Hyperbilirubinemia or elevation of serum bilirubin levels is related to hemolysis of RBCs and subsequent re-absorption of unconjugated bilirubin from the small intestines. The condition may be benign or may place the neonate at risk for multiple complications/untoward effects.
1. Prevent injury/progression of condition.
2. Provide support/appropriate information to family.
1. Maintaining physiological homeostasis with bilirubin levels declining.
2. Complications prevented/resolving.
3. Parent(s) understand condition/prognosis and therapeutic regimen.
4. Plan in place to meet needs after discharge.
Nursing diagnosis: INJURY, risk for CNS involvement may be related to prematurity, hemolytic disease, asphyxia, acidosis, hypoproteinemia, and hypoglycemia
Nursing care plan intervention with rationale:
1. Note infant/maternal blood group and blood type.
Rationale: ABO incompatibilities affect 20% of all pregnancies and most commonly occur in mothers with type O blood, whose anti-A and anti-B antibodies pass into fetal circulation, causing RBC agglutination and hemolysis. Similarly, when an Rh-negative mother has previously been sensitized by Rh-positive antigens, maternal antibodies cross the placenta and attach to fetal RBCs, causing immediate or delayed hemolysis.
2. Review intrapartal record for specific risk factors, such as low birth weight (LBW) or IUGR, prematurity, abnormal metabolic processes, vascular injuries, abnormal circulation, sepsis, or polycythemia.
Rationale: Certain clinical conditions may cause a reversal of the blood-brain barrier, allowing bound bilirubin to separate either at the level of the cell membrane or within the cell itself, increasing the risk of CNS involvement.
3. Note use of vacuum extractor for delivery. Assess infant for presence of cephalhematoma and excessive ecchymosis or petechiae.
Rationale: Resorption of blood trapped in fetal scalp tissue and excessive hemolysis may increase the amount of bilirubin being released and cause jaundice.
4. Review infant’s condition at birth, noting need for resuscitation or evidence of excessive ecchymosis or petechiae, cold stress, asphyxia, or acidosis.
Rationale: Asphyxia and acidosis reduce affinity of bilirubin to albumin.
5. Keep infant warm and dry; monitor skin and core temperature frequently.
Rationale: Cold stress potentiates release of fatty acids, which compete for binding sites on albumin, thereby increasing the level of freely circulating (unbound) bilirubin.
6. Initiate early oral feedings within 4–6 hr following birth, especially if infant is to be breastfed. Assess infant for signs of hypoglycemia. Obtain Dextrostix levels, as indicated.
Rationale: Establishes proper intestinal flora necessary for reduction of bilirubin to urobilinogen; decreases enterohepatic circulation of bilirubin (bypassing liver with persistence of ductus venosus); and decreases reabsorption of bilirubin from bowel by promoting passage of meconium. Hypoglycemia necessitates use of fat stores for energy-releasing fatty acids, which compete with bilirubin for binding sites on albumin.
7. Evaluate maternal and prenatal nutritional levels; note possible neonatal hypoproteinemia, especially in preterm infant.
Rationale: Hypoproteinemia in the newborn may result in jaundice. One gram of albumin carries 16 mg of unconjugated bilirubin. Lack of sufficient albumin increases the amount of unbound circulating (indirect) bilirubin, which may cross the blood-brain barrier.
8. Observe infant in natural light, noting sclera and oral mucosa, yellowing of skin immediately after blanching, and specific body parts involved. Assess oral mucosa, posterior portion of hard palate, and conjunctival sacs in dark-skinned newborns.
Rationale: Detects evidence/degree of jaundice. Clinical appearance of jaundice is evident at bilirubin levels >7–8 mg/dl in full-term infant. Estimated degree of jaundice is as follows, with jaundice progressing from head to toe: face, 4–8 mg/dl; trunk, 5–12 mg/dl; groin, 8–16 mg/dl; arms/legs, 11–18 mg/dl; and hands/feet, 15–20 mg/dl. Note: Yellow underlying pigment may be normal in dark-skinned infants.
9. Note infant’s age at onset of jaundice; differentiate type of jaundice (i.e., physiological, breast milk–induced, or pathological).
Rationale: Physiological jaundice usually appears between the 2nd and 3rd days of life, as excess RBCs needed to maintain adequate oxygenation for the fetus are no longer required in the newborn and are hemolyzed, thereby releasing bilirubin, the final breakdown product of heme. Breast milk jaundice usually appears between the 4th and 6th days of life, affecting only 1%–2% of breastfed infants. The breast milk of some women is thought to contain an enzyme (pregnanediol) that inhibits glucuronyl transferase (the liver enzyme that conjugates bilirubin), or to contain several times the normal breast milk concentration of certain free fatty acids, which are also thought to inhibit the conjugation of bilirubin. Pathological jaundice appears within the first 24 hr of life and is more likely to lead to the development of kernicterus/bilirubin encephalopathy.
10. Apply transcutaneous jaundice meter.
Rationale: Provides noninvasive screening of jaundice, quantifying skin color in relation to total serum bilirubin.