Neonatal jaundice is a major complication for newborn

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