JAUNDICE Just Call Me Yellow Mary Johnson RNC/MSN Gwinnett Hospital System

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Transcript JAUNDICE Just Call Me Yellow Mary Johnson RNC/MSN Gwinnett Hospital System

JAUNDICE
Just Call Me Yellow
Mary Johnson RNC/MSN
Gwinnett Hospital System
Objectives
• At the end of the presentation; the participant will
be able to:
• List 2 factors that place a neonate at risk for
jaundice
• Describe the common treatment modalities for
jaundice
• Discuss the difference between physiologic
jaundice and pathologic jaundice
Jaundice
• Jaundice: An elevated bilirubin level
• Bilirubin: Results from the breakdown of
hemoglobin
Bilirubin Metabolism
• The breakdown of “heme” is usually a
normal physiologic process…
• Heme is initially converted to biliverdin via
the enzyme heme oxygenase
• Biliverdin is then further reduced to
bilirubin by biliverdin reductase
Bilirubin Metabolism
• Bilirubin is insoluble in water and must be
placed into the plasma circulation by being
bound to albumin
• In the liver, bilirubin is changed to a water
soluble compound by being conjugated by
the enzyme UDPGT (uridine
diphosphylgluronosyn transferase)
Bilirubin Metabolism
• This changed (or conjugated) bilirubin is
released, after several enzymatic reactions,
from the liver into the bile duct and then to
the GI tract for elimination. Some bilirubin
is also excreted through the urine via similar
processes. This all depends on adequate
amounts of oxygen and glucose.
Bilirubin Binding
• Bilirubin/albumin binding explains how bilirubin
can be toxic to the brain.
• Small amounts of unconjugated (unchanged)
bilirubin are not bound to albumin, but circulate as
free bilirubin.
• This unbound, insoluble bilirubin crosses the lipid
containing cell membranes-including the blood
brain barrier and causes kernicterus
Before Birth
• Metabolism and clearance of fetal bilirubin
is accomplished through the maternal liver
• There is limited conjugation in the fetus
because there is limited fetal blood flow in
the fetal liver
• Unconjugated bilirubin in the fetus is
cleared by the placenta
Before Birth
• Conjugated bilirubin in the fetus is not
cleared by the placenta and may accumulate
in fetal tissues
Factors influencing bilirubin
levels
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Racial and ethnic groups
Perinatal events
Maternal Diabetes
Higher bilirubin production in neonates
Limited conjugation of bilirubin in neonates
Delayed excretion due to increased
enterohepatic circulation
Enterohepatic Circulation
• Excretion is delayed because the small intestine of
the neonate contains an enzyme (B-glucoronidase)
which converts conjugated bilirubin back to its
unconjugated form. Bilirubin is then re-absorbed
into the circulation
• Neonatal intestines are slow to become colonized
with bacteria that degrade bilirubin into non-reabsorbable urobilogen
Measurement of Jaundice
• May be serum blood level- most accurate
• Trancutaneous bilirubin monitoring
acceptable.
Physiologic Jaundice
• Almost universally observed in all neonates
due to:
• Larger RBC mass
• Shorter RBC lifespan
• Greater amount of bilirubin produced from
sources other than RBCs
• Increased enterohepatic circulation
• Defective conjugation
• Decreased excretion
Physiologic Jaundice
• Bilirubin levels generally peak on day 3 to 5
of life in term babies and day 5 to 6 in
preterm babies
• Hyperbilirubinemia in premies is an
exaggerated form of physiologic jaundice
because of decreased glucuronyl transferase
activity in the liver.
Treatment of Physiologic
Jaundice
• Phototherapy
• Works by “photoisomerization”: a process that
converts bilirubin to a water soluble component
excreted by the liver
Optimal Phototherapy
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Expose as much skin as possible
Eye patches except for feeding
Turn frequently
Monitor temperature
Monitor intake and output: increased
insensible water loss is common
• Monitor for diarrhea
Phototherapy Information
• Place lights at the distance from the infant
recommended by the manufacturer
(generally 8 to fourteen inches from the
baby)
• Place lights so that they are centered over
the baby
Phototherapy Information
• Use radiometer: Place parallel to the light
unit and directly under the light at the level
of the baby’s skin.
• An irradiance level of 20 microwatts or
greater is acceptable
• An irradiance level of 30 microwatts or
greater is considered to “intensive” or
double phototherapy
Phototherapy Information
• Higher levels of irradiance are not known to
be detrimental to the infant
Bili Blankets
• Acceptable to use bili blankets in
conjunction with regular phototherapy
• If only bili blanket used: eye patches are not
needed
Phototherapy
• Side effects
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Loose stools/diarrhea/dehydration
Hyper/hypothermia
Skin rashes
lethargy
Pathologic Jaundice
• Differs from physiologic jaundice:
• Begins earlier (sometimes before 24 hours)
• Rises more quickly (>5 mg/dl/day)
• Lasts longer (> 1 week in term babies and
greater than 2 weeks in preterms)
Pathologic Jaundice
• Causes
• Hemolytic disease
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Rh incompatibility
ABO incompatibility
G6PD deficiency
Breastfeeding Jaundice
Breastmilk Jaundice
Rh Incompatibility
• Fetal blood cells containing Rh antigen
(Rh + cells) enter the maternal circulation.
The maternal cells have no Rh antigen (Rh-)
and the maternal immune system then
produces antibodies against the fetal
antigens. Finally, the maternal antibodies
enter the fetal circulation and hemolyze
(destroy) the fetal red cells.
Rhogam
• Given to protect hemolysis in the neonate
• Given at 28 weeks and within 72 hours after
delivery
ABO Incompatibility
• Less severe; more frequent than Rh
• Most often seen in mothers with Blood type
O with blood type A or B babies
• Fetal cells enter the maternal circulation as
with Rh disease
• Infant presentation includes:
• Hemolysis; anemia
• Jaundice
G6PD Deficiency
• A deficiency of the enzyme glucose 6 phosphate
dehydroginase
• Autosomal dominant
• Caused by:
• Impaired conjugation
• Hemolysis: G6PD protects the RBC membranes from
oxidation. In G6PD deficiency; the red cell is very
likely to hemolyze
G6PD Deficiency
• More common in
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African Americans
Greeks
Italians
Sephardic Jews
Asians
Males
G6PD Deficiency
• Once diagnosed: usually a good outcome
• Diagnosis with G6PD testing
• Treatment includes dietary restrictions
• No fava beans
Breastfeeding Jaundice
• Breastfeeding is associated with more
significant and prolonged jaundice than
formula feeding
• Early onset (2 to 4 days of age)
• Inadequate nursing (inadequate feeding and
calories)
• Encourage nursing/pumping 10-12 times a day
• No water supplement needed
Breastmilk Jaundice
• Late onset (4-7 days of life)
• Prolonged physiologic jaundice
• Related to the ingredients in breast milk
• Decreased conjugation from
• Interference of UDGT enzyme
• Increased concentration of free fatty acids because
of the lipoprotein in human milk
• Increased enterohepatic circulation because of
lipoprotein in breast milk
Breastmilk Jaundice: Treatment
• Discontinue breastfeeding for 24 hours
• Have mom pump and then resume
breastfeeding
Kernicterus
• Bilirubin induced neurological dysfunction
with yellow staining and neuronal injury in
the ganglia
• Classic signs
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Cerebral palsy
Gaze abnormalities
Hearing impairment
Dental dysplasia
Kernicterus
• Usually associated with bilirubin levels
• Greater than 30 in term babies
• Greater than 20 in preterm babies
• Severity of symptoms varies from baby to baby
Other Treatments
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Early feedings
Phenobarbital
IVIG
Exchange transfusion
• Decision based on bili level; age in hours of
baby; gestational age; rate of rise of bilirubin
• Blood removed from UAC and replaced with
whole blood as ordered by the physician
Exchange Transfusion
• Major complication is hypocalcemia
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