the yellow baby

1. Name: Ghaida alrashed
The yellow baby
Presented by:
Ghiada Al-Rashed

2. Case summary
•Three day old baby
•Was yellow ( jaundice)
•Not drinking very well
•Was difficult to wake up
•When touched, he groans softly
•labour and birth were without problems
•Fist child of the both parents
•Birth weight: 3450 grams
•Gestation week : 39

3. Learning objectives
•Physiological- pathological mechanisms.
•The most probable causes for the patient.
•How to reach to the probable diagnosis by the history taking
questions ?

4. Neonatal Jaundice (Hyperbilirubinemia)
 Neonatal jaundice is the term used when a newborn has an
excessive amount of bilirubin in the blood characterized by
jaundice.
 Jaundice is the visible manifestation of increased level of
bilirubin in the body.
 Is a yellowish pigmentation of the skin, the conjunctival
membranes over the sclera.
 Jaundice not a disease rather a symptom of diseases.

5. Bilirubin
 Bilirubin is a product of hemoglobin break-down.
 Hemoglobin is contained in the red blood cells.
 Normal TSB level in a newborn would be under 5 mg/dL.
• TSB level usually rises in term infants to a peak level of 12
mg/dL by 3 days of age.
• In preterm infants, the peak level occurs on the 5th day of age
and TSB can rise over 15 mg/dL
 Bilirubin can cross the BBB Lead to permanent, Damage
irreversible, which is why high SBR is so dangerous

6. Normal Bilirubin Metabolism

7. Objectives:
Predisposing Causes of Neonatal
Jaundice :

8. Causes of Neonatal Jaundice:
Physiologic
Jaundice
Pathological
Jaundice

9. # Physiologic Jaundice:
 DUE TO elevation of unconjugated bilirubin
concentration.
 OCCURS IN the first few days after birth.
 CLEARED BY day 10.
 It is the consequences of 2 factor:
Related to : immature liver enzymes
Related to : when fetus breath the oxygen

10. Physiologic Jaundice mechanism
Newborn baby has a
hemoglobin (HB) level
of
18-19g/dl.
(necessary during fetal
life to facilitate oxygen
carrying capacity)
When baby is BORN
and able to breath
oxygen
High HB level is not
needed THEN starts
to drop.
In the first week of life the baby’s HB will drop to
about 11g/dl  Breakdown of the fetal RBC’s 
cause bilirubin to exceed the plasma.
Physiological
JAUNDICE
What is the mechanism of dropping HB???

11. Physiologic Jaundice mechanism
 Glucuronosyl-transferase enzyme (UDP-GT)  percent in the liver
and normally converts unconjugated bilirubin to conjugated bilirubin
Before birth this enzyme is actively down-regulated
 bilirubin needs to remain unconjugated
in the fetus in order to cross the placenta =
to avoid being accumulated in the fetus
BECAUSE
After birth it takes some time for this enzyme to gain
function.
( This time the fetus will increase unconjugated
bilirubin in circulation  lead to : jaundice )

12. #Pathological Jaundice:
 It is significant in the first 24hrs of life.
 It may persist more than 2 weeks
 Refers to : jaundice that arises from factors that alter the
usual process in bilirubin metabolism in the liver.
Pathological
Jaundice
hemolytic
Intrinsic Extrinsic
Non-
hemolytic

13. Hemolytic cause
Intrinsic :
 Membrane condition of RBC.
 spherocytosis
 Enzyme condition :
 G6PD deficiency
 Globin synthesis defect :
 Sickle cell disease
 Thalassemia
Extrinsic :
 RH hemolytic incompatibility.
 ABO incompatibility
Unconjugated
bilirubin
hemolytic
Intrinsic Extrinsic
Non-
hemolytic

14. Hemolytic cause
Intrinsic :
 Membrane condition of RBC.
 spherocytosis
 Enzyme condition :
 G6PD deficiency
 Globin synthesis defect :
 Sickle cell disease
 Thalassemia
Extrinsic :
 RH hemolytic incompatibility.
 ABO incompatibility
• Hereditary familial disease .
• Morphologic hallmark is the
microspherocyte of RBC.
( sphere- shaped rather than bi-
concave shape)
Unconjugated
bilirubin
hemolytic
Intrinsic Extrinsic
Non-
hemolytic

15. Hemolytic cause
Intrinsic :
 Membrane condition of RBC.
 spherocytosis
 Enzyme condition :
 G6PD deficiency
 Globin synthesis defect :
 Sickle cell disease
 Thalassemia
Extrinsic :
 RH hemolytic incompatibility.
 ABO incompatibility
• Hereditary abnormality in the
activity of an erythrocyte.
• This enzyme is essential for
assuring a normal life span for
red blood cells.
Unconjugated
bilirubin
hemolytic
Intrinsic Extrinsic
Non-
hemolytic

16. Hemolytic cause
Intrinsic :
 Membrane condition of RBC.
 spherocytosis
 Enzyme condition :
 G6PD deficiency
 Globin synthesis defect :
 Sickle cell disease
 Thalassemia
Extrinsic :
 RH incompatibility.
 ABO incompatibility
Rh incompatibility  (Rh may
occur if mother is Rh Negative and
fetus is Rh positive….
ABO incompatibility ABO may
occur if mother blood group is O and
fetus blood group is either A or B)
Unconjugated
bilirubin
hemolytic
Intrinsic Extrinsic
Non-
hemolytic

17. Non- Hemolytic cause
 Breastfeeding failure jaundice.
 Breast milk jaundice.
 Polycythemia
• Caused by insufficient breast milk
intake.
• Because of difficulty in feeding or
if the mother does not have an
adequate milk supply
• leading to dehydration or low
caloric intake.
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

18. Non- Hemolytic cause
 Breastfeeding failure jaundice.
 Breast milk jaundice.
 Polycythemia
• Mother Breast milk may contain
inhibitor of bilirubin conjugated
• Interruption of breastfeeding for
1-2 day result in rapid decline in
bilirubin level
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

19. Non- Hemolytic cause
 Breastfeeding failure jaundice.
 Breast milk jaundice.
 Polycythemia
• An excessively high hematocrit >
65%
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

20. Non- Hemolytic cause
 Sepsis
 Gilbert’s syndrome.
 Crigler- najjar syndrome
• Caused by: mutation of promoter
rigon of Glucu-ronosyl-
transferase enzyme .
• hepatic enzyme dysfunction
• Lead to mild hyperbilirubinmia
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

21. Non- Hemolytic cause
 Sepsis
 Gilbert’s syndrome.
 Crigler- najjar syndrome
• Serious, rare disease.
• Autosomal receive .
• Permanent deficiency and
absent of Glucu-ronosyl-
transferase enzyme
• Lead to saver hyperbilirubinmia.
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

22. Non- Hemolytic cause
 Sepsis
 Gilbert’s syndrome.
 Crigler- najjar syndrome
• Lead to kernicterus ( bilirubin
encephalopathy):
• Deposition of indirect bilirubin
in brain cells especially in basal
ganglia.
• Jaundice , lethargy, poor feeding,
high pitched cry, hypotonia and
sizures
Unconjugated
bilirubin
hemolytic
Non-
hemolytic

23. Differences:
Physiologic Jaundice: Pathological jaundice:
 Appear after 24 hours (on the
2nd/3rd day(
 Maximum intensity between the
3RD and 4TH days.
 Serum bilirubin <12 mg/ dl.
 Duration 8-14 days of life
( not detected after 14 day)
 No treatment is require.
 Appear within 24 hours.
 Serum bilirubin is rising at a
rate > 0.5 mg/dL/24 hr.
 Serum bilirubin > 13 mg/ dl.
 Jaundice persists after 14
days of life.
 Treatment is require.

24. Objectives:
Causes of neonatal jaundice by age..

25. Causes of neonatal jaundice by age
After 72 hours24-72 hours<24 hours of age
Neonatal hepatitisHemolytic disease
• G6PD deficiency.
• spherocytosis.
• Pyruvate kinase
deficiency .
Hemolytic disease
• Rh incompatibility.
• ABO incompatibility.
SepsisInfections
• Congenital infection (TORCH)
• Sepsis
Breast feeding
jaundice
PolycythemiaG6PD deficiency
Breast feeding
jaundicePathological jaundice Physiological Jaundice:
OR
Pathological jaundice
Physiological Jaundice:
OR
Pathological jaundice

26. Com..
 If the jaundice Prolonged ( >1 week):
Pathological
• Breast milk jaundice
• Gilbert syndrome
• Crigler- najjar syndrome
• Biliary tract obstruction

27. The most probable causes for our
..patient

28. The most probable causes
for our patient
•Three day old baby
•Was yellow ( jaundice)
•Not drinking very well
•Was difficult to wake up
•When touched, he groans softly

29. Three day old baby .
after72 hours24-72 hours<24 hours of age
Neonatal hepatitisHemolytic disease
• G6PD deficiency.
• spherocytosis.
• Pyruvate kinase
deficiency .
Hemolytic disease
• Rh incompatibility.
• ABO incompatibility.
SepsisInfections
• Congenital infection (TORCH)
• Sepsis
Breast feeding
jaundice
PolycythemiaG6PD deficiency
Breast feeding
jaundicePathological jaundice Pathological jaundice
OR
Pathological jaundice
Pathological jaundice
OR
Pathological jaundice

30. We could suspect the diagnosis by the time
BUT we couldn’t confirm it
 HAVE to do
#additional investigation to the baby+
#Take Postnatal history / Perinatal History
#Family History ( if suspect hereditary disease).
#know the duration ( if prolonged or no !)

31. :
•How to reach to the probable diagnosis by the history
taking questions ?

32. History Taking
Postnatal
history
Perinatal
History
Family
History

33. Postnatal history
In which day the jaundice is presents and for how long
?
Because it will be pathological if it starts from 1st day ( within 24 hours )
of life or if it is starts from 2nd or 3rd but it is continue for more than 1- 2
weeks .
Feeding: breast milk or formula?
Because there is a type of jaundice related to problem in breast milk
itself.

34. - Is jaundice relieved after interruption of breastfeeding
for about 2 days ?
Because if there is reliving of jaundice it is indicate breast milk jaundice.
How adequate your breastfeeding for your baby ?-
Because there is type of jaundice occur when babies do not nurse well
or the mother's milk is slow to come in.
What is the current weight compared to birth weight ?
To know the progress of growth

35. Infections or fever?
Because High fever indicates infections
Urine and stool production ?
Because if there is decreased feeding which represents by decrease
urination maybe it will be ( breastfeeding jaundice).
what is the color of stool & Urine?
Because if the bilirubin excreted in stools for newborn in high amount
lead white colored stool and/or dark urine.
Associated symptoms?
lethargy, hypotonia, poor feeding

36. Family History
Previous sibling with jaundice in the neonatal period ?
(particularly if the jaundice required treatment)
Presence of ( Anemia, liver disease or bile stones ) in
family members or known heredity for hemolytic
disorders?
( because all of that previous conditions can lead to
accumulation of bilirubin in circulating blood )

37. Perinatal History
Maternal infections ?
(TORCH infection ? Sepsis ? )
Maternal illness ? ( maternal diabetes )
Maternal blood group? (ABO incompatibility, Rh Disease, other )
Maternal medicine or drug intake?
Delayed cord clamping ?

38. Summary
• Jaundice < 24 hrs is always pathologic
• lethargy and poor feeding, hypotonia may indicate
kernicterus
• A detailed history is an essential part to reach the
probable diagnosis

39. References
 https://www.nlm.nih.gov/medlineplus/ency/article/001
559.htm
 http://www.health.vic.gov.au/neonatalhandbook/cond
itions/jaundice-in-neonates.htm
 http://emedicine.medscape.com/article/178841-
overview#a2