This presentation on neonatal jaundice focuses on the meaning, causes, types and nutritional guidelines.

1. ~ Arwa H Ujjainwala
M.S. Foods, Nutrition and
Dietetics
NEONATAL JAUNDICE
And Kernicterus

2. INTRODUCTION
• Neonatal Jaundice is a yellow discoloration of the
skin cause by too much bilirubin in the blood
(hyperbilirubinemia).
• At least 60% of full-term and 80% of pre-term infants
will become visibly jaundiced with their serum
bilirubin levels exceeding 5-7 mg/dL.
• In most cases it is benign and no intervention is
required.
• Approximately 5-10% of them have clinically
significant hyperbilirubinemia mandating the use of
phototherapy.
• If hyperbilirubinemia does not resolve and becomes
sufficiently severe, the elevated bilirubin levels can
cause permanent neurological damage.
It is visible in
the new-born
skin if:
Serum bilirubin
> 5 mg/dl

3. BILIRUBIN METABOLISM
• Higher levels of hemoglobin are necessary in utero to carry the
oxygen delivered to the fetus by the placenta, therefore, the normal
full-term infant has a hematocrit of 50-60%.
• As soon as the infant is born and begins to breathe room air, the need
for high levels of haemoglobin is gone, and excess erythrocytes are
destroyed.
• The released hemoglobin is broken down, and bilirubin, which is an
insoluble by-product of hemoglobin breakdown is released into the
circulation.(bilirubin is bound or albumin or other transport proteins)
• The insoluble form of bilirubin is removed from the circulation by the
liver which conjugates the bilirubin to a water soluble form and
excretes it via the bile through the stools.

4. GH

5. Before birth, the maternal
liver is responsible for
metabolism and clearance
of fetal bilirubin. After
birth, unique developmental
factors that control the
production, conjugation and
excretion of bilirubin pre-
dispose the neonate to
hyperbilirubinemia:
Bilirubin
production
in neonate is
double that
of an adult
Uptake of
insoluble
bilirubin by
the liver is
limited.
Conjugation
to a water-
soluble form
is limited
Excretion of
bilirubin is
delayed.

7. PHYSIOLOGIC JAUNDICE
 Neonates tend to produce more bilirubin then they can eliminate. Pre-
maturity magnifies this balance.
 Retention of unconjugated bilirubin by the new-born is known as
normal new-born jaundice or physiologic jaundice of the new born.
 Excessive bilirubin is deposited in the various tissues including the skin,
muscles and mucous membranes of the body causing the skin to take on a
yellowish colour.
 In healthy new-borns this condition is temporary and usually resolves
within a few days without treatment. Bilirubin levels rise steadily in the
1st 3-4 days of life and peak around the 5th day of life and then
decline.(pre-term peaks later day 6-7 and takes longer to resolve).
 Bilirubin levels in physiologic jaundice are usually less than 10-14 mg in
infants.

8. PATHOLOGIC JAUNDICE
 Pathologic jaundice begins earlier(sometimes it is observed before 24 hours o0f age),
rises faster, and lasts longer.
 A TSB greater than 8 mg/dl in the first 24 hours should be investigated for pathologic
origin.

9. Causes of pathologic jaundice include:
• Hemolytic disease
• Erythrocyte disorders
• Extravasation of blood
• Inborn errors of metabolism/conjugation of defects
• Hypothyroidism
• Polycythemia
• Macrosomic infant of diabetic mother
• Intestinal obstruction; delayed passage of meconium
• Sepsis

10. • Colostrum and mature human milk stimulates bowel
movements, which speeds elimination of bilirubin.
• * If Galactosemia is the cause for the jaundice,
breastfeeding in such a case is contra-indicated.
In most cases, frequent
breastfeeding can continue during
diagnosis and treatment of
pathologic jaundice.*

11. DIAGNOSIS
• The presence of jaundice can be determined by
examining the infant in a well-lit room and blanching
the skin with digital pressure to reveal the color of the
skin and subcutaneous tissue. Neonatal dermal icterus is
not noticeable at total serum bilirubin levels below 4 mg
per dL (68 μmol per L)
• Increasing total serum bilirubin levels are accompanied
by the cephalocaudal progression of dermal icterus,
predictably from the face to the trunk and extremities,
and finally to the palms and soles
• The total serum bilirubin level can be estimated
clinically by the degree of caudal extension: face, 5 mg
per dL; upper chest, 10 mg per dL (171 μmol per L);
abdomen, 12 mg per dL; palms and soles, greater than
15 mg per dL.

12. The physical examination should focus on
identifying one of the known causes of
pathologic jaundice. The infant should be
assessed for pallor, petechiae, extravasated
blood, excessive bruising, hepatosplenomegaly,
weight loss, and evidence of dehydration.

13. JAUNDICE AND BREASTFEEDING

14. EARLY-ONSET BREAST FEEDING
JAUNDICE
• “Breast-nonfeeding Jaundice”
• Results from reduced volume of milk transfer to
the infant, limiting caloric intake and resulting in
partial starvation.
• Early discharge of infants from the hospital in less
than 72 hours of life has raised concerns about the
ability to evaluate breastfeeding and the
opportunity to evaluate infants for jaundice.
• The AAP strongly recommends that all breastfed
infants be evaluated by a trained observer .

16. LATE-ONSET BREAST FEEDING
JAUNDICE
• Prolonged elevation of unconjugated bilirubin associated with the
ingestion of breast milk is called “breast milk jaundice syndrome”.
• Becomes apparent after the 3rd day and peaks any time from 7th to the
10th day.
• No correlation with weight loss or gain and stools are normal.
• Research demonstrates at lest 1/3rd of all breastfed infants may
suffer from breast milk jaundice syndrome.
• The underlying cause of breast milk jaundice is not entirely
understood. It is believed to be a combination of factors: A substance
In maternal milk, that increases intestinal absorption of bilirubin
and individual variations in the infant’s ability to process bilirubin.
• To establish the diagnosis of breast milk jaundice firmly when the
bilirubin level is above 16mg/dl for more than 24 hours, a short,
temporary interruption of breastfeeding (12-24 hours) while
monitoring bilirubin levels is recommended. Breastfeeding may then
be resumed.

17. KERNICTERUS or BILIRUBIN
ENCEPHALOPATHY
• “Kernicterus” refers to the neurologic
consequences of the deposition of
unconjugated bilirubin in brain tissue.
Subsequent damage and scarring of
the basal ganglia and brainstem nuclei
may occur.
• They brain and brain cells if
destroyed by bilirubin deposits, do not
regenerate.
• Has a mortality rate of 50%.
• Survivors may face severe problems
such as cerebral palsy, hearing loss,
paralysis of upward gaze, intellectual
and other handicaps.

18. PREVENTION AND TREATMENT OF
SEVERE HYPERBILIRUBINEMIA
• The AAP Guidelines.
• Phototherapy: Involves placing the infant
new-born under special fluorescent lights
(blue wavelengths of light) that like sunlight,
alters unconjugated bilirubin in the skin. The
bilirubin is converted to less toxic water-
soluble photoisomers that are excreted in the
bile and urine without conjugation. The
decision to initiate phototherapy is based on
the new-born's age and total serum bilirubin
levels.

20. AAP GUIDELINES
The following are the key elements of the recommendations provided by this guideline:
• Promote and support successful breastfeeding.
• Establish nursery protocols for the identification and evaluation of hyperbilirubinemia.
• Measure the total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) level on infants
jaundiced in the first 24 hours.
• Recognize that visual estimation of the degree of jaundice can lead to errors, particularly
in darkly pigmented infants.
• Interpret all bilirubin levels according to the infant’s age in hours.
• Recognize that infants at less than 38 weeks’ gestation, particularly those who are
breastfed, are at higher risk of developing hyperbilirubinemia and require closer
surveillance and monitoring.
• Perform a systematic assessment on all infants before discharge for the risk of severe
hyperbilirubinemia.
• Provide parents with written and verbal information about newborn jaundice.
• Provide appropriate follow-up based on the time of discharge and the risk assessment.
• Treat newborns, when indicated, with phototherapy or exchange transfusion.

21. RESEARCH ON PREVALENCE IN THE
INDIAN SCENARIO
Study of neonatal jaundice in a tertiary care centre of
South India
• The present study was a prospective hospital based study involving all
neonates who were born at ASRAM Medical College and Hospital, a
tertiary care centre, Eluru, West Godavari District, Andhra Pradesh.
• Observation: Out of 560 new-borns, 273 (48.8%) new-borns developed
clinical jaundice. Out of 273 new-borns with clinical jaundice, 166 (61%)
new-borns developed physiological jaundice and 107 (39%) new-borns
developed non physiological jaundice requiring therapeutic intervention
in the form of phototherapy or exchange transfusion.
• Conclusion: Present study concludes that the leading cause of
pathological jaundice is breastfeeding jaundice, ABO incompatibility and
prematurity.

22. REFERENCES:
• Brown,J.E., Sugarman, I.J.(2002). Nutrition through the Life Cycle,
Wadsworth Thomson Learning
• aafp.org/afp/2002/0215/p599.html
• www.omicsonline.org/etiologis-oand-initial-evaluation-of-neonatal-jaundice-
2167-0897-1000220.php?aid=72906
• http://pediatrics.aappublications.org/content/114/1/297
• RESEARCH ARTICLE LINK:
medresearch.in/index.php/IJPR/article/view/818/1533

23. THANK YOU.