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Approach to jaundice
- 1. By DR Ahmad Zulfahmi Sha’ari Hospital Kemaman APPROACH TO JAUNDICE
- 2. Outline Definition Epidemiology Pathophysiology Etiology Presentation Examination Investigation Management
- 3. Definition Yellowish discoloration of the skin, sclerae and mucous membrane due to hyperbilirubinaemia. Normal bilirubin level 0.3-1.3mg/dL. Manifested when serum bilirubin level >3mg/dL. Besides a rise in the bilirubin level, yellowness of the skin can be due to carotenemia (excess in diet) or, use of drug quinacrine. It’s not a disease, rather it’s a clinical SIGN of many diseases.
- 4. Neonatal Jaundice In NNJ serum bilirubin levels are >85 μmol/L (5 mg/dl). This occurs in approximately 60% of term infants and 80% of preterm infants. First becomes visible in the face and forehead. Blanching reveals the underlying colour. Jaundice then gradually becomes visible on the trunk and extremities.
- 5. Pathophysiology Bilirubin Metabolism Bilirubin is a yellowish pigment found in bile. It is result from the breakdown of mature RBCs in reticuloendothelial system. 15% of bilirubin comes from the catabolism of other haem-containing proteins, such as myoglobin. 250 – 300 mg of bilirubin are produced daily. Released to plasma bound to albumin. Hepatocytes conjugate it and excrete through bile channels into small intestine.
- 7. Etiology
- 8. Types of Jaundice Prehepatic / hemolytic jaundice Hepatic jaundice Posthepatic / obstructive jaundice
- 10. Biliary Function
- 14. Prehepatic / Hemolytic Jaundice The increased breakdown of RBCs leads to an increase in production of bilirubin. Level of unconjugated bilirubin is raised. The serum transferase and ALP are normal. Causes: Hemolytic disorders: spherocytosis, sickle cell anemia, G6PD deficiency Inherited: Crigler Najjar syndrome (deficient of UDPGT), Gilbert syndrome (defective uptake) Drugs: rifampicin, probenecid, ribavirin Infection: malaria Transfusion reaction Hemoglobinopathy
- 15. Hepatic Jaundice Inability of liver to transport bilirubin across hepatocytes into bile due to liver disease. Increase level of unconjugated and conjugated bilirubin. Usually associated with increased level of transaminase.
- 16. Examples: Infection: Viral hepatitis, Epstein Barr virus (infectious mononucleosis), Leptospirosis Alcohol Drug toxicity: Acetaminophen, isoniazid Environment toxin: Vinyl chloride, wild mushrooms (Amanita phalloides)-amanita toxins Liver cirrhosis Autoimmune: Wilson’s disease (disorder Cu metabolism), autoimmune hepatitis Inherited: Dubin Johnsons Syndrome (defective excretion), Rotors Syndrome (abnormal excretion) Miscellanous: Fatty liver of pregnancy, Amyloidosis, Postop cholestasis
- 17. Posthepatic Jaundice Condition which there is blockage of the flow of bile out of liver. Commonly gallstones, PBC, bile ducts stricture Charecteristically a/w tea-colored urine, pale-colored stool and pruritis. Intrahepatic Extrahepati c
- 18. Intrahepatic: Primary biliary cirrhosis • Sclerosing cholangitis
- 19. Extrahepatic: Benign: Choledocholithiasis (bile duct stones), choledochal cyst, pancreatitis Malignancy: Carcinoma of head of pancreas, cholangiocarcinoma, gallbladder CA
- 20. Presentation Associated symptoms: Abdominal pain Fever Fat intolerance Change in urine and stool colour Pruritis LOA and LOW Bleeding tendency Abdominal distension Pedal edema
- 21. Medication history Family history – hemolytic anemia, hepatitis, congenital hyperbilirubinaemia Social history Occupational history – contact with rats/rodents Travel history Tattoos, sexual activity Alcohol history Parenteral exposures: IV drug abuse, blood transfusion
- 22. Physical Examination Vital signs General inspection: Temporal and proximal muscle wasting Scratch marks, purpura, fetor hepaticus Stigmata of chronic liver disease: Finger clubbing (toxemia/cyanosis) Palmar erythema Flapping tremor Spider naevi Gynaecomastia Ascites first Caput medusa Testicular atrophy
- 23. Enlarged left supraclavicular lymph node – Virchow’s node Parotid gland enlargement (endemic parotitis) Raised JVP – right heart failure Abdominal examination: Size and consistency of liver and spleen Tender hepatomegaly – viral/alcoholic hepatitis Enlarged nodular liver – malignancy Murphy’s sign – cholecystitis Palpable gallbladder Ascites Pedal edema
- 25. Investigations Blood: Full blood count (FBC) –anemia/thrombocytopenia/leucopenia/leucocytosis Liver function test (LFT) Albumin Total bilirubin, direct and indirect Transaminase ALT found mainly in liver, while AST also found in other muscles like skeletal and cardiac ALT is more specific in detecting liver disease Alkaline phosphatase – increased in obstructive jaundice/cholestasis (response of the liver to any form of biliary tree obstruction) Hepatitis screening Leptospira serology, creatinine kinase Coagulation profile
- 27. Imaging: Ultrasound Dilatation of bile duct Presence of gallbladder stone CT abdomen ERCP Liver biopsy
- 31. References CPG management of Neonatal Jaundice (second edition) https://www.emedicinehealth.com/jaundice/article_em.htm emedicine.medscape.com/article/974786-overview
Editor's Notes
- Quinacrine: antiprotozoal, antirheumatic and an intrapleural sclerosing agent Phenols: a class of chemical compounds consisting of a hydroxyl group (—OH) bonded directly to an aromatic hydrocarbon group
- UDP glucuronosyltransferase
- Probenecid: is a medication that increases uric acid excretion in the urine. It is primarily used in treating gout and hyperuricemia. Ribavirin: is an anti-viral medication used to treat RSV infection, hepatitis C, and viral hemorrhagic fever.
- PBC begins with loss of immune self tolerance, leading to damage of the biliary epithelial cells of small bile ducts. Ongoing immunologic events perpetuate the biliary epithelial cell destruction via direct cytotoxicity or lymphokine-mediated cell damage, leading to disease progression. Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by a progressive course of cholestasis with inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts.