Transcript Clinical Approach to Neonatal Jaundice

Clinical Approach to
Neonatal Jaundice
Dr. Siddeeg Addow
Pediatric Resident
Khartoum, Sudan
CONTENTS:
INTRODUCTION
PATHOPHYSIOLOGY
DIFFERENTIAL DIAGNOSIS
HISTORY
EXAMINATION
INVESTIGATION
INTRODUCTION
Bilirubin is the end product of heme
degradation
Most of the daily production comes from the
breakdown of RBCs in the RES
Heme
biliverdin
bilirubin
Bilirubin is released & bound to serum
albumin
Bilirubin is uptake & conjugated with
glucuronic acid
Finally conjugated bilirubin is excreted in bile
PATHOPHYSIOLOGY
UNCONJUGATED B.
Tightly compounded
to s. albumin
Normally very small
amount is present as
albumin free
Insoluble in water
can not be excreted
in urine
Toxic
CONJUGATED B.
Non toxic
Water soluble
Loosely bound to
albumin. Delta fraction
Both conjugated & unconjugated bilirubin
may accumulate systemically & deposit in
tissues
Normally s. bilirubin level vary b/w 0.3 &
1.2mg/dl.
The rate of systemic bilirubin production
is = to the rate of hepatic uptake,
conjugation & biliray excretion .
Jaundice becomes evident when the
s.bilirubin levels rise above 2.0 to
2.5mg/dl
Levels as high as 30 to 40mg/dl can occur
with sever disease
Jaundice occurs when the = b/w bilirubin
production &clearance is disturbed by one
or more of the following mechanisms:
1. Excessive production of bilirubin
2. Reduced hepatic uptake
3. Impaired conjugation
4. Decreased hepatocellular excretion
5. Impaired bile flow
CAUSES OF JAUNDICE
PRDOMINATLY INDIRECT HYPERBILIRUBINEMIA
 Excessive production of bilirubin
hemolytic anemia's
resorption of blood from internal hemor.
ineffective erythropoiesis
 Reduced hepatic uptake:
drugs
some cases of Gilbert syndrome
Impaired bilirubin conjugation:
physiologic jaundice
breast milk jaundice
genetic deficiency of glcuronosyl transferase
decreased expression of glcuronosyl
transferase
diffuse hepatocellular diseases
PREDOMINATLY DIRECT HYPERBILIRUBINEMIA
Decrease excretion of conjugated
bilirubin:
deficiency in canalicular membrane
transport
drug induced canalicular membrane
dysfunction
hepatocelluler damage or toxicity
Decreased intrahepatic bile
flow :
inflammatory destruction of
intrahepatic bile ducts
Extra hepatic biliary obstruction:
gall stone obstruction of biliary tree
extra hepatic biliary atresia
biliary stricture & choledochal cyst
primary sclerosing cholangitis
liver fluke infestation
carcinoma
HISTORY
 onset / duration
 pain
 nausea & vomiting
 loss of weight
 itching
 color of stool
 color of urine
 past history
 ttt &family history
EXAMINATION
 color of skin
 severity of jaundice
 anemia
 liver
 spleen
 gall bladder
 ascites
INVESIGATION
 CBC
 LFT
 Prothrombin time
 Alfa feto proteins
 UG
 SG
 U/S
 ERCP & PTC
 Liver biopsy
The End