Physiologic jaundice is a common cause of hyperbilirubinemia in newborns resulting from increased bilirubin production, shortened RBC lifespan, and hepatic immaturity. It presents between 2-10 days of life with indirect bilirubin levels <12 mg/dL in term infants peaking on day 3. Kernicterus is a neurological syndrome caused by bilirubin deposition in the brain and can be prevented by avoiding excessively high indirect bilirubin levels >25 mg/dL. Diagnosis of hyperbilirubinemia involves history, physical exam, and laboratory tests including total, direct and indirect bilirubin levels as well as blood typing if levels are

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬

2. Neonatal jaundice
‫عماد‬ ‫علياء‬
‫احمد‬ ‫فاطمة‬
‫حسين‬ ‫فاطمة‬
‫حسن‬ ‫فاطمة‬

3. Definition:is a yellowing of the skin and sclera
of a newborn infant caused by accumulation of
Bilirubin( Hyperbilirubinemia) in the skin &
mucous mambrene

4. Hyperbilirubinemia is a common and in most
cases benign problem in neonates. Jaundice is
observed during the 1st wks. of life in
approximately 50- 60% of term newborns and
80% of premature infants.
Its clinically visible when exceeds 5 mgm/dl.

5. Metabolism and secretion of bilirubin
Bilirubin -breakdown of hemoglobin
Unconjugated bilirubin (insoluble in water)
transported to liver- Bound to albumin
Transported into hepatocyte (Ligandin / y- protein ) &
conjugated - With glucuronic acid → now water
soluble
Secreted into bile
In ileum & colon, converted to stercobilin
10-20% (Deconjugated by β glucuronidase)
reabsorbed into portal circulation (Enterohepatic
circulation )and re-excreted into bile or into urine by
kidneys - urobilinogen

7. Clinical Manifestations
• Yellow skin and sclera
• Poor feeding
• Brown urine
• Fever
• High pitch cry
• Vomiting
• without treatment
can progress to acute
bilirubin
Encephalopathy
(kernicterus)

8. Physiologic jaundice : (Icterus Neonatorum)
Physiologic jaundice is a common cause of
hyperbilirubinemia among newborns. It is adiagnosis
of exclusion, made after careful evaluation has ruled
out more serious causes of jaundice, such as
hemolysis, infection, and metabolic diseases.

9. Physiological jaundice is jaundice that is
present between day 2 and day 10

10. Characteristics:-
1-The clinical pattern of physiologic jaundice in
term infants includes a peak indirect-reacting
bilirubin level of no more than 12 mg/dL on day 3
of life. In premature infants, the peak is higher (15
mg/dL) and occurs later (fifth day).
2-its disappears by one weak in full term infants &
two weeks in preterm infants.
3-serum bilirubin is rarly rising at
a rate faster than 5 mg/dL/24 hr
4- Healthy baby.

11. Pathologic jaundice
• Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Total Serum bilirubin > 13 mg / dl in term
infant or 10 mg/dl in preterm
.The direct bilirubin fraction is greater than
1.5 mg/dL
May associated with
acute hemolysis
• Signs of an
underlying illness

12. Risk factors for jaundice
1-low birth wt & prematurity
2-polycythemia
3-A sibling affected
4-male sex
5-hemolytic conditions
6-sepsis
7-ABO incompatibility

13. Types of neonatal jaundice

15. In Hemolytic disease of the
newborn (ABO / Rh)
Rh incompitability:
• is the most common cause
• < 1 mL of Rh-positive fetal blood is sufficient to sensitize the
Rh negative mother
• 90% sensitization during delivery/abortion
So , most first born infants are not affected due to the short
period of exposure which is insufficient to produce a
significant maternal IgG antibody response.
Sensitized mother produces Ab –IgG types—crosses placenta
sensitized –small doses of Ag stimulate high Ab titer .
So, risk and severity of sensitization response increases with
each subsequent pregnancy with Rh-positive blood fetus

16. Not all mother produce hemolysis in their
baby ??
1. The baby may be Rh negative
2. Not all mother produce enough Abs
3. The mother might have been immunized
by anti D immunoglobin
4. Fetomaternal trasfusion occurs only in 50%
of preg
5. When mother and baby ABO
incompatibale

17. ABO incompatibility
• if Mother is type O and the baby is either type A
or B. O +ve Mothers makes antibodies which are
IgM & IgG types , IgG types crosses the placenta
• No effects if the mother & baby have same blood
group or baby is grp O, as there is nothing to
make antibodies against.
• If mother - type A or B Makes antibodies (IgM)
type so does not cross the placenta
So, even if baby has a different blood type no effect

18. Physiologic jaundice is a common cause of hyperbilirubinemia
among newborns. It is a diagnosis of exclusion, made
after careful evaluation has ruled out more serious causes of
jaundice, such as hemolysis, infection, and metabolic diseases.
Physiologic jaundice is the result of many factors that
are normal physiologic characteristics of newborns:
1- increased bilirubin production resulting from an increased RBC
mass,
2- shortened RBC life span,
3- hepatic immaturity of ligandin and glucuronosyltransferase.
Physiologic jaundice

19. Crigler-Najjar syndrome is a serious, rare, autosomal
recessive, permanent deficiency of glucuronosyltransferase
that results in severe indirect hyperbilirubinemia.
Type II
responds to enzyme induction by phenobarbital, producing
an increase in enzyme activity and a reduction of bilirubin
levels.
Type I
does not respond to phenobarbital and manifests
as persistent indirect hyperbilirubinemia, often leading to kernicterus
Gilbert disease is caused by a mutation of the promoter
region of glucuronosyltransferase and results in a mild
indirect hyperbilirubinemia. In the presence of another icterogenic
factor (hemolysis), more severe jaundice may develop

20. Breast milk jaundice
may be associated with unconjugated hyperbilirubinemia without
evidence of hemolysis during thefirst to second week of life.
Bilirubin levels rarely increase to more than 20 mg/dL.
Interruption of breastfeeding for 1 to 2 days results in a rapid decline
of bilirubin levels, which do not increase significantly after
breastfeeding resumes.
Breast milk may contain an inhibitor of bilirubin conjugation or may
increase enterohepatic recirculation of bilirubin because of
breast milk glucuronidase

21. Direct-reacting hyperbilirubinemia (defined as a direct bilirubin
level >2 mg/dL or >20% of the total bilirubin) is never
physiologic and should always be evaluated thoroughly
according to the diagnostic categories
Etiology of Direct Conjugated Hyperbilirubinemia
Direct-reacting bilirubin (composed mostly
ofconjugated bilirubin) is not neurotoxic to the
infant but signifies a serious underlying
disorder involving cholestasis or hepatocellular
injury.

23. Best classified by age of onset and duration:
Early: within 24 hrs of life
Intermediate: 2 days to 2 weeks
Late: persists for >2 weeks
Causes of neonatal jaundice

24. Causes of neonatal jaundice
Early Intermediate Late/prolonged
• Haemolytic causes:
– Rh isoimmunisation
– ABO incompatibility
– G6PD deficiency
• Congenital infection
• Physiological jaundice
• Breast milk jaundice
(inadequate intake)
• Sepsis
• Haemolysis
• Crigler-Najjar syndrome
(glucuronyl transferase
absent/reduced)
• Polycythaemia, bruising
• Conjugated (dark urine, pale
stools):
– Bile duct obstruction
– Biliary atresia
– Neonatal hepatitis
• Unconjugated:
– Physiological
– Breast milk jaundice
– Infection
– Hypothyroidism

25. Kernicterus ( bilirubin encephalopathy):
is a neurologic syndrome results when indirect bilirubin is
deposited in brain cells and disrupts neuronal metabolism and
function, especially in the basal ganglia.
Indirect bilirubin may cross the blood-brain barrier because of
its lipid solubility. Other theories propose that a disruption of
the blood-brain barrier permits entry of a bilirubin-albumin
or free bilirubin–fatty acid complex
Its characterized by severe athetoid
cerebral palsy, paralysis of upward gaze,
hearing loss & intellctual impairment
& its preventable
Kernicterus

26. Kernicterus usually is noted when the bilirubin level is
excessively high for gestational age. It usually does not
develop
in term infants when bilirubin levels are less than 20 to25
mg/dL, but the incidence increases as serum bilirubin levels
exceed 25 mg/dL

27. Pathalogy
Yellow staining of the brain with neuronal injury, there are necrosis, neuronal
loss and gliosis
Its commonly seen in the basal ganglia, hypocampus,cerebellum,brainstem &
spinal cord

28. Risk factor for Kernicterus
1. Sever hyperbilirubinemia
2. Prematurity
3. Asphyxia
4. Acidosis ,hemolysis, hypoxia, hypothermia
5. Hypoglycemia, sepsis, meningitis,
Other risks for kernicterus in term infants are
hemolysis, jaundicenoted within 24 hours of birth, and
delayed diagnosis of hyperbilirubinemia

29. Clinical feature
The earliest clinical manifestations of kernicterus are
lethargy
Hypotonia
irritability
poor Moro response
poor feeding.
A high-pitched cry and emesis also may be present.
Early signs are noted after day 4 of life.
Later signs include
bulging fontanelle
opisthotonic posturing
pulmonary hemorrhage
Fever
Hypertonicity
paralysis of upward gaze and seizures

30. Complication of Kernicterus
Infants with severe cases of kernicterus die in the neonatal
period.
Spasticity resolves in surviving infants, who may
manifest later nerve deafness
choreoathetoid cerebral palsy
mental retardation
enamel dysplasia
and discoloration of teeth as permanent sequelae
Prevention
Kernicterus may be prevented by
-avoiding excessively high indirect bilirubin levels
-avoidingconditions or drugs that may displace bilirubin from
albumin.

31. Diagnosis of hyperbilirubiniemia

32. :
• History
 ask about Antenatal history
 Drugs
 Trauma
 Family H/O of jaundice
 Liver disease
 H/O delayed feeding
 Sepsis
 Sibling jaundice
 Splenectomy in family

33. Examination :
• Look for yellowish discoloration of the skin,
sclera and mucous membrane
• Gently pressing by finger on the tip of the
nose
• Examination of liver and spleen for
hepatosplenomegaly
• Look for the color of urine and
• stool

34. Kramer index:
1.Face-5 mg/dl
2.Abdomen 15 mg/dl
5.Palms & sloes 20 mg/dl

35. LABORATORY TESTS
Physical evidence of jaundice is observed in infants when
bilirubin levels reach 5 to 10 mg/dL (versus 2 to 3 mg/dL in
adults). When jaundice is observed, the laboratory evaluation
for hyperbilirubinemia should include
a total bilirubin measurement to determine the magnitude of
hyperbilirubinemia.
Bilirubin levels greater than 5 mg/dL on the first day of life
or greater than 13 mg/dL thereafter in term infants should be
evaluated further with
measurement of indirect and direct bilirubin levels
blood typing
Coombs test
complete blood count, blood smear
and reticulocyte count.

36. These tests must be
performed before treatment of hyperbilirubinemia with
phototherapy
or exchange transfusion. In the absence of hemolysis
or evidence for either the common or the rare causes of
nonhemolytic indirect hyperbilirubinemia,
the diagnosis is
either physiologic or breast milk jaundice. Jaundice present
after 2 weeks of age is pathologic and suggests a direct-reacting
Direct-reacting hyperbilirubinemia (defined as a direct
bilirubin
level >2 mg/dL or >20% of the total bilirubin) is never
physiologic and should always be evaluated thoroughly
according to the diagnostic categories
Direct-reacting bilirubin (composed mostly of conjugated
bilirubin)
is not neurotoxic to the infant but signifies a serious underlying
disorder involving cholestasis or hepatocellular injury.

37. Treatment

38. phototherapy
•is an effective and safe method for reducing indirect bilirubin
levels, particularly when initiated before serum bilirubin increases
to levels associated with kernicterus.
•In term infants, phototherapy is begun when indirect
bilirubinlevels are between 16 and 18 mg/dL.
• Under the effects of phototherapy light with maximal
irradiancein the 425- to 475-nm wavelength band, bilirubin is
transformed into isomers that are water soluble and easily
excreted.
• Blue lights and white lights are effective in reducing bilirubin

39. The therapeutic effect of phototherapy depends on
1. the light energy emitted in the effective range of wavelengths
2. the distance between the lights and the infant
3. the surface area of exposed skin,
4. the rate of hemolysis
During phototherapy :
1. Cover the eyes and Genitals
2. Supplemental hydration
3. monitoring for side effects
4. Monitering of bilirubin level

40. Serum bilirubin levels and hematocrit should be monitored every
4-8 hr in infants with hemolytic disease and those with
bilirubin levels near toxic range .
Complications of phototherapy
Early complication:
1. loose stools
2. erythematous macular rash
3. dehydration (increased insensible water loss, diarrhea)
4. bronze baby syndrome (which occurs in the presence of direct
hyperbilirubinemia)
5. lethargy, masking of cyanosis, nasal obstruction by eye pads

41. Late complication:
• Risk of skin malignancies
• Damage to intracellular DNA
• Retinal damage
• Testicular damage

42. Intensive phototherapy
using light source above and beneath the infant using
in sever cases with risk of kernicterus
Home phototherapy
This is an option way of treatment where facilities are
available and fiber optic blankets are commonly used
.the family should be well instructed and a well trained
nurse should be present it is usually used for simple
jaundice

43. Intravenous Immunoglobulin
The administration of intravenous immunoglobulin
use in treatment for hyperbilirubinemia due to
isoimmune hemolytic disease.
(0.5-1.0 g/kg/dose; repeat in 12 hr) has been shown to
reduce the need for exchange transfusion in both ABO
and Rh hemolytic disease, by reducing hemolysis

44. Exchange blood transfusion
usually is used for infants with dangerously high
indirect bilirubin levels who are at risk for kernicterus .
The exchange transfusion usually is performed
through an umbilical venous catheter placed in the
inferior vena cava or,if free flow is obtained, at the
confluence of the umbilical veinand the portal system.

45. Indication:
• The appearance of clinical signs suggesting
kernicterus
• Rh and ABO incompatibility
• Unconjugated billirubin > 20 -25mg/dl in
term, >15 -18mg/dl preterm babies.
• Other disease :Septicemia ,DIC,Severe
anemia,…

46. Complications
1. Problems related to the blood (transfusion reaction,
metabolic instability,or infection)
2. Problems related to the catheter (vessel perforation or
hemorrhage)
3. problems related to the procedure (hypotension or
necrotizing enterocolitis )
4. Unusual complications include thrombocytopenia and
graft-versus-host disease.

47. Prevention of neonatal jaundice :
1. Promote and support breast feeding
2. Establish nursery protocols for identifying and evaluating
hyperbilirubinemia
3. Measure bilirubin levels in all neonate with jaundice in the first 24
hrs
4. Recognize that visual estimation of bilirubin level inaccurate
5. Interpret all bilirubin levels according to baby age in hrs
6. Identify preterm ,breast fed infant and provide close monitoring
7. Risk assessment for all newborn baby .
8. Give written and verbal information to familly
9. Treat newborns when indicated and appropriate follow up

49. ‫علي‬&‫فاطمة‬
•‫لكما‬ ‫هللا‬ ‫بارك‬
‫عليكما‬ ‫وبارك‬
‫بينكما‬ ‫وجمع‬
‫خيـــر‬ ‫في‬
‫الخطوبة‬ ‫مبروك‬