Neonatal jaundice is a very common condition in baby. It should be evaluated thoroughly and properly.

2. Lecture-08
Neonatal Jaundice
Prof. Dr. Sunil Natha Mhaske
Dean
Dr. Vithalrao Vikhe Patil Foundation’s Medical College
and Hospital,
Ahmednagar (M.S.) India-414111
Mo- 7588024773
Mail-sunilmhaske1970@gmail.com

3. History
• The term jaundice is from the French word "jaune”
• Neonatal jaundice may have first been described in
a Chinese textbook 1000 years ago.
• Earliest work on jaundice from Baumes-1785 and
Hervieux-1847
• Medical theses, essays, and textbooks from the
18th and 19th centuries contain discussions about
the causes and treatment of neonatal jaundice.
• Kernicterus was first described by Johannes
Orth, 1875, He postulated that jaundice might have
hematologic origins. He noted that the brain in
jaundiced adults wasn’t affected.
• Christian Schmorl coined the term in 1904,
Translated, Kernicterus means jaundice of the
“kern” or nuclear region of the brain.

4. • It is a yellowish discoloration of the white part of the eyes and skin in
a newborn baby due to high bilirubin levels.
• About 60% of full term newborn and 80% of premature babies are
jaundiced.
• 3% of normal term infant show bilirubin level more than 15mg/dl
• Jaundice is the most common condition that requires medical attention
and hospital readmission in newborns.
Neonatal jaundice or Neonatal Hyperbilirubinemia-

5. Bilirubin
• Non-polar, water insoluble compound requiring conjugation with
glucuronic acid to form a water soluble product that can be
excreted.
• It circulates to the liver reversibly bound to albumin

6. Pathophysiology
• Bilirubin comes from the breakdown in heme, which is produced from the
breakdown of hemoglobin.
• Heme is converted to biliverdin, iron, and carbon monoxide by the enzyme heme
oxygenase.
• biliverdin is then converted to bilirubin by biliverdin reductase.
• The conversion of heme to bilirubin takes place in the reticuloendothelial system.
• The unconjugated bilirubin is hydrophobic and is transported to the liver bound to
albumin where it is conjugated by the enzyme uridine diphosphate-
glucuronosyltransferase (UGT).
• Conjugated bilirubin, which is water-soluble, is excreted in bile and into the
gastrointestinal (GI) tract and mostly excreted in feces after being metabolized by
bacterial flora.
• Some conjugated bilirubin is deconjugated to unconjugated bilirubin and reabsorbed
through the enterohepatic circulation.

8. • Ligandins{y} responsible for transport from plasma membrane to
endoplasmic reticulum.
• Bilirubin conjugated in presence of UDPGT (uridine diphosphate
glucuronyl transferase) to mono and diglucoronides, which are
then excreted into bile canaliculi.
• Phenobarbitol Increases the conc. of Ligandin and also induces
UDPGT.
• Conjugated” bilirubin is water soluble and is secreted by the
hepatocytes into the biliary canaliculi.
• Converted to stercobilinogen (urobilinogen) (colorless) by
bacteria in the gut.
• Oxidized to stercobilin which is colored, Excreted in feces.
• Some stercobilin may be re-adsorbed by the gut and re-excreted
by either the liver or kidney.

9. Enterohepatic circulation-
• Meconium contains 100-200mg of conjugated bilirubin at
birth.
• Conjugated bilirubin is unstable and easily hydrolyzed to
unconjugated bilirubin.
• This process occurs non-enzymatically in the duodenum
and jejunum and also occurs in the presence of beta-
glucuronidase, an enteric mucosal enzyme, which is found
in high concentration in newborn infants and in human
milk.
Factors enhancing enterhepatic circulation
- Decrease entral intake
- Intestinal atresia
- Meconium ileus
- Hiruschsrung disease

10. Jaundice is visible-
- in adults at STB > 2mg/dl
- in neonates if STB> 5 mg/dl
Physiological Mechanisms of Neonatal Jaundice-
•Increased synthesis
•Less efficient binding and transport
•Less efficient hepatic conjugation and excretion
•Enhanced absorption via enterohepatic circulation

11. Risk factors for Neonatal Jaundice
 Premature birth. A baby born before 38 weeks of gestation may not be able to
process bilirubin as quickly as full-term babies do. Premature babies also may
feed less and have fewer bowel movements, resulting in less bilirubin eliminated
through stool.
 Significant bruising during birth. Newborns who become bruised during
delivery gets bruises from the delivery may have higher levels of bilirubin from
the breakdown of more red blood cells.
 Blood type. If the mother's blood type is different from her baby's, the baby may
have received antibodies through the placenta that cause abnormally rapid
breakdown of red blood cells.
 Breast-feeding. Breast-fed babies, particularly those who have difficulty nursing
or getting enough nutrition from breast-feeding, are at higher risk of jaundice.
Dehydration or a low caloric intake may contribute to the onset of jaundice.
However, because of the benefits of breast-feeding It's important to breast feed.
 Race. Studies show that babies of East Asian ancestry have an increased risk of
developing jaundice.

12. Classification Neonatal Hyperbilirubinemia
Based on Mechanism of Accumulation
Increased bilirubin
load
(prehepatic)
1. Haemolytic-
• coomb positive
• coomb negative:-
2. Non haemolytic
• Extravascular source
• Polycythemia
• Exaggerated
enterohepatic
circulation
Decreased bilirubin
conjugation
(Hepatic)
1. Physiologic
jaundice
2. Crigler-Najjar
syndrome 1 and 2
3. Gilbert syndrome
4. Hypothyroidism
5. Breast milk
jaundice
Impaired bilirubin
Excretion
(post hepatic)
1. Biliary
obstruction:
2. Metabolic
disorder
3. Chromosomal
abnormality:
4. Infection
5. Drugs

13. Classification

16. • Pathologic jaundice may occur in the first 24 hours of life and
• It is characterized by a rapid rate of rising in the bilirubin level
more than 0.2 mg/dl per hour or 5 mg/dl per day.
• Causes - due to increased bilirubin production, decreased bilirubin
clearance, and increased enterohepatic circulation.
a. Immune-mediated hemolysis - ABO and rhesus
incompatibility.
b. Non-immune mediated - cephalhematoma, red blood cell
membrane defects like hereditary spherocytosis and
elliptocytosis, enzyme defects like glucose-6-phosphate
dehydrogenase (G6PD) deficiency and pyruvate kinase.
Pathological jaundice (Pathologic unconjugated
Hyperbilirubinemia.)

17. Signs of Pathological Jaundice –
• Intrauterine growth restriction
• Stigma of intrauterine infections (e.G. Cataracts, small head,
and enlargement of the liver and spleen)
• Cephalohematoma
• Bruising
• Signs of bleeding in the brain's ventricles
• Family history of jaundice and anemia
• Family history of neonatal or early infant death due to liver
disease, maternal illness suggestive of viral infection
• Maternal drugs (e.G. Sulphonamides, anti-malarials causing red
blood cell destruction in G6PD deficiency)

18. Red flags for pathologic jaundice
•Jaundice in first 24 hours
•Rapidly rising total bilirubin concentration (>86umol/L/day)
•Early gestational age
•Previous sibling with jaundice
•Significant bruising
•Jaundice persisting for more than 2-3 weeks
•East Asian ethnicity

19. Physiological jaundice
• It is also referred to as non-pathologic jaundice.
• It is mild and transient.
• This occurs because of differences in the metabolism of bilirubin in the
neonatal period leading to an increased bilirubin load.
• The increased bilirubin load in the newborn arises from increased
production of bilirubin due to a higher mass of red blood cells with a
decreased lifespan in the neonate, a decreased bilirubin clearance from a
deficiency of the uridine diphosphate glucuronosyltransferase (UGT)
enzyme, which in the newborn has the activity of about 1% of the adult
liver and increased enterohepatic circulation.
• Physiologic jaundice usually occurs on days 2 to 4, peaks between 4 to
5 days, and resolves in 2two weeks. Physiologic jaundice never occurs in
the first 24 hours.
• Visible jaundice due to elevation of unconjugated bilirubin during first
week.

20. • Phase one-
- Term infants - jaundice lasts for about 10 days with a rapid
rise of serum bilirubin up to 204 μmol/l (12 mg/dL).
- Preterm infants - jaundice lasts for about two weeks, with a
rapid rise of serum bilirubin up to 255 μmol/l (15 mg/dL).
• Phase two –
- bilirubin levels decline to about 34 μmol/l (2 mg/dL) for
two weeks, eventually mimicking adult values.
• Preterm infants - phase two can last more than one
month.
• Exclusively breastfed infants - phase two can last more
than one month.

21. 1) Increase bilirubin load over liver cell
• Increase RBC volume/kg as compared to adult
• Decrease RBC survival:-90 dayS
• Increase early labelled bilirubin from haem,haem proteins ,
myoglobin, haem containing liver enzyme or ineffective
erythropoesis,.
• Increase enterohepatic circulation of bilirubin:
- No bactericidal activity in gut ,bilirubin can not converted into
urobillinogen.
- Beta glucronidase which unconjugate bilirubin diglucronide
present in intestine and helps in reabsoportion of bilirubin in portal
circulation.
2) Defective hepatic uptake of bilirubin from plasma
Decrease ligandin (Y protein)
Binding of Y & Zn protein by other anions
3) Defective bilirubin conjugation- Decrease UDP Glucronyl
transferase activity and decrease UDP glucose dehydrogenase activity.
4) Defective Bilirubin excretion.

23. ABO incompatibility
ABO incompatibility occurs in mother’s with blood group O
who have anti-A and anti-B IgG antibodies that cross the
placenta and cause hemolysis in newborns with blood group A
or B.
ABO incompatibility
 Type O mothers
 Type A or B fetuses
 Presence of IgG anti-A or Anti-B antibodies in type O mother
 Frequently occurring during the first pregnancy without prior
sensitization

24. Rhesus (Rh) incompatibility
• Pathophysiology of alloimmune hemolysis resulting from Rh incompatibility
 An Rh-negative mother
 An Rh-positive fetus
 Leakage of fetal RBC into maternal circulation
 Maternal sensitization to D antigen on fetal RBC
 Production and transplacental passage of maternal anti-D antibodies into fetal
circulation
 Attachment of maternal antibodies to Rh-positive fetal RBC
 Destruction of antibody-coated fetal RBC
Rh hemolytic disease was rare during the first pregnancy involving an Rh-positive fetus.
• Once sensitization has occurred, re-exposure to Rh D RBC in subsequent
pregnancies leads to an anamnestic response, with an increase in the maternal anti-
Rh D antibody titer.
• The likelihood of an infant being affected increased significantly with each
subsequent pregnancy.
• Using Rhogam (anti-D gamma globulin) as prophylaxis in a mother with prior
exposure has decreased the incidence of Rh hemolysis.

25. Clinical Features Rh ABO`
Frequency Unusual Common
Anemia Marked Minimal
Jaundice Marked Minimal to moderate
Hydrops Common Rare
Hepatosplenomegaly Marked Minimal
Kernicterus Common Rare

26. Laboratory Features Rh ABO
blood type of Mother Rh negative O
blood type of Infant Rh positive A or B
Anemia Marked Minimal
Direct Commb’s test Positive Negative
Indirect Commb’s test Positive Usually positive
Hyperbilirubinemia marked Variable
RBC morphology Nucleated RBC Spherocytes

27. G6PD enzyme deficiency
• The G6PD enzyme, found in red blood cells (RBCs), protects
against oxidative injury by the production of NADPH
(nicotinamide adenine dinucleotide phosphate hydrogenase) from
NADP (nicotinamide adenine dinucleotide phosphate).
• With its deficiency, and in the presence of oxidant stressors like
illness, certain drugs, dyes, and foods like fava beans, there is
hemolysis of RBCs.
• The clinical presentation is varied depending on the variant of the
GGPD, and some newborns may present with neonatal jaundice
with severe hyperbilirubinemia or kernicterus.
• G6PD is an X-linked disorder leading to males mostly being
affected and females mostly being asymptomatic carriers.

28. Crigler- Najjar syndrome
• In Crigler-Najjar syndrome, there is either an absence of UGT
activity (type 1) or low UGT activity (type 2), which leads to
severe hyperbilirubinemia in the first days of life or less severe
disease respectively.
• Neonates with Crigler-Najar 1 need liver transplantation or
long-term use of phototherapy.
• Phenobarbital may be used in type 2 Crigler-Najjar.

29. Gilbert syndrome
• There is a mutation of the UGT1A1 gene in Gilbert
syndrome.
• Causing decreased UGT production and unconjugated
hyperbilirubinemia.
• Gilbert is usually diagnosed in the adolescent period,
although presentation in the neonatal period may occur
and is mostly inherited as an autosomal dominant
condition.
• It can be diagnosed with genetic testing.

30. Breastfeeding jaundice (breastfeeding failure jaundice)
• occurs in the first week of life.
• It is due to failure of adequate intake of breast milk leading to
dehydration and hypernatremia.
• Breastfeeding failure leads to decreased intestinal motility and
decreases the elimination of bilirubin in the stool or meconium.
• This leads to increased enterohepatic circulation, resulting in
increased reabsorption of bilirubin from the intestines.
• most cases can be ameliorated by frequent breastfeeding sessions of
sufficient duration to stimulate adequate milk production

31. Breast milk jaundice
• occurs late in the first week, peaks in the second, and usually resolves by
12 weeks of age.
• It is due to inhibition of UGT activity and a factor in breast milk with
a beta-glucuronidase-like activity that deconjugates conjugated bilirubin
in the intestines leading to increased enterohepatic circulation.
• It is a biochemical occurrence.
• bilirubin uptake in the gut (enterohepatic circulation) is increased in breast
fed babies, possibly as the result of increased levels of epidermal growth
factor (EGF) in breast milk. Breast milk also contains glucoronidase
which will increase deconjugation and enterohepatic recirculation of
bilirubin.
• inhibition of bilirubin conjugation leads to increased levels of bilirubin in
the blood.
• enzyme in breast milk (lipoprotein lipase) produces increased
concentration of nonesterified free fatty acids that inhibit hepatic
glucuronyl transferase, which again leads to decreased conjugation and
subsequent excretion of bilirubin.

32. Conjugated hyperbilirubinemia
Conjugated hyperbilirubinemia is always pathologic and is due to defects in bile formation or
transport, obstruction to its flow, or to systemic conditions that may affect the liver.
Conditions causing conjugated hyperbilirubinemia due to hepatobiliary disease include-
biliary atresia Inborn errors of metabolism like
galactosemia
choledochal cysts genetic disorders like a-1 antitrypsin
deficiency
idiopathic neonatal hepatitis. metabolic disorders such as
tyrosinemia.
Alagille syndrome. Urinary tract infections
TORCH” (toxoplasmosis, other-
syphilis, varicella-zoster, rubella,
cytomegalovirus, and herpes
simplex)
Systemic infections like “infections and
systemic conditions like sepsis, shock,
and birth asphyxia

33. Biliary atresia
• Biliary atresia is the most common cause of conjugated neonatal
hyperbilirubinemia.
• It involves both intra-hepatic and extra-hepatic bile ducts.
• classically presents around 2 to 4 weeks of life with pale stools.
• The initial evaluation is by ultrasonography that may show an
absent gallbladder and the classic "triangular cord" sign.
• percutaneous liver biopsy
• open cholangiogram
• surgical intervention-Kasai procedure (hepatoportoenterostomy) -
performed before eight weeks.

34. Choledochal cysts
• Choledochal cysts involve dilation of the intrahepatic and
extra-hepatic bile duct.
• Ultrasonography

35. Alagille syndrome
• Alagille syndrome is caused by a genetic mutation leading to a
paucity of interlobular bile ducts and hepatic manifestations,
including jaundice and cirrhosis.
• Other clinical features are butterfly vertebrae, peripheral
pulmonic stenosis, renal involvement, dysmorphic features, and
posterior embryotoxon of the eye.
• Alagille syndrome is inherited in an autosomal dominant pattern

36. • Alpha-1-antitrypsin deficiency is a common genetic disorder
that presents with cholestatic jaundice in infants
who are homozygous for the PiZZ genotype.
• Accumulation of anti-trypsin polymers in the endoplasmic
reticulum of hepatocytes of a patient with the PiZZ genotype
leads to apoptosis, neonatal cholestasis, and cirrhosis later in
childhood.
Alpha-1-antitrypsin deficiency

37. • Newborns with galactosemia present with jaundice, cataracts,
hepatomegaly, failure to thrive, renal tubular acidosis,
and Escherichia coli sepsis after the ingestion of milk.
• Galactosemia is due to galactose-1-phosphate
uridyltransferase (GALT) deficiency leading to the
accumulation of toxic metabolites in multiple organs.
• The presence of reducing substances in urine suggests
galactosemia, and GALT activity in the liver or erythrocytes
confirms the diagnosis.
Galactosemia

39. • Originally described by Kramer.
• Dermal staining of bilirubin may be used as a clinical guide to the
level of jaundice.
• Dermal staining in newborns progresses in a cephalo-caudal
direction.
• The newborn should be examined in good daylight.
• The physician should pale the skin by digital pressure and the
underlying color of skin and subcutaneous tissue should be noted.
• Newborns who are detected the yellow skin beyond the thighs should
have an urgent laboratory confirmation for bilirubin levels.
• Clinical assessment is unreliable if a newborn has been receiving
phototherapy and has dark skin.
Clinical Examination of Neonatal Jaundice

42. Diagnosis
1. Biochemical: The gold standard method for bilirubin estimation is the total and
conjugated bilirubin assessment based on the van den Bergh reaction.
2. Bilimeter: Spectrophotometry is the base of Bilimeter and it assesses total
bilirubin in the serum. Because of the predominant unconjugated form of
bilirubin, this method has been found a useful method in neonates.
3. Transcutaneous Bilirubinometer: This method is noninvasive and is based on
the principle of multi wavelength spectral reflectance from the bilirubin staining
in the skin. The accuracy of the instrument may be affected by variation of skin
pigmentation and its thickness
4. Blood grouping and Rh typing
5. Hematocrit, Reticulocyte count, PBS
6. Direct Coomb’s test on baby
7. Sepsis screen
8. Liver function and Thyroid tests
9. Torch assay

43. Complications
1. Kernicterus-
- occurs if acute bilirubin encephalopathy causes permanent damage
to the brain.
- Involuntary and uncontrolled movements (athetoid cerebral palsy)
- Permanent upward gaze
- Hearing loss
- Improper development of tooth enamel

44. 2. Acute Bilirubin Encephalopathy
1st phase: hypotonia, poor suck-present in the first few days
2nd phase: Hypertonia (retrocollis and opisthotonos), fever
3rd phase: Gradual disappearance of the hypertonia-Up to years after
the first week
3. Chronic Encephalopathy:
• Perlstein’s Tetrad: Extrapyramidal Abnormalities, Hearing Loss,
Gaze abnormality, and Dental Dysplasia
• Extrapyramidal abnormalities: Facial grimacing, drooling,
dysarthria, and athetosis--may develop by 18mo or delayed to
8or9 years.
• Hearing loss is usually due to injury of the cochlear nuclei in the
brainstem. It may be the only manifestation
• Gaze abnormalities: Limitation of upward gaze, palsies
• Cerebral cortex is relatively spared, so intelligence is often close
to normal.

45. Physiological Jaundice-
• Benign in nature.
• mother should be encouraged to breast-feed her baby frequently
and exclusively.
• Mother should be told to bring the baby to the hospital if the color
on the legs looks as yellow as the face.
• Any newborn discharged before 48 h of life should be evaluated
again in the next 48 h for breastfeeding sufficiency and
development of jaundice.
Treatment

46. • It is a portable phototherapy device for the treatment of neonatal
jaundice The name is a combination of bilirubin and blanket.
• Biliblankets offer the possibility of treating some degrees of
jaundice at home.
• The baby is tied to the machine, unless they can wheel it around,
and there is a stiff pad between the mother and baby.
• Phototherapy for jaundice involves a blue/white light of varying
intensity placed close to the skin or touching it through a
special, light-permeable fabric.
• The whole setup consists of the light generator, termed the light
box, the fibre-optic cable through which the light
is carried and the light pad, which is a
25cm x13cm (10"x5") pad that's attached to
the baby.
Biliblanket

47. Phototherapy

48. • 1950- The use of phototherapy was first discovered, accidentally, at Rochford
Hospital in Essex, England, when a nurse, Sister Jean Ward, noticed that babies
exposed to sunlight had reduced jaundice.
• Dr. Perryman- a pathologist, who noticed that a vial of blood left in the sun had
turned green.
• Dr. Cremer, Richards and Dobbs put together these observations, leading to a
landmark randomized clinical trial which was published in Pediatrics in 1968; it
took another ten years for the practice to become established.
• Niels Ryberg Finsen- Danish physician, founder of modern phototherapy.

49. • Bilirubin absorbs light optimally in the blue-green range (460 to 490
nm)
• Mechanism: Bilirubin is photoisomerized and excreted in the bile or
converted into lumirubin and excreted in the urine.
- Eyes and genitalias (Boy) of the newborn must be covered and the
maximum body surface area exposed to the light.
- It is important to maintain hydration and urine output as most of the
bilirubin is excreted in the urine as lumirubin.
- The use of phototherapy is not indicated in
conjugated Hyperbilirubinemia and may lead to the “bronze baby
syndrome” with grayish-brown discoloration of the skin, serum, and
urine.
- After phototherapy is discontinued, there is an increase in the total
serum bilirubin level known as the" rebound bilirubin."
- The phototherapy involved is not ultraviolet light therapy.
- Distance - 45 cm.
- The penetration power of phototherapy is 2mm

50. Preferable to use either daylight (provides enhanced clinical observation and
adequate efficacy) or blue light (better efficacy)
Not green light which provides neither

51. • The baby is turned every 2 hrs or after each feed
• Temp is monitored every 2-4 hrs
• Weight is taken daily
• More frequent breast feeds or 10-20% extra IV fluids are
provided
• STB is measured every 12 hrs
• Phototherapy is discontinued if 2 STB values are < 10 mg/dl
Side effects-
 Increased insensible water loss
 Loose green stools
 Hyperthermia / Hypothermia
 Rashes (erythema)
 Oxidative injury
 UV light irradiation
 Bronze baby syndrome

52. • Used for any newborn with a total serum bilirubin of greater than 25 mg/dl
• Indicated if there is a risk of neurologic dysfunction with or without an attempt at
phototherapy.
• It is used to removed bilirubin from the circulation, and in iso-immune hemolysis
removes circulating antibodies and sensitized red blood cells as well.
• A double volume exchange blood transfusion (160 to 180 ml/kg) is performed,
replacing the neonate’s blood in aliquots with crossed-matched blood.
• Complications - electrolyte abnormalities like hypocalcemia and hyperkalemia,
cardiac arrhythmias, thrombocytopenia, blood-borne infections, portal vein
thrombosis, graft versus host disease, and necrotizing enterocolitis (nec)
Exchange transfusions

53. N.B: Blood Volume = 70-90 ml/kg for term and 85-110 ml/kg for preterm
infants
One blood volume removes 65% of baby’s red cells.
Two blood volumes removes 88% of baby’s red cells.
<1000gms Use 5ml aliquots
1000-2000gm 10ml aliquots
>2000gms 15ml aliquots

54. Maisel’s Chart
STB (mg/dl) Birth Wt <24 hrs 24-48 hrs 49-72 hrs >72 hrs
<5` All
5-9 All Phototherap
y if
hemolysis
10-14 <2500G
--------------
>2500 G
Exchange if
hemolysis
Phototherapy
--------------------------------------------------
Investigate if STB > 12 mg/dl
15-19 <2500 g
--------------
>2500 g
Exchange Transfusion
Consider exchange
--------------------------------
Phototherapy
20 and
More
All Exchange Transfusion

56. Pharmacological Treatment
1. Phenobarbitone: Bilirubin processing including hepatic uptake, conjugation and its
excretion are ameliorated by this agent thus helps in decreasing level of bilirubin. When
used for 3–5 days in a dose of 5 mg/kg after birth prophylactically, it has shown to be
effective in babies with hemolytic disease, extravasated blood and in pre-term without any
significant side effects.
2. Intravenous Immunoglobulin (IVIG): High dose IVIG (0.5–1 gr/kg) has shown to be
effective in decreasing the needs of exchange transfusion and phototherapy in babies with
Rh hemolytic disease.
3. Metalloporphyrins: These compounds are still experimental but showing promising
results in various hemolytic and non-hemolytic settings without significant side effects.
4. Administration of agar has been tried in an attempt to decrease the enterohepatic
recirculation of conjugated bilirubin. It has not proved to be clinically useful and may cause
intestinal obstruction.
5. Administration of glycerin suppositories to facilitate stooling has been evaluated as a
potential method of preventing hyperbilirubinemia
6. Enteral prebiotics- Enterohepatic recirculation and delayed stooling contribute to
perpetuation of hyperbilirubinemia.
7. L-aspartic acid and enzymatically hydrolyzed casein are known inhibitors of beta
glucuronidase, the enzyme that promotes enterohepatic recirculation of conjugated bilirubin
in the neonatal intestine.

57. Prevention
• Early and frequent feeding
• Adequate hydration
• Administration of Anti-D injection to Rh negative mother
Follow-up
• Babies having roughly 20 mg/dl serum bilirubin and that
requiring exchange transfusion should be kept under follow-up
in the high risk clinic for neurodevelopmental outcome.
• Hearing assessment (Brainstem Evoked Response Audiometry
(BAER)) should be done at 3 months of corrected age.

58. Prognosis
• With treatment, the prognosis is excellent.
• In those with delayed treatment, brain damage is a major
complication.

59. Thanks a lot