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Reem Ahmed Alyahya
212522156
CLINICAL APPROACH TO
JAUNDICE IN ADULTS
Introduction
• A 66 y/o patient presented to the hospital complaining of
yellowish staining of his eyes over the last 3 months.
• This discoloration is also associated with itching and palpable mass
in the right hypochondrium.
• The history is negative for abdominal pain
• He also reported Wight loss of 10 kg during the last 3 months.
Jaundice
• The word “jaundice” comes from the French word jaune,
which means yellow.
• jaundice is a yellowish discoloration of the skin, sclera, and
mucous membranes by bilirubin.
• The discoloration typically is detected clinically once the
serum bilirubin level rises above 3 mg/dL
• Bilirubin metabolism takes place in three phases—prehepatic,
intrahepatic, and posthepatic. Dysfunction in any of these
phases may lead to jaundice.
Jaundice
Pre-hepatic
hepatic Post-heptic
unconjugated
hyperbilirubinemia
Conjugated
hyperbilirubinemia
Unconjugated hyperbilirubinemia
Mechanism Examples Suggestive findings
Increase bilirubin
production
Hemolysis, resorption of
large hematomas
 Few or no clinical
manifestations of
hepatobiliary disease
 anemia, jaundice
splenomegaly and
gallstones
 Serum bilirubin level (4-6
mg/dl)
 Normal
aminotransferase levels
 Normal urine color
 Features of hemolysis
Decrease hepatic
conjugation
Gilbert syndrome, cirgler
najjar syndrome
Conjugated hyperbilirubinemia
Mechanism examples Suggestive findings
Hepatocellular dysfunction Viral hepatitis , drugs,
cirrhosis, hepatocellular
carcinoma.
Aminotransferase levels >
500 U/L
Intrahepatic cholestasis Alcoholic liver disease,
drugs, toxins, hepatitis,
primary biliary cirrhosis
 Alkaline phosphatase
and GGT > 3 times
normal
 Aminotransferase
levels< 200 U/L
Extrahepatic cholestasis CBD stones, pancreatic
cancer, CBD strictures,
acute cholangitis
 Alkaline phosphatase
and GGT > 3 times
normal
 Aminotransferase levels
< 200 U/L
Hereditary disorders Dubin-Jhonson syndrome,
Rotor’s syndrome
Normal liver enzymes.
Evaluation:
History of
presenting
illness
Past medical
history
Physical
examination
Investigations
History of presenting illness:
•Onset and duration of jaundice
•Urine and stool color
•Prodromal symptoms (e.g. fever, malaise and
myalgia) before jaundice
•Pruritus
•Steatorrhea
•Wight loss
•Abdominal pain (location, severity, duration and
radiation)
Past medical history:
•Hepatobiliary disease: gallstones, hepatitis, cirrhosis
•Disorders that could cause hemolysis:
hemoglobinopathy , G6PD deficiency.
•Infiltrative disorders: amyloidosis, lymphoma,
sarcoidosis , AIDS.
•Drug history
•Vaccination against hepatitis
Past medical history:
•Surgical history: previous surgeries on the biliary
tract ( a potential cause of strictures.)
•Social history: risk factors of hepatitis, amount and
duration of alcohol use, injection drug use and sexual
history.
•Family history: should include questions about
recurrent mild jaundice and hereditary liver disorders.
Physical examination:
• Vital signs are reviewed for fever and signs of
systemic toxicity (e.g. hypotension and
tachycardia)
• General appearance is noted, cachexia and
lethargy
• Head and neck examination includes
inspection of the sclera for icterus and the
eyes for Kayser-Fleischer rings.
• The abdomen is inspected for collateral
vasculatures, spider nevie, ascites and surgical
scars.
Physical examination:
• The abdomen is examined for shifting
dullness, fluid thrill, masses and tenderness.
• The liver should be palpated for
hepatomegaly, masses, nodularity and
tenderness
• The spleen is palpated for splenomegaly.
• Men are checked for testicular atrophy and
gynecomastia.
Physical examination:
• Upper extremities are examined for
Dupuytren’s contractures, and asterixis.
• The skin is examined for jaundice, palmar
erythema, needle tracks, excoriations,
Xanthomas, hyperpigmentation, petechiae, and
purpura.
• Neurologic examination including mental status
assessment.
Investigations
Blood
tests
imaging
Liver
biopsy
Initial laboratory tests:
• Normal alkaline phosphatase and aminotransferases:
hemolysis or inherited disorders of bilirubin metabolism
may be responsible for the hyperbilirubinemia.
• Predominant alkaline phosphatase elevation:
suggests biliary obstruction or intrahepatic cholestasis
• Predominant aminotransferase elevation:
suggests that jaundice is caused by intrinsic hepatocellular
disease
Initial laboratory tests:
• Elevated INR :
- Corrects with Vitamin K administration : impaired intestinal
absorption of fat-soluble vitamins and is compatible with
obstructive jaundice
- does not correct with vitamin K suggests hepatocellular disease
with impaired synthetic function
Subsequent evaluation:
• Suspected hepatocellular injury:
• Serologic tests for viral hepatitis
• Measurement of antimitochondrial antibodies (for primary biliary
cirrhosis)
• Measurement of antinuclear anti-smooth muscle and liver-kidney
microsomal antibodies (for autoimmune hepatitis)
• Serum levels of iron, transferrin, and ferritin (for hemochromatosis)
• Serum and urinary copper , serum levels of ceruloplasmin (for
Wilson disease)
Subsequent evaluation:
• Suspected biliary obstruction or intrahepatic cholestasis:
• Abdominal US: highly accurate in detecting extrahepatic
obstruction (gall stones)
• CT scan: more accurate in pancreatic lesions.
• If the results are positive for extrahepatic cholestasis, other tests
may be necessary to determine the cause: MRCP , ERCP
• Liver biopsy:
• Not commonly required but can help in diagnosing autoimmune
hepatitis or biliary tract disorders (e.g., primary biliary cirrhosis,
primary sclerosing cholangitis)
Treatment:
• The underlying cause and any complications are
treated
• Jaundice itself requires no treatment in adults “
unlike children “
• Itching if bothersome, maybe relieved by
cholestyramine 2-8 g orally twice daily
• However cholestyramine is ineffective in patients
with complete biliary obstruction.
Back to our case:
• A 66 y/o patient presented to the hospital complaining of yellowish
discoloration of his eyes over the last 3 months.
• This discoloration is also associated with mild itching and palpable
mass in the right hypochondrium.
• The history is negative for abdominal pain
• He also reported Wight loss of 10 kg during the last 3 months.
Pancreatic cancer induced biliary
obstruction
Conclusion
• Acute jaundice, particularly with viral prodrome in
the young and healthy suggests acute viral hepatitis
• Painless jaundice in elderly patients with weight loss ,
an abdominal mass and minimal pruritis suggests
biliary obstruction caused by cancer.
• Prodominant increase in Aminotrnsferase suggests
hepatocellular dysfunction.
• Prodominant increase in Aalkaline phosphatase
suggest cholestasis
• Significant hepatic dysfunction is indicated by
altered mental states and coagulopathy.
References:
• The merck manual of diagnosis and therapy. 19th edition. 2011
• Kumar and clark. Clinical medicine.8th edition.2012
• Macleod’s clinical examination.13th edition. 2013
• UpToDate: http://www.uptodate.com/contents/diagnostic-
approach-to-the-adult-with-jaundice-or-asymptomatic-
hyperbilirubinemia
• American Familiy physician:
http://www.aafp.org/afp/2004/0115/p299.html
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clinical approach to jaundice in adults

  • 1. Reem Ahmed Alyahya 212522156 CLINICAL APPROACH TO JAUNDICE IN ADULTS
  • 2. Introduction • A 66 y/o patient presented to the hospital complaining of yellowish staining of his eyes over the last 3 months. • This discoloration is also associated with itching and palpable mass in the right hypochondrium. • The history is negative for abdominal pain • He also reported Wight loss of 10 kg during the last 3 months.
  • 3. Jaundice • The word “jaundice” comes from the French word jaune, which means yellow. • jaundice is a yellowish discoloration of the skin, sclera, and mucous membranes by bilirubin. • The discoloration typically is detected clinically once the serum bilirubin level rises above 3 mg/dL • Bilirubin metabolism takes place in three phases—prehepatic, intrahepatic, and posthepatic. Dysfunction in any of these phases may lead to jaundice.
  • 5. Unconjugated hyperbilirubinemia Mechanism Examples Suggestive findings Increase bilirubin production Hemolysis, resorption of large hematomas  Few or no clinical manifestations of hepatobiliary disease  anemia, jaundice splenomegaly and gallstones  Serum bilirubin level (4-6 mg/dl)  Normal aminotransferase levels  Normal urine color  Features of hemolysis Decrease hepatic conjugation Gilbert syndrome, cirgler najjar syndrome
  • 6. Conjugated hyperbilirubinemia Mechanism examples Suggestive findings Hepatocellular dysfunction Viral hepatitis , drugs, cirrhosis, hepatocellular carcinoma. Aminotransferase levels > 500 U/L Intrahepatic cholestasis Alcoholic liver disease, drugs, toxins, hepatitis, primary biliary cirrhosis  Alkaline phosphatase and GGT > 3 times normal  Aminotransferase levels< 200 U/L Extrahepatic cholestasis CBD stones, pancreatic cancer, CBD strictures, acute cholangitis  Alkaline phosphatase and GGT > 3 times normal  Aminotransferase levels < 200 U/L Hereditary disorders Dubin-Jhonson syndrome, Rotor’s syndrome Normal liver enzymes.
  • 8. History of presenting illness: •Onset and duration of jaundice •Urine and stool color •Prodromal symptoms (e.g. fever, malaise and myalgia) before jaundice •Pruritus •Steatorrhea •Wight loss •Abdominal pain (location, severity, duration and radiation)
  • 9. Past medical history: •Hepatobiliary disease: gallstones, hepatitis, cirrhosis •Disorders that could cause hemolysis: hemoglobinopathy , G6PD deficiency. •Infiltrative disorders: amyloidosis, lymphoma, sarcoidosis , AIDS. •Drug history •Vaccination against hepatitis
  • 10. Past medical history: •Surgical history: previous surgeries on the biliary tract ( a potential cause of strictures.) •Social history: risk factors of hepatitis, amount and duration of alcohol use, injection drug use and sexual history. •Family history: should include questions about recurrent mild jaundice and hereditary liver disorders.
  • 11. Physical examination: • Vital signs are reviewed for fever and signs of systemic toxicity (e.g. hypotension and tachycardia) • General appearance is noted, cachexia and lethargy • Head and neck examination includes inspection of the sclera for icterus and the eyes for Kayser-Fleischer rings. • The abdomen is inspected for collateral vasculatures, spider nevie, ascites and surgical scars.
  • 12. Physical examination: • The abdomen is examined for shifting dullness, fluid thrill, masses and tenderness. • The liver should be palpated for hepatomegaly, masses, nodularity and tenderness • The spleen is palpated for splenomegaly. • Men are checked for testicular atrophy and gynecomastia.
  • 13. Physical examination: • Upper extremities are examined for Dupuytren’s contractures, and asterixis. • The skin is examined for jaundice, palmar erythema, needle tracks, excoriations, Xanthomas, hyperpigmentation, petechiae, and purpura. • Neurologic examination including mental status assessment.
  • 15. Initial laboratory tests: • Normal alkaline phosphatase and aminotransferases: hemolysis or inherited disorders of bilirubin metabolism may be responsible for the hyperbilirubinemia. • Predominant alkaline phosphatase elevation: suggests biliary obstruction or intrahepatic cholestasis • Predominant aminotransferase elevation: suggests that jaundice is caused by intrinsic hepatocellular disease
  • 16. Initial laboratory tests: • Elevated INR : - Corrects with Vitamin K administration : impaired intestinal absorption of fat-soluble vitamins and is compatible with obstructive jaundice - does not correct with vitamin K suggests hepatocellular disease with impaired synthetic function
  • 17. Subsequent evaluation: • Suspected hepatocellular injury: • Serologic tests for viral hepatitis • Measurement of antimitochondrial antibodies (for primary biliary cirrhosis) • Measurement of antinuclear anti-smooth muscle and liver-kidney microsomal antibodies (for autoimmune hepatitis) • Serum levels of iron, transferrin, and ferritin (for hemochromatosis) • Serum and urinary copper , serum levels of ceruloplasmin (for Wilson disease)
  • 18. Subsequent evaluation: • Suspected biliary obstruction or intrahepatic cholestasis: • Abdominal US: highly accurate in detecting extrahepatic obstruction (gall stones) • CT scan: more accurate in pancreatic lesions. • If the results are positive for extrahepatic cholestasis, other tests may be necessary to determine the cause: MRCP , ERCP • Liver biopsy: • Not commonly required but can help in diagnosing autoimmune hepatitis or biliary tract disorders (e.g., primary biliary cirrhosis, primary sclerosing cholangitis)
  • 19. Treatment: • The underlying cause and any complications are treated • Jaundice itself requires no treatment in adults “ unlike children “ • Itching if bothersome, maybe relieved by cholestyramine 2-8 g orally twice daily • However cholestyramine is ineffective in patients with complete biliary obstruction.
  • 20. Back to our case: • A 66 y/o patient presented to the hospital complaining of yellowish discoloration of his eyes over the last 3 months. • This discoloration is also associated with mild itching and palpable mass in the right hypochondrium. • The history is negative for abdominal pain • He also reported Wight loss of 10 kg during the last 3 months. Pancreatic cancer induced biliary obstruction
  • 21. Conclusion • Acute jaundice, particularly with viral prodrome in the young and healthy suggests acute viral hepatitis • Painless jaundice in elderly patients with weight loss , an abdominal mass and minimal pruritis suggests biliary obstruction caused by cancer. • Prodominant increase in Aminotrnsferase suggests hepatocellular dysfunction. • Prodominant increase in Aalkaline phosphatase suggest cholestasis • Significant hepatic dysfunction is indicated by altered mental states and coagulopathy.
  • 22. References: • The merck manual of diagnosis and therapy. 19th edition. 2011 • Kumar and clark. Clinical medicine.8th edition.2012 • Macleod’s clinical examination.13th edition. 2013 • UpToDate: http://www.uptodate.com/contents/diagnostic- approach-to-the-adult-with-jaundice-or-asymptomatic- hyperbilirubinemia • American Familiy physician: http://www.aafp.org/afp/2004/0115/p299.html

Editor's Notes

  1. Bilirubin is formed by a breakdown product of heme rings, usually from metabolized red blood cells. >50 umol/l
  2. Hemolytic Obstructive, surgical
  3. Unconjugated bilirubin is not water soluble and therefore doesn’t pass into urine “ acholuric jaundice LDH increase “ lactase dehydrogenase” haptoglobin is low Most common familial hyperbilirubenemia , asymptomatic , detected incedintally , other biochem normal,AS , UDP- glucotonosyl transferase (UGT-1, HUG-BR1)
  4. Intrahepatic cholestasis: failure of bile secretion Extrahepatic: large duct obstruction of bile flow at any point in the biliary tract. conjugated bilirubin is soluble and filtered by the kidney so the urine is dark brown. Urine is dark Stools is pale in case of biliary obstruction gamma-glutamyl transferase MRP2 transportr genes, black liver melanin deposition
  5. A history of prolonged duration of jaundice with wt loss and elderly may suggest malignancy Short history with prodromal symptoms hepatits
  6. Should identify know causative disoders
  7. travel, IV drug use, tattos, blood transfusion
  8. flapping tremor, or liver flap) is a tremor of the hand when the wrist is extended t can be a sign of hepatic encephalopathy, damage to brain cells presumably due to the inability of the liver to metabolize ammonia to urea. The cause is thought to be predominantly related to abnormal ammonia metabolism.[2] an irregular yellow patch or nodule on the skin, caused by deposition of lipid
  9. Initial laboratory tests include measurements of serum total and unconjugated bilirubin, alkaline phosphatase, aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), prothrombin time/international normalized ratio (INR), and albumin. The presence or absence of abnormalities and the type of abnormalities should help to distinguish the various causes of jaundice. the jaundice is not likely due to hepatic injury or biliary tract disease. In such patients, he inherited disorders associated with isolated unconjugated hyperbilirubinemia are Gilbert and Crigler-Najjar syndromes; the disorders associated with isolated conjugated hyperbilirubinemia are Rotor and Dubin-Johnson syndromes.
  10.  Subsequent studies are guided based on findings from the history, physical examination, and initial laboratory tests
  11. typically the first test ordered, because of its lower cost, wide availability, and lack of radiation exposure, which may be particularly important in pregnant patients. elevated conjugated bilirubin and alkaline phosphatase), the first step in the evaluation is hepatic imaging magnetic resonance cholangiopancreatography [MRCP], endoscopic retrograde cholangiopancreatography [ERCP] ERCP is more invasive but allows treatment of some obstructive lesions ‘ stone, stricture’
  12. Bile acid sequestrant