Jaundice (1)

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Transcript of Jaundice (1)

  • Mohammad MobasheriSpR General Surgery

  • Definition: yellow discolouration of skin and sclera as a result of hyperbilirubinaemia

    Bilirubin >35mmol/L for jaundice to be visible on examination

    Sclera first place to become jaundiced

  • Bilirubin is a product of metabolism of haemoglobin (80%) and other haem containing proteins (e.g. Myoglboin, cytochrome P450: 20%) Degredation of haemoglobin into bilirubin takes place in macrophages. Bilirubin is then excreted into plasma and binds with albumin

    HaemoglobinGlobinHaem (iron + porphyrin)Amino AcidsBiliverdinBilirubin (unconjugated)Bilirubin binds to albumin in the plasmaRBC breakdown

  • Uptake of unconjugated bilirubin into hepatocyteUnconjugated bilirubin converted to conjugated bilirubin by glucuronyl transferase (this is required before bilirubin can be excreted into the bile, as this process makes bilirubin water soluble)Bilirubin secreted (as component of bile) into the small intestineBacterial enzymes deconjugate bilirubin and convert it into urobilinogen90% urobilinogen broken down further into stercobilinogen and stercobilin and excreted in faeces10% urobilinogen absorbed (via portal vein)Majority of absorbed urobilinogen re-enters hepatocyte and re-excreted in bile (entero-hepatic circulation)The rest of the absorbed urolbilinogen bypasses liver and is excreted by kidneys

  • Disruption of bilirubin metabolism and excretion can cause hyperbilirubinaemia and subsequent jaundice

    Hyperbilirubinaemia maybe unconjugated (indirect) or conjugated (direct) depending on the cause

    Some inherited syndromes of bilirubin handling can result in hyperbilirubinaemiaGilberts syndrome reduced activity of glucuronyl transferase therefore reduced conjugated bilirubin therefore elevated unconjugated bilirubin Criggler-Najjar reduction in amount of glucoronyl transferase therefore elevated unconjugated bilirubinRotors/Dubin-Johnson syndrome defective excretion of conjugated bilirubin into the biliary cannaliculi therefore elevated conjugated bilirubin

  • Pre-hepatic: pathology occuring prior to the liverAny cause of increased haemolysis (e.g. Spherocytosis, thalassaemia, sickle cell disease, transfusion reaction, auto-immune, malaria etc.) and some drugsCauses unconjugated hyperbilirubinaemia

    Intra-Hepatic: pathology occuring within the liverAll the causes of hepatitis/cirrhosis (e.g. Alcohol, viral, auto-immune, primray biliary cirrhosis, haemochromatosis, wilsons, alpha-1 antitrypsin deficiency etc.), inherited condition on previous slide and some drugsCan result in hepatocyte destruction and therefore unconjugated hyperbilirubinaemia or in bile cannaliculi destruction and therefore conjugated hyperbilirubinaemia or bothNote/ neonatal jaundice: occurs in most newborns as hepatic machinary for conjugation and excretion of bilirubin not fully matured until 2 weeks of age

    Post-hepatic: pathology occuring after conjugation of bilirubin within the liver (aka obstructive jaundice)Any cause of biliary obstruction (e.g. Gallstones)Causes conjugated hyperbilirubinaemia

  • Following investigations will help to determine nature of jaundice:

    Liver function testsBilirubinALT/ASTALP/GGTConjugated v Unconjugated bilirubin levelsUrine bilirubin and urobilinogen levels

  • Total bilirubin and its conjugated and unconjugated levels help to determine nature of jaundice

    TestPre-hepaticHepaticPost-hepaticTotal bilirubin+++ +++Conjugated bilirubinNormalIncreasedIncreasedUnconjugated bilirubinIncreasedIncreasedNormal

  • Liver EnzymesALT/AST mainly present in hepatocytesALP/GGT mainly present in bile cannaliculi biliary treeDerrangement of particular liver enzymes in association with jaundice can determine nature of the jaundice


  • Urine bilirubin Normally, tiny amount bilirubin (conjugated) excreted in urinePre-hepatic jaundice: Haemolysis causes rise in unconjugated bilirubin (water insoluble) and this is not excreted by the kidney therefore there is no rise in urine bilirubinSome causes of Hepatic jaundice: result in damage to biliary cannaliculi and therefore result in poor biliary drainage and therefore elevated conjugated bilirubin levels in blood, excreted into urine (giving dark urine)Post-Hepatic juandice: Obstruction to biliary drainage and so conjugated bilirubin (water soluble) levels in the blood increase and appear in the urine (giving dark urine)Urine urobilinogenPre-hepatic jaundice: Haemolysis results in increased bilirubin production and subsequent increase bilirubin metabolism and urobilinogen in stool and therefore in the urine. Some causes of Hepatic jaundice : result in hepatocellular destruction and therefore reduced re-excretion of re-absorbed urobilinogen (i.e. Reduction in entero-hepatic circulation of urobilinogen) resulting in elevated levels in urine Post-Hepatic jaundice: Less bilirubin reaching intestine therefore reduction in urobilinogen therefore reduction in urine urobilinogen

    TestPre-hepaticHepaticPost-hepaticUrine BilirubinnegativeNegative (but maybe increased depending on cause)IncreasedUrine urobilinogenIncreasedNormal (but maybe increased depending on cause)Decreased/negativeUrine colourNormalNormal (but maybe dark depending on cause)DarkStool colourNormalNormalPale

  • How long been jaundiced?Ever been jaundiced before?Any associated fevers or abdominal pain or weight loss?Pale stool and dark urine (suggests obstructive/post-hepatic jaundice)?Any recent foreign travel (hepatitis, malaria)?Any risk factors for hepatitis (tattoos, IVDU, high risk professions, blood transfusions, multiple sexual partners)?PMH of blood disorders (e.g. SCD, thalassemia)?DH any new medications that can cause jaundice?SH excess alcohol intakeFH of jaundice (inherited disorders of bilirubin metabolism)

  • If jaundice associated with background of intermittent RUQ pains think gallstones and choledocholithiasisIf jaundice associated with long history of upper abdominal pain and weight loss and patient elderly thing pancreatic cancerIf jaundice associated with recent foreign travel think hepatitis (A,E) or malariaIf jaundice occuring in patient with risk factors think hepatitis B,CIf jaundice occuring on a background of alcohol abuse think alcoholic liver diseaseIf jaundice is painless and family history of blood disorder think pre-hepatic jaundice

  • Blood testsFBC (low HB suggesting haemolysisLFTs (bilirubin, ALT/AST, ALP/GGT, albumin)Conjugated and unconjugated bilirubinClotting (INR)U&E (hepatorenal syndrome)UrineBilirubinUrobilinogen Above tests used to determine if jaundice pre/intra/post hepatic which will determine further investigations

  • Pre-hepaticSickle cell testSerum electrophoresisBlood filmHepaticSerum iron, ferritin, copper, alpha-1 antitrypsin levelsauto-antibody screenHepatitis screenLiver USSPost-hepaticAs surgeons we deal with post-hepatic jaundice

  • CausesLuminalGallstoneIntra-muralBenign stricture (e.g. As complication of cholecystectomy or due to pancreatitis)Malignant stricture: cholangiocarcinomaExtra-muralHead of pancreas cancerPancreatitis (oedema of head of pancreas) Pancreatic pseudocystCompression by malignant lymph nodes at porta hepatis

  • Blood testsFBC (elevated WCC in ascending cholangitis)U&E (monitor renal function in case of hepato-renal syndrome)LFTs (elevated bilirubin, ALP/GGT)Conjugated/unconjugated bilirubinClotting (INR maybe elevated)

    USSLook for gallstones, biliary tree dilatation, stone in CBD (though often not seen due to bowel gas).Look at pancreas to look for cancer (often poor views due to overlying bowel gas)Look at liver to exclude parenchymal disease.

  • PTC (percutaneous transhepatic cholangiogram) performed by interventional radiologistDiagnostic and therepeutic (biliary drain to relieve obstruction) but invasiveMore invasive and Higher complication rate than ERCP (particularly haemorrhage) therefore used in situations where ERCP unavailable (out of hours in patient with cholangitis) or unsuccesful

  • Monitor for acute renal failure (hepato-renal syndrome)Ensure patients well fluid resuscitated and monitor urine output to reduce the risk of the aboveMonitor INRIf derranged give vitamin KDetermine cause of obstructive jaundiceDanger is progression to ascending cholangitis (Charcots triad) can be life threatening!Must un-obstruct Biliary tree to prevent development of cholangitis

  • ERCP preferred methodBalloon trawl or dormia basket (for stones)Sphincterotomy (to prevent future stones from obstructing)Stent (to allow free drainage of bile past a stricture)

    PTCUsed where ERCP unavailable or unsuccesful (as more invasive and higher complication rate)Drain inserted percuteously, trans-hepatically (through the liver) and into the biliary tree to allow free drainage of bile

  • Questions?