Jaundice

Published on 02/04/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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114 Jaundice

Instruction

Would you like to ask this patient a few questions and perform a relevant examination?

Salient features

History

Take a history by asking the patient about the following:

• His or her age: hepatitis is more common in the young and carcinoma in the elderly

• Sore throat and rash: infectious mononucleosis

• Occupation: Weil’s disease in sewerage and farm workers

• Contact with jaundice: hepatitis A

• Drug history: oral contraceptives, phenothiazines

• Blood transfusions, injections, arthritis, urticaria: hepatitis B

• Alcohol consumption

• Pruritus: cholestasis caused by hepatitis A, primary biliary cirrhosis

• Colour of the urine: dark, tea- or cola-coloured urine is caused by renal excretion of conjugated bilirubin

• Colour of the stools: pale stools in obstructive jaundice

• Abdominal pain: cholecystitis, gallstones, cholangitis, carcinoma of the pancreas

• Past history: recurrent jaundice, as in Dubin–Johnson syndrome

• Fever, rigors and abdominal pain: suggests cholangitis.

Diagnosis

This patient is markedly icteric and has spider naevi and gynaecomastia (lesions) caused by alcoholic liver disease (aetiology).

Questions

What do you understand by the term jaundice?

It is the yellowish discoloration of skin, sclera and mucous membrane caused by the accumulation of bile pigments. Scleral icterus suggests that serum biliburin of at least 51 µmol/l (30 mg/l).

How would you differentiate jaundice from carotenaemia?

The discoloration of carotenaemia is differentiated from jaundice by the absence of yellow colour in the sclera and mucuous membranes, normal urine colour and the presence of yellow–brown pigmentation of carotenoid pigment in the palms, soles and nasolabial folds.

What is Murphy’s sign and what does it indicate?

It is the tenderness elicited on palpation at the midpoint of the right subcostal margin on inspiration. It is a sign of cholecystitis.

Have you heard of Courvoisier’s law?

It states that in a patient with obstructive jaundice a palpable gallbladder is unlikely to be caused by chronic cholecystitis.

What is Charcot’s fever?

Intermittent fever associated with jaundice and abdominal discomfort in a patient with cholangitis and biliary obstruction.

Advanced-level questions

What do you know about Dubin–Johnson syndrome?

It is a rare benign condition characterized by jaundice and pigmentation secondary to a failure of excretion of conjugated bilirubin. The defect in this syndrome is mutations in the gene for multiple drug resistance protein 2. The liver is stained by melanin in the centrilobular zone. The bromsulfthalein test shows a late secondary rise at 90 min.

What do you know about Gilbert syndrome?

Gilbert syndrome is very common, with reported incidence of 3–7% of the population and with males predominating females by a ratio of 2–7:1. It is characterized by the impaired conjugation of bilirubin caused by reduced activity of uridine diphosphate glucuronyltransferase (UDPGT). The patients typically have mild unconjugated hyperbilirubinaemia (<103 µmol/l or <30 mg/l).

Mention a few causes of postoperative jaundice

Causes of postoperative jaundice (usually occurring in the first 3 postoperative weeks) include:

• resorption of haematomas, haemoperitoneum, haemolysis of transfused erythrocytes (particularly when stored blood products are used), haemolysis in glucose-6-phosphate dehydrogenase deficiency

• impaired hepatocellular function caused by halogenated anaesthetics, sepsis, hepatic ischaemia secondary to perioperative hypotension

• extrahepatic biliary obstruction caused by biliary stones, unsuspected injury to biliary tree.

How does estimation of serum bilirubin concentration help in discerning the aetiology of jaundice?

Normal serum bilirubin concentration is usually no greater than 15 mg/l and is mainly unconjugated. If jaundice is primarily caused by haemolysis or a disorder of bilirubin conjugation, at least 85% of the bilirubin will be unconjugated. With normal liver function, haemolysis alone does not produce a serum bilirubin level >40 mg/l. A rise in serum bilirubin levels of up to 20 mg/l is compatible with extrahepatic cholestasis, but a greater rate indicates haemolysis, hepatitis or hepatic cell necrosis. The serum bilirubin in pure biliary obstruction seldom exceeds 300 mg/l; a greater value indicates that there is associated hepatocellular jaundice as well.

A Gilbert (1858–1927), Professor of Medicine at l’Hôtel Dieu in Paris.

PSA Weil (1848–1916), Professor of Medicine in Tartu, Estonia and Berlin.

JB Murphy (1857–1916), Professor of Surgery at Northwestern University in Chicago.

J Courvoisier (1843–1918), Professor of Surgery, Basel, Switzerland.

IN Dubin, Professor of Pathology, Pennsylvania, and FB Johnson, pathologist, Veterans Administration Hospital, Washington.

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