NEONATAL

JAUNDICE
By gudeta

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0bjectives

 Under this topic we will try to cover

 Definition of jaundice and hyperbilirubinemia
 Etiology of jaundice and hyperbilirubinemia
 Main distinguishable features of physiologic and
pathologic jaundice
 Possible risk factors for neonatal hyperbilirubinemia
 Differential diagnosis of neonatal jaundice
 Definition ,clinical manifestations of kernicterus and
principles of management of hyperbilirubinemia

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 Introduction
 Definition - Jaundice is a yellowish discoloration of the skin
and or sclera due to bilirubin deposition.

 Jaundice is observed during the 1st wk of life in

approximately 60% of term infants and 80% of preterm
infants

 An elevation of serum bilirubin concentration >2 mg/dL is

found in virtually all newborns in the first several days of life.
 Jaundice becomes clinically apparent at serum bilirubin
concentration of >5 mg/dL.

ZeikoBilirubin
is the end product of the catabolism of heme and is
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produced primarily by the breakdown of red blood cell
hemoglobin.
 Bilirubin is break down product of the RBCs.
 RBCs breakdown produce unconjugated or indirect
 Which is mostly bound to albumin .
 Unconjugated bilirubin is metabolized in the liver
to produce conjugated or direct bilirubin
 Which then passes through gut and excreted in the
stool.
 Bilirubin can be reabsorbed again from remaining
stool.

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  Hyperbilirubinemia is raised level bilirubin in
the blood.
 Newborn babies RBCs have shorter life span than
those of adults.
 The concentration of RBCs also higher than adult
 So bilirubin is higher than the later in life.
 The degree of hyperbilirubinemia as result of
these normal physiology

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 Cont ,,,
 Inside liver cells, unconjugated bilirubin is bound to
ligandin, Z protein, and other binding proteins;
 Conjugated bilirubin is water soluble and can be
excreted in the urine, but most of it is rapidly excreted
as bile into the intestine.
 Conjugated bilirubin is further metabolized by
bacteria in the intestine and excreted in the feces.
 Hyperbilirubinemia presents in the neonate as either:
1. unconjugated Hyperbilirubinemia or
2. conjugated Hyperbilirubinemia.

 The two forms involve different pathophysiologic

causes with distinct potential complications.
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 Bilirubin have normal physiological role as
antioxidant
 Elevation of indirect ,unconjugated
bilirubin is neurotoxic
 Although the conjugated form is not
neurotoxic ,potentially serious hepatic
disorder or systemic illness.

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PATHOPHYSIOLOGY
 UNCONJUGATED B.  CONJUGATED B.

Tightly Non toxic

compounded to s.
Water soluble
albumin
Loosely bound to
Normally very
albumin. Delta
small amount is
fraction
present as
albumin free
Insoluble in water
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excreted in urine
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 Etiology
 During the neonatal period, metabolism of
bilirubin is in transition from the fetal
stage,

 during which the placenta is the principal

route of elimination of the lipid soluble,
unconjugated bilirubin,
 to the adult stage, during which the water
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soluble conjugated form is excreted from
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hepatic cells into the biliary system and

 Unconjugated Hyperbilirubinemia may be
caused or increased by any factor that:-

1. Increases the load of bilirubin to be metabolized

by the liver
• Hemolytic anemias,polycythemia,
shortened red cell life as a result of
immaturity or transfused cells, increased
enterohepatic circulation, infection),
2. Damages or reduces the activity of the
transferase enzyme
• Genetic deficiency, hypoxia, infection,
possibly hypothermia and thyroid
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 Cont ,,,
3. Competes for or blocks the transferees
enzyme
• drugs and other substances requiring
glucuronic acid conjugation for
excretion
4. Leads to an absence or decreased amounts
of the enzyme or to reduction of bilirubin
uptake by liver cells
• genetic defect, prematurity.
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 Cont ,,,
 Drugs such as oxytocin (in the mother)
and
 chemicals used in the nursery such as
phenolic detergents may also produce
unconjugated hyperbilirubinemia.
 Clinical Manifestations Jaundice usually
appears during the early neonatal
period, depending on etiology.
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 cause of conjugated

 sepsis
 intra uterine infection
 biliary ateresia
 hepatitis

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 Clinical manifestation
 Whereas jaundice from deposition of indirect
 bilirubin in the skin tends to appear bright
yellow or orange
, jaundice of the obstructive type (direct
bilirubin) has a greenish or muddy yellow cast.
 Jaundice usually becomes apparent in a
 cephalocaudal progression, starting on the
face and progressing to the abdomen and then
the feet, as serum levels increase
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 Cont ,,,

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 Differential Diagnosis
 Jaundice can be divided into physiological or
pathological.
 The distinction between physiologic and
pathologic jaundice
 relates to the timing, rate of rise, and extent of
Hyperbilirubinemia,
 because some of the same causes of physiologic
jaundice (e.g., large RBC mass, decreased
capacity for bilirubin conjugation, increased
enterohepatic circulation) can also result in
pathologic jaundice.
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 Cont ,,,

 Evaluation should be determined on the

 basis of risk factors,
 clinical appearance, and
 severity of the Hyperbilirubinemia

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 Cont ,,,
 Jaundice that is present at birth or appears
withinthe 1st 24 hr after birth should be
considered pathologic and requires immediate
attention.
 Potential diagnoses would include
 erythroblastosis fetalis, concealed hemorrhage,
sepsis, or congenital infections, including
syphilis, cytomegalovirus (CMV), rubella, and
toxoplasmosis.

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 early-onset breastfeeding jaundice are seen
initially on the 2nd or 3rd day.

 jaundice appears on the 2nd or 3rd day is usually

physiologic but may represent a more severe.

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 Cont ,,,
.
 Jaundice appearing after the 3rd day and within the
1st week suggests
bacterial sepsis or urinary tract infection;
it may also be caused by other infection
, notably syphilis, toxoplasmosis, CMV , and
enterovirus.

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 Cont ,,,
 There is a long differential diagnosis for
jaundice first recognized after the 1st week of
life,
 including breast milk jaundice,
septicemia,congenital atresia or paucity of
the bile ducts, hepatitis, galactosemia,
hypothyroidism, , and congenital hemolytic
anemia crises related to RBC morphology
and enzyme deficiencies.

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 Risk Factors for Development of
Severe Hyperbilirubinemia
MAJOR RISK FACTORS
• Predischarge TSB or TcB level in the high-risk zone
• Jaundice observed in the 1st 24 hr
• Blood group incompatibility with positive direct
antiglobulin test, other known hemolytic disease (G6PD
deficiency), elevated end-tidal CO concentration
• Gestational age 35-36 wk
• Previous sibling received phototherapy
• Cephalohematoma or significant bruising
• Exclusive breastfeeding, particularly if nursing is not
going well and weight loss is excessive
• East Asian race
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 MINOR RISK FACTORS
• Predischarge TSB or TcB level in the high
intermediate-risk zone
• Gestational age 37-38 wk
• Jaundice observed before discharge
• Previous sibling with jaundice
• Macrosomic Infant of a diabetic mother
• Maternal age ≥25 yr
• Male gender
DECREASEDRISK
• TSB or TcB level in the low-risk zone
• Gestational age ≥41 wks
• Exclusive bottle feeding Black race
• Discharge from hospital after 72 hr.
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 Evaluation of the Neonate With Significant
Jaundice
CONCERN POSSIBLE INITIAL
DIAGNOSIS LABORATORY
TESTS

Jaundice on day 1 Hemolysis CBC, smear Total

TORCH/sepsis and direct bilirubin
Hepatic failure Blood type and
syndromes Coombs test
Internal hemorrhage

Jaundice Hemolysis As above

requiring TORCH/sepsis
phototherapy

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 Direct/conjugat TORCH/sepsis Hepatic
ed Biliary atresia enzymes, INR,
Hyperbilirubine Other causes check newborn
mia of cholestasis screen for
Hepatic failure metabolic
syndromes disease, blood
glucose, blood
ammonia and
lactate, urine
and blood
cultures, CMV
and HSV PCR

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 Physiologic jaundice

 In almost every newborn infant,

particularly premature infants, a
physiologic elevation of serum
unconjugated bilirubin develops during
the first week of life, usually in the
second or third day, and resolves
spontaneously.

 Jaundice that develops in the 24 h of life

is to be considered pathologic until
proven otherwise.
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 The features

 Appears after 24hrs

 Maximum intensity by 4th -5th day in terms and 7th day in preterm
 Serum level less than 15mg/dl
 Clinically not detectable after 14days
 Disappear without any treament

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 Why does physiological
jaundice develop ?
 Increased bilirubin load
 Defective uptake from plasma
 Defective conjugation
 Increased enter –hepatic circulation

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 Pathologic Hyperbilirubinemia
 It appears in the 1st 24hrs of life
 Serum bilirubin is >5mg/dl /24hr
 Serum bilirubin is >12mg/dl in full term
 Jaundice persistent after 10-14 days of life
 Direct reacting bilirubin is >2mg/dl

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 Cont ,,,
 The greatest risk associated with indirect
hyperbilirubinemia

 is the development of bilirubin-induced neurologi

dysfunction, which typically occurs with high
indirect bilirubin levels.
 The development of kernicterus (bilirubin
encephalopathy) depends on the level of indirect
bilirubin, duration of exposure to bilirubin
elevation, the cause of jaundice, and the infant's
well-being.
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 Cont ,,,
 Neurologic injury including kernicterus may
occur
 at lower bilirubin levels in preterm infants and in
the presence of asphyxia, intraventricular
hemorrhage, hemolysis, or drugs that displace
bilirubin from albumin.
 The exact serum indirect bilirubin level that is
harmful for VLBW infants is unclear

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 Investigations for pathological
jaundice
 The clinical impression of jaundice should be confirmed by a
bilirubin measurement, where possible. The investigations depend
on the likely diagnosis and what tests are available, but may
include:
 Haemoglobin or PCV
 Full blood count to look for signs of serious bacterial infection
(high or low neutrophil count with >20% band forms), and to look
for signs of haemolysis
 total serum bilirubin with conjugated (direct) fraction
 Blood type of baby and mother, and Coombs test, reticulocyte
count , peripheral morphology
 Syphilis serology such as VDRL tests
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 Clinical Presentation
A. History
1. Family history.
 Family history of jaundice, anemia,
splenectomy, or metabolic disorders is
significant.
 A history of a sibling with jaundice may
suggest blood group incompatibility,
breast milk jaundice, or G6PD deficiency.
 A familial tendency of neonatal
Hyperbilirubinemia is present.
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 Cont,,,

2. Maternal history.
 Neonatal jaundice is increased with a
history of maternal diabetes or infection.
 Use of drugs
 Delivery trauma, asphyxia, delayed cord
clamping, and prematurity are associated
with an increased risk of
hyperbilirubinemia in the infant.

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 Cont ,,,
3. Infant's history.
a. Breast-feeding. Poor breast-feeding may
result in poor caloric intake, leading to
"starvation jaundice.“
b. Factors affecting the gastrointestinal tract,
such as obstruction, decreased motility
(ileus), and delayed passage of meconium
c. Check for clinical symptoms such as
vomiting and lethargy. Metabolic disorders,
infection, and bowel obstruction can present
in this manner.

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 Physical signs of prematurity, IUGR, and
postmaturity may be helpful in elucidating a
cause for Hyperbilirubinemia.
Plethora is seen with polycythemia, pallor
with hemolytic disease, and large infants with
maternal diabetes, all of which are associated
with Hyperbilirubinemia.
The appearance of abnormal neurologic signs
heralds the onset of early bilirubin
encephalopathy.

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 Management of new born
with jaundice
 The principle in management is
 avoid any drug that may increase
bilirubin in the infants
 give the infant adequate feeding
 lowering serum bilirubin by
phototherapy and/or exchange
transfusion
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 Cont ,,,
 Phototherapy
 It is one method of lowering the serum (indirect)
bilirubin level by exposing the infant skin to
measured light source (white, blue)
 Phototherapy is indicated to a baby when TSB is
more than normal and
 but it is not a substitute for exchange
transfusion.
 While baby is under phototherapy monitor the
following
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 Cont ,,,
 Baby’s eye should be securely covered
 Distance between body and light source shall be 45cm
 Baby should be taken out from the phototherapy every 2-3 hrs
for breast feeding and every time the position should be changed
 Monitor fluid and electrolyte status
 Monitor temperature regularly (prevent hyperthermia)
 Monitor level of bilirubin at least once daily
 Continue phototherapy until serum bilirubin level is lower than
threshold
 If the bilirubin level is very elevated and you can safely do
exchange transfusion, consider doing so

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 Cont ,,,
 Common side effects of
phototherapy
 Increased insensible water loss,
dehydration and overheating (baby need
extra fluid - 20ml/kg/day)
 Damage to the retina (cover the eyes)
 Skin rashes
 Loose stool or diarrhea
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 Cont ,,,
 Exchange transfusion
 It is one of the treatment for pathological jaundice
where the infants blood is drawn and replaced with
donated cross matched blood in volume to volume .
Exchange may be beyond the scope of this pocket book.
a. Exchange transfusion is not described in this pocket
book. These serum bilirubin levels are included in case
exchange transfusion is possible or in case the baby can
be transferred quickly and safely to another facility where
exchange transfusion can be performed

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 Cont ,,,
b. Risk factors include small size (less than 2.5 kg at
birth or born before 37 weeks gestation), haemolysis,
and sepsis
c. Visible jaundice anywhere on the body on day 1
 Antibiotics
 If suspected infection, treat for serious bacterial
infection
 Antimalarials
 If fever is present and the baby is from a malarious
area, check blood films for malaria parasites and
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 kernicterus

 Kernicterus is neurologic syndrome resulting

from the deposition of unconjugated bilirubin in
the brain cells.
 The risk of kernicterus rise with
 serum unconjugated bilirubin and
• preterm and newborns with
infection
• Have greater susceptibility to kernicterus

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 The pathogenesis of kernicterus is multifactorial
and involves
 an interaction between unconjugated bilirubin
levels, albumin binding and
 unbound bilirubin levels, passage across the
blood-brain barrier (BBB), and
 neuronal susceptibility to injury. Disruption of the
BBB by disease, asphyxia,
 and other factors and maturational changes in BBB
permeability affect risk
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 Clinical manifestation

 Sign and symptoms usually appear 2-5 days after

birth term
 As late as 7days in preterm birth infants
 Common c/m is ; lethargy
 poor feeding
 loos of moro reflex
 bulging fontanel
 And convulsion occur in advanced cases.
 Many children progress to sever sings dies.
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ACUTE FORM
• Phase 1 (1st 1–2 days): poor sucking
stupor, hypotonia, seizures
• Phase 2 (middle of 1st wk) hypertonia
of extensor muscles, opisthotonos,
fever
• Phase 3 (after the 1st wk): hypertonia

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CHRONIC FORM
• First year: hypotonia, active deep
tendon reflexes, obligatory tonic neck
reflexes, delayed motor skills
• After 1st yr: movement disorders
(choreoathetosis, ballismus, tremor)
sensor neural hearing loss

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 Treatment

 The goal of therapy is to avoid

kernicterus.
 The principles of treatment are;
 phototherapy
 exchange transfusion
 treatment of underlying
cause

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 The End
The End

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