Physiologic Jaundice of the

Newborn
Presented by:
Cruz, Prince Lloyd Isabelo III G.
Siazon, Dwight Laurence S.
Shah, Isharajul

PRESENTED TO:
Dr. Grandeelee Taquiqui

DATE OF DISCUSSION:
26TH JULY, 2011
Discussion

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 Physiologic jaundice of the newborn

 Jaundice

 Yellowish staining of the skin and whites

of the newborn's eyes (sclerae) by
pigment of bile (bilirubin).

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 Pathophysiology
 In newborn babies, a degree of jaundice
is normal.
 indirect-reacting bilirubin is 1–3 mg/dL
(umbilical cord serum) - Normal
 The level rises at a rate of <5 mg/dL/24
hr
 Visible on the 2nd–3rd day
 Peaks - between the 2nd and 4th days at
5–6 mg/dL
 Decreases - between the 5th and 7th
days of life (below 2 mg/dL) Company Logo
 Jaundice associated with these changes
is designated physiologic and is believed
to be the result of increased bilirubin
production from the breakdown of fetal
red blood cells combined with transient
limitation in the conjugation of bilirubin by
the immature neonatal liver.

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 Etiology
 Neonatal period: metabolism of bilirubin
is in transition from the fetal to adult
stage.
 fetal stage (the placenta is the principal
route of elimination of the lipid-soluble,
unconjugated bilirubin)

 adult stage ( the water-soluble conjugated

form is excreted from hepatic cells into the
biliary system and gastrointestinal tract).

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 Unconjugated hyperbilirubinemia may be
caused or increased by any factor that:

1. increases bilirubin load to be metabolized

by the liver
 hemolytic anemias
 Polycythemia
 shortened red cell life (immature, transfused)

 increased enterohepatic circulation

 infection

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 Unconjugated hyperbilirubinemia may be
caused or increased by any factor that:

2. Damages or reduces the activity of the

transferase enzyme or other related
enzymes
 genetic deficiency
 Hypoxia
 Infection
 thyroid deficiency

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 Unconjugated hyperbilirubinemia may be
caused or increased by any factor that:
3. Competes for or blocks the transferase
enzyme (drugs and other substances
requiring glucuronic acid conjugation)

4. Leads to an absence or decreased

amounts of the enzyme or to reduction
of bilirubin uptake by liver cells
(genetic defect, and prematurity).

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 Neurotoxic effects are directly related to
the permeability of the blood-brain barrier
and nerve cell membranes, and neuronal
susceptibility to injury.
 All are adversely influenced by asphyxia,
prematurity, hyperosmolality, and
infection.

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 Breast-feeding and dehydration increase
serum levels of bilirubin.
 Delay in passage of meconium, which
contains 1 mg bilirubin/dL, may contribute
to jaundice by enterohepatic circulation
after deconjugation by intestinal
glucuronidase.
 Additional risk factors include
polycythemia, infection, prematurity, and
being an infant of a diabetic mother.
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The neonatal production rate of bilirubin is 6–8 mg/kg/24 hr
(in contrast to 3–4 mg/kg/24 hr in adults Company Logo
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 Diagnostics
 Preclude known causes of jaundice on
the basis of the history, clinical findings,
and laboratory data

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 Diagnostic evaluation
 determinations of:
 bilirubin levels (direct and indirect reacting
levels)
 Hemoglobin
 reticulocyte count

 blood type

 Coombs test
 examination of peripheral blood smear.

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 Indirect reacting hyperbilirubinemia,
reticulocytosis and red blood cell
destruction indicate hemolysis.

 Direct reacting hyperbilirubinemia

suggests hepatitis, cholestasis, inborn
errors of metabolism, cystic fibrosis,
sepsis.

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 A search to determine the cause of jaundice
should be made if:

1. it appears in the 1st 24–36 hr of life

2. serum bilirubin is rising at a rate faster than 5
mg/dL/24 hr
3. serum bilirubin is >12 mg/dL in full-term infants
(especially in the absence of risk factors) or 10–
14 mg/dL in preterm infants
4. jaundice persists after 10–14 days of life
5. direct-reacting bilirubin is >2 mg/dL at any time

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Factors suggesting a nonphysiologic
cause of jaundice are
 family history of hemolytic disease
 Pallor

 Hepatomegaly
 Splenomegaly

 failureof phototherapy to lower bilirubin

 Vomiting

 Lethargy

 poor feeding
 excessive weight loss

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Factors suggesting a nonphysiologic
cause of jaundice are
 Apnea

 Bradycardia

 abnormal vital signs (including hypothermia)

 light-colored stools

 dark urine positive for bilirubin

 signs of kernicterus.

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 Treatment
 Goal: to prevent indirect-reacting bilirubin
related neurotoxicity while not causing
undue harm
 Phototherapy and exchange transfusion
remain the primary treatment modalities
used to keep the maximal total serum
bilirubin below the pathologic levels
 The risk of injury to the central nervous
system from bilirubin must be balanced
against the potential risk of treatment.
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 Phototherapy
 may require 6–12 hr to have a
measurable effect
 must be started at bilirubin levels below
those indicated for exchange transfusion.
 Clinical jaundice and indirect
hyperbilirubinemia are reduced by
exposure to a high intensity of light in the
visible spectrum.
 Broad-spectrum white, blue, and special
narrow-spectrum (super) blue lights
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 Bilirubin absorbs light maximally in the
blue range (420–470 nm).


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 Bilirubin in the skin absorbs light
energy, causing several photochemical
reactions.
 Reversible photo-isomerization reaction
converting the toxic native unconjugated
bilirubin into an unconjugated
configurational isomer which can be
excreted in bile without conjugation.
 Lumirubin, converted from native bilirubin
and can be excreted by the kidneys in the
unconjugated state.

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 Applied continuously, and the infant is
turned frequently for maximal skin
surface area exposure.
 discontinued as soon as the indirect
bilirubin concentration has reduced to
levels considered safe
 Serum bilirubin levels and hematocrit
should be monitored every 4–8 hr in
infants with hemolytic disease or those
with bilirubin levels near toxic range for
the individual infant.
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 Skin color – not a reliable measure of
effectiveness of phototherapy
 intravenous fluid supplementation added
to oral feedings may be beneficial in
dehydrated patients or those with high
bilirubin levels nearing exchange
transfusion.

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 Complications
 loose stools
 erythematous macular rash
 purpuric rash associated with transient
porphyrinemia
 Overheating
 dehydration (increased insensible water loss,
diarrhea)
 hypothermia from exposure
 a benign condition called bronze baby
syndrome.

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 Complications
 corneal damage
 pressure injury to the closed eyes
 Body temperature should be monitored,
and the infant should be shielded from
bulb breakage.
 Irradiance should be measured directly
and details of the exposure recorded
(type and age of the bulbs, duration of
exposure, distance from the light source
to the infant).
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 Clinical experience suggests that long-
term adverse biologic effects of
phototherapy are absent, minimal, or
unrecognized.

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 Exchange Transfusion

Double volume exchange transfusion

 If intensive phototherapy fails

 If the risk of kernicterus exceeds the

risk of the procedure

 

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 Potential complications
 metabolic acidosis
 electrolyte abnormalities
 Hypoglycemia
 Hypocalcemia
 Thrombocytopenia
 volume overload
 Arrhythmias
 Infection
 graft versus host disease
 death
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 Indications:
 (+) clinical signs of kernicterus (at any
level of serum bilirubin)
 A level approaching that considered
critical for the individual infant during
the 1st or 2nd day of life when a further
rise is anticipated
 hepatic conjugating mechanism becomes
more effective on the 4th day (term
infants) or on the 7th day (premature
infants) – an imminent fall may be
anticipated
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