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JAUNDICE
Dr J. Njoku
MBBS, FWACP(Gastroenterology)
• Jaundice is the yellowish discoloration of the skin,
sclera and mucous membranes due to elevated
bilirubin levels
• Normal serum bilirubin is 0.3 – 1mg/dl
• It becomes visible/detectable at 3mg/dl
• Due to an imbalance between production and
clearance of bilirubin
• Sclera- high affinity because of elastin content
Epidemiology
• The incidence varies with age: common in
newborns and elderly
• Incidence is approximately 40,000 per 100,000
individuals in ICU
• Incidence would vary with the prevailing underlying
aetiology
• The knowledge, proper evaluation & early diagnosis
of the underlying cause in jaundice is essential in
improving patients prognosis.
Bile metabolism
Bilirubin metabolism
• Unconjugated bilirubin is produced ( 250-300mg daily)
from catabolism of haemoglobin after removal of its iron
component.
• Bilirubin in the ciculating blood is mostly unconjugated
and it is not water-soluble, bound to albumin and does
not pass into urine.
• Unconjugated -> conjugated(bilirubin mono and
diglucuronide) by UDP glucuronyl transferase
• This glucuronide (conjugated form) is more water-
soluble than free bilirubin, is then transported into
the bile canaliculi
• Small amounts escape into blood, and is excreted in
urine
• Most of the bilirubin glucuronide passes via the bile
ducts to the intestine
• Intestinal mucosa is impermeable to conjugated
but permeable to unconjugated and to
urobilinogens (colorless derivates of bilirubin
formed by the action of bacteria in the intestine)
• Consequently, some of the bile pigments and
urobilinogens are reabsorbed in the portal
circulation, and excreted by the liver via the
enterohepatic circulation
• Small amounts of urobilinogen enter the circulation
and are excreted in urine
• Hyperbilirubinemia may be due to
• 1. Excess production of bilirubin
• 2. Decreased uptake of bilirubin into hepatic cells
• 3. Disturbed intracellular protein binding or
conjugation
• 4. Disturbed secretion of conjugated bilirubin into
the bile canaliculi
• 5. Intrahepatic/ extrahepatic bile duct obstruction
Bilirubin Metabolism
Classification: depends on
A. Type of Circulating Bilirubin:
1.Conjugated
2.Unconjugated
B. Site of the Problem:
1.Prehepatic
2.Intrahepatic/Hepatocellular
3.Post-hepatic/Cholestatic/ Obstructive
Aetiopathogenesis
• Pre-hepatic Jaundice: Excess Bilirubin production from
excessive breakdown of RBCs or defective bilirubin
conjugation in the liver
• Causes:
• Sickle cell crisis
• Spherocytosis
• Haemolytic anaemia
• Gilbert’s disease: partial deficiency of UDP-glucoronyl
transferase, 1 copy of UGT1A gene mutated
• Criggler-Najar syndrome- inability of liver to conjugate
bilirubin with glucuronic acid due to almost total deficiency
of the enzyme. 2 copies of the UGT1A gene are mutated
• Clinical Features: Jaundice not really severe
• Increased unconjugated plasma bilirubin
• Increased urobilinogen in urine
• ALP, ALT, AST – usually normal
• Intrahepatic/Hepatocellular Jaundice: -
• There is hepatocellular damage leading to decreased
conjugation
• There is both unconjugated and conjugated
hyperbilirubinemia
• Causes:
• Viruses: HAV, HBV, HCV, HDV, HDV, CMV, EBV
• Drugs eg Rifampicin, Phenothiazine, Acetaminophen
• Alcoholic Hepatitis, Cirrhosis, Liver
metastases/abscesses,
• Hemochromatosis, Wilson’s disease, Alpha-1
antitrypsin deficiency
• Sepsis
• Leptospirosis
• Budd Chiari Syndrome
• Failure to Excrete Bilirubin (Dubin – Johnson &
Rotor Syndromes)
• Right Heart Failure
• Toxins( Carbon Tetrachloride)
• Fungi – Aspergillus flavus
• Mushroom poisoning (Amanita phyloides)
• Post-
hepatic/Cholestatic/Obstruct
ive Jaundice:
• Obstruction to passage of
conjugated bile-> Conjugated
Hyperbilirubinemia.
• Conjugated Bilirubin cannot
pass into intestine.
• Causes: Choledocholithiasis,
Pancreatic cancer, ,
Cholangiocarcinoma, Primary
Sclerosing Cholangitis,
Primary Biliary cirrhosis,
Choledochal cysts, Biliary
atresia
Clinical features
• Yellowness of the eyes
• Dark urine
• Pale stool
• Pruritus
• Abdominal pain +/- swelling
• +/-fever
• Weight loss
• Lethargy
• +/- Vomiting
EVALUATION OF A JAUNDICED
PATIENT
• History
• Biodata
• Hx of yellowness of the eyes and associated symptoms
• Examination: Vital signs, Physical exam, Abdominal exam,
DRE
• Investigation:s
• LFT + Serum albumin, total proteins
• FBC
• Clotting profile
• Viral Hepatitis screening
• EUCr
• Urinalysis
• Abdominal imaging-USS, CT
• Other serologic markers for other disease conditions eg ANA, Anti-
LKM
Laboratory tests
Abdominal uss
• Detects diffuse/focal liver masses, abscesses,
cirrhosis etc
• Evaluates Intrahepatic bile ducts
• CBD
• gallbladder wall
• CBD diameter increases with age and after previous
biliary surgery
• For obstructive jaundice ultrasound has a
sensitivity 70 - 95% and specificity 80 - 100%
GENERAL MEASURES
• Rehydrate -IVF 10% Dextrose
• Broad spectrum Antibiotics
• IM/IV Vitamin K 10mg dly for 4-5days
• Antihistamines
• Cholestyramine for obstructive jaundice
• Urethral catherization for strict I/O monitoring
• Monitor plasma glucose
• Analgesics for tumor pain
• Serial urine chart
• Specialist care depends on underlying aetiology
Complications
• Kernicterus
• GI bleeding
• Impaired wound healing
• Coagulopathy
• Impaired Immune function
THANK YOU

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JAUNDICE Dr Njoku.pptx

  • 1. JAUNDICE Dr J. Njoku MBBS, FWACP(Gastroenterology)
  • 2.
  • 3. • Jaundice is the yellowish discoloration of the skin, sclera and mucous membranes due to elevated bilirubin levels • Normal serum bilirubin is 0.3 – 1mg/dl • It becomes visible/detectable at 3mg/dl • Due to an imbalance between production and clearance of bilirubin • Sclera- high affinity because of elastin content
  • 4. Epidemiology • The incidence varies with age: common in newborns and elderly • Incidence is approximately 40,000 per 100,000 individuals in ICU • Incidence would vary with the prevailing underlying aetiology • The knowledge, proper evaluation & early diagnosis of the underlying cause in jaundice is essential in improving patients prognosis.
  • 6. Bilirubin metabolism • Unconjugated bilirubin is produced ( 250-300mg daily) from catabolism of haemoglobin after removal of its iron component. • Bilirubin in the ciculating blood is mostly unconjugated and it is not water-soluble, bound to albumin and does not pass into urine. • Unconjugated -> conjugated(bilirubin mono and diglucuronide) by UDP glucuronyl transferase
  • 7. • This glucuronide (conjugated form) is more water- soluble than free bilirubin, is then transported into the bile canaliculi • Small amounts escape into blood, and is excreted in urine • Most of the bilirubin glucuronide passes via the bile ducts to the intestine • Intestinal mucosa is impermeable to conjugated but permeable to unconjugated and to urobilinogens (colorless derivates of bilirubin formed by the action of bacteria in the intestine)
  • 8. • Consequently, some of the bile pigments and urobilinogens are reabsorbed in the portal circulation, and excreted by the liver via the enterohepatic circulation • Small amounts of urobilinogen enter the circulation and are excreted in urine
  • 9. • Hyperbilirubinemia may be due to • 1. Excess production of bilirubin • 2. Decreased uptake of bilirubin into hepatic cells • 3. Disturbed intracellular protein binding or conjugation • 4. Disturbed secretion of conjugated bilirubin into the bile canaliculi • 5. Intrahepatic/ extrahepatic bile duct obstruction
  • 11. Classification: depends on A. Type of Circulating Bilirubin: 1.Conjugated 2.Unconjugated B. Site of the Problem: 1.Prehepatic 2.Intrahepatic/Hepatocellular 3.Post-hepatic/Cholestatic/ Obstructive
  • 12. Aetiopathogenesis • Pre-hepatic Jaundice: Excess Bilirubin production from excessive breakdown of RBCs or defective bilirubin conjugation in the liver • Causes: • Sickle cell crisis • Spherocytosis • Haemolytic anaemia • Gilbert’s disease: partial deficiency of UDP-glucoronyl transferase, 1 copy of UGT1A gene mutated • Criggler-Najar syndrome- inability of liver to conjugate bilirubin with glucuronic acid due to almost total deficiency of the enzyme. 2 copies of the UGT1A gene are mutated
  • 13. • Clinical Features: Jaundice not really severe • Increased unconjugated plasma bilirubin • Increased urobilinogen in urine • ALP, ALT, AST – usually normal
  • 14. • Intrahepatic/Hepatocellular Jaundice: - • There is hepatocellular damage leading to decreased conjugation • There is both unconjugated and conjugated hyperbilirubinemia • Causes: • Viruses: HAV, HBV, HCV, HDV, HDV, CMV, EBV • Drugs eg Rifampicin, Phenothiazine, Acetaminophen • Alcoholic Hepatitis, Cirrhosis, Liver metastases/abscesses, • Hemochromatosis, Wilson’s disease, Alpha-1 antitrypsin deficiency
  • 15. • Sepsis • Leptospirosis • Budd Chiari Syndrome • Failure to Excrete Bilirubin (Dubin – Johnson & Rotor Syndromes) • Right Heart Failure • Toxins( Carbon Tetrachloride) • Fungi – Aspergillus flavus • Mushroom poisoning (Amanita phyloides)
  • 16. • Post- hepatic/Cholestatic/Obstruct ive Jaundice: • Obstruction to passage of conjugated bile-> Conjugated Hyperbilirubinemia. • Conjugated Bilirubin cannot pass into intestine. • Causes: Choledocholithiasis, Pancreatic cancer, , Cholangiocarcinoma, Primary Sclerosing Cholangitis, Primary Biliary cirrhosis, Choledochal cysts, Biliary atresia
  • 17. Clinical features • Yellowness of the eyes • Dark urine • Pale stool • Pruritus • Abdominal pain +/- swelling • +/-fever • Weight loss • Lethargy • +/- Vomiting
  • 18. EVALUATION OF A JAUNDICED PATIENT • History • Biodata • Hx of yellowness of the eyes and associated symptoms • Examination: Vital signs, Physical exam, Abdominal exam, DRE • Investigation:s • LFT + Serum albumin, total proteins • FBC • Clotting profile • Viral Hepatitis screening • EUCr • Urinalysis • Abdominal imaging-USS, CT • Other serologic markers for other disease conditions eg ANA, Anti- LKM
  • 20. Abdominal uss • Detects diffuse/focal liver masses, abscesses, cirrhosis etc • Evaluates Intrahepatic bile ducts • CBD • gallbladder wall • CBD diameter increases with age and after previous biliary surgery • For obstructive jaundice ultrasound has a sensitivity 70 - 95% and specificity 80 - 100%
  • 21. GENERAL MEASURES • Rehydrate -IVF 10% Dextrose • Broad spectrum Antibiotics • IM/IV Vitamin K 10mg dly for 4-5days • Antihistamines • Cholestyramine for obstructive jaundice • Urethral catherization for strict I/O monitoring • Monitor plasma glucose • Analgesics for tumor pain • Serial urine chart • Specialist care depends on underlying aetiology
  • 22.
  • 23. Complications • Kernicterus • GI bleeding • Impaired wound healing • Coagulopathy • Impaired Immune function