View Entire Collection
By Clinical Topic
Diabetes – Summer 2012
Future of Nursing Initiative
Heart Failure - Fall 2011
Influenza - Winter 2011
Nursing Ethics - Fall 2011
Trauma - Fall 2010
Traumatic Brain Injury - Fall 2010
Fluids & Electrolytes
Sometimes in nursing, we encounter a clinical problem so frequently that it becomes so routine, expected, and familiar that we are lulled into thinking it unimportant. This is often the case with neonatal jaundice. Two of 3 full-term newborns, and virtually all premature newborns will develop jaundice, so what is the big deal?
Nature has left us with a bit of a conundrum when it comes to neonatal jaundice. Bilirubin, the source of jaundice, is a well-known antioxidant,1 with protective effects that rival those of vitamin E. The newborn's intestine secretes an enzyme that actually encourages the return of bilirubin to the circulation.2,3 Breastfed babies have higher bilirubin levels than formula-fed babies.4 Is Mother Nature trying to tell us something? Have we overlooked an evolutionary advantage-could bilirubin actually be good for babies?
An intriguing notion, but even if some bilirubin is good for babies, regrettably, the dividing line between "harmless" (or even beneficial) and "toxic" bilirubin levels is unknown. This fact compels us to treat practically any significant jaundice as potentially harmful. No matter how many jaundiced babies we see in a day, or a week, or a year, we must approach every single one as the baby who, if the bilirubin level is permitted to rise unchecked, could suffer permanent neurological damage.
I love the "stopped-up sink" analogy for viewing the problem of hyperbilirubinemia in the newborn.5 A baby's bilirubin level stems from the balance between production and elimination of bilirubin in the body.6 Bilirubin production is like water running from the faucet, and bilirubin elimination is the drain. If the water is running (bilirubin being produced) and the drain is open (bilirubin being eliminated), the sink does not fill up, and bilirubin does not accumulate in the body. However if the water is running too fast (overproduction) or the drain is clogged (underelimination), the bilirubin level climbs. Many factors can increase the bilirubin load (such as hemolysis or bruising), and others can impair its elimination (such as insufficient feeding intake, bowel obstruction, or immature liver conjugation), and all are additive. With so many variables in the mix, is it any wonder that jaundice is so common?
It is our responsibility as nurses to recognize these variables as risk factors for a rising serum bilirubin concentration after an infant is discharged from the nursery and is no longer under our watchful eyes. We must supplement our subjective assessment skills with objective technology and, combined with the latest and best evidence, identify newborns who require closer monitoring or treatment to eliminate the threat of bilirubin encephalopathy. We must use education to make parents our partners in protecting their infants from harm. When treatment is indicated, we must implement it efficiently, effectively, and safely. Above all, we must guard against the complacency that might lead us to ignore jaundice simply because it is so common.
In this special supplement of Advances in Neonatal Care, 3 articles are presented to assist us to achieve these goals. In "Managing jaundice in full-Term Infants," nurse practitioner Susan Simmons Holcomb summarizes the latest guidelines from the American Academy of Pediatrics for managing jaundice in newborn infants of 35 or more weeks' gestation. These guidelines focus on prevention and enumerate detailed strategies for hospitals to implement as they develop their standards of care for managing this common clinical condition.
The article "Fundamentals of Phototherapy for Neonatal Jaundice," originally written in 2006, has been updated for 2011 to reflect the state of the science in phototherapy for the treatment of neonatal hyperbilirubinemia. The effectiveness of phototherapy is greatly influenced by the skills, knowledge, and attention to detail on the part of the nurse who implements this treatment.
Finally, this compilation includes NANN's original position statement, "Prevention of Acute Bilirubin Encephalopathy and Kernicterus in Newborns," which reiterates the organization's support of recent national guidelines for the assessment and management of severe hyperbilirubinemia in newborn infants. This important document emphasizes the role of neonatal nurses and nursing leaders in developing and adhering to organizational policies consistent with these guidelines. We hope that you will find these articles interesting as well as instructive. This supplement has been generously supported by an educational grant from Draeger.
1. Stocker R, Yamamoto Y, McDonagh AF, Glazer AN, Ames BN. Bilirubin is an antioxidant of possible physiological importance. Science. 1987;235:1043-1046. [Context Link]
2. Baranano DE, Rao M, Ferris CD, Snyder SH. Biliverdin reductase: a major physiologic cytoprotectant. Proc Natl Acad Sci USA. 2002;99:16093-16098. [Context Link]
3. Gourley GR, Arend RA. Beta-glucuronidase and hyperbilirubinaemia in breast-fed and formula-fed babies. Lancet. 1986;1:644-646. [Context Link]
4. Adams JA, Hey DJ, Hall RT. Incidence of hyperbilirubinemia in breast- vs. formula-fed infants. Clin Pediatr (Phila). 1985;24:69-73. [Context Link]
5. Stevenson DK, Dennery PA, Hintz SR. Understanding newborn jaundice J Perinatol. 2001;21:S21-S24 [Context Link]
6. Kaplan M, Muraca M, Hammerman C, Rubaltelli FF, Vilei MT, Vreman HJ. Imbalance between production and conjugation of bilirubin: a fundamental concept in the mechanism of neonatal jaundice. Pediatrics. 2002;110:e47. [Context Link]
NANN Board of Directors March 2010
Assessment and management of hyperbilirubinemia in the newborn is critical in order to prevent associated complications, including acute bilirubin encephalopathy (ABE) and bilirubin-related brain damage, or kernicterus.
As the professional voice of neonatal nursing, the National Association of Neonatal Nurses (NANN) recommends the practice of universal screening using total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) measurements, as well as efforts by neonatal nurses to educate parents and identify strategies within their institutions and practices to enhance the processes of diagnosing and managing hyperbilirubinemia.
National Assocation of Neonatal Nurses
Neonatal nurses must be proactive in the assessment and management of hyperbilirubinemia in the newborn, and screening is a key intervention in the prevention of ABE and kernicterus. NANN supports universal screening using TSB or TcB measurements, which help to assess the risk of subsequent severe hyperbilirubinemia. A top priority for neonatal nurses is to provide written and verbal information about newborn jaundice so that all families are educated about this condition. Neonatal nurses must continue to take steps to increase awareness and identify strategies within their institutions and practices to enhance the processes of diagnosing and managing hyperbilirubinemia.
During the first week after birth, more than 60% of apparently healthy full-term and late-preterm newborns develop hyperbilirubinemia, and most are discharged from their birth hospitals before the usual peak of TSB (age 72-120 hours). Hyperbilirubinemia typically resolves by 7-10 days of age, and the outcome is usually benign. However, approximately 5%-ll% of infants will develop severe hyperbilirubinemia, defined as having TSB above the 95th percentile for age in hours, that requires treatment with phototherapy (Bhutani, Johnson, & Keren, 2004; Ebbesen et al., 2005; Manning, Todd, Maxwell, & Piatt, 2007). Without appropriate intervention, a progressive increase in hyperbilirubinemia to TSB values greater than 25 or 30 mg/dl_ (above the 99th percentile for age in hours) places otherwise healthy neonates at risk of kernicterus (Smitherman, Stark, & Bhutani, 2006). In 2002 the National Quality Forum declared kernicterus and TSB concentrations greater than or equal to 30 mg/dL to be "never events" adverse, preventable medical occurrences that should never happen. The relationship between the extremely high levels of hyperbilirubinemia and bilirubin neurotoxicity is not known because routine surveillance is not available. It has been estimated that the risk of kernicterus in infants with TSB greater than 30 mg/dL is about one in seven infants (Ebbesen et al.; Manning et al.).
Neonates at risk for the development of severe hyperbilirubinemia include
* those of 35-36 weeks' gestational age
* those with indications of inadequate breast-feeding or dehydration
* those having siblings who had jaundice
* those having predischarge TSB or TcB in the high-risk zone
* those in whom jaundice was observed in the first 24 hours
* those having isoimmune or other hemolytic disease (e.g., glucose-6-phosphate dehydrogenase [G6PD] deficiency)
* those with significant bruising or cephalhematoma
* those with G6PD deficiency (which may be present in as many as 12.8% of African-American males [Kaplan, Herschel, Hammerman, Hoyer, & Stevenson, 2004])
* those of East Asian or Mediterranean heredity.
The initial neurotoxicity of extremely elevated bilirubin levels results in ABE, which may progress to kernicterus. No evidence exists that neurotoxicity occurs at a specific bilirubin concentration. The critical level in an otherwise healthy neonate is likely influenced by postnatal age, maturity, duration of hyperbilirubinemia, and rate of TSB rise (Bhutani, Johnson, & Keren, 2005). The presenting signs of ABE are subtle and nonspecific and can be discerned by assessing the infant's mental status, muscle tone, and cry. Some signs are feeding difficulties; lethargy, with an altered awake-sleep pattern; irritability, fussiness, being difficult to console; and intermittent arching.
Advanced signs of ABE are cessation of feeding, bicycling movements, inconsolable irritability and shrill crying, seizures, fever, and coma. Long-term morbidity-including choreoathetoid palsy, sensorineural hearing loss, gaze paresis, dental hypoplasia, and cognitive impairment-can result if the elevated bilirubin levels are not reduced during the time when neurotoxicity may be reversible (Johnson, Bhutani, & Brown, 2002; Soorani-Lunsing, Woltil, & Hadders-Algra, 2001).
In 2001, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO, known since 2007 simply as the Joint Commission) issued a sentinel event alert notifying hospitals and healthcare providers that kernicterus threatens otherwise healthy newborns (JCAHO, 2001). A warning on the danger of kernicterus was also issued by the Centers for Disease Control and Prevention (CDC) in 2001, and the National Quality Forum (2002) declared kernicterus and TSB concentrations equal to or greater than 30 mg/dL "never events" In July 2004, the Subcommittee on Hyperbilirubinemia of the American Academy of Pediatrics (AAP) published its clinical practice guideline "Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation" and a similar guideline was published in 2007 by the Canadian Paediatric Society. In a commentary on and update of AAP's 2004 guideline, Maisels and colleagues recommended universal discharge screening, combined with an assessment of clinical risk factors (of which gestational age and exclusive breast-feeding are the most important) and a targeted follow-up (Maisels et al., 2009).
In 2004 JCAHO released a second sentinel event alert regarding hyperbilirubinemia and the prevention of kernicterus in which it recommended that all hospital and healthcare professionals caring for newborns follow the 2004 AAP clinical guideline (JCAHO, 2004).
NANN supports the recommendations of JCAHO (2004), AAP (2004), the Canadian Paediatric Society (2007), and Maisels and colleagues (2009), the key elements of which are listed below:
1. Successful breastfeeding should be promoted and supported because research shows that frequent breast-feeding (8-12 times per day) decreases the incidence of severe hyperbilirubinemia.
2. Nursery protocols for the identification and evaluation of hyperbilirubinemia should be established.
* Hospitals should adopt facility-wide policies and procedures that maintain an adequate standard of care for all newborns in order to prevent ABE and kernicterus.
* Bilirubin levels should be carefully monitored in infants found to be jaundiced in the first 24 hours of life.
* Jaundice should be assessed regularly at least every 8-12 hours, and nurses should have independent authority to obtain a TSB or TcB level.
3. Education for healthcare providers must emphasize that visual inspection is not reliable as the sole method for assessing jaundice.
4. Bilirubin levels must be interpreted according to the infant's age in hours.
5. Closer surveillance of infants with a gestational age of less than 38 weeks is necessary because of their higher risk for severe hyperbilirubinemia.
6. All infants should be assessed for adequacy of breast-feeding and for the risk of severe hyperbilirubinemia before discharge. Universal discharge screening should be combined with an assessment of clinical risk factors (of which gestational age and exclusive breast-feeding are the most important) and a targeted follow-up.
7. Parents should receive written and verbal information about jaundice.
8. Follow-up care should be based on time of discharge and risk assessment.
9. Phototherapy or exchange transfusions are to be used for treatment when indicated.
* All nurseries should have the equipment to provide intensive phototherapy.
* Breast-feeding should continue if possible for the infant receiving phototherapy or nutritional supplementation.
Neonatal nurses should be knowledgeable about identifying, tracking, and, when necessary, testing and treating infants for severe hyperbilirubinemia in order to prevent ABE and kernicterus. Predischarge measurement of the bilirubin level by TSB or TcB, combined with an assessment of clinical risk factors, should be used to assess for the risk for severe hyperbilirubinemia for all full-term and late-preterm infants discharged from an institution. Nursing leaders can promote patient safety by ensuring that their facility's protocols support nurses in performing a TSB or TcB measurement without an order from a physician or neonatal nurse practitioner. Neonatal nurses should ensure that protocols have been established for the routine assessment of jaundice, reporting of bilirubin levels according to a newborn's age in hours, and documentation through the use of an hour-specific bilirubin nomogram.
Neonatal nurses should also promote breast-feeding and provide lactation support to mothers and families. Neonatal nurses play a pivotal role in providing discharge instructions to the family. Written and verbal instructions should include basic facts about jaundice, the risk factors for jaundice, the significance of jaundice, instructions on checking for jaundice, information on follow-up appointments, and conditions or changes in the infant about which the family should notify healthcare providers.
Further prospective research is needed to identify the potential long-term outcomes of infants with hyperbilirubinemia and the risk of undertreatment. Optimal breast-feeding is an important preventive strategy for severe hyperbilirubinemia. Neonatal nurse researchers should continue to focus on conducting well-designed studies that produce evidence needed to guide best practice on improving breast-feeding support for mothers.
American Academy of Pediatrics, Subcommittee on Hyperbilirubinemia. (2004). Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics, 114(1), 297-316.
Bhutani V. K., Johnson L. H., Keren R. (2004). Diagnosis and management of hyperbilirubinemia in the term neonate: For a safer first week. Pediatric Clinics of North America, 51(4), 843-861 [Context Link]
Bhutani V., Johnson L. H., Keren R. (2005, ). Treating acute bilirubin encephalopathy-Before it's too late. Contemporary Pediatrics. Retrieved January 15, 2010, from http://www.modernmedicine.com/modernmedicine/article/articleDetail.jsp?id=161379. [Context Link]
Canadian Paediatric Society. (2007). Guidelines for detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants (35 or more weeks' gestation). Paediatrics and Child Health, 12(5), 1B-12B.
Centers for Disease Control and Prevention. (2001). Kernicterus in full-term infants: United States, 1994-1998. MMWR Morbidity and Mortality Weekly Report, 50, 491-494.
Centers for Disease Control and Prevention. (2009). Jaundice/Kernicterus. Retrieved January 8, 2010, from http://www.cdc.gov/ncbddd/dd/kernichome.htm.
Ebbesen F., Andersson C., Verder H., Grytter C., Pedersen-Bjergaard L., Petersen J. R., et al.. (2005). Extreme hyperbilirubinaemia in term and near-term infants in Denmark. Acta Paediatrica, 94, 59-64. [Context Link]
Johnson L. H., Bhutani V. K., Brown A. K. (2002). System-based approach to management of neonatal jaundice and prevention of kernicterus. Journal of Pediatrics, 140(A), 396-403. [Context Link]
Joint Commission on Accreditation of Healthcare Organizations. (2001, ). Kernicterus threatens healthy newborns. Sentinel Event Alert, 18. Retrieved January 8, 2010, from http://www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_18.htm. [Context Link]
Joint Commission on Accreditation of Healthcare Organizations. (2004, ). Revised guidance to help prevent kernicterus. Sentinel Event Alert, 31. Retrieved January 8, 2010, from http://www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_31.htm. [Context Link]
Kaplan M., Herschel M., Hammerman C., Hoyer J. D., Stevenson D. K. (2004). Hyperbilirubinemia among African American, glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics, 114(2), e213-e219. [Context Link]
Maisels M. J., Bhutani V. K., Bogen D., Newman T. B., Stark A. R., Watchko J. F. (2009). Hyperbilirubinemia in the newborn infant >=35 weeks' gestation: An update with clarifications. Pediatrics, 124(A), 1193-1198. [Context Link]
Manning D., Todd P., Maxwell M., Piatt M. (2007). Prospective surveillance study of severe hyperbilirubinaemia in the newborn in the UK and Ireland. Archives of Disease in Childhood, Fetal and Neonatal Edition, 92, F342-F346. [Context Link]
National Quality Forum. (2002). Serious reportable events in healthcare: A consensus report. Washington, DC: Author. Retrieved December 7, 2009, from http://www.qualityforum.org/Publications/2002/Serious_Reportable_Events_in_Healt.
Smitherman H., Stark A. R., Bhutani V. K. (2006). Early recognition of neonatal hyperbilirubinemia and its emergent management. Seminars in Fetal and Neonatal Medicine, 11(3), 214-224. [Context Link]
Soorani-Lunsing I., Woltil H. A., Hadders-Algra M. (2001). Are moderate degrees of hyperbilirubinemia in healthy term neonates really safe for the brain? Pediatric Research, 50(6), 701-705. [Context Link]
Bhutani V. K., Johnson L. H., Schwoebel A., Gennaro S. (2006). A systems approach for neonatal hyperbilirubinemia in term and near-term newborns. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 35(4), 444-455.
Eggert L. D., Wiedmeier S. E., Wilson J., Christensen R. D. (2006). The effect of instituting a prehospital-discharge newborn bilirubin screening program in an 18-hospital health system. Pediatrics, 117(5), e855-e862.
Ip S., Chung M., Kulig J., O'Brien R., Sege R., Glicken S., et al.. (2004). An evidence- based review of important issues concerning neonatal hyperbilirubinemia. Pediatrics, 114(1), el30-el53.
Keren R., Bhutani V. (2007). Predischarge risk assessment for severe hyperbilirubinemia. NeoReviews, 8(2), e68-e76. Retrieved January 15, 2010, from http://ne0reviews.aappublicati0ns.0rg/cgi/c0ntent/full/8/2/e68.
Keren R., Luan X., Friedman S., Saddlemire S., Cnaan A., Bhutani V. K. (2008). A comparison of alternative risk-assessment strategies for predicting significant neonatal hyperbilirubinemia in term and near-term infants. Pediatrics, 121(1), el70-el79.
Kuzniewicz M. W., Escobar G. J., Newman T. B. (2009). Impact of universal bilirubin screening on severe hyperbilirubinemia and phototherapy use. Pediatrics, 124(4), 1031-1039.
Newman T. B. (2009). Universal bilirubin screening, guidelines, and evidence. Pediatrics, 124(4), 1199-1202.
Riskin A., Tamir A., Kugelman A., Hemo M., Bader D. (2008). Is visual assessment of jaundice reliable as a screening tool to detect significant neonatal hyperbilirubinemia? Journal of Pediatrics, 152(6), 782-787.
Schwoebel A., Gennaro S. (2006). Neonatal hyperbilirubinemia. Journal of Perinatal and Neonatal Nursing, 20(1), 103-107.
Stark A. R., Lannon C. M. (2009). Systems changes to prevent severe hyperbilirubinemia and promote breastfeeding: Pilot approaches. Journal of Perinatology, 29, S53-S57.
Stokowski L. A. (2002). Family teaching toolbox: Newborn jaundice. Advances in Neonatal Care, 2(2), 115-116.
Trikalinos T. A., Chung M., Lau J., Ip S. (2009). Systematic review of screening for bilirubin encephalopathy in neonates. Pediatrics, 124(A), 1162-1171.
U.S. Preventive Services Task Force, Agency for Healthcare Research and Quality. (2009). Screening of infants for hyperbilirubinemia to prevent chronic bilirubin encephalopathy: U.S. Preventive Services Task Force recommendation statement. Pediatrics, 124(4), 1172-1177.
Copyright (C) 2010 by the National Association of Neonatal Nurses. No part of this statement may be reproduced without the written consent of the National Association of Neonatal Nurses.
4700 W. Lake Avenue, Glenview, IL 60025-1485, 800/451-3795 * 847/375-3660 * Fax 866/927-5321 http://www.nann.org
Phototherapy is the use of visible light for the treatment of hyperbilirubinemia in the newborn. This relatively common therapy lowers the serum bilirubin level by transforming bilirubin into water-soluble isomers that can be eliminated without conjugation in the liver. The dose of phototherapy is a key factor in how quickly it works; dose in turn is determined by the wavelength of the light, the intensity of the light (irradiance), the distance between the light and the baby, and the body surface area exposed to the light. Commercially available phototherapy systems include those that deliver light via fluorescent bulbs, halogen quartz lamps, light-emitting diodes, and fiberoptic mattresses. Proper nursing care enhances the effectiveness of phototherapy and minimizes complications. Caregiver responsibilities include ensuring effective irradiance delivery, maximizing skin exposure, providing eye protection and eye care, careful attention to thermoregulation, maintaining adequate hydration, promoting elimination, and supporting parent-infant interaction.
Phototherapy is the use of visible light for the treatment of hyperbilirubinemia, or jaundice, in the newborn.1 It is perhaps the most common nonroutine therapy applied in the newborn population. How phototherapy came to be is a fascinating story, with a nurse at its center.2
Sister Ward, the nurse in charge of the Premature Unit at Rochford General Hospital in Essex, England, firmly believed in the restorative powers of fresh air and sunshine (Figure 1). On sunny days, she would wheel the infants outdoors into the hospital courtyard, returning them to the nursery just before the doctors-who were not as keen on this practice-arrived for ward rounds. One day in 1956, Sister Ward showed the physicians an undressed infant whose skin was pale except for a triangular area that appeared much yellower than the rest of its body. Dr R. H. Dobbs asked her if she had painted the baby's skin with iodine. She denied having done so, telling him that what she held in her arms was a jaundiced infant whose color had faded except in an area that had been covered by the corner of a sheet.2
Subsequently, physicians and scientists at Rochford Hospital discovered that the levels of bilirubin pigment in tubes of blood left sitting in the sun also dropped dramatically. Putting these observations together, the idea of phototherapy for neonatal jaundice was born. The very first phototherapy unit incorporating an artificial light source instead of natural sunlight was devised and tested by Cremer et al3 at Rochford Hospital, and the results were reported in The Lancet, in 1958 (Figure 2).
Phototherapy was not used in the United States until the landmark study of Lucey et al4 was published in Pediatrics a full decade later. This randomized controlled trial demonstrating the effectiveness of phototherapy led to its acceptance as a simple, inexpensive, and relatively safe way to prevent hyperbilirubinemia in premature infants.
Humans continuously form bilirubin, and newborn infants produce relatively more bilirubin than any other age group. The typical bilirubin load of the newborn is quite high, 2 to 3 times that of an adult. Bilirubin is a product of the normal destruction of circulating erythrocytes (which have a shortened lifespan in the newborn infant) and increased turnover of cytochromes.5 Some infants have excessive bilirubin production, and a correspondingly elevated load of unconjugated bilirubin (Table 1).
Unconjugated bilirubin is lipid-soluble and must be transported to the liver in the plasma, bound reversibly to albumin.6 In the liver, bilirubin is transported across hepatic cell membranes, where it binds to ligandin for conjugation. A liver enzyme, uridine diphosphoglucuronate glucuronosyltransferase, conjugates bilirubin, converting it to water-soluble bilirubin pigments that can be excreted into the bile and exit the body via the intestines, or, to a lesser degree, filtered through the kidneys (Figure 3). Bilirubin pigments in the gut that are not eliminated can be reabsorbed into the circulation as unconjugated bilirubin, essentially recycling the bilirubin load, a process called enterohepatic recirculation. Thus, babies with reduced conjugation or elimination of bilirubin are also at risk for hyperbilirubinemia (Table 1). A more detailed explanation of newborn bilirubin metabolism can be found in an article in the April 2002 issue of this journal.7
Phototherapy converts bilirubin that is present in the superficial capillaries and interstitial spaces of the skin and subcutaneous tissues to water-soluble isomers that are excretable without further metabolism by the liver (Figure 4). Neonatal jaundice expert Maisels suggests that phototherapy is much like a percutaneous drug.6,8 When phototherapy illuminates the skin, an infusion of discrete photons of energy are absorbed by bilirubin much like a drug molecule binds to a receptor. Bilirubin molecules in light-exposed skin undergo relatively quick photochemical reactions-configurational isomerization, structural isomerization, and photooxidation-to form nontoxic, excretable isomers. These bilirubin isomers have different shapes than the native isomer, are more polar, and can be excreted from the liver into the bile without undergoing conjugation or requiring special transport for their excretion.9 Urinary and gastrointestinal elimination remain important to the process of reducing the bilirubin load.
The aim of phototherapy is to curtail rising serum bilirubin and prevent its toxic accumulation in the brain, where it can cause the serious, permanent neurological complication known as kernicterus. Where the technology is readily available, phototherapy has nearly abolished the need for exchange transfusion to treat hyperbilirubinemia. Phototherapy is typically used either prophylactically or therapeutically.
* In preterm infants or those with a known hemolytic process, it is often used prophylactically, to prevent a significant rise in serum bilirubin.
* In late-preterm and full-term infants, it is administered at therapeutic doses to reduce excessive bilirubin levels and avoid development of bilirubin encephalopathy.
The photoisomerization of bilirubin begins almost instantaneously when the skin is exposed to light.8 Unlike unconjugated bilirubin, the photoproducts of these processes are not neurotoxic.8 Therefore, the most important intervention for the severely hyperbilirubinemic infant is to initiate phototherapy without delay.
A robust relationship exists between the dose of phototherapy and the rate of decline in serum bilirubin level.8 Dose of phototherapy is determined by several key factors:
* Spectral qualities of the light source used (wavelength range and peak);
* Intensity of the light (irradiance);
* Distance between the light and the infant's skin;
* Body surface area exposed by the irradiated field or "footprint."
The most effective light sources for degrading bilirubin emit light in a relatively narrow wavelength range (400 to 520 nanometers, or nm), with a peak of 460 +/- 10 nm.1 At these wavelengths, light penetrates the skin well and is maximally absorbed by bilirubin.8 Blue, green, and turquoise light (the blue-green spectrum) are considered the most effective, and some evidences suggest that given equal irradiance levels, the turquoise spectral range is more efficient in reducing bilirubin than blue because of greater skin penetration.9
A popular, but mistaken belief holds that phototherapy delivers ultraviolet light. The phototherapy systems currently used for newborn infants do not emit significant amounts of ultraviolet radiation.8
Irradiance is the light intensity, or number of photons delivered per square centimeter of exposed body surface. The delivered irradiance determines the effectiveness of phototherapy; the higher the irradiance, the faster the decline in serum bilirubin level.10 Spectral irradiance, quantified as [mu]W/cm2/nm, varies with the design of the light source. It can be measured with a spectral radiometer sensitive to the effective wavelength of light. Intensive phototherapy requires a spectral irradiance of 30 [mu]W/cm2/nm, delivered over as much of the body surface as possible.
Light intensity is inversely related to the distance between the light and the body surface. A simple way to increase irradiance is to move the light closer to the infant. Caution must be exerted when positioning halogen phototherapy lamps, which cannot be positioned closer to the infant than recommended by their manufacturers without incurring the risk for a burn.11
The greater the body surface area exposed to light, the faster the decline in serum bilirubin. Many light sources used in neonatal care do not expose a sufficient area of skin to the light. The light source may have an adequate spectral irradiance in the center of the light's footprint; however, irradiance decays significantly at the periphery of the light.12 The result is that only an insufficient proportion of the infant's body surface area receives effective treatment. This problem can be solved by positioning the infant properly within the footprint of the light or using multiple light sources for coverage of at least 80% of the body surface13 (Figure 5).
The size of the exposed body surface area, along with the level of irradiance, determines the spectral power of the phototherapy application, which in turn influences its effectiveness.14 The larger the exposed body surface and stronger the light, the higher the spectral power.
A number of different light sources are commercially available for neonatal phototherapy. Each has its own advantages and disadvantages. Different neonatal phototherapy systems achieve vastly different irradiance levels, and this can influence their clinical effectiveness.12
Combined phototherapy is often the treatment of choice for very preterm infants with hyperbilirubinemia, because it has been shown to achieve lower serum bilirubin levels with a shorter duration of treatment, and to significantly reduce exchange transfusions.15 One method frequently employed to provide combination phototherapy is to use an overhead unit above the infant (fluorescent bank light, gallium nitride light-emitting diode [LED], or halogen lamp) and a fiberoptic mattress underneath the infant. A commercially available system combines banks of fluorescent tubes on each side, with a transparent mattress containing fan-cooled fluorescent bulbs (Bili-Bassinet, Natus Medical Incorporated, San Carlos, California) (Figure 6).
The gallium nitride LED is one of the most recent innovations in phototherapy (Figure 7). These devices provide high irradiance in the blue to blue-green spectrum without excessive heat generation.6 Light-emitting-diode units are efficient, long-lasting, and cost-effective.1 The latest models incorporate amber LEDs to counteract the "blue hue" effect that can irritate caregivers.1
Halogen lamp sources deliver phototherapy using 1 or more quartz halogen bulbs (Figure 8). It is possible to achieve sufficient irradiance with halogen light sources; however, devices designed with a single lamp produce a circle of light with high irradiance only in the center. Halogen systems are compact and caregiver-friendly; however, quartz halogen bulbs carry the disadvantage of generating significant amounts of heat. Manufacturer's recommendations for safe maximal distance should be followed.11 A newer device that incorporates a metal halide bulb (Giraffe SPOT PT Lite, GE Healthcare, Waukesha, Wisconsin) is an improvement over earlier halogen spotlights. The light source is located in a light box, away from the infant, resulting in a cooler light surrounding the infant. This high-intensity light is transmitted through a light pipe in a flexible gooseneck that can be adjusted for maximum light footprint.
Often referred to as "bank lights," fluorescent tube phototherapy devices have been around the longest (Figure 9). It is vital to realize, however, that not all fluorescent tubes are the same. Dramatic differences exist in the irradiance produced by different types of fluorescent tubes, even within the same 425- to 475-nm wavelength.11 Bulbs used in this type of phototherapy unit include daylight, cool-white, blue, "special blue" (the most effective), or a combination of these. One system contains 6 blue tubes and 2 white tubes with an optional on/off switch. Caregivers are often bothered by the blue-hue effect produced by all blue tubes, and the blue light can impair assessment of infant skin color. The white light tubes in this unit can be switched on to minimize the blue-hue effect without hindering the effectiveness of the phototherapy treatment.
Fluorescent tube units are often positioned too far away from the infant to be effective. They should be positioned as close to the infant as possible.8 Maisels recommends that these units be placed 10 cm above nude full-term infants in bassinets for effective phototherapy. This method achieves an irradiance of 50 [mu]W/cm2 while maintaining normal body temperature8 and has been successfully implemented in jaundiced infants 37 or more weeks' gestation.16
Fiberoptic devices contain a tungsten-halogen bulb that delivers light via a cable into a plastic pad containing fiberoptic fibers (Figure 10). The pad remains cool and can be placed directly under an infant to increase the skin surface area that is exposed. The pad can also be wrapped around the infant's midsection to provide phototherapy while the infant is being held. Because the spectral power of the pad alone is low, it is commonly used in conjunction with overhead lights to provide double phototherapy.
Phototherapy is much more than just switching on a light. The efficiency with which phototherapy achieves a decline in serum bilirubin level is in large part determined by nursing care. Appropriate nursing care also minimizes the potential side effects and complications of phototherapy.
Position phototherapy lamps or mattresses to provide the most complete skin exposure possible. Light sources should be as close to the infant as possible, with the exception of halogen-lamp phototherapy units. Overhead units that incorporate rubberized feet to rest on the incubator surface should be lowered until they are in contact with the top of the incubator.
Periodic checks of spectral irradiance produced by different phototherapy units should be conducted to ensure adequate irradiance delivery.11 Irradiance is measured with a radiometer, an instrument that gauges light in the effective wavelength for phototherapy (Figure 11). Measurements do vary among different radiometers; use the instrument recommended by the manufacturer of the corresponding phototherapy system.
Measured irradiance can vary widely depending on where the measurement is taken.11 Irradiance in the center of the illuminated area can be double that of the periphery.11 It is preferable to take several measurements in the illuminated area at infant skin level and average them for a determination of overall effective irradiance.8
It is fairly common to see terms such as "single," "double," and "triple" used in orders prescribing phototherapy. Such terms refer only to how many pieces of equipment should be used to deliver phototherapy, and not to a specific target dose, or irradiance level. In other words, "single phototherapy" is 1 phototherapy unit, "double" is 2 units, and so forth. Naturally, it is hoped that 2 phototherapy units will deliver more efficient phototherapy than a single unit, probably through improved skin coverage. However, no standard definitions of "single," "double," and "triple" phototherapy describe phototherapy dosages in terms of target irradiance levels.
Opaque eye shields must be used during phototherapy to protect the infant's eyes from retinal damage (Figure 12). To adequately block the transmission of light, carefully apply eye coverings by first closing the infant's eyes and then applying shields securely. Avoid eye patches that are too tight, as they may apply undue pressure to the infant's delicate eye. Turn off the phototherapy unit and remove eye patches periodically to assess eyes for drainage, edema, and evidence of infection, to provide visual stimulation, and to encourage parent-infant interaction as appropriate on the basis of the infant's clinical status.
Complications of using eye patches include apnea (from displaced eye patches obstructing the nares), eye irritation, corneal abrasion, blocked tears ducts, and conjunctivitis.17 Proper eye care is essential. Gently clean the infant's eyes with sterile cotton or soft gauze moistened with sterile water or saline, starting with the inner canthus of the eye and moving outward in a single, smooth stroke. A separate cleansing pad should be used for each eye. Gloves should be worn when providing eye care. A clean internal layer should be inserted or patches should be changed at regular intervals.
The largest surface area of the infant's body, the trunk, should be positioned in the center of the light, where irradiance is highest. In most cases, it is not necessary to remove diapers or boundary materials used for postural support while providing phototherapy. Removing diapers and nesting materials around jaundiced, low-risk preterm infants weighing more than 1500 g at birth does not shorten the length of treatment.18 It is not known, however, whether diapers and/or boundary materials affect the bilirubin decline in smaller, less mature infants or in larger, more mature infants with severe hyperbilirubinemia.
The American Academy of Pediatrics recommends removing diapers for intensive phototherapy, when the serum bilirubin is approaching exchange transfusion level.11 Light-permeable diapers are also commercially available (BiliBottoms, CAS Medical Systems, Inc, Branford, Connecticut).
Frequent turning to expose different areas of skin has not been shown to improve the effectiveness of conventional (single) phototherapy.19-21
One study actually reported that the serum bilirubin levels of infants maintained in a supine position without turning declined significantly faster than those of infants who were turned prone/supine every 2 to 3 hours.20
Some phototherapy units can cause a significant increase in the infant's body temperature.22 When phototherapy is directed over an incubator, immediate and sustained fluctuations can occur in the thermal environment.23 Thermal instability can occur when using either the skin- or air-control mode of the incubator. With inadequate monitoring, vigilance, and adjustments to the thermal environment, the infant can easily develop hypothermia or hyperthermia during phototherapy.
When phototherapy is initiated during air control mode, a rapid rise in body temperature usually necessitates a downward adjustment in the air temperature set point. When phototherapy is discontinued, the air temperature set point may require an upward readjustment to compensate for the loss of heat from the phototherapy lights.
During skin control mode, the air temperature usually drops when phototherapy is initiated because the additional heat warms the infant, and less environmental heat support is required. Using skin control mode is generally preferred during phototherapy because this automatic compensatory mechanism keeps the infant's body temperature within normal limits as long as the lights remain on. However, if the lights are turned off abruptly, the infant's temperature can also drop precipitously. It will then take some time for the air temperature to rise again and rewarm the infant.
The photoproducts of bilirubin require elimination from the body in the stool or urine. Some of the photochemical reactions induced by phototherapy are reversible, meaning that the isomers can be converted back to unconjugated bilirubin if they are not eliminated in the stool.6 Enteral feeding is essential to promote stooling in hyperbilirubinemic infants. Lumirubin, an irreversible product of structural isomerization of bilirubin, is excreted in the urine as well as in the bile, so an adequate urine output is also important. An ongoing assessment of the infant's urine output is an important measure not only of hydration but also of elimination of bilirubin. The infant's urine may appear dark in color as bilirubin elimination increases.
Watery stools and diarrhea have been observed in infants undergoing phototherapy. These characteristic dark greenish stools are related to the increased excretion of unconjugated bilirubin from the intestines.6 Protective skin care is necessary to prevent perianal skin breakdown from watery stools.
Several studies have documented an increase in transepidermal water loss during phototherapy.24,25 Excessive fluid losses via the skin are of particular concern in the smallest, most immature infants during the first week of life. These losses can be exacerbated by phototherapy, although insensible water losses are not as high with fiberoptic or LED phototherapy devices.5 Increasing fluid intake has been shown to shorten the duration of phototherapy in full-term neonates.26 Some infants may experience intestinal fluid losses from a high volume of loose stools during phototherapy. Although it is important to maintain adequate hydration, routine supplementation with intravenous fluids is not recommended.6 For breastfed infants with evidence of dehydration, supplementation with a milk-based formula inhibits the enterohepatic circulation of bilirubin and may improve the efficacy of phototherapy.6
Maintaining fluid balance by increasing incubator humidity might also be counterproductive, especially if high levels of humidity are used. A recent study27 found that when humidification was set at more than 90%, irradiance delivery from an LED phototherapy unit was reduced by 15% and that from a halogen phototherapy unit by 45%. The mist and water condensation within the incubator are postulated to interfere with irradiance delivery.
Phototherapy necessarily separates the neonate from its mother and may interfere with the process of establishing lactation. Unless jaundice is severe, phototherapy can be safely be interrupted at feeding time to allow continuation of breastfeeding, parental visits, and skin-to-skin care.6 Remove the eye patches during these visits. If the serum bilirubin level is approaching the exchange transfusion threshold, and/or if the infant has escalating pathologic jaundice, phototherapy should be continuously maintained.6
The most significant decline in bilirubin level occurs in the first 4 to 6 hours after initiating phototherapy. Conventional (single) phototherapy can decrease the serum bilirubin by up to 22% in the first 24 hours of treatment. Double phototherapy can produce a fall of as much as 29% in the first 24 hours,28 and intensive phototherapy can lower the bilirubin level by as much as 5 mg/dL/h (85 [mu]mol/L/h) In infants with rapidly rising bilirubin levels, stabilizing the bilirubin level or slowing its rate of rise should be considered valid measures of the success of therapy.29
Phototherapy lamps must be turned off while drawing blood samples for serum bilirubin testing, because the lights will act on the bilirubin pigments in the blood sample, causing the bilirubin level to decline, thereby providing erroneous data to the care team.3 Transcutaneous bilirubinometry can also be used for the evaluation of bilirubin levels in infants receiving phototherapy by using the unexposed skin of the forehead, under the infant's eye patches, for these measurements.30
After discontinuing phototherapy the bilirubin level often rises slightly, a phenomenon known as "rebound." Rebound hyperbilirubinemia is usually an elevation of no more than 1 to 2 mg/dL31,32; however, postphototherapy rebound to clinically significant levels can occur.33 Infants at greatest risk of significant postphototherapy rebound in serum bilirubin levels requiring closer follow-up include the following:
* Premature infants;
* Infants with ongoing hemolysis (ie, positive direct Coombs tests);
* Infants treated before 72 hours of age.33
A serum bilirubin measurement obtained 24 hours after discontinuation of phototherapy will detect rebound hyperbilirubinemia.32
When an infant's serum bilirubin is rising rapidly or approaching exchange transfusion level, intensive phototherapy must be instituted at maximal spectral power. This entails delivering high levels of irradiance (usually 30 [mu]W/cm2/nm or higher) to as much of the infant's surface area as possible.1 The most efficient phototherapy units available should be used, and they should be positioned for maximum skin coverage. In these situations, additional surface-area exposure can be achieved by removing the infant's diaper and lining the sides of the bassinet, incubator, or radiant warmer with light-reflecting material such aluminum foil or white linens.34 Intensive phototherapy can produce a decline in serum bilirubin of as much as 10 mg/dL within a few hours in severely hyperbilirubinemic infants.35
Intensive phototherapy may have another, even more important benefit in an infant with a bilirubin level high enough to increase the risk for neurological damage.36 Almost as soon as the lights are switched on, the process of isomerization of bilitubin begins, converting bilirubin molecules into more polar photoisomers, that are unable to cross the blood-brain barrier independently to gain access to the neurons.35 Well before a measurable decline in serum bilirubin occurs, the effects of phototherapy are believed to protect the brain from the neurotoxic effects of bilirubin, although no studies have yet proved this hypothesis.
The irradiance and surface area exposure produced by home phototherapy units are lower than those produced by typical hospital units11 making them less efficient at lowering the serum bilirubin level. Whether a valid indication for home phototherapy exists is questionable; current guidelines state that a bilirubin high enough to warrant treatment should be managed in the hospital.11 In the past, parents have sometimes been told to expose their jaundiced infants to sunlight. Notwithstanding phototherapy's beginnings in the sunny courtyard of an English hospital, this practice is not considered a safe or reliable way to treat jaundice.11 There are reports in the literature of infants developing kernicterus after their parents were instructed to treat their infants' jaundice at home by exposing them to sunlight, in some cases for as little as 15 minutes per day.37 Not only was this very likely to be ineffective but also it probably contributed to delays in recognition of the severity of the hyperbilirubinemia as well as delays in proper treatment.
The most noticeable clinical complication of phototherapy is "bronze baby syndrome," a grayish-brown discoloration of the skin that occurs exclusively in infants with cholestatic jaundice.11 Bronze baby syndrome is believed to occur when the brown photoproducts of porphyrins, especially copper porphyrins, accumulate in the skin and their excretion is impaired by cholestasis.5 Phototherapy can damage red-blood-cell membranes, increasing their susceptibility to lipid peroxidation and hemolysis.1 These effects may contribute to the pathogenesis of disorders common in the very low-birth-weight infant, including bronchopulmonary dysplasia, retinopathy of prematurity, and necrotizing enterocolitis.1 Phototherapy has been associated with patency of the ductus arteriosus38 and ileus in very low-birth-weight infants,39 as well as retinopahty of prematurity.40 Recent evidence also suggests that phototherapy impairs immune system function through alterations of cytokine production.41 Phototherapy has been linked to the development of abnormal melanocytic nevi when the children become older. The evidence for this association is not definitive and has been debated, but at this time, this possible effect cannot be ruled out.42 Although it is not always possible to separate the effects of phototherapy from the effects of hyperbilirubinemia itself, recent research has implicated phototherapy as a risk factor for childhood asthma.43 Other rare side effects include purpura and bulbous eruptions, which can occur in infants with elevated direct bilirubin. Phototherapy is contraindicated in infants with congenital erythropoietic porphyria, because blistering and photosensitivity can result.5
For more than 40 years, phototherapy has been the standard of care for the treatment of hyperbilirubinemia in the newborn. In retrospect, phototherapy may have prevented nearly as much morbidity and mortality in neonatal care as the use of oxygen and has certainly done so with fewer complications. Because we have become so comfortable with this simple therapy, however, we must guard against becoming complacent about the disorder that we are treating. Hyperbilirubinemia in term and preterm infants can, in rare instances, lead to serious complications. It is essential that neonatal caregivers utilize phototherapy to its fullest potential when treating the common but not always benign problem of neonatal hyperbilirubinemia.
1. Vreman HJ, Wong RJ, Stevenson DK. Phototherapy: current methods and future directions. Semi Perinatol. 2004;28:326-333. [Context Link]
2. Dobbs RH, Cremer RJ. Phototherapy. Arch Dis Child. 1975;50:833-836. [Context Link]
3. Cremer RJ, Perryman PW, Richards DH. Influence of light on the hyperbilirubinemia of infants. Lancet 1958;1:1094-1097. [Context Link]
4. Lucey J, Ferriero M, Hewitt J. Prevention of hyperbilirubinemia of prematurity by phototherapy. Pediatrics. 1968;41:1047-1054. [Context Link]
5. Wong RJ, DeSandre GH, Sibley E, Stevenson DK. Neonatal jaundice and liver disease. In: Fanaroff AA, Martin RJ, Walsh MC, eds. Fanaroff and Martin's Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. Philadelphia, PA: Mosby; 2006:1419-1452. [Context Link]
6. Maisels MJ. Jaundice. In: MacDonald MG, Mullett MD, Seshia MMK, eds. Avery's Neonatology. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:768-846. [Context Link]
7. Stokowski LA. Early recognition of neonatal jaundice and kernicterus. Adv Neonatal Care. 2002;2:101-114. [Context Link]
8. Maisels MJ, McDonagh AF. Phototherapy for neonatal jaundice. N Engl J Med. 2008;358:920-928. [Context Link]
9. Ebbesen F, Madsen P, Stovring S, Hundborg H, Agati G. Therapeutic effect of turquoise versus blue light with equal irradiance in preterm infants with jaundice. Acta Paediatr. 2007;96:837-841. [Context Link]
10. Tan KL. The pattern of bilirubin response to phototherapy for neonatal hyperbilirubinemia. Pediatr Res. 1982;16:670-674. [Context Link]
11. American Academy of Pediatrics, Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004;114:297-316. [Context Link]
12. Hart G, Cameron R. The importance of irradiance and area in neonatal phototherapy. Arch Dis Childhood Fetal Neonatal Ed. 2005;90:F437-F440. [Context Link]
13. Buhatin VK. Performance evaluation for neonatal phototherapy. Indian Pediatr. 2009;46:19-21. [Context Link]
14. Hansen TW. Twists and turns in phototherapy for neonatal jaundice. Acta Paediatr. 2010;99:1117-1118 [Context Link]
15. Romagnoli C, Zecca E, Pappaci P, Vento G, Girlando P, Latella C. Which phototherapy system is most effective in lowering serum bilirubin in very preterm infants? Fetal Diagn Ther. 2006;21:204-209. [Context Link]
16. Walker L, Vroman L, Becker J, Anderson F. Open crib phototherapy: using evidence to change practice. Nurs Womens Health. 2007;11:402-404. [Context Link]
17. Fok TF, Wong W, Cheng AF. Use of eye patches in phototherapy: effects on conjunctival bacterial pathogens and conjunctivitis. Pediatr Infect Dis J. 1995;14:1091-1094. [Context Link]
18. Pritchard MA, Beller EM, Norton B. Skin exposure during conventional phototherapy: a randomized controlled trial. J Paediatr Child Health. 2004;40:270-274. [Context Link]
19. Chen C, Liu S, Lai C, Hwang C, Hsu H. Changing position does not improve the efficacy of conventional phototherapy. Acta Paediatr Tw. 2002;43:255-258. [Context Link]
20. Shinwell ES, Sciaky Y, Karplus M. Effect of position changing on bilirubin levels during phototherapy. J Perinatol. 2002;22:226-229. [Context Link]
21. Donneborg ML, Knudsen KB, Ebbesen F. Effect of infants' position on serum bilirubin level during conventional phototherapy. Acta Paediatr. 2010;99:1131-1134. [Context Link]
22. Pezzati M, Fusi F, Dani C, Piva D, Bertini G, Rubaltelli FF. Changes in skin temperature of hyperbilirubinemic newborns under phototherapy: conventional versus fiberoptic device. Am J Perinatol. 2002;19:439-444. [Context Link]
23. Dollberg S, Atherton HB, Hoath SB. Effect of different phototherapy lights on incubator characteristics and dynamics under three modes of servocontrol. Am J Perinatol. 1995;12:55-60. [Context Link]
24. Maayan-Metzger A, Yosipovitch G, Hadad E, Sirota L. Transepidermal water loss and skin hydration in preterm infants during phototherapy. Am J Perinatol. 2001;18:393-396. [Context Link]
25. Grunhagen DJ, De Boer MGJ, De Beaufort AJ, Walther FJ. Transepidermal water loss during halogen spotlight phototherapy in preterm infants. Pediatr Res. 2002;51:402-405. [Context Link]
26. Mehta S, Kumar P, Narang A. A randomized controlled trial of fluid supplementation in term neonates with severe hyperbilirubinemia. J Pediatr. 2005;147:781-785. [Context Link]
27. de Carvalho M, Torrao CT, Moreira ME. Mist and water condensation inside incubators reduce the efficacy of phototherapy. Arch Dis Child Fetal Neonatal Ed. 2011;96:F138-F140. [Context Link]
28. Tan KL. Comparison of the efficacy of fiberoptic and conventional phototherapy for neonatal hyperbilirubinemia. J Pediatr. 1994;125:607-612. [Context Link]
29. Hansen TW. Acute management of extreme neonatal jaundice-the potential benefits of intensified phototherapy and interruption of enterohepatic bilirubin circulation. Acta Paediatr. 1997;86:843-846. [Context Link]
30. Nanjundaswamy S, Petrova A, Mehta R, Hegyi T. Transcutaneous bilirubinometry in preterm infants receiving phototherapy. Am J Perinatol. 2005;22:127-131. [Context Link]
31. Maisels MJ, Kring E. Bilirubin rebound following intensive phototherapy. Arch Pediatr Adolesc Med. 2002;156:669-672 [Context Link]
32. Lazar L, Litwin A, Merlob P. Phototherapy for neonatal nonhemolytic hyperbilirubinemia. Analysis of rebound and indications for discontinuing therapy. Clin Pediatr (Phila). 1993;32:264-267. [Context Link]
33. Kaplan M, Kaplan E, Hammerman C, et al. Post-phototherapy neonatal bilirubin rebound: a potential cause of significant hyperbilirubinemia. Arch Dis Child. 2006;91:31-34 [Context Link]
34. Djokomuljanto S, Quah BS, Surini Y, et al. Efficacy of phototherapy for neonatal jaundice is increased by the use of low-cost white reflecting curtains. Arch Dis Child. 2006;91:F439-F442. [Context Link]
35. Hansen TW. The role of phototherapy in the crash-cart approach to extreme neonatal jaundice. Semin Perinatol. 2011;35:171-174. [Context Link]
36. Ruud Hansen TW. Phototherapy for neonatal jaundice-therapeutic effects on more than one level? Semin Perinatol. 2010;34:231-234 [Context Link]
37. Centers for Disease Control and Prevention. Kernicterus in full-term infants-United States, 1994-1998. Morbid Mortal Wkly Rep. 2001;50:491-494. [Context Link]
38. Barefield ES, Dwyer MD, Cassady G. Association of patent ductus arteriosus and phototherapy in infants weighing less than 1000 grams. J Perinatol. 1993;13:376-380. [Context Link]
39. Raghavan K, Thomas E, Patole S, Muller R. Is phototherapy a risk factor for ileus in high-risk neonates? J Matern Fetal Neonat Med. 2005;18:129-131. [Context Link]
40. Xiong T, Qu Y, Cambier S, Mu D. The side effects of phototherapy for neonatal jaundice: what do we know? What should we do? [published online ahead of print April 1, 2011]. Eur J Pediatr. DOI: 10.1007/s00431-011-1454-1. [Context Link]
41. Kurt A, Aygun AD, Kurt AN, Godekmerdan A, Akarsu S, Yilmaz E. Use of phototherapy for neonatal hyperbilirubinemia affects cytokine production and lymphocyte subsets. Neonatology. 2009;95:262-266. [Context Link]
42. Brewster DH, Tucker JS, Fleming M, et al. Risk of skin cancer after neonatal phototherapy: retrospective cohort study. Arch Dis Child. 2010;95:826-831. [Context Link]
43. Aspberg S, Dahlquist G, Kahan T, Kallen B. Confirmed association between neonatal phototherapy or neonatal icterus and risk of childhood asthma. Pediatr Allergy Immunol. 2010;24(4 part 2):733-739. [Context Link]
bilirubin; hyperbilirubinemia; jaundice; neonatal intensive care; newborn; phototherapy; premature infant
Neonatal hyperbilirubinemia can have serious consequences, including bililrubin encephalopathy and ker- nicterus.1 Bilirubin encephalopathy can be reversed, whereas kernicterus is permanent. Elevated levels of bilirubin lead to the accumulation of unconjugated bilirubin within the brain, which can result in encephalopathy. The consequences of encephalopathy include disability due to deafness, gaze paresis, decreased intelligence, and choreoathetoid cerebral palsy, and rarely, death.2
A newborn produces up to 10 mg/kg/day of bilirubin, most of which is created from the destruction of hemoglobin from red blood cells. Approximately 35 mg of unconjugated, or indirect, bilirubin is formed from each gram of hemoglobin. Bilirubin production is elevated in neonates during the first 24 to 48 hours of life because of their relatively higher hematocrit and more rapid turnover of red blood cells. Conjugation of bilirubin is delayed in newborns during the first hours after birth but increases by about 24 hours of age in the term newborn, reaching adult levels by about 4 days of age. Elimination of bilirubin is further delayed in the preterm infant. An excess of unconjugated bilirubin can result in hyperbilirubinemia.3
Approximately 50% of term infants - those 38 weeks gestation or greater - will develop increased serum total bilirubin levels and visible signs of jaundice in the first 3 to 4 days of life, dissipating by the 6th day. Physiologic jaundice/hyper - bilirubinemia is defined as a serum total bilirubin level of <13 mg/dl or a rise of less than 0.5 mg/dl/hour.3
The incidence of kernicterus peaked in the 1950s and 1960s. Subsequently, kernicterus essentially vanished until the 1990s, when a sudden a rise was again noted. Factors leading to the reappearance of kernicterus are thought to be early discharge, an increase in home births, and an increase in exclusive breast-feeding.4-6
Because hyperbilirubinemia can lead to permanent brain damage, in 2001 the Centers for Disease Control (CDC) urged more stringent identification and management of hyperbilirubinemia in newborns,6 In response to that challenge, in 2004 the American Academy of Pediatrics (AAP) developed its Clinical Practice Guideline: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation.1 The guideline has not been officially updated since its 2004 release; however, as the guideline has been used and new research has become available, recommendations for updating or clarifying the guideline have surfaced. The two works that add to the knowledge base of the guideline include the 2009 US Preventive Services Task Force (USPSTF) guideline, Screening of Infants for Hyperbilirubinemia to Prevent Chronic Bilirubin Encephalopathy,2 and the 2010 work by Maisels, Screening and Early Postnatal Management Strategies to Prevent Hazardous Hyperbilirubinemia in Newborns of 35 or More Weeks of Gestation.4
The 2004 AAP guideline contains four key recommendations for reducing the risk of severe hyperbilirubinemia. The recommendations are aimed not only at reducing the incidence of hyperbilirubinemia but also at minimizing maternal anxiety through education and support; encouraging breastfeeding; and decreasing unnecessary costs and treatment through appropriate identification, follow-up, and therapy. The four recommendations in clude:
* Promote and support breast-feeding.
* Develop nursery protocols to identify hyperbilirubinemia.
Measure total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) level on newborns who become jaundiced within the first 24 hours following birth and interpret the level according to the newborn's age in hours (Figure 2).
Visual determination of jaundice is unreliable.
Complete a thorough assessment of the newborn before discharge to identify risk factors of hyperbilrubinemia (Table 1).
Direct special attention to newborns less than 38 weeks gestation, especially if exclusively breast-fed, because these infants are at greater risk for developing hyperbilirubinemia.
Educate parents about newborn jaundice.
* Initial follow-up, after discharge, is determined by risk of hyperbilirubinemia.
* Phototherapy or exchange transfusions are indicated for treatment of newborns with hyper - bilirubinemia to prevent severe hyperbilirubinemia and possibly bilirubin encephalopathy (kernicterus).
A seeming contradiction of the guideline is seen in the recommendation to promote and support breast-feeding. Exclusive breastfeeding has been identified as potentially one of the major risk factors in the development of hyperbilirubinemia. Although a biologically natural act, breast-feeding requires time for both the mother and the infant to adjust so that the mother supplies sufficient calories and nutrients and the infant ingests enough milk to receive adequate calories and nutrients.4 Therefore, breast-feeding is a risk factor because of insufficient caloric and nutrient intake in the newborn.
Other concerns with breastfeeding include formation of stools that contain less bilirubin when compared to stools of formula-fed infants, as well as smaller cumulative stool output and decreased formation of urobilin in the gastrointestinal tract. Breast-fed infants also demonstrate increased intestinal fat absorption, which permits uptake of bilirubin by adipose cells. In addition, activity of B-glucuronidase is increased in breast milk, which may lead to more rapid absorption of unconjugated bilirubin from the intestine. All of these situations can elevate total serum bilirubin levels.5
To promote and support breastfeeding while at the same time reducing the risk of hyperbilirubinemia associated with breast feeding, mothers should be encouraged to feed 8 to 12 times a day for the first 48 to 72 hours. Although no randomized, controlled trial exists, there appears to be enough supporting evidence to suggest this practice, because increasing the number of feeding times encourages caloric and fluid intake as well as weight gain. Maisels notes that in the kernicterus registry, 123 of the 125 infants who developed kernicterus were exclusively breastfed.4
In order to manage hyperbilirubinemia, the condition must first be identified. As can be seen in the recommendations of the 2004 AAP guideline, screening by total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) level is suggested because visual identification of jaundice is not considered reliable.1 The newer USPSTF guideline, "concludes, that there is not enough evidence to recommend screening; risk-factor assessment, measurement of bilirubin level either TcB or TSB, or a combination, of hyperbilirubinemia in order to prevent chronic bilirubin encephalopathy.' This rather bold statement is based on an extensive review of the literature, conducted from September 2001 through August 2007, that found screening evidence insufficient in four domains: burden of suffering from the condition, potential of harm from the intervention, cost, and current practice.2 These statements should be kept in mind when caregivers develop protocols to enhance and improve patient outcomes.
Nursing protocols that enable the bedside nurse to think critically and intervene when necessary will ensure that the patient experiences the best care and outcome. For hyperbilirubinemia, it is suggested that part of the nursery protocol include standing orders that authorize the nurse to order a TSB when hyperbilirubinemia is suspected either by visual observation or by TcB.4 As stated in the recommendations by the 2004 guideline, visual determination of jaundice is neither a refined nor an accurate skill and therefore cannot be used as the sole means for detecting hyperbilirubinemia.1,4 However, research has provided a scale that can be used to objectify and quantify visual jaundice.3 Jaundice appears as bilirubin levels increase, beginning cephalically and moving caudally; or literally, moving from head to toe.
As jaundice progresses cephalo-caudally, association with TSB values has been made and can be noted in Table 2.4 A clinical pearl may be that if jaundice is not seen below the nipple line, it is unlikely that the TSB is >12 mg/dl, and if jaundice does not extend below the umbilicus it is unlikely that the TSB is >14.6 mg/dl.4
If jaundice is noted on visual inspection before obtaining a TSB level, which is an invasive procedure, the nurse should obtain a TcB if the facility provides this mode of evaluation. TcB measurements can be performed not only in an inpatient setting but also in outpatient settings because of their non-invasiveness and ease of use. Evidence supports the use of TcB in estimating TSB values, but not as a substitute for obtaining TSB values. TcB measures the yellow color of blanched skin and subcutaneous tissues, and thus can be used only to estimate the TSB value and to determine whether a TSB should be drawn. TcB measurements are plotted on the same nomogram as TSB measurements, noting the value of the measurement and the infant s age in hours.4
It should be noted that screening by TSB or TcB is a billable event and thus has the potential to increase insurance premiums, as well as place increased financial burden on the parents.
Prior to discharge, the newborn should be assessed for risk factors for the development of hyperbilirubinemia, especially if the infant is being discharged less than 72 hours after birth. Major risk factors include exclusively breast-feeding, a family history of neonatal jaundice, bruising of the neonate during birth, presence of cephalohematoma, East Asian ethnicity, maternal age >25 years, male gender, glucose-6-phosphate dehydrogenase deficiency, and a gestational age less than 38 weeks.1,4,5 Even though East Asian ethnicity is considered a major risk factor, almost 60% of infants who develop hyperbilirubinemia in the United States are Caucasian.5 Additional risk factors are presented in Table 1.
Before the infant is discharged, parents should be given both written and verbal information about jaundice, including risk factors, identification, and treatment. Preprinted educational materials are readily available. The American Academy of Pediatrics offers a kit covering breast-feeding and jaundice, Sate and Healthy Beginnings, which can be found at http://www.aap.org/bookstore. Stanford Medical University has a web-based tool, the Bili-Tool, which can be found at http://www.bilitool.org. The CDC has also developed a teaching home page for families of newborns with kernicterus. The information can be found at http://www.cdc.gov/ncb-ddd/jaundice/index.html.
Re-evaluation of the newborn is, in large part, determined by when the patient was discharged from the hospital. Recommendations include the infant s first outpatient office visit two days after discharge, if the infant was discharged 72 hours or sooner after birth.4 However, this first visit can be later if the infant is not at risk for hyperbilirubinemia (Table 1) and no other concerns related to birth or discharge have been identified.1,4 At the initial outpatient evaluation, the caregiver should reiterate to the parents the information regarding jaundice and hyperbilirubinemia and answer any questions the parents may have.
The USPSTF found that even though early treatment of hyperbilrubinemia reduces bilirubin levels, there is inadequate evidence that treatment subsequently reduces bilirubin encephalopathy and kernicterus.2 Evidence for definitive harm associated with phototherapy is also incomplete. Potential side effects of phototherapy includes weight loss, gastrointestinal problems, interference with feeding and bonding, and potential development of melanocytic nevi.2 Because of the invasiveness of exchange transfusions, considerable risks to the infant can occur and even though the increased morbidity affects only 5% of patients, even that small a risk in a newborn is too high. Severe side effects include apnea, bradycardia, vasospasm, thrombosis, and necrotizing enterocolitis.3
It should be recognized that hyperbilirubinemia is not a standalone factor for the development of kernicterus. Not all infants with high serum bilirubin levels develop bilirubin encephalopathy or kenicterus. Harm may occur with frequent bilirubin determination include pain from venipuncture or heel sticks, interference with routines of eating and bonding, and increased parental anxiety, as well as the potential for weight loss, gastrointestinal concerns, and possible development of melanocytic nevi.
The USPSTF found significant variations in current methods and practice of screening across the United States and that is why the committee concluded that current evidence does not support universal screening.2 Therefore treatment must be individualized. Initiation-of-treatment considerations include risk factors, TSB levels, and potential for harm from treatment cost.
A pharmaceutical agent for the prevention of hyperbilirubinemia is currently being investigated. The agent, tin mesoporphyrin, is a potent inhibitor of heme oxygenase which can effectively reduce TSB levels. At this time, its costs, side effects, and burden of proof vs. harm have yet to be realized.4
Severe sequelae from hyperbilirubinemia, bilirubin encephalopathy, and kernicterus, although rare, when they occur lead to morbidity and mortality in neonates. Recent research has modified how the 2004 guidelines are practiced in an effort to continue to reduce the potential for harm, while we await an official guideline update.
1. Subcommittee on Hyperbilirubinemia. Clinical practice guideline: management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004; 297-316. [Context Link]
2. US Preventive Services Task Force (USPSTF): Screening of infants for hyperbilirubinemia to prevent chronic bilirubin encephalopathy: US Preventive Services Task force recommendation statement. Agency for Healthcare Research and Quality (AHRQ) 2009. Guideline Summary NGC-7376. Retrieved July 20, 2011 from http://www.guidelines.gov/content.aspx?id=14890&search=hyperbilirubinemia[Context Link]
3. Hartley P: Neonatal Jaundice: Hyperbilirubinemia. http://CEFast.com 2007. Retrieved July 20, 2010 from http://www.guidelines.gov/content.aspx?id=14890&search=hyperbilirubinemia[Context Link]
4. Maisels JJ: Screening an early postnatal management strategies to prevent Hazardous hyperbilirubinemia in newborns 35 or more weeks gestation. Seminars in Fetal & Neonatal Medicine 2010. 15:129-135. [Context Link]
5. Springer SC. WebMD July 1, 2010. Retrieved July 20, 2011 from http://emedicine.medscape.com/article/975276-overview[Context Link]
6. Centers for Disease Control. Kernicterus in full-term infants - United States, 1994-1998. MMWR. 2001;40:491. [Context Link]
Back to Top