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Jaundice . Presented by Dr. Pollock Prepared by Christopher Edwards Tintanalli Chapter 84, pgs. 560-561 October 2005. Jaundice. Clinical marker of defect in metabolism &/or excretion of bilirubin.

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Presented by Dr. Pollock

Prepared by Christopher Edwards

Tintanalli Chapter 84, pgs. 560-561

October 2005

  • Clinical marker of defect in metabolism &/or excretion of bilirubin.
  • ER task to initiate lab eval or imaging studies to identify cause and determine admission or outpt therapy.
  • Yellow discoloration of sclera, skin, mucous membranes due to deposition of bile pigment
  • Clinically detected with serum bilirubin 2-2.5mcg/dL or  (2 times nl)
what is bilirubin
What is bilirubin?
  • The breakdown product of Hgb from injured RBCs and other heme containing proteins.
  • Produced by reticuloendothelial system
  • Released to plasma bound to albumin
  • Hepatocytes conjugate it and extrete through bile channels into small intest.
what causes bilirubin
What causes  bilirubin?
  • Overproduction by reticuloendothelial system
  • Failure of hepatocyte uptake
  • Failure to conjugate or excrete
  • Obstruction of biliary excretion into intestine
unconjugated vs conjugated

 production exceeds ability of liver to conjugate

Ex. Hemolytic anemias, hemoglobinopathies, in-born errors of metab., transfusion rxn.


Can produce but not excrete

Metabolic defect

Intra- or extrahepatic obstruction

Unconjugated vs. Conjugated
clinical features
Clinical Features
  • Careful history and PE
  • Family history (Gilbert, Rotor, Crigler-Najjar, Dubin-Johnson, Sickle Cell)
  • Healthy young person with fever, malaise, myalgias = viral hepatitis (try to locate source)
clinical features8
Clinical Features
  • Gradually develops symptoms = hepatic/bile duct obstruction (consider ETOH liver dz/cirrhosis)
  • Develops acutely with abd pain = acute cholangitis 2° to choledocholithiasis
clinical features9
Clinical Features
  • Painless jaundice in older person with epigastric mass & weight loss = biliary obstruction from malignancy
  • Hepatomegaly with pedal edema, JVD, and gallop = CHF
laboratory tests
Serum bilirubin level (total and direct)

Liver aminotransferase levels

Alk. Phos

U/A for bilirubin and urobilogen



Other labs pertinent to history

Coombs test

Hgb electrophoresis

Viral hepatitis panel

U/S Gallbladder

Laboratory Tests
  • Hemodynamically stable, new-onset jaundice, no evidence of liver failure or acute biliary obstruction  discharge with follow up
  • If one of above violated  admission with surgery consult
cholecystitis and biliary colic

Cholecystitis and Biliary Colic

Tintanalli Chapter 85

Pages 561-566

biliary tract emergencies related to gallstones
Biliary Tract Emergencies Related to Gallstones
  • 1) Biliary Colic
  • 2) Cholecystitis
  • 3) Gallstone pancreatitis
  • 4) Ascending cholangitis
  • Most gallstones are asymptomatic
  • Usually seen in obese females 20-40 yoa and pregnancy (Remember fat, fertile, flatulent, female, forty)
  • Associated with upper abdominal pain
  • Uncommon in children (seen with hemolytic d/o, idiopathic, cystic fibrosis, obesity, ileal resection, long term use of TPN)
  • Elderly
    • 14-27% symptomatic gallstone dz.
    • More likely biliary sepsis/gangrenous GB
    •  perioperative morbidity
    • Mortality rate 19%
gallstone risk factors
Gallstone Risk Factors
  • Familial
  • Asian descent
  • Chronic biliary tract infections
  • Parasitic infections (ascaris lumbricoides)
  • Chronic liver dz (ETOH)
  • Chronic intravasular dz (Sickle Cell, Hereditary Scherocytosis)
  • Hepatitis A, B, C, E
  • HIV
  • Herpesvirus
  • Bile
    • Manufactured & secreted from hepatocytes GB storage in canaliculi, ductiles, & bile ducts bile ducts enlarge form R and L hepatic ducts form common hepatic duct joins cystic duct from GB to form CBD Ampulla of Vater duodenum
  • Release of bile stimulated by cholecystokinin secreted from small int. mucosal cells when fats & AA enter duodenum
  • Symptomatic cholelithiasis = stone migration from GB into biliary tract with eventual obstruction obstruction of hollow viscus pain, nausea & vomiting acute cholecystitis
pathogens involved in acute cholecystitis
Pathogens Involved in AcuteCholecystitis
  • E. coli/Klebsiella-70%
  • Enterococci-15%
  • Bacteroides-10%
  • Clostridium-10%
  • Group D Strep
  • Staphylococcal species
clinical features21
Clinical Features
  • Overlap of s/s of PUD, gastritis, GERD, nonspecific dyspepsia
  • RUQ pain
  • Upper abd/epigastric pain
  • Radiation to L upper back
  • Pain persisant lasting 2-6h
clinical features22
Clinical Features
  • Clinical studies show no coorelation with fatty food
  • Peak symptoms 9PM-4AM –follows circadium rhythm
  • Infrequent pain-intervals more than 1wk
  • Not related to meals in 1/3 of pts.
clinical features of acute cholecystitis
Clinical Features of Acute Cholecystitis
  • Pain lasts beyond 6h
  • N,V
  • Anorexia
  • Fever, chills
  • +Murphy’s sign ( pain or inspiratory arrest with deep, subcostal palpation on inspiration)
  • See Table 85-2
acalculous cholecystitis
5-10% incidence



Multiple trauma

Extensive burns

Prolonged Labor

Major surgery

GB torsion

Systemic vasculitis states

Bacterial or parasitic infection of biliary tract

Acalculous Cholecystitis
differential diagnosis





AMI in elderly

Acute renal colic

Acute pyelo

Appendicitis (pregnancy, retrocecal)


Fitzhugh-Curtis Syn.



Pleural Effusion

Differential Diagnosis
diagnostic studies
Diagnostic Studies
  • Most important is high clinical suspicion and U/S.
  • Usually labs nl. (CBC, bilirubin, Alk. Phos, LFTs, U/A, UHCG, Lipase)
  • CXR- r/o pneumonia, pleural effusion
  • 12 Lead EKG- r/o ACS
  • U/S shows stones small as 2mm
  • CT when ? other intraabdominal path
  • HIDA Scan
  • Fluid & Electrolyte deficiencies- due to vomiting & anorexia
  • Upper GI hemorrhage- Mallory-Weiss tears
  • Gallstone pancreatitis
  • Ascending cholangitis
  • Cholecystitis
  • GB Empyema
  • Emphysematous (gangrenous) GB
  • Uncomplicated Symptomatic Cholelithiasis– No immediate surgery, Elective cholecystectomy, Control symptoms
    • Antispasmodics
    • Opiates (Meperidine preferred)
    • Antiemetics
    • Ketorolac (relieves GB distention)
    • Replace fluids & electrolytes
  • Acute Acalculous/Calculous Cholecystitis
  • If septic – wide spectrum abx and immediate surgery
  • If not septic – single agent abx (3rd gen cephalosporin), surgery within 24-72 hours
hepatic disorders hepatic failure

Hepatic Disorders & Hepatic Failure

Tintanalli Chapter 86

Pages 566-573

acute chronic liver disease
Acute & Chronic Liver Disease
  • CLD- 12th leading cause of death in US
  • However, decreased inf with hepatitis viruses A, B, & C in last decade.
  • Other causes: ETOH, CMV, HSV, Coxsackie, EBV, Drugs, autoimmune, metabolic
  • Hepatocellular
  • Cholestatic
  • Immunologic
  • Infiltrative Disorder
clinical features33
Clinical Features
  • Acute Viral –anorexia, N, V, low-grade fever
  • Cholestatic –jaundice, pruritis, clay-colored stools, dark urine
  • Chronic –complications of advanced cirrhosis, portal HTN (abd pain, ascites, GI bleed, fever, AMS)
history history history
History, History, History
  • Sexual behaviors
  • Travel
  • ETOH
  • Illicit drug use
  • Natural supplements (Vitamin A)
  • Herbal remedies
  • Mushroom ingestion
  • Raw oysters
  • Family history
physical findings
Physical Findings
  • Acute
    • Moderate liver enlargement, tenderness, +/- jaundice
  • Chronic
    • Sallow complexion, extremity muscle atrophy, palmar erythema, cutan spider nevi, parotid enlargement, testicular atrophy, gynecomastia, splenomegaly, ascites
  • 1) Markers of acute hepatocyte injury & death: AST (SGPT), ALT (SGOT), Alk Phos.
  • 2) Measures of hepatocyte synthetic fxn : PT, Albumin
  • 3) Indicators of hepatocyte catabolic activity: direct & indirect bilirubin, ammonia
  • 4) Others: Lactate dehydrogenase, viral hepatitis serology
cirrhosis complications of end stage liver dz
Cirrhosis & Complications of End Stage Liver Dz
  • Gastroesophageal Varices & Hemorrhage
  • Medical literature shows no evidence of  risk of iatrogenic hemorrhage from placement of naso- or orogastric catheters!!!
  • Tx: Hemodynamic & airway stabiliz.
  • Endoscopy-banding/sclerotherapy
  • Vasoactive drugs: Somatostatin, Octreotide
  • Abx. to cover enteric organisms
ascites spontaneous bacterial peritonitis
Ascites & Spontaneous Bacterial Peritonitis
  • Paracentesis (U/S guided or not)
  • Lab Testing of Ascitic Fluid (WBC, diff, glucose, protein, gram stain, C&S)
    • SBP = WBC>1000/L, low glucose, high protein
    • Abx coverage of enterobacteriaceae (63%), S. Pneumoniae (15%), Enterococci (6-10%), Anaerobes (<1%)
    • See table 86-4
hepatorenal syndrome
Hepatorenal Syndrome
  • Acute renal failure with acute or chronic hepatic failure
  • Etiology unknown
  • Median survival 21 days
  • Tx: Liver transplant & kidneys will spontaneously recover
hepatic encephalopathy
Hepatic Encephalopathy
  • Accumulation of nitrogenous waste products
  • Diagnosis of exclusion
  • Tx: Decreased protein intake, lactulose (traps ammonia & allows stool excretion), neomycin
the end
  • Questions???????
  • 1) Unconjugated hyperbilirubinemia usually results from a intra- or extrahepatic biliary obstruction.
    • A. True
    • B. False
  • 2) All patients with jaundice should be admitted to the hospital for further workup.
    • A. True
    • B. False
3) All of the following are risk factors for development of gallstones except:
    • A. Pregnancy
    • B. >50 yoa
    • C. Female
    • D. Obesity
    • E. Asian descent
4) Clinical features of cholecystitis include all of the following except:
    • A. RUQ abdominal pain
    • B. Radiation to R upper back
    • C. Nausea, Vomiting
    • D. + Murphy’s sign
    • E. Fever
5) A marker of acute hepatocyte injury &/or hepatocyte death is:
    • A. PT
    • B. ALT
    • C. Albumin
    • D. Direct bilirubin
    • E. Ammonia
  • All answers are B!!