APPROACH TO A PATIENT WITH JAUNDICE
WHAT IS JAUNDICE
• Yellowish discoloration of sclera, skin, mucous membranes due to deposition of bile
pigment
• Jaundice (icterus) is detectable clinically when the serum bilirubin is greater than 50
μmol/L (3 mg/dL).
DIFFERENTIAL ON YELLOWING OF SKIN
CAROTENODERMA
Seen in tha patient with excessive intake of fruits and vegetables rich in carotene (carrots, squash,
peaches, oranges).
DRUGS (QUINACREINE) : in it sclera is also involved like in jaundice.
Bilirubin metabolism
Cause for hyperbilirubinemia
1. overproduction of bilirubin
2. impaired uptake, conjugation, or excretion of bilirubin
3. regurgitation of unconjugated or conjugated bilirubin from damaged hepatocytes
or bile ducts.
HISTORY
The onset of Jaundice in viral hepatitis is associated with a prodrome of nausea and vomiting,
malaise & myalgia.
The onset of cholestasis is insidious, it is associated with pruritus.
A history of fever with rigors, Rt upper abd. pain or a past history of biliary surgery suggest
cholangitis.
Dark urine & pale stool suggest the obstructive feature.
A history of multiple sex partners, travel, ethanol intake, drugs, bl. transfusion, needle stick
exposure & tattooing is also important.
contd...
Previous biliary surgery with subsequent jaundice may suggest stricture, residual
stones or hepatitis.
A family history of jaundice or liver disease suggests the possibility of hereditary
hyperbilirubinaemia or genetic disorder such as Wilson disease.
Features of types of jaundice
Hemolytic jaundice:
Stool is high colored( due to excess stercobillinogen and stercobillin)
Acholuric urine
Mild jaundice (lemon yellow tinge)
ANEMIA
Splenomegaly
Obstructive jaundice
Deep yellow urine ( due to presence of conjugated bilirubin)
Stool--- pale or clay colored
Greenish yellow tinge in bulbar conjunctiva
Generalized pruritus
Xanthelasma (hypercholesterolemia)
Gall bladder may be palpable
Rarely hepatosplenomegaly
Hepatocellular jaundice
Urine- yellowish
Stool – high colored
Orange yellow tinge of bulbar conjunctiva
Anorexia, nausea, vomiting , fever
Tender hepatomegaly
Examination
Patient nutritional status----- e.g temporal and proximal muscle wasting: pancreatic
ca./cirrhosis
Enlargement of left supraclavicular LN OR Periumbilical nodes suggest abdominal
malignancy.
Stigmata of CLD ------- jaundicde is hepatocellular in origin.
High fever, right upper abdominal tenderness------cholangitis & choledocholithiasis.
A systemic illness should be excluded e.g. distended jugular veins in constrictive
pericarditis or Rt. Heart Failure in patient with hepatomegaly & ascites.
Hard nodular liver--------Primary or Secondary malignancy.
Diffuse lymphadenopathy-----infectious mononucleosis or lymphoma.
Rt. upper abd. scar or palpable gallbladder------Obstructive Jaundice
Certain physical findings may suggest a particular liver disease:
Hyperpigmentation--------haemochromatosis.
Xanthoma-------PBC
Kayser-Fleischer rings --------Wilson disease.
The clinical assessment & basic biochemical parameters lead
to three broad subgroups of patients:
1. Isolated elevation of s. bilirubin: when AST, ALT & ALP levels are normal.
2. Hepatocellular jaundice: when the AST & ALT levels are elevated out of
proportion to the ALP levels.
3. Cholestatic jaundice: when the ALP level is elevated out of proportion to the
AST & ALT levels.
Isolated elevation of serum Bilirubin
Unconjugated Hyperbilirubinaemia
Increase bilirubin production (e.g. haemolysis)
Decrease hepatocellular uptake (e.g. rifampicin)
Decrease conjugation (Gilbert Syndrome, Criggler Najjar Syndrome)
Conjugated Hyperbilirubinemia
Dubin-Johnson syndrome
Rotor syndrome
Hepatocellular Jaundice
Acute or subacute hepatocellular injury
Viral hepatitis, alcohol, drugs, ischemic hepatitis, Wilson's disease
Chronic hepatocellular disease
Viral hepatitis, alcoholic, autoimmune hepatitis, Wilson’s, haemochromatosis, NASH,
alpha 1 antitrypsin deficiency.
Hepatic disorders with prominent cholestasis
Diffuse infiltrative disorders (e.g. granulomatous disease, TB, sarcoidosis, lymphoma,
drugs) Amyloidosis, malignancy.
Inflammation of intrahepatic bile ductules (PBC), Drugs (chloropromazine)
Miscellaneous e.g. use of oestrogen & steroids, TPN, bacterial Infection.
Obstruction of The bile duct
Benign----------Choledocholithiasis, pancreatitis
Malignant----carcinoma gallbladder, periampullary carcinoma, cholangiocarcinoma,
Ca head of pancreas
Investigations
Serum Biochemical Tests:
Bilirubin:
The normal serum bilirubin is <1.5mg/dl of which <0.5% is conjugated.
In haemolysis or genetic disorders e.g. Gilbert syndrome there is
unconjugated hyperbilirubinaemia (>90%).
In hepatocellular jaundice >50% of bilirubin is conjugated.
In obstructive jaundice the circulating bilirubin is mainly conjugated.
Enzymes raised in hepatocellular injury:
Aminotransferases include ALT (located in cytosol) & AST (located in mitochondria & cytosol).
ALT is found mainly in liver while AST is also found in other tissues such as skeletal & cardiac muscle.
ALT is more specific than AST in detecting liver disease.
AST & ALT are released following hepatocyte necrosis.
A marked raise in transaminases > 1000 U/L, is seen in Autoimmune viral hepatitis, ischaemic
hepatitis & drug-induced liver disease.
In alcoholic liver disease, the enzyme levels are rarely raised > 200-300 U/L, with AST:ALT ratio
>2:1.
Enzymes raised in cholestasis:
Alkaline Phosphatase (ALP), gamma-glutamyl transpeptidase (GGT) & 5’-
nucleotidase (5’NT).
ALP isoenzymes are also present in bone & placenta.
Increase in ALP, GGT & 5’NT suggest hepatobiliary origin.
GGT levels are often disproportionately elevated in alcoholic liver disease.
Albumin:
Albumin is synthesized by liver & has a half-life of 15-20 days.
Decreased level of albumin are seen in advanced hepatic cirrhosis &
signify severe hepatic dysfunction.
Serum albumin usually remain normal in acute hepatitis; falling values in
this setting imply an unusual sever course.
Globulins:
Non-specific diffuse elevation is common in CLD.
There is a disproportionate elevation of IgG in autoimmune hepatitis, IgM in Primary
biliary cholangitis & IgA in alcoholic liver disease.
INR & Prothrombin time (PT):
INR/PT is a valuable index of the ability of liver to synthesize vit. K-
dependent clotting factors.
An increasing PT/INR implies relatively severe hepatocellular dysfunction.
The PT/INR may be deranged in cholestasis as well, but this is due to the
malabsorption of vit. K & is rapidly corrected by parenteral administration of
vit K.
Other tests:
Antimitochondrial antibody (AMA) for PBC
Antinuclear factor (ANA), anti-smooth muscle antibody (ASMA) & anti-
liver kidney microsome (LKM) antibody seen in autoimmune hepatitis
alpha-fetoprotien which is raised in HCC
serum caeruloplasmin for Wilson disease
Imaging Procedures
Radiological imaging is important for the diagnosis of a focal liver mass
or biliary disease. However, imaging plays little role in the evaluation of
diffuse hepatocellular e.g. hepatitis
Ultrasonography (US)
It is a valuable but operator-dependent investigation.
It has sensitivity of 55-91% & specificity of 82-95% for biliary obstruction.
Although US may not detect stones in the extrahepatic bile duct, which
may be obscured by overlying gas, it reliably establishes the presence of
a dilated bile ducts
Besides it can differentiate intrahepatic from extrahepatic cholestasis, US
can also detect the associated abnormalities such as portal hypertension,
focal lesions & fatty liver.
ERCP
ERCP not only permits direct visualization of the biliary tree but also
allows therapeutic intervention e.g. removal of CBD stones or biliary
stenting.
It is the gold standard test for the evaluation of extrahepatic biliary
disease causing jaundice.
PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY
IN PTC, direct contrast visualization of the biliary tree is obtained via a percutaneous
needle puncture of the liver. It is useful if there is high biliary obstruction e.g. a
tumour at the bifurcation of the hepatic ducts.
It also permits therapeutic intervention such as stent insertion to bypass a ductal
malignancy.
MRCP
MRCP is superior to US & CT in detecting biliary obstruction. It has a sensitivity of 82-100% &
a specificity of 92-98% to detect biliary obstruction.
CT Scan
CT has a sensitivity of 63-96% & a specificity of 93-100% to detect biliary
obstruction.
Non-calcified cholestrol gall stones can be easily missed on CT because they may
be isodense with bile.
LIVER BIOPSY
It has relatively low risk, it is needed in only a minority of cases with
hepatic dysfunction.
Major indications include
• chronic hepatitis
• cirrhosis
• unexplained liver enzyme abnormalities
• hepatosplenomegaly of unknown aetiology
• suspected infiltrative disorder
• suspected granulomatous disease.
Relative contraindications include a tendency for clinical bleeding,
• INR>1.5 or PT >3 sec above the control,
• severe thrombocytopenia &
• marked ascites.
Thank you…….
