resourceful!

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
2

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
8
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
9
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
11
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
19

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
21

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
22

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
24

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
25

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
26

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
27

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
28

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
29

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
30

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
31

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
32

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
33

34. Clinical progression of encephalopathy
34

35. Thank you!
35