Neonatal Jaundice Pediatrics Phototherapy

1. APPROACH TO A CHILD
WITH JAUNDICE
APPROACH TO A CHILD
WITH JAUNDICE
S.BALASANKAR
S.BALASANKAR
2009 MBBS
2009 MBBS

2. JAUNDICE
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

3. 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)

4. 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
&

6. Hyperbilirubinemia
-Direct( Conjugated)
-Indirect( Un-conjugated)
Conjugated Hyperbilirubinemia is present,
* >20% of total bilirubin is conjugated
* >2mg/dl is conjugated
If neither criteria is met, hyperbilirubinemia is
classified as Un-conjugated.

7. NEONATAL JAUNDICE

9. Jaundice after 1 week:
a) Prolonged direct Jaundice
› Neonatal hepatitis (common)
› Extra-hepatic biliary atresia
› Breast milk jaundice
› Metabolic disorders
› Intra-hepatic biliary atresia
› Amino acid toxicity
› Inspissated bile syndrome (uncommon)

10. b) Prolonged Indirect Jaundice
> Criggler Najjar Syndrome
> Breast milk jaundice
> Hypothyroidism
> Pyloric stenosis
> Ongoing hemolysis, malaria

11. CLINICAL CLASSIFICATION:
PHYSIOLOGICAL JAUNDICE
PATHOLOGICAL JAUNDICE

12. PHYSIOLOGICAL JAUNDICE:
•
In new born babies bilirubin
metabolism is immature which results in the
occurrence of hyperbilirubinemia in the first
few days of life. Also there is increased
bilirubin load on the hepatic cell due to
physiological polycythemia.

13. Immaturity could be at various steps of
bilirubin metabolism like:
 Defective uptake from plasma into liver
cell( deficiency of LIGANDIN)
 Defective conjugation( UDP-glucoronosyl
transferase: <1% of adult activity during
the first 10 days of life)
 Decreased excretion
 Increased entero-hepatic circulation

14. Increased Bilirubin production:
Larger circulating red blood cell volume
Shortened RBC lifespan (70-90 days vs 120
days in adult)
Substantial production from other sources

15. Characteristics:
 First appears between
hours of age
 Maximum intensity seen on 4-5th day in
term and 7th day in preterm neonates
 Does not exceed 15 mg/dl
 Clinically undetectable after 14 days.
 No treatment is required but baby should be
observed closely for signs of worsening
jaundice.

16. PATHOLOGICAL JAUNDICE
Presence of any of the following signs
denotes that the jaundice is pathological.
 Clinical jaundice detected before 24 hours
of age
 Rise in serum total bilirubin by more than 5
mg/dl/ day (>5mg/dl on first day , 10 mg/dl
on second day and 12- 13 mg/dl thereafter
in term babies)

17.  Serum bilirubin more than 15 mg/dl
 Clinical jaundice persisting beyond 14 days
of life
 Clay/white colored stool and/or dark urine
staining the nappy yellow
 Direct bilirubin >2 mg/dl at any time.
Treatment is required in the
form of phototherapy or exchange blood
transfusion. One should investigate to find the
cause of pathological jaundice.

18. It can be
Overproduction Hyperbilirubinemia
Under-secretion Hyperbilirubinemia

19. Overproduction Hyperbilirubinemia:
Blood group incompatibilities
Maternal-fetal or feto-fetal transfusions
Non Immune Hemolytic anemias
Structurally Abnormal Red cells
Extra-vascular Hemolysis

20. Blood Group Incompatibilities:
Rh negative mother & Rh positive infant
ABO incompatibilities
Strongly considered if there is jaundice in
the first 24 hours of life

21. Non-Immune Hemolytic Anemias:
1. G6PD Deficiency:
Deficiency-decreased NADPHdecreased reduced Glutathione –
decreased protection of RBCs from
oxidants-hemolysis.
2. Excess of Vitamin K given IM

22. Structurally Abnormal RBCs:
Spherocytosis
Pyknocytes ( irregular borders)

23. Under-secretion Hyperbilirubinemia:
Enzymatic Deficiency( Glucoronyl
transferase)
Hormonal suppression (Breast milk
jaundice)
Inhibition of conjugation
Hepatic cell injury due to Infections
Substrate deficiency (hypoglycemia)
Mechanical obstruction (biliary atresia)

24. Hormonal Suppression:
Pregnandiol present in maternal breast milk
suppresses bilirubin conjugation.
Breast feeding may be stopped and
restarted in a period of 48hours.

26. Thyroxine Deficiency:
Thyroxine increases the activity of
Glucoronyl transferase which promotes
conjugation of bilirubin.

27. Inhibition of Conjugation:
Sulfonamides and Vitamin K results in
competitive conjugation inhibition of bilirubin.
GALACTOSEMIA:
Absent or deficient Galactose 1phosphoate uridyl transferase which is
needed in glucoronidaton of indirect bilirubin.

28. APPROACH

29. HISTORY
Maternal and Perinatal History:
Delivery at period of gestation, Postnatal
age in hours.
Maternal illness during pregnancy which
also includes diabetes; drug use.
Previous history of malaria.
Traumatic delivery, delayed cord
clamping, oxytocin use.
Birth asphyxia, delayed feeding, delay in
meconium passage.

30. Family history of jaundice, liver disease
Previous sibling with jaundice for blood
group incompatibility.
Kernicterus: Lethargy, poor feeding, and
hypotonia. Some advanced signs are
seizures, retrocollis, paralysis of upward
gaze and shrill cry.
Breast feeding.

31. ON EXAMINATION:
Baby lethargic, poor feeding, temperature
instability, with apnea: Sepsis
Small for gestation: polycythemia
Cataract, rash: TORCH infections
Extra vascular bleed: Cephalhematoma
Pallor: hemolysis, blood loss

32. Petechiae: sepsis, TORCH infections.
Hepatosplenomegaly: Rh-isoimmunization,
sepsis, TORCH infections.
Dysmorphic features, congenital heart
disease (pulmonary stenosis), Intra-hepatic
biliary atresia :Alagille syndrome

33. HOW DO YOU LOOK FOR
ICTERUS?
1. Dermal staining :progresses from head to
toe
Examined in good day light skin of
forehead, chest, abdomen, thigh, legs,
palms, and soles.
Blanched with digital pressure and the
underlying color of the skin and
subcutaneous tissue should be noted.

36. Clinical Jaundice
Measure Bilirubin
> 12 mg/dl and infant <
24 hr old
< 12 mg/dl and infant > 24
hr old
Fraction of Bilirubin
Follow bilirubin level
Indirect
Direct

37. Direct bilirubin
Evaluate for treatable causes
1.Infections-blood, urine culture, VDRL.
2.Metabolic disorders-urine reducing substances, serum
amino acids,T4,TSH.
If no abnormality ;screen for Identifiable causes
*α-1 antitrypsin deficiency
*cystic fibrosis
*congenital viral infections
If no abnormality; evaluate for anatomical abnormalities
*Stool color
*USG
*Hepato-biliary scintigraphy
*Liver biopsy

38. Indirect
Hematocrit
High(>65%)
Polycythemia
Low/Normal
Reticulocyte count
Blood Type
Coomb’s test
Platelets
Evaluate smear

39. Normal Reticulocyte
count
Look for evidence of,
*Infections-blood, urine culture
*Enclosed hemorrhage
*Congestive cardiac failure
*Hypoxia
*Hypothyroidism
*Drugs/toxins
None found
Familial Disorders
*Criggler Najjar
*Gilbert
Elevated Reticulocyte Count
Consider:
1.Iso-immunization
2.Erythrocyte membrane
defect
3.Erythrocyte enzyme defect

40. MANAGEMENT

41. 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.

42. PATHOLOGICAL JAUNDICE
Mainly 2 modalities of Treatment:
PHOTOTHERAPY
EXCHANGE TRANSFUSION

43. PHOTOTHERAPY
Mainstay of treatment
Under blue-green light(460490nm), insoluble bilirubin is converted into
soluble isomers that can be excreted in
urine & feces.
To be effective, bilirubin must be present in
skin; hence nor role for prophylactic
phototherapy

45. Term & near term neonates:
The American Academy of Pediatrics (AAP)
has laid down criteria for managing babies
with elevated serum bilirubin based on
gestational age and other risk factors(
hemolysis , asphyxia, low albumin level,
hypothermia)

47. MECHANISMS:
CONFIGURATIONAL ISOMERIZATION
STRUCTURAL ISOMERIZATION
PHOTO OXIDATION

48. Configurational Isomerization
Z-isomer converted to E-isomer
Reaction is instantaneous but reversible.
After exposure of 8-12 hrs, this constitutes
about 25% of the TSB which is non-toxic.
Excreted slowly from the body; hence not a
major mechanism for decrease in TSB.

49. Structural Isomerization
Irreversible reaction
Bilirubin is converted into Lumirubin.
This product forms 2-6% of TSB which is
rapidly excreted from body thus is mainly
responsible for phototherapy induced
decline in TSB.

50. Photo oxidation
Minor reaction

51. Administering Phototherapy:
Optimum ambient room temperature( 2528celcius) to prevent hypothermia.
Remove all clothes of baby except diaper
Cover baby’s eyes with an eye patch(to
prevent retinal degeneration) ensuring that it
does not block the baby’s nostrils.
Place the baby under the lights in a cot if
weight is more than 2kg or in an incubator if
baby is small(<2kg)

52. Keep the distance between the baby & the
light 30-45cm.
Ensure optimum breastfeeding as
intermittent feeding sessions.
Monitor temperature of the baby every 24hrs
Measure TSB every 12-24hrs.
Discontinue, once 2 TSB values 12hr apart
fall below current age-specific cut-offs.
Monitor for rebound bilirubin rise within
24hrs.

53. Complications of Phototherapy:
Loose stools
Erythematous macular rash
Purpuric rash associated with transient
porphyrinemia
Over-heating
Dehydration
Bronze baby syndrome

54. Bronze Baby Syndrome
Intense grey-brown discoloration
of the skin, serum, and urine,
especially in premature infants;
when phototherapy was used to
reduce hyperbilirubinemia. Preexisting hepatic disease is
suspected as a cause of the
jaundice and may have
prevented the biliary excretion of
the photo oxidation products of
bilirubin; their retention resulted
in the bronze discoloration.

55. EXCHANGE TRANSFUSION
Double Volume Exchange Transfusion
(DVET) : 160-180ml/kg; is to be performed if
TSB levels reach age-specific cut-offs or if
the infant shows signs of bilirubin
encephalopathy, irrespective of TSB levels.
If baby shows signs of cardiac
decompensation at birth, partial exchange
transfusion with 50ml/kg of packed red cells
should be done to quickly restore oxygen
carrying capacity of blood.
Umbilical venous route.

57. FOLLOWUP
Babies with serum bilirubin>20 mg/dl &
those who required ET should be kept under
follow-up in high-risk clinic for neurodevelopmental outcome.
Hearing assessment should be done at
3months of age.

58. PREVENTION
Ante-natal screening to detect Rh isoimmunization & prompt administration of
Anti D after first obstetric event.
Ensure adequate breast feeding.
Educate parent about danger signs to
ensure immediate checkup.
Follow-up high risk babies( large cephalohematoma, family history of jaundice) for 2-3
days of discharge.

59. JAUNDICE IN THE CHILD &
ADOLESCENT
HISTORY:
Age at onset of symptoms. E.g.: Wilson’s
disease commonly manifests in preadolescents & adolescents.
Past/present use of any drugs
H/o of blood transfusion/ dialysis
Exposure to viral hepatitis
Any h/o of chronic illness;
hemoglobinopathies.

60. DDs of Un-conjugated
Hyperbilirubinemia:
Auto-immune hemolytic anemias
Drug induced hemolytic anemias
Erythrocyte membrane defects
Erythrocyte enzyme defects
Hemoglobinopathies
Congestive cardiac failure
Sepsis
Gilbert syndrome.

61. DDs of Conjugated
Hyperbilirubinemia:
1.




2.





Obstructive
Gall stones
Primary sclerosing cholangitis
Choledochal cyst
Tumors
Infections
Hepatitis A, B, C, D, E
EBV,CMV
Varicella zoster
HIV
Leptospirosis

62. THANK YOU