A nurse caring for a term newborn. which assessment finding predispose occurrence of jaundice?

Hyperbilirubinemia is the elevation of serum bilirubin levels that is related to the hemolysis of RBCs and subsequent reabsorption of unconjugated bilirubin from the small intestines. The condition may be benign or place the neonate at risk for multiple complications/untoward effects.

The newborn‘s liver is immature, which contributes to icterus, or jaundice. The liver cannot clear the blood of bile pigments that result from the normal postnatal destruction of red blood cells. The higher the blood bilirubin level is, the deeper jaundice and the greater risk for neurological damage. Physiological jaundice is normal, while pathological jaundice is more serious, which occurs within 24 hours of birth, and is secondary to an abnormal condition, such ABO-Rh incompatibility. The normal rise in bilirubin levels in preterm infants is slower than in full-term infants. It lasts longer, which predisposes the infant to hyperbilirubinemia or excessive bilirubin levels in the blood.

Physiological jaundice is the most common type of newborn hyperbilirubinemia. This unconjugated hyperbilirubinemia presents in newborns after 24 hours of life and can last up to the first week. Pathological jaundice is defined as the appearance of jaundice in the first 24 hours of life due to an increase in serum bilirubin levels greater than 5 mg/dl/day, conjugated bilirubin levels ≥ 20% of total serum bilirubin, peak levels higher than the normal range, and the presence of clinical jaundice greater than two weeks. Breast milk jaundice occurs in breastfed newborns between the first and third day of life but peaks by day 5 to 15, with a decline occurring by the third week of life (Morrison, 2021).

In the past, hemolytic disease of the newborn was most often caused by an Rh blood type incompatibility. Because the prevention of Rh antibody formation has been available for almost 50 years, the disorder is now most often caused by an ABO incompatibility. In both instances, because the fetus has a different blood type than the mother, the mother builds antibodies against the fetal red blood cells, leading to hemolysis of the cells, severe anemia, and hyperbilirubinemia.

The nursing care plan for clients with hyperbilirubinemia involves preventing injury/progression of the condition, providing support/appropriate information to family, maintaining physiological homeostasis with bilirubin levels declining, and preventing complications.

Risk For Injury (CNS Involvement)

Bilirubin-induced brain injury in the neonatal period has detrimental effects on neurodevelopment that persist into childhood, contributing to childhood developmental disorders. Unconjugated bilirubin is a potent antioxidant that may be useful for protecting against oxidative injuries, but it becomes a potent neurotoxin once it crosses the blood-brain barrier. Because bilirubin toxicity involves a myriad of pathological mechanisms, can damage most types of brain cells, and affect brain circuits or loops that influence cognition, learning, behavior, sensory, and language, the clinical effects of bilirubin-induced neurotoxicity are likely to be manifold (Amin et al., 2018).

Nursing Diagnosis

• Risk for Injury (CNS involvement)

Risk factors

• Prematurity 
• Hemolytic disease 
• Asphyxia
• Acidosis 
• Hypoproteinemia 
• Hypoglycemia

Possibly evidenced by

• [Not applicable]

Desired Outcomes

• The neonate will display indirect bilirubin levels below 12 mg/dl in term infants at three days of age.
• The neonate will show resolution of jaundice by the end of the 1st wk of life.
• The neonate will be free of CNS involvement.

Nursing Assessment and Rationales

1. Assess infant/maternal blood group and blood type.
ABO incompatibility affects 20% of all pregnancies and most commonly occurs in mothers with type O blood, whose anti-A and anti-B antibodies pass into fetal circulation, causing RBC agglutination and hemolysis. ABO and Rh incompatibilities increase the risk for jaundice. Maternal antibodies cross the placenta in Rh-negative women who had previously sensitized due to Rh-positive infants. Antibodies attach to fetal RBCs and increase the risk of hemolysis.

2. Assess the infant in daylight.
This prevents distortion of actual skin color through the use of artificial lighting. Most infants do not appear jaundiced at birth because the maternal circulation has evacuated the rising indirect bilirubin level. With birth, progressive jaundice, usually occurring within the first 24 hours of life, will begin, indicating that a hemolytic process is occurring in both Rh and ABO incompatibility.

3. Review infant’s condition at birth, noting the need for resuscitation or evidence of excessive ecchymosis or petechiae, cold stress, asphyxia, or acidosis.
Asphyxia and acidosis reduce the affinity of bilirubin to albumin. A study found that perinatal asphyxia was negatively associated with neonatal hyperbilirubinemia. This might be explained by acidosis in asphyxia is generally corrected soon after birth before significant hyperbilirubinemia develops in preterm infants. Although one study from Pakistan showed birth asphyxia was a risk factor for severe jaundice (Aynalem et al., 2020).

4. Review intrapartal records for specific risk factors, such as low birth weight (LBW) or intrauterine growth restriction (IUGR), prematurity, abnormal metabolic processes, vascular injuries, abnormal circulation, sepsis, or polycythemia.
Certain clinical conditions may cause a reversal of the blood-brain barrier, allowing bound bilirubin to separate either at the cell membrane level or within the cell itself, increasing the risk of CNS involvement. The higher the blood bilirubin level is, the deeper jaundice and the greater the risk for neurological damage.

5. Observe the infant on the sclera and oral mucosa, yellowing of skin immediately after blanching, and specific body parts. Assess oral mucosa, posterior portion of the hard palate, and conjunctival sacs in dark-skinned newborns.
The yellow discoloration of the skin and sclera in neonates diagnosed with jaundice results from the accumulation of unconjugated bilirubin. Neonatal jaundice first becomes visible on the face and forehead (Hansen & Aslam, 2017). Clinical appearance of jaundice is evident at bilirubin levels >7–8 mg/dl in full-term infants. Note: Yellow underlying pigment may be normal in dark-skinned infants.

6. Evaluate maternal and prenatal nutritional levels; note possible neonatal hypoproteinemia, especially in preterm infants.
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. The binding of compounds to albumin may reduce their toxicity, such as in the case of unconjugated bilirubin in the neonate. Albumin is also involved in maintaining acid-base balance as it acts as a plasma buffer (Gounden et al., 2021).

7. Note infant’s age at onset of jaundice; differentiate the type of jaundice (i.e., physiological, breast milk–induced, or pathological).
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. Some women’s breast milk is thought to contain an enzyme (pregnanediol) that inhibits glucuronyl transferase (the liver enzyme that conjugates bilirubin) or contain several times the normal breast milk concentration of certain free freezer 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.

8. Assess infant for progression of signs and behavioral changes.
Excessive unconjugated bilirubin (associated with pathologic jaundice) has an affinity for extravascular tissue, including the basal ganglia of brain tissue. Behavior changes associated with kernicterus usually occur between the 3rd and 10th days of life and rarely occur before 36 hours of life. The characteristic clinical manifestations of kernicterus that are routinely described and are consistent with neuropathological findings include athetoid cerebral palsy, paralysis of upward gaze, and hearing disorders. However, these may represent only “the tip of the iceberg” (Amin et al., 2018).

9. Evaluate infant for pallor, edema, or hepatosplenomegaly
These signs may be associated with hydrops fetalis, Rh incompatibility, and in utero hemolysis of fetal RBCs. With Rh incompatibility, an infant may not appear pale at birth despite the red cell destruction that occurred in utero because the accelerated production of red cells during the last few months in utero compensates to some degree for the destruction. The liver and spleen may be enlarged from attempts to destroy damaged blood cells. Suppose the number of red cells has significantly decreased. In that case, the blood in the vascular circulation may be hypotonic to interstitial fluid, causing fluid to shift from the lower to higher isotonic pressure by osmosis, resulting in extreme edema. Hydrops fetalis is a Greek term that refers to a pathologic accumulation of at least two or more cavities with a fluid collection in the fetus.

10. Assess the neonate’s bilirubin blood levels regularly.
Phototherapy success is determined by frequently measuring serum bilirubin levels. Neonatal hyperbilirubinemia is extremely common because almost every newborn develops an unconjugated serum bilirubin level of more than 1.8 mg/dL during the first week of life. Significant jaundice was defined according to gestational and postnatal age and leveled off at 14 mg/dL at four days in preterm infants and 17 mg/dL in the term infants (Hansen & Aslam, 2017).

11. Assess infant for signs of hypoglycemia.
Hypoglycemia necessitates fat stores for energy-releasing fatty acids, which compete with bilirubin for binding sites on albumin. A study reported that 70.8% of late preterm neonates and 29.1% of term neonates has at least one neonatal morbidity like neonatal jaundice, hypoglycemia, respiratory morbidities, and sepsis. They observed jaundice in 55.1% of late preterm neonates who required phototherapy, and hypoglycemia was found in 8.8% of late preterm neonates (Salman et al., 2021).

Nursing Interventions and Rationales

1. Initiate early oral feedings within 4–6 hours following birth, especially if the infant is breastfed. 
This establishes proper intestinal flora necessary for reducing bilirubin to urobilinogen; decreases the enterohepatic circulation of bilirubin (bypassing the liver with the persistence of ductus venosus), and decreases reabsorption of bilirubin from the bowel by promoting passage of meconium. A delay in enteral feeding may limit intestinal motility and bacterial colonization, resulting in decreased bilirubin clearance (Aynalem et al., 2020).

2. Keep infant warm and dry; frequently monitor skin and core temperature.
Cold stress potentiates the release of fatty acids, which compete for binding sites on albumin, thereby increasing freely circulating (unbound) bilirubin. A neutral thermal environment permits the infant to maintain a normal core temperature with minimum oxygen consumption and caloric expenditure. Preterm infants have little or no muscular activity; they remain in an extended posture because of a lack of muscle tone; they cannot shiver.

3. Apply transcutaneous jaundice meter.
Since visual assessment of jaundice is not accurate, both the American Academy of Pediatrics and the Spanish Association of Pediatrics recommend that all newborns as of 35 weeks of gestation undergo screening for hyperbilirubinemia by measuring either total serum bilirubin (SB) or transcutaneous bilirubin (TcB). Transcutaneous bilirubinometry measures the bilirubin subcutaneously, and therefore, TcB is not the same value as SB. although current jaundice meters have been designed to agree as closely as possible with SB (Maya-Enero et al., 2021).

4. Discontinue breastfeeding for 24–48 hr, as indicated. Assist mother as needed with the pumping of breasts and reestablishment of breastfeeding.
Opinions vary as to whether interrupting breastfeeding is necessary when jaundice occurs. However, formula ingestion increases GI motility and excretion of stool and bile pigment, and serum bilirubin levels begin to fall within 48 hours after discontinuation of breastfeeding. Certain factors present in the breast milk of some mothers may also contribute to the increased enterohepatic circulation of bilirubin (breast milk jaundice). Beta-glucuronidase may play a role by uncoupling bilirubin from its binding to glucuronic acid, thus making it available for reabsorption (Hansen & Aslam, 2017).

5. Monitor laboratory studies, as indicated: 

• Direct and indirect bilirubin.
  Bilirubin appears in two forms: direct bilirubin, which is conjugated by the liver enzyme glucuronyl transferase, and indirect bilirubin, which is unconjugated and appears in a free form in the blood or bound to albumin. Elevated levels of indirect bilirubin best predict the infant’s potential for kernicterus. Elevated indirect bilirubin levels of 18–20 mg/dl in the full-term infant or13–15 mg/dl in preterm or sick infants are significant (Hansen & Aslam, 2017).

• Total serum bilirubin level.
  Usually, a total serum bilirubin level test is the only one required in an infant with moderate jaundice who presents on the typical second or third day of life without a history or physical findings suggestive of a pathologic process (Hansen & Aslam, 2017).

• Direct/indirect Coombs’ test on cord blood.
  Positive results of the indirect Coombs test indicate the presence of antibodies (Rh-positive or anti-A, anti-B) in the mother’s and newborn’s blood; positive results of the direct Coombs test indicate the presence of sensitized (Rh-positive, anti-A, or anti-B) RBCs in the neonate.

• CO2-combining power; Reticulocyte count and peripheral smear.
  A decrease is consistent with hemolysis. Excessive hemolysis causes reticulocyte count to increase. Smear identifies abnormal or immature RBCs. The reticulocyte count provides an indirect insight into the bone marrow condition by distinguishing if the anemia is related to inadequate RBC production or accelerated loss/destruction (Szigeti & Staros, 2014).

• Hemoglobin/hematocrit (Hb/Hct).
  Elevated Hb/Hct levels (Hb 22 g/dl; Hct 65%) indicate polycythemia, possibly caused by delayed cord clamping, maternal-fetal transfusion, twin-to-twin transfusion, maternal diabetes, or chronic intrauterine stress and hypoxia, as seen in low birth weight (LBW) infant or infant with compromised placental circulation. Hemolysis of excess RBCs causes elevated bilirubin levels with 1 g of Hb yielding 35 mg of bilirubin. Low Hb levels (14 mg/dl) may be associated with hydrops fetalis or Rh incompatibility occurring in utero and causing hemolysis, edema, and pallor.

• Total serum protein or serum albumin levels.
  Low serum protein levels (3.0 g/dl) indicate a reduced binding capacity for bilirubin. Serum albumin levels appear to be a useful adjunct in evaluating the risk of toxicity levels because albumin binds bilirubin in a ratio of 1:1 at the primary high-affinity binding site (Hansen & Aslam, 2017).

6. Calculate plasma bilirubin-albumin binding capacity.
This aids in determining the risk of kernicterus and treatment needs. When the total bilirubin value divided by total serum protein level is <3.7, the danger of kernicterus is very low. However, the risk of injury is dependent on the degree of prematurity, presence of hypoxia or acidosis, and drug regimen (e.g., sulfonamides, chloramphenicol) (Hansen & Aslam, 2017).

7. Initiate phototherapy per protocol, using fluorescent bulbs above the infant or bile blanket (except for newborns with Rh disease).
Phototherapy causes photooxidation of bilirubin in subcutaneous tissue, thereby increasing the water solubility of bilirubin, which allows rapid excretion of bilirubin in stool and urine. The rate of bilirubin reduction is related to phototherapy, so an exchange transfusion is the only appropriate treatment. Phototherapy is discontinued when the bilirubin level steadily declines to 14 mg/dL.

8. Administer enzyme induction agent  (phenobarbital, ethanol) as appropriate.
Medications are not usually administered in infants diagnosed with physiologic neonatal jaundice. However, in certain instances, phenobarbital, an inducer of hepatic bilirubin metabolism, has been used to enhance bilirubin metabolism. Several studies have shown that phenobarbital effectively reduces mean serum bilirubin values during the first week of life (Hansen & Aslam, 2017).

9. Assist with preparation and administration of exchange transfusion.
Exchange transfusion can be used as therapy for blood incompatibility, wherein it removes approximately 85% of sensitized red cells. It reduces the serum concentration of indirect bilirubin and can prevent heart failure in infants with severe anemia or polycythemia. The type of blood used for transfusion is O Rh-negative blood, even if an infant’s blood type is positive; if Rh-positive or type A or B blood was given, the maternal antibodies that entered the infant’s circulation would destroy this blood also, and the transfusion would be ineffective.

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