Surgery - Obstructive Jaundice

Question 1

Obstructive Jaundice

The normal enterohepatic circulation

Answer 1

• The haem component of spent red cells is broken down to bilirubin (mainly in spleen and bone marrow), bound to albumin and transported to the liver.
• This protein–pigment complex is insoluble in water and is not excreted in urine.
• In the liver, the complex is split and the bilirubin conjugated with glucuronic acid which makes it water-soluble, before being excreted into the bile canaliculi.
• The normal concentration of both conjugated and unconjugated bilirubin in the blood is very low.
• Bacterial action in the bowel converts conjugated bilirubin into colourless urobilinogen and pigmented urobilin which imparts the brown colour to normal faeces.
• Some urobilinogen is reabsorbed, passing to the liver in the portal blood, and is then re-excreted in the bile.
• The entire process is called an enterohepatic circulation.
• A small amount of urobilinogen escapes into the systemic circulation and is excreted in the urine, colouring it yellow.

Question 2

Obstructive Jaundice

The normal enterohepatic circulation

Bile Salts

Answer 2

Bile acids (salts)

• Are synthesised in the liver from cholesterol-based precursors.
• These are excreted in bile to the duodenum and facilitate lipid digestion and absorption in the small intestine.
• About 95% of the bile acids are reabsorbed in the distal ileum and returned to the liver via the portal vein, only to be re-excreted in the bile.
• Thus both bilirubin and bile acids are involved in enterohepatic circulations.

Question 3

Obstructive Jaundice

Pathophysiology

Answer 3

• If biliary outflow becomes obstructed, conjugated bilirubin is dammed back in the liver from where it enters the bloodstream and causes a gradual rise in plasma bilirubin.
• Once the plasma bilirubin level exceeds about 30 µmol/L, jaundice should be clinically detectable. Conjugated bilirubin, being water-soluble, is excreted in the urine, turning it dark.
• In obstructive jaundice there is diminished or absent excretion of bile into the bowel, causing changes in the faeces.
• There is less urobilin to darken the stool and fewer bile acids, resulting in defective fat absorption and characteristic ‘putty’ coloured stool.
• A consequence of poor dietary fat absorption is malabsorption of fat soluble vitamins A, D, E and K.
• Lack of vitamin K leads to decreased hepatic synthesis of clotting factors, notably prothrombin (factor II), factors VII, IX, and X, and proteins C, S, and Z.
• Impaired blood clotting leads increases the risk of haemorrhage during invasive procedures, so a clotting screen must be checked beforehand.
• The coagulopathy is corrected with parenteral vitamin K or, in an urgent procedure, fresh frozen plasma.
• Biliary obstruction also dams back bile acids, which raises their blood concentration leading to deposition in the skin; this can cause intense itching.

Question 4

Obstructive Jaundice

History and examination of patients with obstructive jaundice

History

Answer 4

Enquiry about episodes of pain typical of gallstone disease, previous episodes of obstructive jaundice, biliary tract surgery or attacks

Include:

• Change in colour of urine and stools, i.e. dark urine and pale stools
• Drug history, e.g. oral contraceptive pill—potential for intrahepatic cholestasis
• Risk factors for viral hepatitis—blood product transfusion, intravenous drug abuse, tattoos, shellfish ingestion, sexual exposure
• Alcohol intake—if excessive, predisposes to pancreatitis and cirrhosis
• Symptoms associated with malignancy—anorexia, weight loss and non-specific upper GI disturbance is common in carcinoma of the pancreas, a disease of later life
• A history of inflammatory bowel

Question 5

Obstructive Jaundice

History and examination of patients with obstructive jaundice

Examination

Answer 5

• Early jaundice is a subtle physical sign and can be missed unless the patient is examined in a good light, preferably daylight.
• Jaundice is first detectable in the sclera and soon afterwards in abdominal wall skin.
• In some cases of obstructive jaundice, the patient develops generalised itching (pruritus) and scratch marks may be evident.
• The general stigmata of liver disease, such as spider naevi and liver ‘flap’ of the wrists are found only when jaundice is caused by primary liver disease rather than extrinsic obstruction.
• Examine abdomen for ascites, hepato/splenomegaly
• Ascites in a patient with obstructive jaundice is almost always due to disseminated intra-abdominal malignancy.

Question 6

Obstructive Jaundice

History and examination of patients with obstructive jaundice

Examination

Courvoisier’s ‘law’

Answer 6