elevated total serum bilirubin level 

yellow color caused by the  

    deposit of bilirubin in the skin

Bilirubin toxicity: direct correlation with elevated levels of unconjugated bilirubin and symptoms

Phase 1: lethargy, hypotonia

Phase 2: fever, retrocollis, hypertonia, opisthotonos, high pitched cry

Phase 3: shrill cry, hearing and visual impairment, athetosis (involuntary, abnormal movements), apnea, seizures, coma, death

Irreversible, chronic sequelae of bilirubin toxicity

Yellow staining of brain tissue caused by transfer of free bilirubin into brain cells

Neuronal necrosis, atrophy and loss

indirect bilirubin, fat soluble, produced by RBC destruction

Direct bilirubin,transformed by liver to water soluble form

is the metabolic end product of erythrocyte (RBC) breakdown

One gram of heme produces 34 mg of bilirubin

Normal neonates produce 8 – 10mg/kg/day

binds reversibly to albumin

Transported to liver as an unconjugated, fat soluble product 

Propensity for fatty tissues like subcutaneous and brain tissue

Amount of serum bilirubin

Other drugs such as salicylates, sulfa products

Acidosis and hypoxemia

In the liver, bilirubin, is bound to hepatic proteins

Transformed into a water soluble form that can be excreted by the neonate

The conjugated bilirubin is excreted into the bile, into the small intestine

Converted by bacteria into urobilinogen  

Converted to stercobilin and excreted in the stool

In the intestine, the enzyme β- glucuronidase may break down the  conjugated bilirubin causing it to become unconjugated and reabsorbed from the intestine into the blood stream (enterohepatic recirculation) – in the fetus eliminated by placenta

Increased RBC volume

Increased hematocrit

Increased RBC destruction

Fetal RBC’s have a shorter life span

Hemolysis 

OA or OB, Rh incompatibilities

Infection (bacterial or viral)

Red Cell membrane defects (spherocytosis, elliptocytosis)

RBC enzyme defects (Glucose-6-phosphate dehdydrogenase deficiency (G6PD), pyruvate kinase deficiency) 

Delayed meconium passage

Delayed feeding

Bruising, cephalohematoma

Perinatal complications-asphyxia

Impaired hepatic functioning-Prematurity,liver disease,

inborn errors of metabolism

Endocrine Disorders

Lucey-Driscoll syndrome (familial neonatal jaundice)

Enzyme inhibition of hepatic conjugation of bilirubin

Hypothyroidism

Breast milk jaundice

Diagnosis of exclusion

Otherwise healthy infant

Direct coombs negative

Does not have hemolytic disease

Develops at > 24 hours of age

Total bilirubin is < 12mg%

Daily increase of <5mg%

Peaks at day 3 – 4 (term infant) or 5 – 6 (preterm infant)

Appears at < 24 hours of age (term)

Appears at < 48 hours (preterm)

Persists beyond normal time frame

Rate of rise > 0.5mg% per hour

History of hemolytic disease or blood group incompatibility

Other signs/symptoms of illness

Mother’s blood type incompatible with fetus’s blood type

Mother O with A or B type fetus

Mother A with B or AB fetus

Mother B with A or AB fetus

Rh -  mother with Rh + fetus

Maternal sensitization usually occurs during delivery or abortion of first Rh + fetus

Maternal antibodies (IgG) to Rh+ blood cross placenta and attack and destroy fetal RBC’s

Fetus compensates by increasing rate of RBC production

Severe cases – fetal anemia, hydrops, death

RhoGAM:  anti-D human gamma globulin given to mothers following the birth or abortion of an Rh+ fetus or neonate

Prevents maternal production of anti-Rh antibodies

Current recommendations:  routine administration at 28 weeks to all Rh – women and within 24 hours after birth of Rh+ newborn.  

Later onset

Peaks at day 10 – 15

Gradual resolution

Range from 12 mg% to 27 mg%

Diagnosis by history and exclusion of other causes

Answer unknown

Depends on

Gestational age

Weight

Other contributing factors

Acidosis

Infection

Feeding

Evidence of hemolysis

Jaundice in first 24 hours after birth

Suboptimal breast feeding

Late preterm infants

Bruising and cephalohematoma

Hemolysis, blood type incompatibilities

G6PD deficiency

Genetic or ethnic risk factors

gestation

    - age of infant

    - onset of jaundice

    - birth history

    - maternal blood type

    - family history

    - feeding and stooling  

      patterns

Color

Tone

Degree of jaundice

Contributing factors

Cephalhematoma

bruising

Liver and spleen

Other S/S of illness

Indirect and direct bilirubin levels

Blood type (know maternal blood type)

Indirect coombs (antibody screen):  measures the red cell antibody (A,B, or Rh) in the serum

Direct coombs (antibody screen): measures the presence of the antibody on the surface of the red blood cell

May initially be negative if antibody load is not high enough

CBC and differential with smear (to look at red cell morphology)

Reticulocyte count

Consider G6PD screen

Less than 38 weeks

Blood incompatibility (ABO/Rh)

Exclusive breastfeeding

Male infant

Mediterranean or African American descent

Previous infant with jaundice

Visible jaundice less than 24 hours of age

Birth trauma

Ensure adequate intake (weight, voids, stools)

Lactation consult

Breast feed, then pump and supplement with pumped breast milk or with formula

Do not use sterile water or glucose water

Remember that 35 to 37 week infants are not full term

3 types of chemical reactions occur when bilirubin is exposed to light, changing the bilirubin into less toxic form that is rapidly excreted into the bile without conjugation:

Photoisomerization

Structural isomerization

Photo-oxidation

Maximize light level:  use bilimeter and keep lights within the recommended range (>10)

Maximize skin exposure

Ensure adequate hydration

Ensure stooling

Follow bilirubin level

Protect eyes with patches 

Frequent position changes

Temperature instability

Increased insensible water loss

GI hypermotility:  loose stools

Lethargy or irritability

Retinal damage

Photosensitivity

? Potential cellular damage

? Hypocalcemia, thrombocytopenia

Bronze color if high conjugated bilirubin level

Correct anemia and improve CHF in infants with hydrops

Stop hemolysis and bilirubin production by removing antibody and sensitized RBC’s

Double volume exchange (160 mL/kg) will reduce the TSB by  50%

has been used to reduce bilirubin in infants with isoimmune hemolytic disease.  

Mechanism unknown

Possibly prevents receptors in reticuloendothelial cells from taking up and lysing antibody-coated RBC’s  

Increase enteral feeds

Do not supplement with water or glucose

Rule out other causes

Treat underlying condition

Aggressive phototherapy

Exchange transfusion

IVIG

Follow-up must be provided to all neonates discharged at less than 72 hours after birth by a health care professional in an office, clinic, or at home within 24 to 48 hours after discharge.