This document provides an overview of neonatal jaundice, including its definitions, clinical classification, clinical assessment, and principles of management. It discusses the definitions of jaundice and physiologic versus pathologic jaundice. Pathologic jaundice can be caused by increased production, decreased clearance, or increased enterohepatic circulation of bilirubin. The clinical assessment of jaundice involves examining the progression of color change. Workup includes history, physical exam, total serum bilirubin with conjugated fraction, and additional tests depending on suspected causes. Management aims to lower bilirubin levels and involves phototherapy, exchange transfusion, or addressing underlying factors. Kernicterus results from deposition of bil

1. 1
Approach to the diagnosis of
Neonatal jaundice
By
Gelaye
M
andefro
Am
bo
University
Departm
ent of
M
edicine
August 2015

2. outline
 Definitions
 Clinical classification
 Clinical Assessment
 Principles of management
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3. Definition and Basic concept
Jaundice is the visible manifestation of increased level of
bilirubin in the body
 It is not a disease rather a symptom of diseases
In adults sclera appears jaundiced when serum bilirubin
exceeds 2 mg/dl
However it is difficult to see sclera in newborn due to
difficulty in opening eye
 But in new born it is very easy to see jaundice in skin.

4. Definition and Basic concept…
Burden:
 Important problem in the 1st
week of life
 Almost all neonates (60% Term and 80% Preterm) will have bilirubin >
5 mg/dl in the 1st
week of life and become visibly jaundiced, vast
majority being benign
 Some of the term babies (8 to 9%) have levels exceeding 15 mg/dl in 1st
7 days of life
 High bilirubin level is toxic to the developing CNS(KERNICTERUS;
Bilirubin≥25mg/dl)

5. Definition and Basic concept…
Bilirubin:
End product of hemoglobin metabolism that is excreted in bile
In neonates
-75% : from catabolism of circulating RBCs
-25% :*from ineffective erythropoiesis (bone marrow)
*from turnover of heme proteins & free heme(liver).

6. Normal Bilirubin Metabolism
 Hemoglobin----Bilivervdin-----Bilirubin---Uptake in the liver---
Conjugation----Excretion
 Unconjugated bilirubin bind albumin
 Unconjugated and un bound bilirubin cross blood brain barrier
 Conjugated bilirubin (direct bilirubin) is non toxic to the brain and
not cross blood brain barrier
 Conjugated bilirubin is excreted via bile ducts to the gut and pass
through feces
 Conjugated bilirubin damages liver if not excreted

7. Neonatal jaundice

8. Clinical classification
1. Physiologic Jaundice
Jaundice becomes evident as physiologic in neonates B/c :
 Short life span of RBCs(70-90days)
 RBC mass is increased
 Immature ligandine
 Less UDPGT
 High activity β-glucuronidase (gut)
 Decreased flora in the gut
common neonatal problems
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07/30/16

9. Preterm Term
Peaktime 4th
-7th
days 2nd
– 4th
day
Peaklevel 8 – 12 mg/dl 5 -6 mg/dl
Resolution time Before 10th
day 5th
– 7th
day
common neonatal problems
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Clinical classification…
Physiologic jaundice ( Icterus
neonatorum)
07/30/16

10. Clinical classification…
2. Pathologic jaundice
Jaundice detected on the first day of life
Jaundice persisting more than two weeks
Jaundice rising at a rate more than 0.5mg/dl/hr
Direct bilirubin more than 2mg/dl
Underlying systemic illness

11. Clinical classification…
Physiologic Vs pathologic
Signs PhysiologicJx Pathologic Jx
Clinical Jx Visible in 2-3day With in 24hrs
TSB rise <5mg/dl/day >5mg/dl/day
TSB Term<12mg/dl
Preterm<15mg/dl
Term>12g/dl
Preterm>15mg/dl
Conj BBn <1.5mg/dl >1.5(2)mg/dl
Jaundice
persisting
Term <1 week
Preterm <2weeks
Term >1week
Preterm >2weeks
common neonatal problems
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07/30/16

12. Causes of pathologic jaundice
Increased production
 Hemolytic diseases (ABO and RH)
 Enclosed hemorrhage
 Polycythemia
Decreased clearance
 Sepsis
 Prinatal asphyxia
 Prematurity
 Hypothyroidism
 Crigler-Najjar syndrome

13. Causes of pathologic jaundice
Increased enterohepatic circulation
Breast milk jaundice
Gastro intestinal obstruction
Breast feeding jaundice
Obstructive lesions (Direct Bilirubin)
Choledochal cyst
Biliary atresia
Sepsis and congenital infections

14. Causes of pathologic jaundice…
Blood Group Incompatibilities
Rh negative mother & Rh positive infant
ABO incompatibilities
Strongly considered if there is jaundice in the first 24 hours of life
Non-Immune Hemolytic Anemias:
 G6PD Deficiency:
Deficiency-decreased NADPH- decreased reduced Glutathione –
decreased protection of RBCs from oxidants-hemolysis

15. Causes of pathologic jaundice…
Structurally Abnormal RBCs:
 Spherocytosis
 Pyknocytes ( irregular borders)
Thyroxine Deficiency:
 Thyroxine increases the activity of Glucoronyl transferase which promotes
conjugation of bilirubin.
Inhibition of Conjugation:
 Sulfonamides and Vitamin K results in competitive conjugation inhibition of bilirubin.
 GALACTOSEMIA:
 Absent or deficient Galactose 1-phosphoate uridyl transferase which is needed in
glucoronidaton of indirect bilirubin.

17. RH hemolytic disease
 RH negative woman conceiving RH positive fetus
 IgG crosses the placenta and results in fetal red blood cell hemolysis
 Anemia, jaundice, heart failure and generalized edema (hydrops fetalis)
develop in utero
 Affected new borns are delivered prematurely and may be still birth
 Moderately affected new borns may show anemia, hepatosplenomegaly and
signs of congestive heart failure
 Early exchange transfusion is life saving
 Unsensitized woman should take anti –D every delivery of RH positive
neonate

18. Jaundice Risk Factors for Neonatal
Hyperbilirubinemia
 Jaundice visible on the 1st day of life
 A sibling with neonatal jaundice or anemia
 Unrecognized hemolysis (ABO, Rh, other blood group, incompatibility); UDP-
glucuronyl transferase deficiency (Crigler-Najjar, Gilbert disease)
 Non-optimal feeding (formula or breast-feeding)
 Deficiency of glucose-6-phosphate dehydrogenase
 Infection (viral, bacterial). Infant of diabetic mother. Immaturity (prematurity)
 Cephalohematoma or bruising. Central hematocrit >65% (polycythemia)
 East Asian, Mediterranean, Native American heritage

19. Clinical assessment of jaundice
Jaundice in the newborn progresses in cephalocaudal
direction
 Face =5-7mg/dl
Chest =10mg/dl
lower abdomen /thigh= 12mg/dl
Sole/palms≥15mg/dl
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21. Work up neonates with Jx
History
 Age of onset
 Family history of Jaundice,pallor,splenectomy
 Previous sibling with Jaundice
 Maternal illness during pregnancy
 Maternal drug intake
 Delivery history e.g. PROM ,sepsis, prolonged labor
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22. Cont’d
P/E
Proper classification of the newborn according to GA, & wgt.
Pallor, petechea
Bruises and cephalhematoma
Dark urine and clay colored stool
Examination geared to specific cause
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23. Schematic approach to the diagnosis of neonatal jaundice

24. Investigations
 TSB with conjugated fraction
 Hct with RBC morphology and reticulocyte count
 Bg of the baby with direct coomb’s test
 Bg of the mother with indirect coomb’s test.
 Specific investigations for suspected specific problems
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25. Management
 Aim
 lower serum billirubin
 decrease neurtoxicity
 Principles of treatment
 Avoid drugs w/c interfere with BBn metabolism
 Treat factors w/c↑ neurotoxicity
 Give adequate feeding
 Specific therapy
 Decrease serum billirubin
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26. Management…
Physiological jaundice
 Explain about benign nature of the disease
 Encourage to breastfeed frequently & exclusively
 Ask Mother to bring baby back if baby looks deep yellow or palms &
soles have yellow staining.
Pathological jaundice
Mainly 2 modalities of treatment:
Phototherapy
Exchange transfusion
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27. Management…
Lower serum Billirubin
 Phototherapy
 Exchange transfusion
1. Phototherapy
 Mainstay of treatment
 Under blue-green light(460-490nm), insoluble bilirubin is converted
into soluble isomers that can be excreted in urine & feces.
 Indicated when TSB rises more than normal but not exchange
transfusion level
 May be therapeutic or prophylactic
 To be effective, bilirubin must be present in skin; hence nor role for
prophylactic phototherapy
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28. Prophylactic phototherapy
INDICATIONS
RH isoimmunization with sever hemolysis
Birth weight<1000gm(EVLBW)
Sever multiple bruises
SIDE EFFECTS
Erythematous skin rash
Retinal damage
Increased insensible water loss
Bronze baby syndrome
Loose stool
Low calcium
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29. Exchange transfusion( ET)
Most effective way of treating Jaundice and
anemia
Could be partial or double exchange
transfusion
INDICATIONS
Rh isoimmunization with hydrops fetalis
Cord blood Billirubin >5mg/dl
Rise in Billirubin >0.5mg/dl/hr despite
phototherapy
Hemoglobin <11gm/dl
TSB >20mg/dl
VLBW, preterm, sepsis
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30. Choice of blood forexchange BT
 ABO incompatibility
 Use O blood of same Rh type
 Rh isoimmunization
 Emergency 0 -ve blood
 Ideal 0 -ve suspended in AB plasma
 or baby's blood group but Rh –ve
 Other situations
 Baby's blood group
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31. Exchange transfusion
COMPLICATIONS
 Portal vein thrombosis
 Umbilical vein perforation/bleeding
 Necrotizing enterocolitis
 Cardiac arrest/arrhythmia
 Hypoglycemia, hypocalcemia, hypomagnisemia,
hyperkalemia
 Increased risk of infection
 Respiratory and metabolic acidosis
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32. KERNICTERS (Billirubin encephalopathy)
 Definition: neurologic syndrome resulting from
deposition of unconjugated billirubin in brain cells .
 Sites of billirubin staining and necrosis include
-Basal ganglia , Hippocampal cortex, Sub thalamic
nucleus & cerebellum
 Cerebral cortex is spared
 Half of the neonates with kernicters at autopsy have
extra neuronal lesions
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33. Pathophysiologic mechanism
 Unconjugated BBn is nonpolar ,lipid soluble and can
traverse BBB.
 Factors that ↑billirubin toxicity
 Hypoxia (asphyxia)
 Hypothermia & hypoglycemia
 sepsis
 Prematurity
 Acidosis
 Hypoalbuminemia
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34. Clinical progression of encephalopathy
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35. Thank you!
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