JAUNDICE Just Call Me Yellow

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JAUNDICEJust Call Me Yellow

• Mary Johnson RNC/MSN
• Gwinnett Hospital System

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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

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Jaundice

• Jaundice An elevated bilirubin level
• Bilirubin Results from the breakdown of
  hemoglobin

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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

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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)

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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.

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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

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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

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Before Birth

• Conjugated bilirubin in the fetus is not cleared
  by the placenta and may accumulate in fetal
  tissues

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Factors influencing bilirubin levels

• 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

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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-re-absorbable urobilogen

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Measurement of Jaundice

• May be serum blood level- most accurate
• Trancutaneous bilirubin monitoring acceptable.

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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

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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.

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Treatment of Physiologic Jaundice

• Phototherapy
• Works by photoisomerization a process that
  converts bilirubin to a water soluble component
  excreted by the liver

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Optimal Phototherapy

• 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

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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

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Phototherapy Information

• Use radiometer Place parallel to the light unit
  and directly under the light at the level of the
  babys 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

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Phototherapy Information

• Higher levels of irradiance are not known to be
  detrimental to the infant

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Bili Blankets

• Acceptable to use bili blankets in conjunction
  with regular phototherapy
• If only bili blanket used eye patches are not
  needed

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Phototherapy

• Side effects
• Loose stools/diarrhea/dehydration
• Hyper/hypothermia
• Skin rashes
• lethargy

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Pathologic Jaundice

• Differs from physiologic jaundice
• Begins earlier (sometimes before 24 hours)
• Rises more quickly (gt5 mg/dl/day)
• Lasts longer (gt 1 week in term babies and greater
  than 2 weeks in preterms)

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Pathologic Jaundice

• Causes
• Hemolytic disease
• Rh incompatibility
• ABO incompatibility
• G6PD deficiency
• Breastfeeding Jaundice
• Breastmilk Jaundice

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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.

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Rhogam

• Given to protect hemolysis in the neonate
• Given at 28 weeks and within 72 hours after
  delivery

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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

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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

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G6PD Deficiency

• More common in
• African Americans
• Greeks
• Italians
• Sephardic Jews
• Asians
• Males

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G6PD Deficiency

• Once diagnosed usually a good outcome
• Diagnosis with G6PD testing
• Treatment includes dietary restrictions
• No fava beans

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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

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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

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Breastmilk Jaundice Treatment

• Discontinue breastfeeding for 24 hours
• Have mom pump and then resume breastfeeding

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Kernicterus

• Bilirubin induced neurological dysfunction with
  yellow staining and neuronal injury in the
  ganglia
• Classic signs
• Cerebral palsy
• Gaze abnormalities
• Hearing impairment
• Dental dysplasia

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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

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Other Treatments

• 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

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Exchange Transfusion

• Major complication is hypocalcemia
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