JAUNDICE

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JAUNDICE

• Ayman Linjawi, MD, FRCS

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jaundice

• Icterus is a yellowish pigmentation of the
  skin, the conjuctival membranes over the sclerae,
  and other mucous membranes caused by
  hyperbilirubinemia.
• Pale stools and dark (tea color) urine.
• Causes could be pre-hepatic, hepatic and
  post-hepatic.

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Pre-hepatic causes

• Anything which causes an increased rate of
  hemolysis.
• Tropical diseases as malaria
• Certain genetic diseases, such as sickle cell
  anemia, spherocytosis, thalassemia and G6PD
  deficiency.
• Drugs very long list

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Hepatic causes

• jaundice causes include acute hepatitis,
  hepatotoxicity, Gilbert syndrome.
• Crigler-Najjar syndrome.
• Alcoholic liver disease

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Post-hepatic (cholestatic)

• obstructive jaundice.
• The most common causes are gallstones in the
  common bile duct, and tumors in the head of the
  pancreas.
• Parasites known as liver flukes can live in the
  common bile duct, causing obstructive jaundice.
• Strictures of the common bile duct,biliary
  atresia, ductal carcinoma, pancreatitis and
  pancreatic pseudocysts.
• A rare cause of obstructive jaundice is Mirizzi
  syndrome.

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Function test Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal / Increased Increased Increased
Conjugated bilirubin Normal Increased Increased
Unconjugated bilirubin Normal / Increased Increased Normal
Urobilinogen Normal / Increased Increased Decreased / Negative
Urine Color Normal (urobilinogen) Dark (urobilinogen conjugated bilirubin) Dark (conjugated bilirubin)
Stool Color Normal Normal Pale
Alkaline phosphatase levels Normal Increased Increased
Alanine transferase and Aspartate transferase levels Normal Increased Increased
Conjugated Bilirubin in Urine Not Present Present Present
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Pathophysiology

• Hemoglobin's are released into the blood when
  fragile RBC rupture.
• The hemoglobin is phagocytosed by macrophages,
  and split into its heme and globin portions.
• Heme is oxidized to biliverdin then reduction to
  bilrubin.
• Bilirubin is conjugated in the liver.

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Pathophysiology

• Intestinal bacteria convert the bilirubin into
  urobilinogen.
• urobilinogen can take two pathways. It can either
  be further converted into stercobilinogen, which
  is then oxidized to stercobilin and passed out in
  the feces, or it can be reabsorbed by the
  intestinal cells, transported in the blood to the
  kidneys, and passed out in the urine as the
  oxidised product urobilin.
• Stercobilin and urobilin are the products
  responsible for the coloration of feces and
  urine, respectively

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Diagnosis of obstructive jaundice

• Symptoms and signs
• Blood test increase total and direct bilirubin,
  disturbe liver enzymes, increase alk phos and
  GGT, prolong INR.
• Radiology US to assess GB, CT to assess
  pancreas, MRCP to assess biliary tract,
  Endoscopic US to assess pancreatic masses.
• ERCP assess biliary tract, brush biopsy,
  drainage (papillotomy)

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Management of obstructive jaundice

• According to the cause
• Biliary stones
• Benign stricture of hepatic or common bile duct.
• Tumor at the hepatic or common bile duct.
• Tumor at the head of pancreas.

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Complications

• Complications of obstructive jaundice include
  sepsis especially cholangitis, biliary cirrhosis,
  pancreatitis, coagulopathy, renal and liver
  failure.