Donna M. Schultz

Mary F. Terhaar


Destruction of old red blood cells (RBCs) is a normal and adaptive process in newborns as it is across the life span. When RBCs die, they are lysed and bilirubin is released as a by-product. Under certain conditions, the rate of RBC destruction exceeds the body’s ability to eliminate bilirubin, which results in excess levels of the waste product circulating in the bloodstream. This condition is called hyperbilirubinemia, or jaundice. Jaundice is the yellow coloration of skin and sclera that results when excessive bilirubin levels accumulate in skin and mucous membranes.

During pregnancy, the placenta, attached to the fetus, removes bilirubin along with other waste from the fetal bloodstream. Once delivery is complete and the umbilical cord is cut, the newborn must activate his or her own hepatic pathways to conjugate and eliminate bilirubin along with other wastes through the gastrointestinal system (Cohen, Wong, & Stevenson, 2010). It is the imbalance of RBC destruction and hepatic function that produces hyperbilirubinemia.


Hyperbilirubinemia has two distinct presentations, physiologic and pathologic, which are distinguished by the timing, etiology, and severity of the jaundice. Approximately 60% to 85% of all term newborns will develop clinical signs of hyperbilirubinemia (Azzuqa & Watchko, 2015).

Physiologic jaundice in the newborn is a normal, adaptive process; commonly it is self-correcting, time-limited, and lacking in clinical significance. The condition results during normal transition to extrauterine life when the newborn breaks down fetal RBCs even as the kidneys, liver, and gastrointestinal system are assuming responsibility for elimination of waste. This increase in waste product generation precedes functional capacity for elimination. Bilirubin levels usually peak between 3 and 5 days of life and start to decrease by the end of the first week. This is the presentation of physiologic jaundice.

Pathologic jaundice occurs in a relatively small group of newborns. The jaundice presents before 24 hours of life, with total bilirubin levels rising to exceed 5 mg/dL, or greater than the 95th percentile on the Bhutani nomogram (Bhutani, Vilms, & Hamerman-Johnson, 2010). Multiple factors increase the risk for pathologic jaundice, including prematurity, polycythemia, hemolytic disease, genetic abnormalities such as G6PD or Gilbert’s disease, sepsis, blood cell irregularities, extensive bruising, abnormal pooling of blood as seen in cephalohematoma, family history of jaundice, inefficient feeding, and dehydration. Newborns of Asian, Arabic, or Mediterranean ethnicity face greater risk as well. 161A thorough medical history from the mother is important so that health care providers can identify risk factors and monitor the baby for pathologic jaundice (Cohen et al., 2010).

The first cases of jaundice, icterus neonatorum, were described in the late 19th century as a benign and self-limiting yellowing of the skin and the sclera that generally disappeared by the end of the baby’s stay in the hospital (which was 10–14 days in the late 19th century; Cashore, 2010). A second, more severe form of jaundice icterus gravis was associated with significant anemia, neurologic abnormalities, and increased mortality (Cashore, 2010). The acute phase of this condition is named bilirubin-induced encephalopathy (BIND) and the resultant long-term sequelae are identified as kernicterus. Bilirubin is a neurotoxin in large doses. Both BIND and kernicterus result when bilirubin levels become too high, allowing the toxin to cross the blood–brain barrier and deposit in the basal ganglia producing serious neurologic damage (American Academy of Pediatrics [AAP] Subcommittee on Hyperbilirubinemia, 2004). Kernicterus has not been reported in infants with peak TSB levels less than 20 mg/dL (Bhutani et al., 2004). However, it has not been determined at what level kernicterus can occur.

Because length of hospital stay for the mother–baby dyad has radically decreased, careful monitoring for hyperbilirubinemia is key to newborn well-being. In the case of spontaneous vaginal delivery, mother and newborn are commonly discharged to home by 48 hours after the birth. In the case of birth by cesarian section, mother and newborn are commonly discharged to home at approximately 72 hours. In both cases, discharge takes place before bilirubin levels can be expected to peak. This discrepancy motivated The Joint Commission to issue a sentinel event detailing the rise in BIND and kernicterus. In response, the AAP revised guidelines for the management of hyperbilirubinemia and rates began to decline (2004). As a result, The Joint Commission retired their sentinel alert. Best practice now calls for all newborns to be screened for hyperbilirubinemia before discharge to home.

Clinical Aspects


Early assessment of risk for hyperbilirubinemia is essential. Family history, maternal history, and progression of the pregnancy and labor are all relevant to risk assessment. It is important to make note of any discrepancy between maternal, paternal, and newborn blood and Rh type; use of antibiotics or oxytocin during pregnancy or labor; prolonged second stage of labor; use of mechanical assistance with delivery (vacuum or forceps); any trauma or bruising to the fetus or newborn; as well as presence of cephalohematoma. Each of these findings is associated with increased risk.

A transcutaneous bilirubin (TcB) level is routinely obtained within the first 12 to 24 hours of life. TcB measurements are a noninvasive way to obtain a cutaneous bilirubin level and to determine if a serum bilirubin level needs to 162be drawn (Maisel, Coffey, & Kring, 2015). Abnormal values are brought to the attention of the responsible health care provider.

Use of the Bhutani nomogram for infants 35 or more weeks gestational age, with the four risk-zone stratification, is best practice for monitoring newborns with hyperbilirubinemia (AAP Committee on Hyperbilirubinemia, 2004). Infants whose total bilirubin levels are plotted in the high-risk zone should receive phototherapy. The number of banks of lights is determined by the bilirubin level. An infant’s discharge should be delayed until a pattern of declining bilirubin levels is documented (Bhutani et al., 2010).

Infants whose bilirubin levels rise to the high–intermediate risk zone should be sent home only if feeding, voiding, and stooling appropriately. A bilirubin level at discharge must be documented. A follow-up appointment should be scheduled for the following day after discharge with the family’s primary care provider (PCP) to monitor the bilirubin level.

Phototherapy promotes conjugation of bilirubin, which allows it to be eliminated in urine and stool. Aside from hydration and monitoring, phototherapy is the most commonly used intervention for the jaundiced newborn (American Academy of Pediatrics, 2004). Blue to green light (wavelengths 460–490 nm) most effectively facilitates conjugation of bilirubin and is used in treatment of the newborn (Muchowski, 2014). Fluorescent or halogen lights and light emitting diodes (LED) are commonly used (Muchowski, 2014). Exposure to these lights with as much skin exposed as possible for as much time as possible maximizes effect. Eye shields are used to protect the infant and need to be placed carefully to prevent them from becoming loose, leaving the eyes unprotected. Phototherapy can lead to burns, retinal damage, temperature instability, dehydration, rashes, and loose stools.


Frequent breastfeeding (or bottle feeding if the parents choose) is key. A delay in breast milk production can lead to mild dehydration in the infant. Skin-to-skin contact between mother and newborn is begun in the delivery room or birthing suite and continued unless the newborn or maternal conditions prohibit the practice. Monitoring of urine and stool output helps to determine sufficiency of intake.

Care pathways and electronic health record (EHR) documentation systems, which incorporate checklists, help assure proper identification of all risk factors and support provision of individualized care. These approaches have been established as effective means to reduce errors of omission and promote early identification of newborns who require vigilant monitoring and careful discharge planning. Care pathways and the EHR should capture and report the initial transcutaneous bilirubin (TcB) level within the first 12 to 24 hours of life. Abnormal values documented over time, measured in hours of life, should be brought to the attention of the responsible health care provider.

163Educating families about hyperbilirubinemia by nursing is key. Families need to understand the need for phototherapy and to be supported as they experience separation from the infant during treatment (Muchowski, 2014). Parents should understand the importance of close primary care follow-up, because often the infant should be discharged before normal bilirubin peak levels. Families must require understanding about the effects of hyperbilirubinemia such as sleepiness, decreased wet diapers, stooling, and feeding as well as when to call their PCP.


Parents should be given a copy of the infant’s discharge summary and the bilirubin nomogram so the PCP has accurate information to transition the baby into the primary care setting and develop an appropriate plan of care. Parents should be provided with education and resources to consult after discharge to home. Many health care systems provide home health team visits and lactation support.

Early identification of risk, early detection of rising bilirubin levels, and early treatment are key to, and timely resolution of, the problem. These same elements of care are key to avoiding readmissions.


Hyperbilirubinemia is one of the most common complications seen in newborn infants. Hydration, monitoring, and phototherapy are usual practices. Nonetheless, the evidence to support phototherapy is based largely on consensus and expert opinion. Limited strong evidence is available to support the current practice. Research is needed to support meaningful risk assessment and to evaluate treatment options. More important, little evidence is available to predict risk for severe hyperbilirubinemia, kernicterus, or readmission.

American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. (2004). Clinical practice guideline: Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics, 114(1), 297–316. doi:10.1542/peds.114.1.297

Azzuqa, A., & Watchko, J. F. (2015). Bilirubin concentrations in jaundiced neonates with conjunctival icterus. The Journal of Pediatrics, 167(4), 840–844. doi:10.1016/j.jpeds.2015.06.065

Bhutani, V. K., Vilms, R. J., & Hamerman-Johnson, L. (2010). Universal bilirubin screening for severe neonatal hyperbilirubinemia. Journal of Perinatology, 30(Suppl.), S6–S15. doi:10.1038/jp.2010.98

Cashore, W. (2010). A brief history of neonatal jaundice. Medicine and Health, Rhode Island, 93(5), 154–155. Retrieved from www.rimed.org/medhealthri/2010-05/2010-05-154.pdf


Only gold members can continue reading. Log In or Register to continue

Jun 30, 2018 | Posted by in NURSING | Comments Off on Hyperbilirubinemia
Premium Wordpress Themes by UFO Themes