1. Neonatal Jaundice.
Valmiki Seecheran.
Year V MBBS.

2. Introduction.
• A bilirubin level of more than 5mg/dl
manifests clinical jaundice in neonates.
• Cranio-caudal progression.
• 50-60% of babies affected in the first week of
life.

3. Physiological
• Most infants develop visible jaundice due to elevation
of unconjugated bilirubin concentration during their
first week.
• Phase I.
– Term infants – lasts up to 10 days with rapid rise of serum
bilirubin up to (12mg/dL).
– Preterm infants – lasts up to two weeks with rapid rise of
serum bilirubin up to (15mg/Dl).
• Phase II – bilirubin levels decline to 2mg/Dl for 2
weeks.
– Preterm infants – phase II can last more than 1 month.
– Breastfed infants – phase I can last more than 1 month.

4. Causes.
• Low enzymatic activity of
glucruonosyltransferase. (converts
unconjugated to conjugated bilirubin).
• Shorter life span of fetal red blood cells.
(90days).
• Low conversion of bilirubin to urobilinogen by
intestinal flora.

5. Pathological.
• Clinical jaundice appearing in the 1st 24 hours
or greater than 14 days of life.
• Increases in the level of total bilirubin by more
than (0.5 mg/dL) per hour or 5 mg/dL per 24
hours.
• Total bilirubin more than (19.5 mg/dL)
• Direct bilirubin more than (2.0 mg/dL).

6. Pathological vs. Physiological.
• Presence of intrauterine growth restriction.
• Family history of jaundice and anemia.
(Neonatal or early infant death.)
• Maternal drugs (sulphanoamides, anti-
malarials).
• Stigma of intrauterine infections
– Cataracts, microcephaly, cephalohematomas.

7. Causes of jaundice.
• Breakdown of fetal hemoglobin.
• Immature hepatic metabolic pathways.
• In the event if neonatal jaundice is not
alleviated with phototherapy, biliary atresia,
progressive familial intrahepatic cholestasis
and other pediatric liver diseases should be
considered.

8. Causes of jaundice.
• Unconjugated bilirubin.
– Pathologic.
• Hemolytic. – G6PD, spherocytosis, sickle cell, sepsis,
ABO.
• Non-hemolytic. –Breast milk, UTI, Sepsis.
– Physiological
• Conjugated bilirubin.
– Hepatic. – Sepsis, Hep A & B, Alpha 1 antitrypsin
deficieny.
– Post-hepatic. – Bile duct obstruction.

9. Causes of jaundice.
• Breast milk jaundice is a biochemical
occurrence. Bilirubin levels peaks 6-14days of
life.
• Enzymes such as 3 alpha 20 beta pregnanediol
and lipoprotein lipase prevents conjugation
leading to higher levels of bilirubin in blood.

10. Clinical assessment.
• Ingram icterometer.
– 5 transverse strips of graded yellow lines.
– Pressed against the nose and the corresponding
yellow colour of the blanched skin is match and
level is assigned.
• Transcutaneous bilirubinometer.
– Pressure applied to photoprobe, generates light,
the intensity of the yellow colour in the light is
measured and displayed.

11. Treatment.
• Phototherapy
– Discovered in Essex, England by a nurse.
– Process of isomerization that changes trans-
bilirubin into water soluble bilirubin isomer.
– Blue light more effective at breaking down
bilirubin.
– Biliblanket.
• Exchange transfusions.
– Indicated for a total serum bilirubin >25mg/Dl.

12. Complications.
• Kernicterus – chronic bilirubin
encephalopathy.
– Neurotoxic.
– Gray matter of the brain.
– Brain damage/death.
• Fever/ Seizures.

13. Thank you.