summary expanation on Jaundice

2. Jaundice - icterus
• Jaundice also known as icterus, from the Greek word ίκτερος;
adjectival form icteric - is a yellowish pigmentation of the
 skin
 theconjunctival membranes over the sclerae (whites of the eyes),
 and other mucous membranes caused by high blood bilirubin levels.
• This hyperbilirubinemia subsequently causes increased levels of
bilirubin in the extracellular fluid.
• Concentration of bilirubin in blood plasma is normally below
1.2 mg/dL (<25µmol/L).
• The term jaundice comes from the French word jaune, meaning
yellow.

3. Jaundice
Bilirubin is a yellow pigment which causes discoloration
of the skin and when serum levels exceed 35-40 µmol/L.
Concentrations may increase for three reasons:
- the production rate of bilirubin is increased, exceeding
the excretory capacity of the liver (prehepatic jaundice);
- conjugating and / or excretory functions are reduced,
(hepatic
or hepatocellular jaundice);
- biliary obstruction interferes with the flow of bile and thus
bilirubin excretion (posthepatic, obstructive or
cholestatic jaundice).
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4. Pathogenesis of Jaundice
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6. 1.Pre hepatic jaundice
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7. Prehepatic Jaundice
• Prehepatic jaundice is caused by increased destruction of
erythrocytes either:
- mature cells or
- precursors (ineffective erythropoiesis).
• The breakdown of mature cells can be caused by:
- haemolysis, or
- as a result of the metabolism of blood
following internal haemorrhage, e.g. into
a soft tissue injury or fracture.
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8. Prehepatic Jaundice
• Ineffective erythropoiesis occurs in conditions such as:
- pernicious anaemia, where the
maturation of red cells is impaired, or
- thalassaemia, where the structure
of haemoglobin is abnormal.
• Hyperbilirubinaemia in prehepatic jaundice results from
the accumulation of unconjugated bilirubin; this is not
excreted by the kidney.
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9. Prehepatic Jaundice
• Jaundice occurs because the conjugating capacity of the liver is
saturated,
- the capacity of the liver for conjugation is
greater than the normal rate of bilirubin production.
• Increased fluxes of bilirubin through the liver into the gut
• Greater amounts of urobilinogen are produced, with
- increased urobilinogen excretion in urine.
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10. 2.Hepatic Jaundice
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11. Hepatic Jaundice
• Congenital disorders of bilirubin transport lead to
jaundice because of:
- defective uptake, reduced conjugation
or impaired excretion of bilirubin.
• Generalized hepatocellular dysfunction may occur in
hepatitis and hepatic cirrhosis.
• Drugs may cause hepatocellular damage, either due
to dose-dependent hepatoxicity (e.g. paracetamol).
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12. Hepatic Jaundice
• The pathogenesis of jaundice in these
conditions is complex,
- reduced hepatic uptake,
- decreased conjugation and,
- impaired intracellular transport
of bilirubin, all contributing.
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13. Hepatic Jaundice
• When hyperbilirubinaemia is caused by impaired
conjugation of bilirubin;
- unconjugated bilirubin, and no
increased fluxes of bilirubin through the liver,
- bilirubinuria does not occur and
- urinary urobilinogen is not increased.
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14. Hepatic Jaundice
• Serum bilirubin may be unconjugated or conjugated, as UDP
glucuronyl transferase and intracellular transport may be
defective.
• If the rate of conjugation exceeds excretory capacity;
- conjugated hyperbilirubinaemia will
occur and bilirubin may be excreted,in urine,
- this is sometimes seen in recovery from acute
viral hepatitis.
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15. 3.Cholestatic Jaundice
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16. Cholestatic Jaundice
• Cholestatic jaundice results from interference to biliary flow
between the sites of secretion by the hepatocyte and
drainage into the duodenum.
• It may be caused by lesions;
- within the liver (intrahepatic cholestasis),
or in the biliary tree or head of the
pancreas (extrahepatic cholestasis);
- the term cholestatic is preferable to post-hepatic
to describe this pattern of jaundice.
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17. Cholestatic Jaundice
• Intra- and extra-hepatic cholestasis can be differentiated by;
- ultrasound examination or
- liver biopsy, but not by liver function tests.
• Intrahepatic cholestasis may result from generalized hepatocellular
dysfunction, such as occurs in;
- Hepatitis,
- Hepatic cirrhosis
• Hepatic malignancies may block branches of the biliary tree.
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18. Cholestatic Jaundice
• Some drugs may cause intrahepatic cholestasis such as:
- anabolic steroids, and
- phenothiazines
• Extrahepatic obstruction may be due to tumours in:
- major branches of the biliary tract,
- head of pancreas.
• Gallstones may obstruct biliary flow.
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19. Cholestatic Jaundice
• Jaundice is due to impaired excretion and
accumulation of conjugated bilirubin which can be
filtered by the kidney and appear in urine.
• If obstruction is complete bilirubin does not reach
the gut, therefore urobilinogen:
- is not produced, and
- is absent in urine.
• Under such circumstances the stools are pale.
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20. SUMMARY IN LIVER FUNCTION TESTS IN THE
DIFFERENTIAL DIAGNOSIS OF JAUNDICE
Test Prehepatic Hepatic Cholestatic
Serum bilirubin Uncojugated Mixed Conjugated
Urine bilirubin Absent//Present Present Present
Urine Urobilinogen Increased Increased Decreased
ALT & AST Normal Marked Slight
increase increase
ALP Normal Slight Marked
increase increase
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21. NEONATAL JAUNDICE

22. Neonatal jaundice
• is usually harmless
• this condition is often seen in infants around the second day
after birth, lasting until day 8 in normal births, or to around
day 14 inpremature births.
• Typical causes for neonatal jaundice include normal
physiologic jaundice, jaundice due to formula
supplementation, and hemolytic disorders that
includehereditary spherocytosis, glucose-6-phosphate
dehydrogenase deficiency, pyruvate kinase deficiency, ABO/Rh
blood type auto antibodies, or infantile pyknocytosis.
• Serum bilirubin normally drops to a low level without any
intervention required.

23. Neonatal jaundice
• In cases where bilirubin rises higher, a brain-damaging
condition known as kernicterus can occur, leading to
significant disability.
• This condition has been rising in recent years due to less
time spent outdoors. A Bili light is often the tool used for
early treatment, which often consists of exposing the
baby to intensive phototherapy.
• Sunbathing is effective treatment, and has the
advantage of ultra-violet-B, which promotes Vitamin
D production. Bilirubin count is lowered through bowel
movements and urination, so frequent and effective
feedings are especially important

24. Hemolytic jaundice
• Congenital: Known also as hereditary
spherocytosis (HS), this is a genetic disorder of
the red blood cell membrane clinically
characterized by anemia, jaundice (yellowing)
and splenomegaly (enlargement of the
spleen).
• It is also condition which is characterized by
jaundice due to an increased production of
bilirubin from degradation of red blood cells.

25. The risk factors for developing
jaundice
• Certain individuals with hereditary conditions (for
example, thalassemia or hereditary spherocytosis)
jaundice from hemolysis.
• Individuals who consume alcohol heavily are at an
increased risk of developing alcoholic hepatitis,
pancreatitis, and cirrhosis leading to jaundice.
• exposure to the different types of viral hepatitis (for
example, hepatitis B and hepatitis C) are also at risk
of developing jaundice at the time of infection or
subsequently if liver disease occurs or if liver cancer
develops later.

26. What problems does jaundice cause?
1. Skin and sclerae - yellow
2. Stool - light colour, clay coloured
3. Dark urine
4. Pain in abdomen
5. Itching
6. Trouble with sleeping
7. Fatigue
8. Swelling
9. Ascites
10. Mental confusion
11. Coma
12. Bleeding

27. • History
• Physical examination
• Blood tests - laboratory
• Ultrasonography
• CT
• MRI
• Liver biopsy
• ERCP (endoscopic retrograde
cholangiopancreatography)
• Endoscopic ultrasound
Diagnosis

28. Laboratory Tests
• Bilirubin level in
serum (total and
direct)
• Aminotransferase
• Alkaline phosphatase
• U/A for bilirubin and
urobilogen
 Complete blood count
 Prothrombin time
 Other laboratory tests
pertinent to history
 Coombs test
 Electrophoresis of
hemoglobin
 Viral hepatitis panel

29. Treatment
• Treatment requires a precise diagnosis of the
specific cause and should be directed to the
specific problem

30. Treatment
• In certain individuals with jaundice, the treatment will consist
of supportive care and can be managed at home. For
example, most cases of mild viral hepatitis can be managed at
home with watchful waiting and close monitoring by your
doctor (expectant management).
• Alcohol cessation is necessary in patients with cirrhosis,
alcoholic hepatitis, or acute pancreatitis secondary to alcohol
use.
• Jaundice caused by drugs/medications/toxins requires
discontinuation of the offending agent. In cases of intentional
or unintentional acetaminophen (Tylenol) overdose, the
antidote N-acetylcysteine (Mucomyst) may be required.
• Various medications may be used to treat the conditions
leading to jaundice, such as steroids in the treatment of some
autoimmune disorders. Certain patients with cirrhosis, for
example, may require treatment with diuretics and lactulose.

31. Treatment
• Antibiotics may be required for infectious causes of
jaundice, or for the complications associated with certain
conditions leading to jaundice (for example, cholangitis).
• Blood transfusions may be required in individuals
with anemia from hemolysis or as a result of bleeding.
• Individuals with cancer leading to jaundice will require
consultation with an oncologist, and the treatment will vary
depending on the type and extent (staging) of the cancer.
• Surgery and various invasive procedures may be required
for certain patients with jaundice. For example, certain
patients with gallstones may require surgery. Other
individuals with liver failure/cirrhosis may require a liver
transplant

32. Treatment
• Antihistamines may be used for the
symptomatic treatment of pruritus,
particularly as a sedative at night. Their
effectiveness is modest. Endogenous opioids
have been suggested as possibly playing a role
in the development of pruritus of cholestasis.
Treatment with parentally administered
naloxone and, more recently, nalmefene, has
improved pruritus in some patients.

33. THE NEED FOR SURGICAL INTERVENTION DEPENDS ON
THE CAUSE OF BILIARY OBSTRUCTION.
• Cholecystectomy is the recommended treatment in
cases of symptomatic cholelithiasis because these
patients have an increased risk of developing
complications.Open cholecystectomy is relatively safe,
with a mortality rate of 0.1-0.5 %.
• Laparoscopic cholecystectomy remains the treatment
of choice for symptomatic gallstones, partially because
of the shorter recovery period (return to work in an
average of 7 d), decreased postoperative discomfort,
and improved cosmetic result.
• Approximately 5% of laparoscopic cases are converted
to an open procedure secondary to difficulty visualizing
the anatomy or a complication.

34. RESECTABILITY OF NEOPLASTIC CAUSES OF BILIARY
OBSTRUCTION
• Varies with respect to the location and extent of the
disease. Photodynamic therapy (PDT) has been shown
to have good results in the palliative treatment of
advanced biliary tract malignancies, particularly when
used in conjunction with a biliary stenting procedure.
• PDT produces localized tissue necrosis by applying a
photosensitizing agent, which preferentially
accumulates in the tumor tissue, and then exposing
the area to laser light, which activates the medication
and results in destruction of tumor cells.
• Liver transplantation may be considered in appropriate
patients.

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