neonatal jaundice dr. mohamed haseen basha assistant professor ( pediatrics) faculty of medicine...
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Neonatal Jaundice
Dr. Mohamed Haseen BashaAssistant professor ( Pediatrics)
Faculty of MedicineAl Maarefa College of Science and
Technology
Visible jaundice occurs in about 75% of term infants and 80% of preterm
infants during the first week of life. It is caused by a raised level of bilirubin, a
breakdown product of red blood cells.
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
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
Pathological Jaundice
• TSB concentrations have been 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.
Increased Bilirubin Load
• Elevated unconjugated bilirubin
• Hemolytic Disease
– Features: elevated reticulocytes, decreased Hgb
– Coomb’s + Rh incompatibility, ABO incompatibility, minor antigens
– Coomb’s - G6PD, spherocytosis, etc.
• Non-hemolytic Disease
– Features: normal reticulocytes
– Extravascular sources i.e. cephalhematoma
– Polycythemia
– Exaggerated enterohepatic circulation – I.e. CF
Decreased Bilirubin Conjugation
• Elevated unconjugated bilirubin
• Genetic Disorders
– Criggler-Najjar
• 2 types
• Severe hyperbilirubinemia
– Gilbert Syndrome
• Mild hyperbilirubinemia
• Hypothyroidism
Impaired Bilirubin Excretion
• Elevated unconjugated and conjugated bilirubin (> 2 mg/dL or > 20% of TSB)
• Biliary Obstruction
– Structural defects i.e. biliary atresia
– Genetic defects – Rotor’s & Dubin-Johnson syndromes
• Infection – sepsis, TORCH
• Metabolic Disorders – i.e. alpha1 antitrypsin deficiency
• Chromosomal Abnormalities – Turner’s syndrome
• Drugs – i.e. ASA, Sulfa, Erythromycin
Causes of jaundice by age of onset.
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?
• Basic pathophysiology of jaundice is same in term and preterm neonates but
at lower gestation babies are at higher risk of developing hyperbilirubinemia
and require closer surveillance and monitoring.
Is there evidence of hemolysis?
• In the setting of Rh or less frequently ABO incompatibility, onset of
jaundice within 24 hours, presence of pallor and hydrops, presence of
hepatosplenomegaly, presence of hemolysis on the peripheral blood smear,
raised reticulocyte count (>8%), rapid rise of bilirubin (>5 mg/dl in 24 hours
or >0.5 mg/dl/hr) or a suggestive family history of significant jaundice
should raise a suspicion of hemolytic jaundice.
Does the infant have an underlying serious disease? (sepsis,
Galactosemia)
• Presence of lethargy, poor feeding, failure to thrive, hepatosplenomegaly,
temperature instability or apnea may be a marker of an underlying serious
disease.
Does the infant have cholestatic jaundice?
• Presence of jaundice (>10 mg/dl) beyond 3 weeks, presence of dark urine
(staining the clothes) or pale colored stools would suggest 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• High irradiance (usually ≥ 30 μ W/cm 2 per nm)• 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.
Nomogram for determination of risk of development of severe hyperbilirubinemia for infants ≥ 35 weeks ’ gestation and ≥ 2.5 kg birthweight.
Indications for phototherapy in infants ≥ 35 weeks ’ gestation
Management of neonatal hyperbilirubinemia in low birth weight babies based on bilirubin levels (mg/dl)
Disadvantages of Phototherapy
• Separates baby and parents.
• Eye coverage necessary, which may be disturbing to parents.
• Bronze - baby syndrome if phototherapy given with elevated conjugated bilirubin.
• Unstable body temperature possible while in open bassinet (cot) with majority of
skin exposed.
• Increased insensible water loss, but less with use of LED light sources.
• 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 thrombosis, embolus, volume overload or depletion,
metabolic abnormalities, infection, coagulation abnormalities.
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.
Indications for exchange transfusion in infants ≥ 35 weeks ’ gestation
Prolonged jaundiceJaundice 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 sensori 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
Thank You
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