General approach to Jaundice during my stay at A&E

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.

6. Heme
Biliverdin
Unconjugated
Bilirubin
Conjugated
Bilirubin
Urobilinogen
Stercobilin
Heme
Oxygenase
Bilirubin
Reductase
UDPGT
Intestinal
Bacteria INTESTINE
LIVER
KIDNEYS
Urinary
Urobilinogen
Globin

7. Etiology

8. Types of Jaundice
 Prehepatic / hemolytic jaundice
 Hepatic jaundice
 Posthepatic / obstructive jaundice

10. Biliary Function

11. Unconjugated/Indirect

12. Conjugated/Direct/Obstructive Jaundice

13. Mixed/ Hepatocellular

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