Asterixis (flapping tremor)
  • 13. Mental confusion, stupor, coma.
  • Jaundice is seen in the sclera in daylight, in the skin and in mucus membrane below tongue.

Hepatic failure

  • Hepatic failure is indicated by presence of signs and symptoms of hepatic encephalopathy in a patient of severe acute or chronic liver disease.
  • Features of hepatic failure:
  • 1. Change in sleep patterns
  • 2. Change in personality
  • 3. Irritability
  • 4. Mental dullness
  • 5. Confusion, disorientation
  • 6. Stupor, coma
  • 7. Asterixis / flapping tremors of body and tongue
  • 8. Fetor hepaticus – sweet ammonia odour in breath
  • 9. Trail making test is positive i.e. patient is unable to connect 25 numbered circles using a pencil within 30 seconds
  • 10. Ascites with umbilical hernia
  • 11. Prominent veins over abdomen and caput me­dusa – veins radiating from umbilicus
  • 12. Widened pulse pressure – Hyperdynamic circu­lation – sodium and fluid retention – increased cardiac output – reduced peripheral resistance.
  • 13. Hepatopulmonary syndrome – Liver disease with hypoxemia and pulmonary arteriovenous shunt­ing. There is dyspnoea and shortness of breath and oxygen desaturation in the upright or sit­ting position.

Skin changes in liver disorders

  • · Hyperpigmentation – Cholestatic liver disease
  • · Xanthelasma
  • · Tendon xanthomata
  • · Gray pigmentation in hemochromatosis
  • · Mucocutaneous vasculitis with purpura in cryo­globulinemia of hepatitis C or B.
  • Eye changes in liver disorders Jaundice.
  • Kayser-Fleischer ring in Wilson’s disease – a golden brown copper pigment in Disemet’s membrane at the periphery of the cornea, seen by slit lamp.
  • Metastatic liver disease and primary hepatocel­lular carcinoma
  • Features are:
  • · Cachexia
  • · Wasting
  • · Hepatomegaly
  • · Hepatic bruit
  • · Hepatic failure.


  • Liver panel tests are:
  • 1. Serum alanine transferase – ALT (SGPT)
  • 2. Serum aspartate aminotransferase – AST (SGOT)
  • 3. Alkaline phosphatase
  • 4. Direct and total serum bilirubin
  • 5. Serum albumin
  • 6. Prothrombin time
  • 7. GGT (Gamma Glutamyl Transpeptidase)
  • 8. Anti mitochondrial antibody – AMA – Autoimmune marker in primary biliary cirrhosis
  • 9. P-ANCA – peripheral anti neutrophil cytoplasmic antibody in sclerosing cholangitis
  • 10. ANA – antinuclear antibody
  • 1 L ASMA – anti smooth muscle antibody; liver, kid­ney, microsomal antibody.
  • Disease

    • Hepatitis A
    • Hepatitis B – Acute
    • Hepatitis B – Chronic Hepatitis C
    • Hepatitis D
    • Hepatitis E
  • Autoimmune hepatitis Primary biliary cirrhosis Primary sclerosing cholangitis Drug-induced
  • Alcoholic
  • Alpha-l antitrypsin disease Wilson’s disease Hemochromatosis Hepatocellular cancer

Diagnostic test

    • Anti HAV IgM
    • HBsAg and anti HBc IgM HBsAg and HBeAg,
    • HBV DNA Anti HCV and HCV RNA HBsAg and Anti HDV
    • Anti HEV
    • ANA or SMA
    • AMA – Anti-mitochondrial antibody P – ANCA
  • History
  • History and histology
  • Reduced alpha 1 antitrypsin levels
  • Decreased serum ceruloplasmin, increased urinary copper Increased iron saturation and serum ferritin
  • Increased alpha fetoprotein level more’than 500, Ultrasound and CT Scan


  • 1. Ultrasound
  • 2. Computed Tomography (CT)
  • 3. Magnetic resonance imaging (MRI)
  • 4. Magnetic resonance cholangiopancreato-graphy (MRCP)
  • 5. Endoscopic retrograde cholangiopancreato­graphy (ERCP)
  • 6. Doppler, ultrasound and MRI for hepatic vascu­lature


  • For chronic liver diseases:
  • • Diagnosis
  • · Severity
  • · Prognosis
  • · Monitoring treatment

Grading and Classification —

  • 1. Child-Pugh classification – Serum bilirubin, se­rum albumin, ProthrombinTime, ascites, hepatic encephalopathy are taken into account and A-B­C staging is done.
  • 2. Liver biopsy is done and amount of fibrosis is staged from 0 to 4+ (histology activity index) or on Ishak scale from 0 to 6+.
  • 3. MELD score – model for end-stage liver disease for assessment for liver transplantation.


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