This document discusses neonatal jaundice (hyperbilirubinemia) in infants. It covers the definition, causes, types (physiological vs pathological), investigations, management including phototherapy and exchange transfusion, and prevention of kernicterus. Key points include: - Jaundice is caused by high bilirubin levels which cause yellowing of the skin and eyes. Bilirubin is produced from the breakdown of red blood cells. - Physiological jaundice appears after 24-72 hours and is common, while pathological jaundice appears within 24 hours and requires treatment. - Management involves phototherapy to reduce bilirubin levels or exchange transfusion for severe

1. JaundiceNeonatal
(Hyperbilirubinemia)
P.Jeyanthi
M.Sc (N) II Year
OBG Department

2. What is the Neonatal Jaundice?
• Neonatal Jaundice(also called Newborn
jaundice) is a condition marked by high levels
of bilirubin in the blood.
The increased bilirubin
cause the infant's skin
and whites of the eyes
(sclera) to look yellow.

3. NJ - 3

4. Incidence
Term—60%
Preterm—80%
• Bilirubin Source –
Hb – 75%
Non Hb – 25% (Myoglobin)

5. Billirubin Metabolism

6. Special characteristic in neonates
1.More billirubin produced
• Much more Hemolysis
• The life-length of hemolysis(70~80)

8. 2.The low capability of albumin on
unconjugated billirubin transportation
• Acid intoxication
• Less albumin in neonates

10. 3.The low capability of heptatocyte
• Less Y protein and Z protein
• The primary development of Hepato-
enzyme system
• Easy-broken hepato-enzyme system
• After-born, the blood glucose level is very low.

12. 4.High workload of the hepato-enteric
circulation
• Less bacterial
• Low enzymatic activity in intestine
• High level of billirubin in
meconium

14. Causes

15. Causes of Jaundice –as per time of onset
Within 24 hrs
• HDN—Rh, ABO Incompatibility
• IU infections-CMV, HSV, Toxo, Syphilis
• RBC Enzyme deficiencies-G-6PD defi,
pyruvate kinase deficiency
• Drugs—large dose of vit k , syntocin drip,
Salicylates, sulphas etc
• Hereditary Spherocytosis
• Criggler-Najjar syndrome
• Alpha thalassemia

16. 24-72 hrs—Physiological Jaundice
Exaggerated Physiological Jaundice
(MATERNAL FACTORS)
• -Blood type ABO or Rh incompatibility
• -Breastfeeding
• -Drugs: Diazepam, Oxytocin
• -Maternal illness: gestational diabetes

17. Exaggerated Physiological
Jaundice
(neonatal factors)
• Birth trauma: cephalohematoma, cutaneous
bruising, instrumented delivery
• Drugs: Erythromycin, Chloramphenicol
• Immaturity ▪ Birth asphyxia
 Acidosis ▪ Cretinism
• Hypothermia
• Hypoglycemia
• Hypothyroidism
• Polycythemia

18. After 72 hrs (within 2 weeks)
• Septicemia
• Neonatal Hepatitis, other IU infections
• Extra hepatic Biliary atresia
• Breast milk jaundice
• Metabolic diseases—galactosaemia, CF,
alpha-1 antitrypsin deficiency, hypothyroidism
• Hypertrophic Pyloric stenosis

20. The general symptom of neonatal
jaundice
• Yellow skin
• Yellow eyes(sclera)
• Sleepiness
• Poor feeding in infants
• Brown urine
• Fever
• High-pitch cry
• Vomiting

21. A little exam
Increased rbc’sIncreased rbc’s
Shortened rbc lifespanShortened rbc lifespan
Immature hepatic
uptake & conjugation
Immature hepatic
uptake & conjugation
Increased enterohepatic
Circulation
Increased enterohepatic
Circulation

22. Brown urine

23. Types

24. Physiological jaundice
Characteristics
• Appears after 24-72 hours
• Seen both in term and preterm
• Develops after 24 hours
• Peaks by day 4- 5 in terms and day 7-8 in preterm
• Peak levels -12mg/dl in term & 15mg/dl in preterm
• Gradually subsides by 10-14 days
• No Treatment necessary
• Note: Baby should, however, be watched for worsening
jaundice.

25. Why does physiological jaundice
develop?
• Increased bilirubin load.
• Defective uptake from plasma.
• Defective conjugation.
• Decreased excretion.
• Increased entero-hepatic circulation.

26. Pathological jaundice
• Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Serum bilirubin > 15 mg / dl
• Jaundice persisting after 14 days
• Stool clay / white colored and urine staining
clothes yellow
• Direct bilirubin> 2 mg / dl

27. Breast feeding jaundice
• In exclusively breast feed infants
• Appears at 24-48 hrs of age
• Peaks by 5-15 days
• Disappears by 3rd
week
• Its related to inadequate B.F
• T/t:Proper & adequate B.F

28. Breast milk jaundice
• In 2-4 % EBF babies
• SBr>10mg/dl beyond 3rd
-4th
week
• Should be differentiated from Hemolytic
jaundice, hypothyroidism, G6PD def
• T/t: Some babies may require PT
Continue breast feeding
Usually declines over a period of time

29. Investigations

38. Investigations in RH incompatibility
• Antenatal - (mother Rh-ve, previous baby Rh
+ ve, father Rh +ve.
1) H/o of abortion, H/o having taken Anti D
gammaglobulin
2) USG for baby maturation ,HSM, ascites,
hydrominos, gen. anasraca

39. Investigations in RH incompatibility
• Antenatal -
- Blood grp (ABO & Rh) of father ,earlier baby
- Indirect Coomb’s test – to detect antibodies in
mother’s serum
IgG Anti body Titre to D TO be estimated at 12-16,28-
32 and 36 weeks. If anti D antibody Titre 1:16 it
should be tested serially
- Ab titre in mother’s blood ->1:64 dignostic of HDN-
TO CONSIDER TERMINATION OF PREGNANCY.

40. Investigations in RH incompatibility
• Anmiocentesis:
- Look for lecithin sphingomyelin ratio to suggest
maturity.
- Shake test for 15 sec. with equal vol etanol 95%-
allowed to stand-ring of buble at the disc
- Optical density-by spectrophotometer OD.>0.15
denotes maturity of lungs
- Alpha feto protein level increased –rh issoimun
- Fetal bloob grp prenatally – amniocentesis

41. POSTNATAL INVESTIGATION BABY
Cord blood—all babies of Rh-ve mothers, all Unknown
blood groups, all with prior h/o jaundice in earlier
babies
Blood group-both mother and baby
- For evidence of hemolysis –
Direct Coombs test
Reticulocyte count - >10 suggest hemolysis.
Hemoglobin cord
Peripheral smear -RBC morphology
Bilirubin

43. Therapeutic Management
• Purposes: reduce level of serum bilirubin and
prevent bilirubin toxicity
• Prevention of hyperbilirubinemia: early feeds,
adequate hydration
• Reduction of bilirubin levels: phototherapy,
exchange transfusion,
• Drugs Use of Phenobarbital promote liver
enzymes and protein synthesis.

44. MANAGEMENT
• Phototherapy
• Drugs
• Exchange transfusion

45. Mechanism To Decrease Bilirubin:
• -↑↑ excretion Phototherapy, ET
- ↑↑ conjugation phenobarbitone
- ↓ enterohepatic circ- Agar, Cholestyramine
- Inhibit Bili production— Metal
metalloporphyrins
- Inhibit haemolysis high dose IVIG
- Inc albumin binding—Albumin

48. Phototherapy
• Safe and effective method for treatment of
neonatal jaundice
• Bilirubin absorbs light maximum at 420-460
nm

49. Mechanism of Action
Conversion of insoluble Bilirubin into soluble
bilirubin
1.Photo-isomerization-conversion into soluble
form – takes place in extravascular space of skin –
conversion to less toxic polar isomer-diffuses into the
blood –excreted easily into bile
2.Structural isomerization - conv to lumirubin
-rapidly excreted in bile and urine
3. Photo-oxidation- of Bilirubin to water soluble
polymers colourless by product.

50. Indications
TSB > 15 mg % in
term
TSB > 12 mg% in
preterm
TSB > 5 mg%
within 24 hours
Adjuvant to
exchange
transfusion
Prophylactic PT –
ELBW, bruised
babies, hemolytic
disease,VLBW
with Perinatal
risk factors

54. Side Effects
• Immediate –
– Loose stools
– Dehydration,
– Hyperthermia,
– ‘Bronze baby’ syndrome,
– Rashes,
– Upsets maternal infant
interactions (bond)

55. • Late –
–Risk of skin malignancies
–Damage to intracellular
DNA
–Retinal damage
–Disturbance in circadian
rhythm
Testicular damage

56. Biliblanket or glow-worm ?
Home phototherapy

58. Definition
• Exchange blood transfusion -- changing
the babies blood with the other blood.
• Usually in hemolytic disease of newborn
it removes partially hemolysed and
antibody coated RBCs and also billirubin.

59. Methods of exchange
• Single volume exchange- 80ml/kg
• Double volume exchange- 160ml/kg
(87% of infant blood volume exchanged
with new blood)
• Triple volume exchange.

60. Blood for exchange transfusion
• Fresh CPD blood
• Rh HDN-
• ABO incompatibility -

61. Roots for exchange
• Umbilical vein cut down- incision
above umbilicus in midline.
• Femoral vein canulation with radial
artery canulation.

63. Investigations
• Pre exchange: Hb%, PCV, billirubin,
glucose K+, Ca+.
• Post exchange: Hb%, PCV, billirubin,
glucose, Calcium, K+, culture.

65. Procedure
• IN NICU OR OT
• Radiant warmer, Monitor HR, BP and other
vitals, infants arms and legs are restrained.
• Assistant to record volume in & out, to
check vitals.
• Blood pre warmed to 37 c
• Dried umbilical cord soaked with wet
gauze.
• Canulation of umbilical vein- 12 o’clock

66. • Catheter inserted till free flow of blood
or SHOULDER UMBILICAL LENGTH.
• Small aliquots of blood removed 5
to10ml -PUSH PULL method.
• Blood in the bag gently mixed.
• Procedure over 1 to 2 hr.
• Tie around the cord for 1 hr, or hold
tightly at the end of procedure.

67. Complications
• Hypocalcemia and Hypomagnesemia -
Citrate in CPD blood.
• Hypoglycemia
• Metabolic alkalosis or acidosis.
• Hyperkelemia.
• CVS: overload and arrythmias
• Infections: HBV HIV
• Hemolysis
• Hypothermia, NEC.

68. Breast milk jaundice
Management
• Stop breast feeding -48 hrs
• Again resume it, bilirubin may rise again but
not reach previous high level

69. Breast feeding jaundice
• Decreased intake of milk leads to increased
enterohepatic circulation
• Higher levels on day 4 compared to
formula fed babies due decreased
intake of milk

71. Kernicterus
• Kernicterus is damage to the brain centers of
infants caused by increased levels of
unconjugated-indirect bilirubin which is free (not
bound to albumin).
• Acidosis affects
bilirubin solubility
• Hyperosmolarity,
anoxia and
Hypercarbia
disrupt BBB

72. • Yellow staining of brain assc with
neuronal injury
• Affects basal ganglia, cranial nerve
nuclei, brain stem nuclei, hippocampus
and AHC of spinal cord (cortex usually
spared)
• Necrosis, neuronal loss and gliosis …
pathological findings

73. TREATMENT
• Phototherapy
• Exchange transfusion
• Albumin infusion
• Anticonvulsants: phenobarbitone
• BERA at follow up

74. Prevention
1. Anti D to be given to the mother after delivery of
the baby-within 48hrs. Also can be given to all
unsensitized mothers at 28-32 weeks of
gestation
2. Amniocentesis and IU transfusion to severely
affected babies
3. Preterm delivery of severely affected babies
4. Cord blood studies-followed by Phototherapy
5. Exchange transfusion

75. Nursing considerations of Hyperbilirubinemia
• Assessment:
 observing for evidence of
jaundice at regular intervals.
 Jaundice is common in
the first week of life and
may be missed in dark skinned
babies
Provide appropriate follow-up based on the time
of discharge
Blanching the tip
of the nose

77. Journal
• Original articles
• Glucose-6-phosphate dehydrogenase
deficiency: a new ætiological factor of severe
neonatal jaundice
•
In vitro and in vivo efficacy of new blue light emitti