Clinical Approach To Neonatal Jaundice: Dr. Siddeeg Addow Pediatric Resident Khartoum, Sudan
Clinical Approach To Neonatal Jaundice: Dr. Siddeeg Addow Pediatric Resident Khartoum, Sudan
Clinical Approach To Neonatal Jaundice: Dr. Siddeeg Addow Pediatric Resident Khartoum, Sudan
Neonatal Jaundice
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. CONJUGATED B.
Tightly Non toxic
compounded to s.
albumin Water soluble
Normally very small Loosely bound to
amount is present albumin. Delta
as albumin free fraction
Insoluble in water
can not be excreted
in urine
Toxic
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
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
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: