A case based approach to Jaundice

27
Jaundice Dr Manoj K Ghoda MD, MRCP Consultant Gastroenterologist Visiting Faculty at GCS Hospital

Transcript of A case based approach to Jaundice

Page 1: A case based approach to Jaundice

Jaundice

Dr Manoj K Ghoda MD, MRCP

Consultant GastroenterologistVisiting Faculty at GCS Hospital

Page 2: A case based approach to Jaundice

18 yrs old femaleConsulted as family noticed her to be yellow.

Fitness fanaticCautious about food

Had no symptoms whatsoever

On examination:She appeared yellow

Physical examination : Normal

S. Bil: 0.8 ( 0.4+0.4)ALT/SGPT: 21 i.u.ALP: 121 i.u.

Page 3: A case based approach to Jaundice

Why does this young lady have yellow discolouration when her bilirubin level is normal?

This young girl was fitness fanatic and diet conscious.Drank lots of carrot juiceDeveloped hypercarotinemia and hence appeared yellow

So.. “All that glitters is not Gold”All yellowness is not jaundice.

Do you know any other compound causing yellow discoloration?

At about 2-3 mg one can appreciate jaundice; in sclera, conjunctiva and mucus membrane

Page 4: A case based approach to Jaundice

Examination of sclera

Sun light is always preferable

Page 5: A case based approach to Jaundice

18 yrs old male

TirednessPallorRecurrent mouth ulcers

On examination:Pallor ++Abdomen was unremarkable, no liver and no spleen

Hb: 5.4MCV: 125MCH: 35.2P.S.: Megalo-ovaloblastic anemia

S. Bil: 3.1 (Conjugated 0.8, unconjugated 2.5)ALT/SGPT: 26 I.U.ALP: 123 I.U.PT: 13/13 sec

Why this young man with megaloblastic anemia is having jaundice?

Page 6: A case based approach to Jaundice

18 yrs old male

Persistent jaundice from birthPallorTiredness

On Examination:Spleen ++

CBC:Hb7.0MCV :75P.S. Uniformly small RBCs without central pallorRetics: 6%

LFT:S. Bil: 3.2 (70% unconjugated)ALT: 18ALP: 100

Why this young man with (hereditary) spherocytosis is having jaundice?

Page 7: A case based approach to Jaundice

18 yrs F

Intermittent jaundice when catches routine illnesses

No complaints

On Examination:Mild icterusLiver and spleen not palpable

CBC: Normal , retics 1.5%

LFTs:S.Bil: 3.5 ( Conjugated 0.2; unconjugated 3.3)ALT: 21 I.U.ALP: 135 I.U.

Why this young lady having jaundice and no anemia?

Page 8: A case based approach to Jaundice

Analysis of all three patients:

• All three have unconjugated hyperbilirubinemia• One has megaloblastic anemia• One has hemolysis ; and • The third has neither of these

So, now we know that unconjugated hyperbilirubinemia is one cause of

jaundice. But what is common between spherocytosis and megaloblastic anemia?The third patient doesn’t have even anemia, but he still has same pattern of jaundice; why?

What could have caused rise in unconjugated bilirubin levels in these three apparently unrelated patients ? What exactly is the underlying mechanism?

To understand this we have to look at bilirubin metabolism

Page 9: A case based approach to Jaundice

Bilirubin Metabolism

Bilirubin Metabolism

Excess production

X

+ Albumin

1

2

1= Heme oxygenase2= Biliverdine reductase

UDP-GTFailure of conversion

Page 10: A case based approach to Jaundice

This is the only reaction in entire body that produces CO

It is easy to break things which are not tightly organized.

Let us look at breakdown of hemoglobin bit more closely

Remember! Biliverdin is GREEN

Page 11: A case based approach to Jaundice

Green jaundice: an unusual case revisited(Gåfvels M, Holmström P, Somell A et al. A novel mutation in thebiliverdin reductase-A gene combined with liver cirrhosis results inhyperbiliverdinaemia [green jaundice].Liver Int 2009; 29:1116–24)

Deficiency of Heme oxygenase would result in hemolysis without unconjugated hyperbilirubinemia

Let me see ..if you brain is working

X

X

Page 12: A case based approach to Jaundice

How to differentiate excessive production from failure of conversion

Excess production•Clinical context

•Low Hb•High retics•High LDH•Hemoglobunuria•Splenomegaly

•Other clinical features of anemia

Failure of conversion•Clinical context

•Hb Normal•Retics normal•LDH normal•No hemoglobinuria•No splenomegaly

•No other features of anemia•May be other features of hyperbilirubinemia

Features of hemolysis

Page 13: A case based approach to Jaundice

Summary:

One reason of jaundice is unconjugated hyperbilirubinemia.

This could be because of

excessive production; or

Failure of conjugation

Therefore when you see unconjugated hyperbilirubinemia it is mandatory that you differentiate between the two.

Hemolytic anemias, Gilbert’s syndrome, Criggler Najjar syndrome, low albumin

Page 14: A case based approach to Jaundice

18 yrs old female

H/o fever 3 daysNauseaVomitingAversion to foodYellowish discolorationEpigastric painYellow urine

O/E: Tenderness in RUQ, mild hepatomegaly

CBC: NormalLFTs:

S. Bil: 5.5 (Direct 70%, indirect 30%)ALT: 1500 i.u.ALP: 135 i.u.

Why this young lady feeling so unwell and has jaundice?

Page 15: A case based approach to Jaundice

48 yrs old female

H/O sudden onset of right upper quadrant pain radiating to the tip of scapulaFever with severe chillsYellowish discoloration

O/E: Tenderness in RUQ

CBC: High WCC, 35,000

LFTs: S. Bil: 5.5 (70% direct, 30% indirect)ALT: 135 i.u.ALP: 1500 i.u.

USG: Dilated CBD with an acoustic shadowing at the lower end.

Why this patient has so much pain and fever with chills with jaundice?

Page 16: A case based approach to Jaundice

Analysis of these two cases:• Both have conjugated hyperbilirubinemia

• The first pt has no pain but is very symptomatic with anorexia, nausea, vomiting and her ALT is elevated

• The second pt had severe pain and fever with dramatic chills with discomfort on touching RUQ

So now we know that Second cause of jaundice is Rise in conjugate bilirubin levels

This could be because of

Hepatocellular damage, or

Obstruction to bile flow

Page 17: A case based approach to Jaundice

Let us see how conjugated bilirubin is formed and disposed off

Page 18: A case based approach to Jaundice

Bilirubin Metabolism

Bilirubin Metabolism

xx

Hepatocellular jaundice

Obstructive jaundice

Conjugated hyperbilirubinemia

Page 19: A case based approach to Jaundice

Conjugated hyperbilirubinemia: Differentiating hepatocellular from obstruction

Hepatocellular damage is detected by high ALT/AST/GGT. USG may show altered echo pattern of liver parenchyma

Obstruction to outflow is detected b high ALP/GGT. USG may show dilatation of Biliary tree

Note: GGT sits on the fence.

With High ALT/AST it suggests hepatocellular damage;

And with high ALP it suggests obstructive jaundice

Page 20: A case based approach to Jaundice

Summary

Any case of jaundice will qualify for label of conjugated hyperbilirubinemia if conjugated bilirubin is above 2 mg.

Usually it constitutes 70% of total bilirubin

Hepatocellular

•Clinical context

•High ALT/AST/GGT•Altered PT which may not be corrected by vitamin K

•USG may show altered parenchymal echo pattern

Obstructive

•Clinical context

•High GGT/ALP•Altered PT easily corrected by vitamin K

•USG may show dilated biliary tree and many times the cause also

Page 21: A case based approach to Jaundice

This was easy. Wasn’t it ?

Let us try some more cases.....

Page 22: A case based approach to Jaundice

18 yrs old female

H/o fever 3 daysYellowish discolorationEpigastric painYellow urine

O/E: Hepatomegaly ++

CBC:

Hb: 5.4MCV: 82 flMCH: 28.2P.S.: suggestive of hemolysisRetics: 5% ( up to 2)

LFTs: S. Bil: 5.5 (Direct 550%, indirect 45%)ALT: 500 i.u.ALP: 135 i.u.

Practically only two conditions are able to produce combined hyperbilirubinemia;

Wilson’s diseaseAutoimmune hepatitis

Page 23: A case based approach to Jaundice

18 yrs old female

H/o fever with rigors for 3 daysHeadacheYellowish discoloration

O/E: mild splenomegaly

CBC: Normal, P.S showed falciparum malaria, retics: normalLFTs:

S. Bil: 5.5 (Direct 70%, indirect 30%)ALT: 15 i.u.ALP: 135 i.u.

Why this young lady is having jaundice when everything else we have discussed so far is normal?

Page 24: A case based approach to Jaundice

TNF-alpha, IL-1,6

X

Transport of conjugated bilirubin from hepatocytes to bile canaliculi

This is cholestasis of inflammationThis is seen in any condition where cytokines are released

Page 25: A case based approach to Jaundice

Jaundice

Viral HepatitisDrug inducedAlcoholicAutoimmuneWilson’s

StoneTumorStricture

HemoglobinopathiesMalaria, Drug inducedAutoimmuneWilson’s

Megaloblastic anemia

PrematurityGilbert’sCriggler Najjar

Page 26: A case based approach to Jaundice

Any questions?

Dr Manoj K Ghoda M.D., M.R.C.P.

Consultant GastroenterologistVisiting faculty at GCS Hospital

Page 27: A case based approach to Jaundice