Arterial health throughout cancer treatment and exercise rehabilitation in wo...
Evaluation of Jaundice by Dr. Sookun Rajeev Kumar
1. CANDIDATE INFORMATION AND TASKS
You are working in a medical outpatient clinic. Your next
patient is a single 25-year-old sales assistant who has
consulted you about general malaise, anorexia, nausea and
fever gradually worsening over the last 10 days. Yesterday he
noted dark urine and pale stools.
On examination you have found icteric conjunctivae, a
temperature of 38.8 °C and tender enlargement of the liver.
Urinalysis was positive for bilirubin and urobilinogen. There
are no other abnormal findings on examination.
2. CANDIDATE INFORMATION AND TASKS
YOUR TASKS ARE TO:
1. Take any further relevant history you require.
2. Tell the examiner what investigations you would
arrange.
3. Explain the nature of the illness and possible
cause to the patient, indicating which you
consider to be the most likely cause.
4. Advise the patient concerning immediate
management.
4. Definition:
• Jaundice is the Yellow colouration of the
skin, sclerae and mucous membrane
which is caused by the deposition of bile
pigment and usually apparent when the
serum bilirubin is more than 35 mmol/l
5. Classification of Jaundice
• Pre Hepatic Jaundice ( causes lemon-yellow skin
colouration) e.g Hemolytic Jaundice
• Hepatic Jaundice (causes deep yellow jaundice
progressing to a greenish tinge)
• Post Hepatic Jaundice
• The sclerae are not coloured in those with yellow skin
caused by hypercarotinaemia.
6. Common Causes of Jaundice
Viral hepatitis
Biliary obstruction from gallstones or carcinoma of the
head of the pancreas
Drugs (Alcohol,Acetaminophen,psy meds,diuretics,etc..
Metastases
Intrahepatic cholestasis (including ascending
cholangitis and primary biliary cirrhosis)
Infectious mononucleosis
Gilbert syndrome
7. Uncommon Causes of Jaundice (cont)
Haemolytic anaemia
Congenital hyperbilirubinaemia
Stricture or carcinoma of the major bile ducts or
ampulla
8. History
• Sudden Onset : Viral hepatitis,acute biliary obstruction,
trauma or toxin-mediated fulminant liver failure.
• Gradual onset : chronic liver disease (including alcoholic
cirrhosis) or malignancy.
• A lifelong history : suggests an inherited metabolic or
haemolytic cause.
9. History (cont)
• Hx of Right Upper Quadrant pain especially after
fatty meal, should suggest Cholestasis or
Cholelithiasis
• Hx of Fever or prior biliary surgery, points to
Cholangitis
• Hx of Anorexia, malaise, or myalgia, a viral etiology
is most probable
10. History (cont)
• Hx of Pruritus or weight loss associated with noninfectious
etiologies.
• Blood transfusion, IVD use, sexual contacts, travel to
endemic areas or ingestion of contaminated foods expose
patients to viral related Hepatocellular injury.
• PMHx,PSHx,FHx of inherited defect in bilirubin conjugation
or transport,wilson’s disease,hemochromatoses
12. Signs & Symptoms in Jaundice (cont)
Yellow coloration of the skin – should be
examined in natural white light
Steatorrhea – suggests no breakdown of fats
Pruritus - suggests chronic disease
Abdominal pain - suggests biliary tract
obstruction from stone or pancreatic tumour
(obstructive jaundice)
13. Signs & Symptoms in Jaundice (cont)
Clay coloured stool
Painless jaundice in the elderly - think of
pancreatic cancer, although most patients with
pancreatic cancer have pain
Kernicterus - rarely seen in adults due to
maturation of blood brain barrier
15. Signs & Symptoms in Jaundice (cont)
Spider Angioma
Caput medusa
Gynecomastia
Testicular Atrophy
Palmar Erythema
Dupuytren’s contracture
• All suggest
Chronic Liver
Disease and
Portal
Hypertension
16. Specific features on examination of the
abdomen in a jaundiced patient include
• Recent operation scars: suggesting
cholecystectomy or surgery for intra-
abdominal carcinoma
• Palpable Enlarged Gall Bladder suggesting bile
duct obstruction caused by carcinoma of the
pancreas (rather than gallstones)
17. Specific features on examination of the
abdomen in a jaundiced patient include (cont)
• Hepatomegaly: irregular
when infiltrated with
carcinoma or in early
cirrhosis, tender in
infectious and acute
alcoholic hepatitis and
occasionally in
congestive heart failure
18. Specific features on examination of the
abdomen in a jaundiced patient include (cont)
• Splenomegaly
in portal
hypertension,
spherocytosis
and infectious
mononucleosis
19. Specific features on examination of the
abdomen in a jaundiced patient include (cont)
• Ascites.
20. Aims for Investigations
1. Investigation aims to discover the site of any
biliary outflow obstruction
2. Determine the degree of impairment of liver cell
function and its cause
3. Eliminate rare causes such as haemolysis
4. Establish potential for treatment.
21. 1. Haematology
Full blood count, reticulocyte count and Coombs’
test
A normal reticulocyte count virtually excludes
haemolytic jaundice.
Leukocytosis may suggest infection or carcinoma.
Abnormal mononuclear cells suggest infectious
mononucleosis or viral hepatitis.
22. 2. Liver Function Tests
Measure the ability of the liver to perform normal functions (e.g.
serum albumin is a measure of protein synthesis; prothrombin
time is a measure of synthetic function; bilirubin is a measure of
bile salt conjugation and excretion).
Liver enzymes (alkaline phosphatase, transaminases) are
indicators of ductal or liver cell damage.
In obstructive jaundice the alkaline phosphatase is greatly
elevated compared with transaminases; in hepatocellular disease
transaminases are predominantly raised.
23. 3. Bilirubin
Bilirubin derived from red cell breakdown is transported to
the liver where it is conjugated to glucuronic acid.
Conjugated bilirubin is secreted in the bile and degraded
in the gut by bacteria to form urobilinogen. Urobilinogen is
either excreted in the stool or reabsorbed from the gut and
excreted by the kidneys.
Serum bilirubin is predominantly unconjugated in
haemolytic jaundice and the other liver function tests are
usually normal. It is mainly conjugated in obstructive
jaundice.
25. 4. Alkaline Phosphatase
Elevated in
Obstructive jaundice
Hepatocellular jaundice
Growth in adolescence
Pregnancy
Normal in
Gilbert syndrome
Myeloma
Alkaline phosphatase is found in high levels in biliary
Canaliculi, osteoblasts, intestinal mucosa and placenta.
26. 4. Alkaline Phosphatase (cont)
• A raised level in the absence of other signs of liver
disease or abnormal liver function tests suggests
the presence of malignant secondary deposits in
the bone or Paget’s disease. Consider measuring
isoenzymes if there is doubt.
27. 4. Alkaline Phosphatase (cont)
Causes of increased hepatic alkaline phosphatase
Extra-hepatic cholestasis
Obstructive jaundice
Intra-hepatic cholestasis (e.g. cirrhosis, drugs, cholangitis, primary biliary
cirrhosis)
Obstructive phase of hepatitis
Causes of increased bone alkaline phosphatase (osteoblastic activity)
Paget’s disease
Bone metastases
Osteomalacia
Hyperparathyroidism
Normal growth in puberty
Fractures
28. 5. Transaminases
Elevated serum transaminases (alanine
aminotransferase, aspartate aminotransferase and
gamma glutamyl transferase) indicate
hepatocellular damage. Slight elevation is
consistent with obstructive jaundice.
29. 5. Transaminases (cont)
Causes of elevated alanine aminotransferase
Active liver cell damage, including drugs, hepatitis and metastatic
infiltration
Acute myocardial infarction (peaks at 24–48 h, may fall to normal
by 72h). The degree of elevation reflects the amount of muscle
damage
Acute pancreatitis
Haemolysis
30. 5. Transaminases (cont)
Elevated aspartate aminotransferase levels parallel the alanine
aminotransferase
-glutamyl transferase
Inducible microsomal enzyme
Most sensitive index of alcohol ingestion
Raised in most forms of liver disease including acute and chronic
hepatitis, cirrhosis and following drugs that induce microsomal
enzymes
31. 6. Urinalysis
Conjugated bilirubin renders the urine dark yellow
Urobilinogen is colourless but on standing the urine turns brown
as urobilinogen is converted to urobilin by oxidation.
Haemolytic jaundice is acholuric (no bilirubin in the urine) but the
urine contains excess urobilinogen because excess bilirubin
reaches the intestine and is re-excreted as urobilinogen.
Obstructive jaundice produces dark brown urine with excess
bilirubin but a reduction of urinary urobilinogen (little or no
bilirubin reaches the gut because of the obstruction and
therefore cannot be reabsorbed and re-excreted).
32. 6. Urinalysis (cont)
In the early stages of acute viral hepatitis, excess
urobilinogen may sometimes be present before clinical
jaundice becomes apparent.
This is a result of failure of the liver to take up the excess
urobilinogen absorbed from the gut.
With increasing severity, biliary obstruction develops and
as conjugated bilirubin appears in the urine it disappears
from the gut and urobilinogen disappears from the urine.
The reciprocal effect also occurs during recovery.
33. 7. Serology
Viral hepatitis serology – hepatitis A–E,
cytomegalo- virus (CMV) and Epstein–Barr
virus (EBV)
Antimitochondrial antibodies (primary biliary
cirrhosis)
Antinuclear factor and smooth-muscle
antibodies (chronic active hepatitis)
35. 8. Abdominal Radiology in jaundice (cont)
Ultrasound, CT and MRI may show prImary or
secondary tumours, pancreatic carcinoma, stones
in the gall bladder and dilated biliary ducts in
obstruction.
Isotope liver scans may demonstrate secondary
deposits.
36. 9. Needle Liver Biopsy
Biliary obstruction is a relative contraindication
because of the potential danger of biliary peritonitis.
Ultrasound and CT-guided biopsy may provide the
histological diagnosis in focal lesions.
Check the prothrombin time and platelet counts are
normal. Fresh frozen plasma will quickly reverse the
prothrombin time for the duration of the procedure.
38. 10. Other investigations
Endoscopic retrograde
cholangiopancreatography (ERCP) is valuable
to define obstruction of the
pancreaticoduodenal tree, for sphincterotomy,
to release stones and to relieve obstruction by
insertion of a stent.
-fetoprotein is raised in hepatocellular
carcinoma.