NEONATAL JAUNDICE
Dr ROBINA ZAFAR
PG PEADS MEDICINE
NEONATAL JAUNDICE
Hyperbilirubinemia refers to an excessive level of
accumulated bilirubin in the blood and is characterized by
jaundice, a yellowish discoloration of the skin, sclera and
mucous membrane
Visible jaundice occurs in about 60% of term infants and 80% of preterm
infants during the first week of life.
Reasons for elevated bilirubin in newborns are:
• The hemoglobin concentration is high at birth so there is considerable
heme degradation
• Lifespan of newborn red blood cells is shorter than that of adult red blood
cells
• Immaturity of liver enzymes impairs bilirubin conjugation and excretion
• Absorption of unconjugated bilirubin by intestines (enterohepatic
circulation).
Metabolism of Bilirubin
Risk factors for jaundice
JAUNDICE
J - jaundice within first 24 hrs of life
A - a sibling who was received phototherapy
U - unrecognized hemolysis
N – non-optimal sucking/nursing
D - deficiency of G6PD
I - infection
C – cephalhematoma /bruising
E - East Asian/North Indian
Causes of jaundice by age of onset.
Physiological Jaundice
Jaundice attributable to physiological immaturity of neonates to handle
increased bilirubin production.
Jaundice usually appears between 24-72 hours of age.
Total serum bilirubin (TSB) level usually rises in full-term infants to a peak
of 6 to 8 mg/dL by 3 days of age and then falls. A rise to 12mg/dL is in the
physiologic range.
In premature infants, the peak may be 10 to 12 mg/dL on the 5 day of life,
possibly rising over 15 mg/dL without any specific abnormality of bilirubin
metabolism.
Levels under 2mg/dL may not be seen until one month of age in both full
term and premature infants.
Safe bilirubin levels in preterms vary according to gestational age.
Breast Milk Jaundice
May persist as a prolonged physiological jaundice or appear de-novo
after 1st week
Common in exclusively breast fed babies
Maximum intensity is between 10-14 days
If STB > 15 mg/dl, temporary cessation of breast feeding for 48 hours
leads to dramatic fall and does not rise thereafter
For higher levels, phototherapy may be needed
The exact cause is still not understood
May be due to glucuronidase in some breast milk
Pathological Jaundice
TSB concentrations defined as non-physiologic if concentration exceeds 5
mg/dl on first day of life in term neonate, 10 mg/dL on second day, or
12-13 thereafter.
Any TSB elevation exceeding 17 mg/dL should be presumed pathologic
and warrants investigation for a cause and possible intervention, such as
phototherapy.
Appearance of jaundice within 24 hours, peak TSB levels above the
expected normal range , presence of clinical jaundice beyond 3 weeks and
conjugated bilirubin (dark urine staining the clothes and light colored
stool) would be categorized under pathological jaundice.
Clinical examination of jaundice
Dermal staining of bilirubin described by Kramer may be used as a
clinical guide to the level of jaundice.
Dermal staining in newborn progresses in a cephalocaudal direction.
The newborn should be examined in good daylight. The skin should be
blanched with digital pressure and the underlying color of skin and
subcutaneous tissue should be noted.
The severity of jaundice cannot be reliably assessed by clinical Examination.
If jaundiced, also check for:
Is the newborn term or preterm?
Is there evidence of hemolysis?
Does the infant have an underlying serious disease? (sepsis,
Galactosemia)
Does the infant have cholestatic jaundice?
Investigations
Total bilirubin, Direct bilirubin, Indirect bilirubin
Reticulocyte count, and smear for red cell morphology.
Blood packed cell volume or hematocrit.
Blood group (mother and baby).
Sepsis Screen
Liver function and Thyroid function tests
TORCH Screening
Direct antibody test (DAT or Coombs test).
G6PD testing
Microbiological cultures of blood, urine and/or cerebrospinal fluid for infection
Management
The need for treatment is ascertained by plotting the total bilirubin level on
a graph of bilirubin against age in hours. This will determine if:
No treatment is needed
Repeat bilirubin is required in 6 – 12 hours
Phototherapy or exchange transfusion is indicated.
Treatment will change according to the absolute level of bilirubin reached and
the rate of rise on serial measurements (if bilirubin rising > 0.5 mg/dL/hour).
Different cut - off criteria are used for preterm infants, for whom the treatment
threshold is lower
Phototherapy
Blue - green light (wavelength 425 – 475 nm) converts unconjugated
bilirubin to harmless isomers. The light is filtered to remove ultraviolet light.
Conventional phototherapy is with a phototherapy light source above the baby.
Continuous multiple phototherapy is used if the serum bilirubin is rising
rapidly or is at a high level or does not fall within 6 hours of starting
conventional phototherapy.
Maintaining adequate hydration and good urine output should help to improve
the efficacy of phototherapy.
Phototherapy requires:
Effective light source
Light as close to the infant as possible (if fluorescent tubes used, can be as
close as about 10 cm from infant)
Widespread skin exposure.
Disadvantages of Phototherapy
• Separates baby and parents.
• corneal damage
• Bronze - baby syndrome if phototherapy given with elevated conjugated bilirubin.
•Unstable body temperature – hypothermia or overheating
• Increased insensible water loss
• Slightly loose, more frequent stools which may contribute to water loss.
Exchange transfusion
Baby’ s blood is removed and replaced with transfused blood. Removes bilirubin
and antibodies and corrects anemia. Blood used for exchange transfusion in neonates
with Rh isoimmunization should always have Rh negative blood group.
Complications include volume overload or depletion, metabolic acidosis, electrolyte
imbalance, hypoglycemia, NEC, infection, thrombocytopenia, graft versus host
disease and death
Phenobarbitone:
It improves hepatic uptake, conjugation and excretion of bilirubin thus helps in
lowering of bilirubin. However its effect takes time.
When used prophylactically in a dose of 5 mg/kg for 3-5 days after birth, it has
shown to effective in babies with hemolytic disease, extravasated blood and in
preterms without any significant side effects.
Intravenous Immunoglobulin ( IVIG )
Can be used in rhesus disease or ABO incompatibility when total bilirubin levels are
rising despite continuous multiple phototherapy or level is near exchange transfusion
level.
0.5 to 1 g\kg\dose, repeat in 12 hours
Metalloporphyrins
Prolonged jaundice
Jaundice present at more than 2 weeks of age for term, 3 weeks for preterm
infants can be considered as prolonged jaundice.
It requires further assessment. First, it needs to be determined if the jaundice is
unconjugated or conjugated.
Unconjugated jaundice causes are:
• Breast milk jaundice – 15% of all breast fed infants are still jaundiced at 2
weeks, gradually decreasing over several weeks
• Hypothyroidism
• Gastrointestinal obstruction, e.g. pyloric stenosis
• Infection
• Liver enzyme disorders.
Conjugated jaundice ( > 1.5 mg/dL, 25 micrograms/L)
may be caused by:
• Biliary atresia – uncommon, but important to identify
as delay in surgery adversely affects outcome
• Neonatal hepatitis syndrome.
The infant will pass pale stools (no stercobilinogen) and
dark urine (from bilirubin).
Detailed investigation of infants with conjugated
jaundice is required.
Discharge and follow up
In view of the re emergence of kernicterus in otherwise healthy infants,
particularly at 35 – 37 weeks ’ gestation, a follow up assessment is considered
for jaundice depending on their length of stay in the nursery.
• Discharge at < 24 hours, follow - up by 72 hours of life
• Discharge at 24 – 48 hours, follow - up by 96 hours of life
• Discharge at 48 – 72 hours, follow - up by 120 hours of life.
Parents should also be given written and verbal information about jaundice.
Clinical judgment should be used in determining follow-up. Earlier or more
frequent follow-up should be provided for those who have risk factors for
hyperbilirubinemia
Kernicterus
Kernicterus describes acute or chronic bilirubin encephalopathy.
Kernicterus is rare in developed countries.
In acute bilirubin encephalopathy there may be hypotonia, lethargy, poor
feeding, irritability, high - pitched cry, fever, apnea, hypertonia with arching of
the neck and trunk (opisthotonus), seizures, coma, and death.
In chronic bilirubin encephalopathy there is permanent neurologic injury
resulting from the deposition of unconjugated bilirubin in the basal ganglia
and brainstem nuclei.
Long term consequences include dental dysplasia with yellow staining of the
teeth, high frequency sensory neural hearing loss, paralysis of upward gaze of the
eyes, choreoathetoid cerebral palsy, and learning difficulties.
Cross - section of the brain at autopsy showing yellow staining,
predominantly in basal ganglia from deposition of unconjugated
bilirubin.
Prevention of Hyperbilirubinemia
1. Early and frequent feeding
2. Adequate hydration
3. Administration of Anti-D injection to Rh negative mother
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