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Tad Kim, M.D.
UF Surgery
(c) 682-3793; (p) 413-3222

• Normal Physiology
• Pathophysiology
• Broad Differential Diagnosis
• DDx of Obstructive Jaundice
• Work-up for “Medical” Jaundice
• Work-up if Obstructive Jaundice
• Treatment of Obstructive Jaundice

Normal Physiology
• Bilirubin is from breakdown of hemoglobin
• Unconjugated bilirubin transported to liver
– Bound to albumin because insoluble in water
• Transported into hepatocyte & conjugated
– With glucuronic acid → now water soluble
• Secreted into bile
• In ileum & colon, converted to urobilinogen
– 10-20% reabsorbed into portal circulation and
re-excreted into bile or into urine by kidneys

• Jaundice = bilirubin staining of tissue @ lvl
greater than ~2
• Mechanisms:
– ↑ production of bilirubin
– ↓ hepatocyte transport or conjugation
– Impaired excretion of bilirubin
– Impaired delivery of bilirubin into intestine
• “surgically relevant jaundice” or obstructive
– “Cholestasis” refers to the latter two, impaired
excretion and obstructive jaundice

Broad Differential Diagnosis

↑production ↓transport or Impaired Biliary
↓conjugation excretion obstruction
↑ Unconjugate ↑ Unconjugate ↑ Conjugated ↑ Conjugated

Hemolysis Gilbert’s Rotor’s CH/CBD stone

Transfusions Crigler-Najarr DubinJohnson Stricture

Txfusion rxn Neonatal Cancer Cancer

Sepsis Cirrhosis Cirrhosis Chronic

Burns Hepatitis Hepatitis PSC

Hgb-opathies Drug inhibition Amyloidosis


DDx: Unconjugated bilirubinemia

• ↑production
– Extravascular hemolysis
– Extravasation of blood into tissues
– Intravascular hemolysis
– Errors in production of red blood cells
• Impaired hepatic bilirubin uptake(trnsport)
– Portosystemic shunts
– Drug inhibition: rifampin, probenecid

DDx: Unconjugated bilirubinemia

• Impaired bilirubin conjugation
– Gilbert’s disease
– Crigler-Najarr syndrome
– Neonatal jaundice (this is physiologic)
– Hyperthyroidism
– Estrogens
– Liver diseases
• chronic hepatitis, cirrhosis, Wilson’s disease

DDx: Conjugated Bilirubinemia

• Intrahepatic cholestasis/impaired excretion
– Hepatitis (viral, alcoholic, and non-alcoholic)
• Any cause of hepatocellular injury
– Primary biliary cirrhosis or end-stage liver dz
– Sepsis and hypoperfusion states
– Pregnancy
– Infiltrative dz: TB, amyloid, sarcoid, lymphoma
– Drugs/toxins i.e. chlorpromazine, arsenic
– Post-op patient or post-organ transplantation
– Hepatic crisis in sickle cell disease

DDx: Obstructive Jaundice

• This is the slide to remember for surgeons
• Obstructive Jaundice– extrahepatic
– Choledocholithiasis (CBD or CHD stone)
– Cancer (peri-ampullary or cholangioCA)
– Strictures after invasive procedures
– Acute and chronic pancreatitis
– Primary sclerosing cholangitis (PSC)
– Parasitic infections
• Ascaris lumbricoides, liver flukes
• Just remember top 5 (not parasites)

Initial Evaluation: History

• Jaundice, acholic stools, tea-colored urine
• Fever/chills, RUQ pain (cholangitis)
– Could lead to life-threatening septic shock
• Reasons to have hepatitis or cirrhosis?
– Alcohol, Viral, risk factors for viral hepatitis
• Exposure to toxins or offending drugs
• Inherited disorders or hemolytic conditions
• Recent blood transfusions or blood loss?
• Is patient septic or on TPN?
• Recent gallbladder surgery? (CBD injury)

Initial Evaluation: Physical Exam

• Signs of end stage liver disease (cirrhosis)
– Ascites, splenomegaly, spider angiomata, and
• Jaundice evident first underneath the
tongue, also evident in sclerae or skin
• Courvoisier’s sign = painless, but palpable
or distended gallbladder on exam
– Could indicate malignant obstruction

Screening Labs
• NL LFT r/o hepatic injury or biliary tract dz
– Consider inherited disorders or hemolysis
• ↑Alk Phos moreso than AST/ALT implies
“cholestasis” (intrahepatic vs obstruction)
– ↑Alk Phos also seen in sarcoid, TB, bone
– In this case, GGT is specific for biliary origin
• Predominant ↑AST/ALT implies intrinsic
hepatocellular disease
– AST/ALT ratio > 2 in alcoholic hepatitis
• ↓albumin or ↑INR c/w advanced liver dz

Subsequent Labs
• If no concern for obstructive jaundice:
– Viral (Hep B&C) serologies for viral hepatitis
– anti-mitochondrial Ab (PBC)
– anti-smooth muscle Ab (Auto-immune)
– iron studies (hemochromatosis)
– ceruloplasmin (Wilson’s)
– Alpha-1 anti-trypsin activity (for deficiency)

Imaging for Obstructive Jaundice

• RUQ Ultrasound
– See stones, CBD diameter
• CT scan
– Identify both type & level of obstruction
– Direct visualization of biliary tree/panc ducts
– Procedure of choice for choledocholithiasis
– Diagnostic –AND- therapeutic (unlike MRCP)
• PTC useul of obstruction is prox to CHD
• Endoscopic Ultrasound or EUS

• If Medical, then treat the etiology
• If Obstructive Jaundice:
– Should r/o ascending cholangitis, ABC/resusc
• For cholangitis: IVF, IV Antibiotics, Decompression
– Stones (remove stones vs stent vs drainage)
• Done via ERCP or PTC or open (surgery)
– Benign stricture (stent vs drainage catheter)
– Cancer (Stent vs drainage +/- resect the CA)
• The key principle is decompression, either
externally(drainage) or internally(stenting)
the duct open to allow better drainage

Take Home Points

• Above is a comprehensive approach
• For surgery clerkship, all you need to
know is:
– 1. Broad categories (no specific diagnoses)
– 2. The four DDx of obstructive jaundice
– 3. H&P (ask about fevers/chills, jaundice,
acholic stools, dark urine, weight loss for CA),
r/o ascending cholangitis = emergency
– 4. Labs (LFT: ?cholestatic, CBC w diff, BMP)
– 5. Imaging (U/S, CT, MRCP, EUS)
– 6. Therapy (ERCP vs PTC vs surgery)