JAUNDICE AFTER THE NEONATAL PERIOD

Definition

Yellow discolouration of skin and mucous membranes due to excess bilirubin. It is also referred to as hyperbiliribinaemia, usually with serum bilirubin at that time of >2mg% (34.2 ìmol/L).

  • Jaundice is a clinical feature and not a diagnosis. Any patient with jaundice should be carefully evaluated to determine the cause of the jaundice so as to institute appropriate management.
  • Hyperbilirubinaemia is categorized according to the location of the abnormality in the metabolism and excretion of bilirubin: pre-hepatic, hepatic, or post-hepatic:
    • Pre-hepatic: This is due to excess intravascular release of bilirubin, often by haemolysis)
    • Hepatic: This is due to hepatocyte dysfunction with faulty uptake, metabolism, or excretion of bilirubin.
    • Post-hepatic: This is due to blockage of bile and its constituents so that they do not exit from the biliary system; this may result from common bile duct obstruction or intrahepatic cholestasis).
  • The common causes of hyperbilirubinaemia include viral hepatitis, haemolytic anaemia (e.g., sickle cell, malaria), cirrhosis, biliary obstruction, hepatoma, drug induced reactions

Clinical Features

Meticulous history and physical examination are important before ordering investigations.

History

  • Exposure to hepatotoxic drugs
  • Known history of haematological disorder
  • History suggestive of viral hepatitis
    • Anorexia
    • Nausea
    • Aversion to fatty foods
  • History suggestive of obstructive jaundice
    • Dark urine
    • Pale stool
    • Pruritus

Physical examination

  • Should look for features suggestive of cirrhosis
    • Spider naevi
    • Gynaecomastia
    • Loss of axillary hair
    • Parotid gland enlargement
    • ascites)
  • Features suggestive of parenchymal liver disease or haemolytic jaundice (splenomegaly). In hepatic encephalopathy in children the early signs may be mild and easy to miss. Child becomes slow and may have disturbed sleep-wake pattern. This progresses through drowsiness, arousable sleep to unconsciousness.

Investigations

  • Full haemoglobin – Polymorphonuclear leucocytosis is found in infections including leptospirosis. Sickle cells may be seen in the peripheral blood smear
  • Reticulocyte count – Increased reticulocyte count indicates a haemolytic anaemia.
  • Blood slide for malaria parasites – Jaundice in a patient with malaria is a medical emergency.
  • Urine – Bilirubin:
    • Absence of bilirubin in a patient suggests haemolytic anaemia.
    • Presence of bilirubin suggests hepatobiliary jaundice.
  • Urine – Urobilinogen:
    • Excessive urobilinogen suggests haemolysis. Urobilinogen is absent in obstructive jaundice.
  • Liver function tests:
    • Gamma Globulin Transaminase (GGT) – Elevated levels suggest primary liver disease.
    • Alkaline phosphatase – Elevated levels suggest obstruction.
    • SGOT (AST) – Elevated levels suggest hepatocellular damage.
    • SGPT (ALT) – Elevated levels suggest hepatocellular damage more specific
      than AST.
    • Serum proteins:
      • Albumin – Low levels in chronic liver disease such as cirrhosis.
      • Globulins – Hyperglobulinaemia is found in chronic active hepatitis,
        cirrhosis.
    • If above investigations are not diagnostic consider:
      • HBs Ag, HAV – Ab. TORCHES in young infants.
    • Ultrasound: Useful in obstructive jaundice, gall stones, differentiating between abscess and tumour.
    • Alpha-foetoproteins: Substantial elevations of alpha-foetoproteins are found in malignancy.
    • Paracentesis of ascitic fluid: Protein content <3g% is found in cirrhosis. Protein content >3g% is found in tuberculosis, peritoneal tumours, peritoneal infection or hepatic venous obstruction. Blood stained ascites usually indicates a malignant disease – cytology is mandatory.
    • Liver biopsy is important in diagnosis of chronic hepatitis, cirrhosis, and hepatocellular malignancy.

Management

  • Patients with history and physical findings suggestive of viral hepatitis can be managed as outpatients requiring advice on bed rest and should be given multivitamins.
  • Conduct diagnostic evaluation and manage according to cause.
  • Admit if patient shows signs of encephalopathy. Refer/consult if not able to manage.
  • Consider hepatic encephalopathy in any patient who has jaundice and mental complaint. Early treatment of hepatic encephalopathy may reduce mortality.

Obstructive Jaundice beyond Neonatal Period

This refers to jaundice caused by obstruction of bile in the biliary tree. It can be due to intrahepatic or extrahepatic causes.

Clinical Features

These include the following features:

  • Jaundice and pruritus, which can be severe, with steady increase in jaundice
  • Distended gall bladder
  • Anorexia
  • Troublesome diarrhoea with pale, foul smelling stool.
  • Dark urine with a history of flatulence.

The causes of obstructive jaundice include the following:

  • Those that are intraluminal include gallstones, which can dislodge from the gallbladder and get impacted in the common bile duct (CBD), and helminthiasis, especially ascaris and liver flukes.
  • Those within the wall or mural include primary sclerosing cholangitis.
  • Those acting outside the wall or extramural include enlarged lymph nodes of any cause, and neoplasms.
  • Other causes include iatrogenic trauma to the ducts during surgery (especially cholecystectomy).

Investigations

  • Full haemogram
  • Liver function tests
  • Prothrombin time index
  • Plain abdominal x-rays may show stones
  • Abdominal ultrasound and CT scan

Management

Appropriately manage the conditions diagnosed and refer those that require surgical management.