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Toward Understanding the Connections Between Infant Jaundice and Infant Feeding
Toward Understanding the Connections Between Infant Jaundice and Infant Feeding Marion Alex, RN, MN, CNM Donna Pierrynowski Gallant, RN, PhD
Parents face a paradox when they are told: Breast is best; bottle-feeding is hazardous to health. But breast-fed babies are more likely to become severely jaundiced than bottle-fed babies, and severe jaundice can lead to brain damage. This article will explore the natural physiology of jaundice with a focus on breast-feeding-associated jaundice, primary prevention of hyperbilirubinemia, and current evidence-based recommendations about feeding jaundice breast-fed infants. © 2008 Elsevier Inc. All rights reserved. Key words: Infant jaundice; Breast-feeding; Bottle-feeding; Acute bilirubin encephalopathy; Fetal neonatal bilirubin metabolism; Primary prevention; Risk for kernicterus
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RIMUM NON NOCERE. Above all, do no harm.—Hippocrates
Case Studies (identities changed and pseudonyms used) Allison, aged 32, tells an office nurse on her 6-week postpartum visit: “I had difficulty nursing my first two babies. And then, with both my children in school, I was determined to get it right this time and exclusively nurse this third baby. Maren was born almost 8 lbs, a beautiful healthy baby girl. A good “nurser,” she had little difficulty catching on. On Day 2 Maren's blood bilirubin levels were slightly elevated, “nothing of concern” I was told. But they kept us in an extra day so that bilirubin levels could be rechecked. The results came back in the night and in the early hours of the morning, a nurse informed me that they were going to give Maren some formula which supposedly would help bring the bilirubin levels down. I was told it was hospital policy. I wanted to speak with my doctor in the morning first, but the nurse persisted and sent another nurse to convince me. No one could explain the physiology, just that it was “policy.” I agreed to give my baby an ounce or two of formula from a cup. Although I was not convinced it was for the baby's benefit, I was not prepared to argue with nurses at 4 in the morning. When my doctor arrived it was decided to place Maren under phototherapy and continue formula feeding until bilirubin levels
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came down. It was an emotional time, as my plan to nurse my child seemed to be slowly slipping away from me. I lacked information, couldn't understand why I couldn't nurse her through the days of phototherapy, and no one seemed able to tell me. I felt I was doing Maren a disservice.” Mary, aged 21 and pregnant with her first baby, tells the public health nurse that she does not want to breast-feed her baby: “My sister tried to breastfeed her baby but her baby got yellow jaundice and needed to be in an incubator for over 3 days. My sister just cried and cried, and when she couldn't make enough breast milk anyway, the doctor said she should switch to formula. I'm not going to bother to try, just in case this problem with breastfeeding jaundice runs in families.” Jane, aged 30, tells a midwife that she is fed up with doctors, nurses, and hospitals and wants a home birth. Jane says that “with my first pregnancy
From the St. Francis Xavier University, Antigonish, Nova Scotia, Canada. Corresponding author: Marion Alex, RN, MN, CNM, St. Francis Xavier University, Box 5000, Antigonish, Nova Scotia, Canada B2G 2W5. E-mail: [email protected] 0882-5963/$-see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.pedn.2007.12.002
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I was clueless, I was induced on my due day, had narcotics in labor, then an epidural, then couldn't push, and then had a vacuum extraction, and then my baby had a cephalohematoma. Then he wouldn't latch, and would scream into my breasts but not suckle. I was so frustrated, and when he got jaundiced I just gave up. The nurses told me not to feel guilty about it, that formula feeding would help his jaundice, but I still feel guilty. Jason has so many allergies and ear infections, and at age 6 he already has a weight problem…. And from what I read it's at least partly due to how I fed him as a baby.” Parents face a paradox when they are told: Breast is best; bottle-feeding is hazardous to health. But breast-fed babies are more likely to become severely jaundiced than bottle-fed babies, and severe jaundice can lead to brain damage. According to Stokowski (2002), the overall incidence of severe jaundice (hyperbilirubinemia) is rising. Severe jaundice is the most common reason for hospital readmission of newborns (Tyler & Hellings, 2003). Jaundice was the principal diagnosis for 27.0% of newborns readmitted to hospitals in Canada in 1991–1992, and 38.8% of newborns in 2000–2001 (Health Canada, 2003). A higher rate of breast-feeding, in conjunction with shorter postpartum hospital stays, is the leading explanation for the high prevalence of jaundice seen today (Stokowski, 2002). With earlier discharge, infants may not be available to health care professionals when bilirubin peaks occur (Bhutani, Johnson, Schwoebel, & Gennaro, 2006). It is imperative to analyze this phenomenon so as not to scuttle breast-feeding efforts but to prevent severe hyperbilirubinemia, promote necessary lactation support, and provide treatment and care to jaundiced breast-fed babies based on the best available evidence. The American Academy of Pediatrics (AAP, 2004, p. 297) calls on clinicians to “reduce the incidence of severe hyperbilirubinemia while minimizing the risks of unintended harm, such as maternal anxiety, decreased breast-feeding, and unnecessary costs of treatment.” Achieving this outcome requires clinicians to understand the physiology of lactation and jaundice and to communicate their knowledge with compassion in a manner that serves to empower parents. This is no easy task when the physiology is complex, the risks are real, and maternal emotions are raw. The terms breast-feeding jaundice or breast milk jaundice are found throughout the published litera-
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ture. Thus, the language health professionals use with childbearing families—of diverse literacy levels— connotes connection between the breast-feeding and/ or the milk and what sounds like a serious medical problem. The above vignettes anecdotally illustrate experiences of mothers who struggle with balancing risks when it is suggested that breast-feeding “causes” jaundice. For nurses also struggling to balance risks, the questions are the following: Why does breast-feeding jaundice happen? How can breast-feeding jaundice be prevented? How can nurses best support breast-feeding mothers whose babies develop severe hyperbilirubinemia? BENEFITS OF BREAST-FEEDING/HEALTH HAZARDS OF BOTTLE-FEEDING The World Health Organization (2003), the AAP (2005), and the Canadian Pediatric Society (Boland, 2005; CPS, 2007) have issued statements calling for exclusive breast-feeding of all infants for the first 6 months of life or longer. These statements are based on extensive evidence of the lifelong benefits of breast-feeding. Factors in human milk promote gastrointestinal mucosal maturation, have immunomodulatory and antiinflammatory functions, and alter gut flora (Oddy, 2002), and breast milk is richer in antioxidants (Aycicek, Erel, Kocyigit, Selek, & Demirkol, 2006). Bottle-feeding is less than ideal. Babies who are not breast-fed are at increased risk of asthma; atopic dermatitis; allergies to foods, pets, or pollens; otitis media; lower respiratory tract infections; gastrointestinal infections; inflammatory bowel disease; obesity; and lower neurodevelopmental and cognitive scores (Anderson, Johnstone, & Remley, 1999; Ball & Wright, 1999; Klement, Cohen, Boxman, & Reif, 2004; Kull, Wickman, Lilja, Nordvall, & Pershagen, 2002; Owen, Martin, Whincup, & Davey-Smith, 2005; Saarinen & Kajosaari, 1995). When breast-feeding does not go as planned for women who intensely want to breast-feed, we must also be concerned with mental health effects. Postpartum depression is prevalent and disabling. Perceiving oneself as “failing” to give birth or breast-feed as hoped for contributes to the etiology of postpartum depression. Many well-meaning people have called for “not making the mother feel guilty.” But as Newman (1998) argues, it is not women who make informed decisions to bottle-feed who feel guilty, but women who want to breastfeed, try, are insufficiently supported, yet know
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bottle-feeding is harmful. Newman (1998) states that what is needed is not avoiding discussion of risks of bottle-feeding, but promotion of breastfeeding coupled with skilled support––something that is not happening in most North American societies. Breast-feeding “failure” associated with jaundice is one reason why women who plan to breast-feed, but cannot, stop breast-feeding. Guilt is what we feel when we know something is wrong; but rather than blame the mother, one could argue that it is our collective culture that is doing something wrong when we fail to appropriately support mothers and babies. Efforts to promote “education of the mother” have been insufficient in enacting change; we also require changes in our collective culture, community, and clinical care systems which honor mother– baby psychophysiology. ACUTE BILIRUBIN ENCEPHALOPATHY AND KERNICTERUS—A BRIEF HISTORY According to AAP (2004), acute bilirubin encephalopathy refers to the acute manifestations of bilirubin toxicity in the first weeks after birth and includes symptoms of lethargy, irritability, hypotonia alternating with hypertonia, and backward arching of neck and trunk. Kernicterus refers to the chronic and permanent sequelae of bilirubin toxicity, which includes severe forms of cerebral palsy, auditory dysfunction, and intellectual handicaps (AAP, 2004). Severe hyperbilirubinemia is a greater problem for infants who are exclusively breast-fed than babies who receive at least some bottled milk (Cohen, 2006; Gourley, 2002). Hyperbilirubinemia, although often benign or even beneficial in babies with jaundice, can on rare occasion be profoundly neurotoxic. Stokowski (2002) notes that preventing kernicterus might be easier if the precise concentration or duration of hyperbilirubinemia leading to neurotoxicity were known. Unfortunately, the mediating variable(s) which leads to kernicterus in a few, but certainly not most, babies with jaundice remain unknown. Wennberg, Ahlfors, Bhutani, Johnson, and Shapiro (2006) note that conclusions about causes of rare events are sparse. In the 1950s, medical literature reported evidence of a link between hyperbilirubinemia and kernicterus and a corresponding search for treatment with exchange transfusions (Mollison & Walker, 1952) and phototherapy (Cremer, Perry-
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man, & Richards, 1958). Hemolytic disease was a common antecedent to kernicterus in these times. As antibody screening and prophylactic use of Rh immune globulin became standard practice in 1983 (Harrod, Hanson, VandeVusse, & Harrod, 2003), the incidence of severe hemolytic disease decreased dramatically. Concomitantly, since the 1950s, formula feeding was the norm in mainstream North America. Massive formula promotion programs led many parents and practitioners to believe formula was superior to breast milk. Even as scientific evidence about benefits of breast-feeding was mounting in the 1970s and 1980s, if there was any concern about breast-feeding not going well, mothers and nurses reached for the baby bottle. With exclusive breastfeeding being rare, breast-feeding-associated jaundice was rare too. By the 1990s, kernicterus seemed to be largely a phenomenon of the past, and calls for a “kinder, gentler” approach to treatment of hyperbilirubinemia emerged (Newman & Maisels, 1992). In 1994, AAP held that many babies were being unnecessarily treated for jaundice and published a practice parameter citing studies that there was no evidence for kernicterus in healthy full-term infants without risk factors for hemolysis such as Rh or ABO incompatibility. AAP (1994) recommended tolerating higher levels of total serum bilirubin before initiation of phototherapy or exchange transfusions. However, in the decade that followed, kernicterus among this population of babies was not eliminated. There was growing concern that some babies with hyperbilirubinemia were “falling through the cracks” and not receiving treatment that could prevent kernicterus. The U.S. Joint Commission on Accreditation of Health Care Organizations (2001) issued a sentinel event alert about the apparent increase in kernicterus in otherwise healthy term and near-term babies. These babies with kernicterus were generally breast-fed and had no other apparent risk factors. Although the incidence was rare, the neurodevelopmental outcomes for those few babies were devastating. Root causes of the rise in kernicterus were seen to be early discharge from hospital with poor follow-up, lack of family education about jaundice, and failure to provide continued lactation support to mothers (Steffansrud, 2004). In 2004, AAP issued an updated clinical practice guideline for management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation to
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provide a framework for the prevention and management of hyperbilirubinemia based on current evidence. According to the guidelines of AAP (2004) and CPS (2007), medical treatment is based on total serum bilirubin levels and involves phototherapy, and in the most severe situations, exchange transfusion in neonatal intensive care. However, AAP (2004) states that the serum bilirubin level by itself, except when it is extremely high and associated with bilirubin encephalopathy, is an imprecise indicator of long-term neurodevelopmental outcome. Most babies with severe hyperbilirubinemia escape without any apparent sequelae, and we do not know why (Wennberg et al., 2006). PHYSIOLOGY OF BREAST-FEEDING JAUNDICE
Forms of Breast-feeding-Related Jaundice Jaundice can occur in both breast-fed and bottle-fed babies. Some causes of hyperbilirubinemia are unrelated to mode of feeding, and the etiology of severe jaundice must be medically investigated. However, regardless of the cause(s), breast-feeding is not contraindicated (AAP, 2004; CPS, 2007). In addition to the disease-related causes of jaundice (e.g., hemolytic disease and liver disease), two forms of breast-feeding-related jaundice occur clinically in otherwise healthy babies and can coexist in the same baby. These two forms are confusingly called breast-feeding jaundice, which is generally of early onset, and breast milk jaundice, which is generally of later onset and lasts longer. Breast-feeding jaundice typically begins on the second or third day of life and is generally due to insufficient milk intake (Steffansrud, 2004). It is perhaps more appropriately termed not-enoughbreast-feeding jaundice. Gartner and Herschel (2001) state that this is the neonatal equivalent of starvation jaundice seen in adults deprived of caloric intake. The other, called breast milk jaundice, begins in healthy weight-gaining babies beginning at 1 to 3 weeks of age and persists for as long as 3 months (Steffansrud, 2004). A reliable diagnosis of breast milk jaundice can be made only on exclusion of pathological causes such as biliary atresia or cystic fibrosis (Ratnavel & Ives, 2005). Newborns with breast milk jaundice appear well and, at present, kernicterus with this type of jaundice has
not been documented (London, Ladewig, Ball, & Bindler, 2007).
Understanding Normal Fetal Neonatal Bilirubin Metabolism To be able to explain these clinical phenomena to parents, infant care providers must understand the physiology involved in bilirubin metabolism. Bilirubin exists in the body in several forms: Unconjugated or indirect bilirubin is lipid soluble. It is generally found bound to albumin in the blood, but some unconjugated bilirubin is not bound to albumin and is called free bilirubin. Conjugated or direct bilirubin is water soluble and ready for excretion in the bile (Thilo, 1999). According to Blackburn (2007), before birth, the placenta efficiently clears bilirubin and, therefore, babies are not born jaundiced. In fetal circulatory anatomy, blood is largely shunted past the liver, and this decreased hepatic circulation limits the capacity of the fetal liver to convert bilirubin to its watersoluble state. With the circulatory changes that occur after birth with the clamping of the cord, hepatic circulation is dramatically increased; the newborn's still-maturing liver then assumes responsibility for bilirubin metabolism, converting lipidsoluble unconjugated bilirubin to water-soluble conjugated bilirubin which can then be excreted. Bilirubin only becomes sufficiently water soluble to enter the bile following hepatic conjugation with glucuronic acid. Once converted to this watersoluble conjugated state, bilirubin passes to the gut. In the gut, it is hydrolyzed by bacteria and converted to urobilinogen, which is oxidized to stercobilin. Stercobilin is what gives feces its characteristic brown color (Blackburn, 2007). Meconium is rich in ready-for-excretion bilirubin. Therefore, babies who stool early and often develop less hyperbilirubinemia. The newborn produces up to 8 to 10 mg/kg/day of bilirubin, more than twice as much as adults do (Blackburn, 2007). This increased bilirubin production is primarily due to a greater circulating red blood cell volume per kilogram. As a physiological adaptation to the relatively oxygen-poor intrauterine environment, the fetus produces comparatively more red blood cells than the newborn does. Fetal hemoglobin and hematocrit levels are significantly higher than infant hemoglobin levels, with cord blood laboratory hematocrit values normally ranging from 43% to 63%, and hemoglobin values normally ranging from 14–20 g/dL (Fanaroff & Martin, 2002). Moreover, neonatal red blood cells
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normally have shorter life spans (80–100 days in term babies and 60–80 days in preterm babies) than do adult red blood cells (120 days; Blackburn, 2007). This comparatively higher fetal red blood cell count becomes unnecessary after birth in the oxygen-richer extrauterine environment, and an expected physiologic catabolism of unnecessary red blood cells occurs. The result is that the healthy newborn has higher bilirubin levels than one would see at any other point in the life span. It is as normal a finding as the twice-as-fast-as-adult's heart and respiratory rates we see in newborns (Maisels, 2006). Visible physiological jaundice is seen in most newborns (AAP, 2004). This phenomenon has been variably described as benign or beneficial. Bilirubin is a potent antioxidant which helps protect the baby from oxidative stress and celldamaging free radicals (Sedlak & Snyder, 2004). Gartner and Herschel (2001) note that the higher range of bilirubin levels in breast-fed infants may be protective because of antioxidant effects. Anthropologically speaking, Thibo (1999) questions why hyperbilirubinemia would be so common in the early days of life unless it conferred some biological advantage. Still, it is the balance of conjugation and elimination of bilirubin that are important. Biliary conversion of bilirubin to its ready-to-excrete form is part of the equation, but the baby must then actually excrete it. Water-soluble bilirubin in the gut is unstable and can be hydrolyzed by the relatively alkaline environment of the intestinal tract and recycled back to the circulation. Absorbed across gut mucosa, this bilirubin is returned to the bloodstream and the portal venous system once again, a process called enterohepatic circulation (Steffansrud, 2004). Hence, the bilirubin reenters the baby's body rather than being excreted and contributes to the load on the neonatal liver once again. Specific enzymes, for example, beta-glucuronidase (Ratnavel & Ives, 2005) or increased amounts of certain fatty acids (Blackburn, 2007) are thought to contribute to prolonging this gutback-to-bloodstream recycling of bilirubin in enterohepatic circulation. Breast milk is rich in beta-glucuronidase; routine infant formula is not (Gourley, Zhanhai, Kreamer, & Kosorok, 2005). The presence of gut flora will minimize enterohepatic circulation as certain intestinal bacteria will change bilirubin to less absorbable forms such as stercobilinogen, but the neonate's gut is sterile at birth and flora are minimal until feeding is
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established. Again, this indicates the need to start breast-feeding as soon as the baby wants to, which for healthy unsedated term babies, is generally in the first hour of life. Bilirubin levels physiologically rise and fall in relation to gestational age, age in hours/days after birth, type of feeding, race (Maisels, 2006), and even altitude. Asian babies overall demonstrate higher bilirubin levels in the first week of life than Caucasian or African American babies (Blackburn, 2007). Babies born at higher altitudes develop higher levels of bilirubin than babies born at sea level; the mechanism is possibly related to elevated hematocrits and hypoxemia at high altitude (Leibson, Brown, & Thibodeau, 1989). The system portrays harmonious and delicate balance between production of and elimination of bilirubin and is an example of the fascinating physiology of the baby's adaptation to extrauterine life. Astute nursing care nurtures mother–baby psychophysiology and strives to appreciate and protect this delicate balance.
Pathological Hyperbilirubinemia and Risk for Kernicterus Pathological imbalance in bilirubin metabolism is of concern. Pathological imbalance, and attendant hyperbilirubinemia and risk of kernicterus, can occur with (a) excess production of bilirubin, (b) insufficient biliary conversion or elimination of bilirubin, (c) irregular binding of bilirubin to albumin in the bloodstream, and/or (d) altered permeability of the blood–brain barrier to bilirubin (Blackburn, 2007; Cohen, 2006; Wennberg et al., 2006). Any factor that increases the catabolism of red blood cells increases bilirubin levels beyond what is physiologically expected. Such excessive destruction of red blood cells can be secondary to hemolytic disease (Rh or ABO incompatibility), prematurity, polycythemia, red blood cell abnormalities, sepsis, excessive blood loss such as in cephalohematoma or other birth injuries, or G6PD deficiency (an X-linked enzyme deficiency). Jaundice related to excessive destruction of red blood cells is called hemolytic jaundice. Any factor which inhibits biliary conversion or elimination of bilirubin also increases bilirubin levels beyond what is physiologically expected. Decreased elimination can be secondary to inadequate stooling, prematurity/hepatic immaturity, intestinal obstruction, or liver disease such as biliary atresia or neonatal hepatitis.
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Any factor which alters the binding capacity or affinity between albumin and bilirubin in the bloodstream can potentially accentuate bilirubin levels. Most bilirubin in the bloodstream is normally bound to albumin—1 gram of albumin binds 8.5 mg to 10 mg of bilirubin (Blackburn, 2007). However, as bilirubin levels rise, the availability of albumin to bind with bilirubin is challenged, particularly in the preterm baby, because of lower albumin concentration, decreased albumin binding capacity, and/or decreased affinity of albumin for bilirubin. The role of this free bilirubin—bilirubin in the bloodstream unbound to albumin—is not well understood, and as AAP (2004) notes, more study is necessary to understand the role of albumin binding in bilirubin neurotoxicity. Recently, Wennberg et al. (2006) stated that albumin binding varies considerably among newborns; it is lower in sick infants and may increase with postnatal age, and the effective concentration of albumin can be reduced by drugs such as sulfonimides that bind to the same locus on bilirubin. Although measurement of free bilirubin may be useful in better identification of jaundiced infants at risk for kernicterus (Wennberg et al., 2006), there is presently no method available for this measurement in serum or plasma (McDonagh & Maisels, 2006). In the meantime, medical guidelines (AAP, 2004; CPS, 2007) for intervention strategies for treatment of hyperbilirubinemia with phototherapy or exchange transfusion remain based on total serum bilirubin levels. Wennberg et al. (2006) also explain that the blood–brain barrier is involved in the risk for kernicterus disruptions in the blood–brain barrier allows bilirubin to move more rapidly into brain tissue. Bilirubin uptake by the brain may involve comorbid factors such as acidosis, dehydration, and infection. More study is clearly needed to understand the basic processes of neuronal toxicity (Bhutani & Johnson, 2006).
(2000) note that significant improvements in preterm birthrates require population health initiatives toward reducing poverty, reducing women's addictions, and ending the epidemic of domestic violence that so many women endure.
PRIMARY PREVENTION OF BREAST-FEEDING-RELATED HYPERBILIRUBINEMIA
Promote Safe Physiological Birth for Babies
Population Health Initiatives to Decrease Preterm Birthrate All other things being equal, the premature baby is more at risk for severe hyperbilirubinemia as the liver, gut, and feeding behaviors are immature. Prematurity rates have not significantly declined in recent decades. Heamon, Sprague, and Stewart
Avoid Iatrogenic Prematurity Buus-Frank (2005) aptly describes near-term babies, many born by elective induction of labor or by elective cesarian days or weeks before term, as “great imposters.” They may fall within normal term weight, some are large for gestational age (LGA) or macrosomic, and many do not face the major respiratory problems of tiny preemies that may keep them in hospital longer. Some may be “estimated” to be at or near term. Bhutani and Johnson (2006) note that clinical practitioners commonly have not recognized late prematurity (34 to 37 weeks) as a risk factor for hazardous hyperbilirubinemia. By not completing all of their third trimester development, these babies are more likely to be challenged in establishing breastfeeding and face prolonged or exaggerated jaundice accompanied by an escalated risk of kernicterus (Sarici et al., 2004). Steffansrud (2004) notes that near-term infants should be considered a separate class from term infants. Breast-feeding difficulty related to decreased energy reserves and more immature hepatic function place these infants at special risk for the development of significantly elevated serum bilirubin levels. In a retrospective review of the Pilot Kernicterus Registry of U.S. births 1992–2003, Bhutani and Johnson (2006) found that breast-fed LGA late preterm babies were disproportionally represented among those who developed kernicterus compared with babies who were term or appropriate for gestational age. Typically these babies were discharged as per routine within 48 hours of age but with insufficient lactation support and delayed follow-up.
Keeping normal birth normal would do much to prevent the risk factors which can lead to hyperbilirubinemia. Vacuum extraction or forceps birth and pitocin induction are risk factors associated with severe hyperbilirubinemia (Bhutani & Johnson, 2006). Use of labor medications and birth by cesarean section impact negatively on baby breastfeeding behavior (Dewey, Nommsen-Rivers, Heinig, & Cohen, 2003; Shealy, Li, Benton-Davis, & Grummer-Strawm, 2005). Rates of elective
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induction of labor and cesarian sections have escalated in recent years (Health Canada, 2003) to the point where true physiologic birth is an increasingly rare event in North American hospitals. Babies whose mothers received intrapartum analgesia had less frequent massage-like hand movements, made fewer hand-to-mouth movements, fewer licking movements, suckled less, and cried more than babies whose mothers who used nonpharmacological pain relief (Ransjo-Arvidson et al., 2001). Women who had epidurals (Torvaldsen, Roberts, Simpson, Thompson, & Ellwood, 2006) or intrapartum fentanyl (Jordan, Emery, Bradshaw, Watkins, & Friswell, 2005) are more likely to stop breast-feeding. Medicated babies may be less behaviorally organized, less able to coordinate latch and suckling behaviors and, therefore, require extra support to establish breast-feeding (Jordan, 2006). In the current birth environment in most North American hospitals, babies frequently require extra support to deal with the “side effects” of common obstetric interventions in the early days of breast-feeding.
Establish Early, Regular, and Sustained Breast-feeding Much of what has been termed breast-feeding jaundice—the significant jaundice that breast-fed babies develop in the first week of life—might more appropriately be termed not-enough-breastmilk jaundice. Doing so might remove the subtle suggestion that the mother inadvertently caused the jaundice by breast-feeding and the baby now requires artificial food (formula), technological wizardry (phototherapy), and highly skilled infant care specialists to take over where her body failed her baby. The solution is not to stop breast-feeding but to understand and honor mother–baby psychophysiology and remedy root problems. As a form of primary prevention, AAP (2004) states that clinicians should advise mothers to nurse their infants at least 8 to 12 times per day for the first several days. Poor caloric intake and/or dehydration associated with inadequate breastfeeding contribute to the development of hyperbilirubinemia. Babies who are effectively transferring adequate amounts of milk rarely develop severe hyperbilirubinemia (AAP, 2004) unless there is another underlying pathology. Breast-feed Within First Hour of Life This time period is a critically sensitive time when mothers' increased oxytocin levels contri-
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butes toward increased milk ejection and promotes maternal nurturing reflex (Matthiesen, RansjoArvidson, Nissen, & Uvnas-Moberg, 2001), and most infants are awake with strong feeding cues (Klaus & Klaus, 1998). Although this first feeding and skin-to-skin contact has less to do with baby's nutrition than nurturing mother to baby interaction, early feeding begins to establish gut flora and helps initiate a cascade of events which promote maternal confidence and infant satiation. Clearly strides have been made toward supporting this initial breastfeeding from days when mothers and babies were routinely separated after birth. But the practice remains particularly challenged among the approximately 30% of North American babies today who are born in an operating room. Feed Baby Early, Feed Baby Often Frequent nursing, beginning in the first hour of life, stimulates maternal breast milk production and neonatal gastrointestinal motility (Biancuzzo, 1999; Blackburn, 2007). Infants fed in the first 1 to 3 hours after birth were found to pass meconium sooner than infants fed after 4 hours (Boyer & Vidyasagar, 1987). Yamauchi and Yamauchi (1990) found bilirubin levels to be lower among babies who were fed more than 8 to 9 times in 24 hours. Blackburn (2007) reports that the neonatal intestines may contain 100 mg to 200 mg of bilirubin; half of this is unconjugated bilirubin and equals 5 to 10 times the daily bilirubin production rate that one expects from heme catabolism in healthy term newborns. Any delay in passage of meconium increases the likelihood that conjugated water-soluble bilirubin will be returned to the circulation. Appropriate Monitoring of the Breast-fed Newborn It is essential that babies' feeding behavior, hydration status, voiding and stooling patterns, and weight changes be observed to either affirm normalcy or identify problems early. If frequency is insufficient or if milk transfer is not occurring, skilled breast-feeding support includes finding alternative methods of maternal expression/neonatal ingestion of breast milk. Teaching mothers how to manually express or pump milk, droplet-feed, finger-feed, or cup-feed expressed milk are acceptable methods of feeding breast milk to babies who are reluctant to nurse in the early days of life. According to CPS (2007), exclusively breast-fed infants experience their maximum
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weight loss by Day 3 and lose, on average, 6% to 8% of their birth weight. Infants who lose more than 10% of their birth weight fall outside of normal physiological expectations and must be carefully evaluated.
Feeding Breast-fed Term Infants With Jaundice The current position statements of AAP (2004) and CPS (2007) state that breast-feeding is not contraindicated in the presence of hyperbilirubinemia and should be continued. Regardless of the cause of jaundice, breast is best, formula feeding involves health risks, and all infants require surveillance that they are meeting normal developmental indicators. Feeding Babies With Early-onset Jaundice A literature review by Shoemaker and Ellis (2003) found no studies demonstrating that cessation of breast-feeding in jaundiced term infants improves clinical outcomes. Whether they require phototherapy or not, continuing breast-feeding in jaundiced babies is not associated with adverse outcomes. Tan (1998) found that exclusively breast-fed infants had slower responses to phototherapy in the first 24 hours of phototherapy than babies who were formula fed or who received supplementation with formula, but there were no significant differences in the total length of phototherapy required by the different groups. Martinez, Maisels, and Otheguy (1989) conducted a randomized clinical trial involving 125 jaundiced (total serum bilirubin z17 mg/dL) breast-fed infants comparing four treatment approaches: (a) continue breast-feeding and observe; (b) discontinue breast-feeding and substitute formula; (c) discontinue breast-feeding, substitute formula, and administer phototherapy; and (d) continue breast-feeding and administer phototherapy. Martinez et al. (1989) did not find a clinically significant difference in serum bilirubin reduction to normal levels at 48 hours between breast-fed and bottle-fed groups undergoing phototherapy or between breast-fed and bottlefed groups who did not have phototherapy. Phototherapy was beneficial, and breast-feeding can be continued during phototherapy. Feeding Babies With Not-Enough-Breast-feeding Jaundice There is no evidence that a trial of formula may solve the problem—the objective is to get more
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breast milk into baby and treat jaundice with phototherapy according to medical guidelines. However, if lactation has been understimulated, little expressed milk is available and a baby is clearly underhydrated, losing weight, and jaundiced, supplementation with formula is appropriate. AAP (2004) does not recommend supplementation with dextrose water which may temporarily satiate the infant but lead to inadequate caloric intake, which increases bilirubin levels. However, mothers can be encouraged to concurrently stimulate breasts with pumping, thereby enhancing milk production and reducing required formula supplementation. Spatz and Goldschmidt (2006) recommend double pumping breasts with a hospital-grade electric pump if milk transfer is not occurring and encouraging mother–baby skin-to-skin contact. We have seen mothers transform feelings of sorrow and inadequacy to joy and renewed confidence in their nurturing abilities as they visualize the increase in milk production after even 1 day of regular pumping. However, reversing discouragement usually takes skilled support by caregivers who honor lactation psychophysiology and “walk the talk” of believing in women's inherent capability of breast-feeding. Feeding Babies With Breast Milk Jaundice Breast milk jaundice is prolonged jaundice in babies who are otherwise thriving. Although other possible pathologies must be ruled out, babies with breast milk jaundice can continue to breast-feed. According to Thilo (1999), it is not known to result in bilirubin encephalopathy. CONCLUSION Breast-feeding is a fundamental step in life span health promotion. The evidence in favor of promoting exclusive breast-feeding is overwhelming, but translating research into practice has not been without barriers. In some cultures, inexperienced mothers receive support from experienced grandmothers, but such resources are frequently unavailable to modern women whose own mothers and grandmothers bottle-fed their babies. In North America, nurses usually advise new mothers about infant feeding, but not all nurses have sufficient expertise and not all maternity units are adequately staffed. Not-enough-breast-feeding jaundice and breastfeeding failure associated with jaundice are largely preventable through a systems-based approach
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(Bhutani, Johnson, Shwoebel & Gennaro, 2006) to ensure that all babies receive skilled lactation support and appropriate surveillance. Breast-fed babies save health care dollars (Ball and Wright, 1999), but we must first invest in saving breast-
feeding. The time to establish breast-feeding is perinatally and in the early postpartum, and we generally only have this one chance to get it right— for the benefit of the baby for a lifetime and, by extension, all of society.
REFERENCES American Academy of Pediatrics. (1994). Management of hyperbilirubinemia in the healthy term newborn. Pediatrics, 94, 558−562. American Academy of Pediatrics. (2004). Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics, 114, 297−316. American Academy of Pediatrics. (2005). Breastfeeding and the use of human milk. Pediatrics, 115, 496−506. Anderson, J. W., Johnstone, B. M., & Remley, D. T. (1999). Breast-feeding and cognitive development: A meta-analysis. American Journal of Clinical Nutrition, 70, 525−535. Aycicek, A., Erel, O., Kocyigit, A., Selek, S., & Demirkol, M. R. (2006). Breast milk provides better antioxidant power than does formula. Nutrition, 22, 616−619. Ball, T. M., & Wright, A. L. (1999). Health care costs of formula-feeding in the first year of life. Pediatrics, 103, 870−876. Bhutani, V., & Johnson, L. (2006). Kernicterus in late preterm infants cared for as term healthy infants. Seminars in Perinatology, 30, 89−97. Bhutani, V., Johnson, L., Schwoebel, A., & Gennaro, S. (2006). A systems approach for neonatal hyperbilirubinemia in term and near-term infants. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 35, 444−454. Biancuzzo, M. (1999). Breastfeeding the newborn: Clinical strategies for nurses. St. Louis, MO: Mosby. Blackburn, S. (2007). Bilirubin metabolism. In S. Blackburn (Ed.), Maternal, fetal, and neonatal physiology: A clinical perspective (pp. 645−668). St. Louis, MO: Saunders. Boland, M. (2005). Exclusive breastfeeding should continue to six months. Retrieved May 15, 2007, from www.cps.ca. Boyer, D. B., & Vidyasagar, D. (1987). Serum indirect bilirubin levels and meconium passage in early fed normal newborns. Nursing Research, 36, 174. Buus-Frank, M. (2005). The great imposter. Advances in Neonatal Care, 5, 233−236. Canadian Pediatric Society. (2007). Position Statement FN 2007-02. Guidelines for detection, management, and prevention of hyperbilirubinemia in term and late preterm newborn infants 35 or more weeks gestation. Pediatrics and Child Health, 12, 1B−12B. Retrieved December 3, 2007, from www.cps.ca. Cohen, S. M. (2006). Jaundice in the full-term newborn. Pediatric Nursing, 32, 202−208. Cremer, R. J., Perryman, P. W., & Richards, D. H. (1958). Influence of light on the hyperbilirubinemia of infants. Lancet, 1, 1094. Dewey, K. G., Nommsen-Rivers, L. A., Heinig, M. J., & Cohen, R. J. (2003). Risk factors for suboptimal infant breastfeeding behavior: Delayed onset of lactation, and excess neonatal weight loss. Pediatrics, 112, 607−619. Fanaroff, A. A., & Martin, R. J. (2002). Neonatal-perinatal medicine (7th ed.) St. Louis, MO: Mosby. Gartner, L. M., & Herschel, M. (2001). Jaundice and breastfeeding. Pediatric Clinics of North America, 48, 389−400. Gourley, G. R. (2002). Breast-feeding, neonatal jaundice, and kernicterus. Seminars in Neonatology, 7, 135−141. Gourley, G. R., Zhanhai, L., Kreamer, B., & Kosorok, M. R. (2005). A controlled, double-blind trial of prophylaxis against jaundice among breastfed infants. Pediatrics, 116, 385−391.
Harrod, K. S., Hanson, L., VandeVusse, L., & Harrod, P. (2003). Rh negative status and isoimmunization update: A casebased approach to care. Journal of Pediatric and Neonatal Nursing, 17, 166. Health Canada. (2003). Canadian Perinatal Health Report 2003. Ottawa, Ontario: Minister of Public Works and Government Services Canada. Heamon, M. I., Sprague, A. E., & Stewart, P. J. (2000). Reducing the preterm birth rate: A population health strategy. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 30, 20−29. Joint Commission on Accreditation of Healthcare Organizations (JCAHO). (2001). Sentinel Event Alert: Kernicterus threatens healthy newborns, 18. Retrieved January 23, 2008 from www.jointcommission.org. Jordan, S. (2006). Infant feeding and analgesia in labour: The evidence is accumulating. International Breastfeeding Journal, 1, 25. Retrieved May 14, 2007, from www.internationalbreastfeedingjournal.com. Jordan, S., Emery, S., Bradshaw, C., Watkins, A., & Friswell, W. (2005). The impact of intrapartum analgesia on infant feeding. British Journal of Obstetrics and Gynecology, 112, 927−934. Klaus, M. H., & Klaus, P. H. (1998). Your amazing newborn. Reading, MA: Perseus Books. Klement, E., Cohen, R. V., Boxman, A. J., & Reif, S. (2004). Breastfeeding and risk of inflammatory bowel disease: A systematic review with meta-analysis. American Journal of Clinical Nutrition, 80, 1342−1352. Kull, I., Wickman, M., Lilja, G., Nordvall, S. L., & Pershagen, G. (2002). Breast feeding and allergic disease in children—A prospective birth cohort study. Archives of Diseases in Children, 86, 478−481. Leibson, C., Brown, M., & Thibodeau, S. (1989). Neonatal hyperbilirubinemia at high altitudes. American Journal of Diseases of Children, 143, 983−987. London, M. L., Ladewig, P. W., Ball, J. W., & Bindler, R. C. (2007). Maternal and child nursing care. Upper Saddle River, NJ: Pearson Prentice Hall. Maisels, M. J. (2006). What's in a name? Physiological and pathologic jaundice: The conundrum of defining normal bilirubin levels in the newborn. Pediatrics, 118, 805−807. Martinez, J. C., Maisels, M. J., & Otheguy, L. (1989). Hyperbilirubinemia in the breast-fed newborn: A controlled trial of four interventions. Pediatrics, 91, 470−473. Matthiesen, A. S., Ransjo-Arvidson, A. B., Nissen, E., & Uvnas-Moberg, K. (2001). Postpartum maternal oxytocin release by newborns: Effects of infant hand massage and sucking. Birth, 21, 13−19. McDonagh, A. F., & Maisels, M. J. (2006). Bilirubin unbound: Deja vu all over again. Pediatrics, 117, 523−525. Mollison, P. L., & Walker, W. (1952). Controlled trials of the treatment of hemolytic disease. Lancet, 1, 429−433. Newman, J. (1998). Breastfeeding and guilt. Retrieved February 2, 2007, from www.breast-feed.com. Newman, T. B., & Maisels, M. J. (1992). Evaluation and treatment of jaundice in the term newborn: A kinder, gentler approach. Pediatrics, 89, 809. Oddy, W. H. (2002). The impact of breastmilk on infant and child health. Breastfeeding Review, 10, 5−18. Owen, C. G., Martin, R. M., Whincup, P. H., Davey-Smith, G., & Cook, D. G. (2005). Effect of infant feeding on the risk of
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obesity across the life course: A quantitative review of the published evidence. Pediatrics, 115, 1367−1377. Ransjo-Arvidson, A. B., Matthiesen, A. S., Lilja, G., Nissen, E., Widstrom, A. M., & Uvnas-Moberg, K. (2001). Maternal analgesia during labor disturbs newborn behavior: Effects on breast-feeding, temperature, and crying. Birth, 28, 20−21. Ratnavel, N., & Ives, N. K. (2005). Investigation of prolonged neonatal jaundice. Current Paediatrics, 15, 85−91. Saarinen, U. M., & Kajosaari, M. (1995). Breastfeeding as prophylaxis against atopic disease: Prospective follow-up study until 17 years old. Lancet, 346, 1065−1069. Sarici, S. U., Serdar, M. A., Korkmaz, A., Erdem, G., Oran, O., et al. (2004). Incidence, course, and prediction of hyperbilirubinemia in near-term and term infants. Pediatrics, 113, 775−780. Sedlak, T. W., & Snyder, S. H. (2004). Bilirubin benefits: Cellular protection by a biliverdin reductase antioxidant cycle. Pediatrics, 113, 1776. Shealy, K. R., Li, R., Benton-Davis, S., & Grummer-Strawm, L. M. (2005). The CDC Guide to Breast-feeding Interventions. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention. Shoemaker, M. D., & Ellis, M. R. (2003). Should jaundiced infants be breastfed? Journal of Family Practice, 52. Retrieved August 27, 2006, from www.jfponline.com. Spatz, D. L., & Goldschmidt, K. A. (2006). Preserving breastfeeding in the rehospitalized infant: A clinical pathway. MCN American Journal of Maternal-Child Nursing, 31, 45−53.
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Steffansrud, S. (2004). Hyperbilirubinemia in term and nearterm infants: Kernicterus on the rise? Newborn and infant nursing reviews, 4, 191−200. Stokowski, L. A. (2002). Early recognition of neonatal jaundice and kernicterus. Advances in Neonatal Care, 2, 101−114. Tan, K. L. (1998). Decreased response to phototherapy for neonatal jaundice in breast-fed infants. Archives in Pediatric and Adolescent Medicine, 152, 1187−1190. Thilo, E. H. (1999). Jaundice. In P. J. Thureen, J. Deacon, P. O'Neill, & J. Hernandez (Eds.), Assessment and care of the well newborn (pp. 245−260). Philadelphia, PA: Saunders. Torvaldsen, S., Roberts, C. L., Simpson, J. M., Thompson, J. F., & Ellwood, D. A. (2006). Intrapartal epidural analgesia and breastfeeding: A prospective cohort study. International Breastfeeding Journal, 11, 24. Tyler, M., & Hellings, P. (2003). Feeding method and rehospitalization in newborns less than 1 month of age. Journal of Obstetrical, Gynecological, and Neonatal Nursing, 34, 70−79. Wennberg, R. P, Ahlfors, C. E., Bhutani, V. K., Johnson, L. H., & Shapiro, S. M. (2006). Toward understanding kernicterus: A challenge to improve the management of jaundiced newborns. Pediatrics, 117, 474−485. World Health Organization & UNICEF. (2003). Global strategy for infant and young child feeding. Geneva: Author. Yamauchi, Y., & Yamauchi, H. (1990). Breastfeeding frequency during the first 24 hours after birth in the full-term neonate. Pediatrics, 86, 171.
Parents face a paradox when they are told: Breast is best; bottle-feeding is hazardous to health. But breast-fed babies are more likely to become severely jaundiced than bottle-fed babies, and severe jaundice can lead to brain damage. This article will explore the natural physiology of jaundice with a focus on breast-feeding-associated jaundice, primary prevention of hyperbilirubinemia, and current evidence-based recommendations about feeding jaundice breast-fed infants. © 2008 Elsevier Inc. All rights reserved. Key words: Infant jaundice; Breast-feeding; Bottle-feeding; Acute bilirubin encephalopathy; Fetal neonatal bilirubin metabolism; Primary prevention; Risk for kernicterus
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RIMUM NON NOCERE. Above all, do no harm.—Hippocrates
Case Studies (identities changed and pseudonyms used) Allison, aged 32, tells an office nurse on her 6-week postpartum visit: “I had difficulty nursing my first two babies. And then, with both my children in school, I was determined to get it right this time and exclusively nurse this third baby. Maren was born almost 8 lbs, a beautiful healthy baby girl. A good “nurser,” she had little difficulty catching on. On Day 2 Maren's blood bilirubin levels were slightly elevated, “nothing of concern” I was told. But they kept us in an extra day so that bilirubin levels could be rechecked. The results came back in the night and in the early hours of the morning, a nurse informed me that they were going to give Maren some formula which supposedly would help bring the bilirubin levels down. I was told it was hospital policy. I wanted to speak with my doctor in the morning first, but the nurse persisted and sent another nurse to convince me. No one could explain the physiology, just that it was “policy.” I agreed to give my baby an ounce or two of formula from a cup. Although I was not convinced it was for the baby's benefit, I was not prepared to argue with nurses at 4 in the morning. When my doctor arrived it was decided to place Maren under phototherapy and continue formula feeding until bilirubin levels
Journal of Pediatric Nursing, Vol 23, No 6 (December), 2008
came down. It was an emotional time, as my plan to nurse my child seemed to be slowly slipping away from me. I lacked information, couldn't understand why I couldn't nurse her through the days of phototherapy, and no one seemed able to tell me. I felt I was doing Maren a disservice.” Mary, aged 21 and pregnant with her first baby, tells the public health nurse that she does not want to breast-feed her baby: “My sister tried to breastfeed her baby but her baby got yellow jaundice and needed to be in an incubator for over 3 days. My sister just cried and cried, and when she couldn't make enough breast milk anyway, the doctor said she should switch to formula. I'm not going to bother to try, just in case this problem with breastfeeding jaundice runs in families.” Jane, aged 30, tells a midwife that she is fed up with doctors, nurses, and hospitals and wants a home birth. Jane says that “with my first pregnancy
From the St. Francis Xavier University, Antigonish, Nova Scotia, Canada. Corresponding author: Marion Alex, RN, MN, CNM, St. Francis Xavier University, Box 5000, Antigonish, Nova Scotia, Canada B2G 2W5. E-mail: [email protected] 0882-5963/$-see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.pedn.2007.12.002
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I was clueless, I was induced on my due day, had narcotics in labor, then an epidural, then couldn't push, and then had a vacuum extraction, and then my baby had a cephalohematoma. Then he wouldn't latch, and would scream into my breasts but not suckle. I was so frustrated, and when he got jaundiced I just gave up. The nurses told me not to feel guilty about it, that formula feeding would help his jaundice, but I still feel guilty. Jason has so many allergies and ear infections, and at age 6 he already has a weight problem…. And from what I read it's at least partly due to how I fed him as a baby.” Parents face a paradox when they are told: Breast is best; bottle-feeding is hazardous to health. But breast-fed babies are more likely to become severely jaundiced than bottle-fed babies, and severe jaundice can lead to brain damage. According to Stokowski (2002), the overall incidence of severe jaundice (hyperbilirubinemia) is rising. Severe jaundice is the most common reason for hospital readmission of newborns (Tyler & Hellings, 2003). Jaundice was the principal diagnosis for 27.0% of newborns readmitted to hospitals in Canada in 1991–1992, and 38.8% of newborns in 2000–2001 (Health Canada, 2003). A higher rate of breast-feeding, in conjunction with shorter postpartum hospital stays, is the leading explanation for the high prevalence of jaundice seen today (Stokowski, 2002). With earlier discharge, infants may not be available to health care professionals when bilirubin peaks occur (Bhutani, Johnson, Schwoebel, & Gennaro, 2006). It is imperative to analyze this phenomenon so as not to scuttle breast-feeding efforts but to prevent severe hyperbilirubinemia, promote necessary lactation support, and provide treatment and care to jaundiced breast-fed babies based on the best available evidence. The American Academy of Pediatrics (AAP, 2004, p. 297) calls on clinicians to “reduce the incidence of severe hyperbilirubinemia while minimizing the risks of unintended harm, such as maternal anxiety, decreased breast-feeding, and unnecessary costs of treatment.” Achieving this outcome requires clinicians to understand the physiology of lactation and jaundice and to communicate their knowledge with compassion in a manner that serves to empower parents. This is no easy task when the physiology is complex, the risks are real, and maternal emotions are raw. The terms breast-feeding jaundice or breast milk jaundice are found throughout the published litera-
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ture. Thus, the language health professionals use with childbearing families—of diverse literacy levels— connotes connection between the breast-feeding and/ or the milk and what sounds like a serious medical problem. The above vignettes anecdotally illustrate experiences of mothers who struggle with balancing risks when it is suggested that breast-feeding “causes” jaundice. For nurses also struggling to balance risks, the questions are the following: Why does breast-feeding jaundice happen? How can breast-feeding jaundice be prevented? How can nurses best support breast-feeding mothers whose babies develop severe hyperbilirubinemia? BENEFITS OF BREAST-FEEDING/HEALTH HAZARDS OF BOTTLE-FEEDING The World Health Organization (2003), the AAP (2005), and the Canadian Pediatric Society (Boland, 2005; CPS, 2007) have issued statements calling for exclusive breast-feeding of all infants for the first 6 months of life or longer. These statements are based on extensive evidence of the lifelong benefits of breast-feeding. Factors in human milk promote gastrointestinal mucosal maturation, have immunomodulatory and antiinflammatory functions, and alter gut flora (Oddy, 2002), and breast milk is richer in antioxidants (Aycicek, Erel, Kocyigit, Selek, & Demirkol, 2006). Bottle-feeding is less than ideal. Babies who are not breast-fed are at increased risk of asthma; atopic dermatitis; allergies to foods, pets, or pollens; otitis media; lower respiratory tract infections; gastrointestinal infections; inflammatory bowel disease; obesity; and lower neurodevelopmental and cognitive scores (Anderson, Johnstone, & Remley, 1999; Ball & Wright, 1999; Klement, Cohen, Boxman, & Reif, 2004; Kull, Wickman, Lilja, Nordvall, & Pershagen, 2002; Owen, Martin, Whincup, & Davey-Smith, 2005; Saarinen & Kajosaari, 1995). When breast-feeding does not go as planned for women who intensely want to breast-feed, we must also be concerned with mental health effects. Postpartum depression is prevalent and disabling. Perceiving oneself as “failing” to give birth or breast-feed as hoped for contributes to the etiology of postpartum depression. Many well-meaning people have called for “not making the mother feel guilty.” But as Newman (1998) argues, it is not women who make informed decisions to bottle-feed who feel guilty, but women who want to breastfeed, try, are insufficiently supported, yet know
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bottle-feeding is harmful. Newman (1998) states that what is needed is not avoiding discussion of risks of bottle-feeding, but promotion of breastfeeding coupled with skilled support––something that is not happening in most North American societies. Breast-feeding “failure” associated with jaundice is one reason why women who plan to breast-feed, but cannot, stop breast-feeding. Guilt is what we feel when we know something is wrong; but rather than blame the mother, one could argue that it is our collective culture that is doing something wrong when we fail to appropriately support mothers and babies. Efforts to promote “education of the mother” have been insufficient in enacting change; we also require changes in our collective culture, community, and clinical care systems which honor mother– baby psychophysiology. ACUTE BILIRUBIN ENCEPHALOPATHY AND KERNICTERUS—A BRIEF HISTORY According to AAP (2004), acute bilirubin encephalopathy refers to the acute manifestations of bilirubin toxicity in the first weeks after birth and includes symptoms of lethargy, irritability, hypotonia alternating with hypertonia, and backward arching of neck and trunk. Kernicterus refers to the chronic and permanent sequelae of bilirubin toxicity, which includes severe forms of cerebral palsy, auditory dysfunction, and intellectual handicaps (AAP, 2004). Severe hyperbilirubinemia is a greater problem for infants who are exclusively breast-fed than babies who receive at least some bottled milk (Cohen, 2006; Gourley, 2002). Hyperbilirubinemia, although often benign or even beneficial in babies with jaundice, can on rare occasion be profoundly neurotoxic. Stokowski (2002) notes that preventing kernicterus might be easier if the precise concentration or duration of hyperbilirubinemia leading to neurotoxicity were known. Unfortunately, the mediating variable(s) which leads to kernicterus in a few, but certainly not most, babies with jaundice remain unknown. Wennberg, Ahlfors, Bhutani, Johnson, and Shapiro (2006) note that conclusions about causes of rare events are sparse. In the 1950s, medical literature reported evidence of a link between hyperbilirubinemia and kernicterus and a corresponding search for treatment with exchange transfusions (Mollison & Walker, 1952) and phototherapy (Cremer, Perry-
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man, & Richards, 1958). Hemolytic disease was a common antecedent to kernicterus in these times. As antibody screening and prophylactic use of Rh immune globulin became standard practice in 1983 (Harrod, Hanson, VandeVusse, & Harrod, 2003), the incidence of severe hemolytic disease decreased dramatically. Concomitantly, since the 1950s, formula feeding was the norm in mainstream North America. Massive formula promotion programs led many parents and practitioners to believe formula was superior to breast milk. Even as scientific evidence about benefits of breast-feeding was mounting in the 1970s and 1980s, if there was any concern about breast-feeding not going well, mothers and nurses reached for the baby bottle. With exclusive breastfeeding being rare, breast-feeding-associated jaundice was rare too. By the 1990s, kernicterus seemed to be largely a phenomenon of the past, and calls for a “kinder, gentler” approach to treatment of hyperbilirubinemia emerged (Newman & Maisels, 1992). In 1994, AAP held that many babies were being unnecessarily treated for jaundice and published a practice parameter citing studies that there was no evidence for kernicterus in healthy full-term infants without risk factors for hemolysis such as Rh or ABO incompatibility. AAP (1994) recommended tolerating higher levels of total serum bilirubin before initiation of phototherapy or exchange transfusions. However, in the decade that followed, kernicterus among this population of babies was not eliminated. There was growing concern that some babies with hyperbilirubinemia were “falling through the cracks” and not receiving treatment that could prevent kernicterus. The U.S. Joint Commission on Accreditation of Health Care Organizations (2001) issued a sentinel event alert about the apparent increase in kernicterus in otherwise healthy term and near-term babies. These babies with kernicterus were generally breast-fed and had no other apparent risk factors. Although the incidence was rare, the neurodevelopmental outcomes for those few babies were devastating. Root causes of the rise in kernicterus were seen to be early discharge from hospital with poor follow-up, lack of family education about jaundice, and failure to provide continued lactation support to mothers (Steffansrud, 2004). In 2004, AAP issued an updated clinical practice guideline for management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation to
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provide a framework for the prevention and management of hyperbilirubinemia based on current evidence. According to the guidelines of AAP (2004) and CPS (2007), medical treatment is based on total serum bilirubin levels and involves phototherapy, and in the most severe situations, exchange transfusion in neonatal intensive care. However, AAP (2004) states that the serum bilirubin level by itself, except when it is extremely high and associated with bilirubin encephalopathy, is an imprecise indicator of long-term neurodevelopmental outcome. Most babies with severe hyperbilirubinemia escape without any apparent sequelae, and we do not know why (Wennberg et al., 2006). PHYSIOLOGY OF BREAST-FEEDING JAUNDICE
Forms of Breast-feeding-Related Jaundice Jaundice can occur in both breast-fed and bottle-fed babies. Some causes of hyperbilirubinemia are unrelated to mode of feeding, and the etiology of severe jaundice must be medically investigated. However, regardless of the cause(s), breast-feeding is not contraindicated (AAP, 2004; CPS, 2007). In addition to the disease-related causes of jaundice (e.g., hemolytic disease and liver disease), two forms of breast-feeding-related jaundice occur clinically in otherwise healthy babies and can coexist in the same baby. These two forms are confusingly called breast-feeding jaundice, which is generally of early onset, and breast milk jaundice, which is generally of later onset and lasts longer. Breast-feeding jaundice typically begins on the second or third day of life and is generally due to insufficient milk intake (Steffansrud, 2004). It is perhaps more appropriately termed not-enoughbreast-feeding jaundice. Gartner and Herschel (2001) state that this is the neonatal equivalent of starvation jaundice seen in adults deprived of caloric intake. The other, called breast milk jaundice, begins in healthy weight-gaining babies beginning at 1 to 3 weeks of age and persists for as long as 3 months (Steffansrud, 2004). A reliable diagnosis of breast milk jaundice can be made only on exclusion of pathological causes such as biliary atresia or cystic fibrosis (Ratnavel & Ives, 2005). Newborns with breast milk jaundice appear well and, at present, kernicterus with this type of jaundice has
not been documented (London, Ladewig, Ball, & Bindler, 2007).
Understanding Normal Fetal Neonatal Bilirubin Metabolism To be able to explain these clinical phenomena to parents, infant care providers must understand the physiology involved in bilirubin metabolism. Bilirubin exists in the body in several forms: Unconjugated or indirect bilirubin is lipid soluble. It is generally found bound to albumin in the blood, but some unconjugated bilirubin is not bound to albumin and is called free bilirubin. Conjugated or direct bilirubin is water soluble and ready for excretion in the bile (Thilo, 1999). According to Blackburn (2007), before birth, the placenta efficiently clears bilirubin and, therefore, babies are not born jaundiced. In fetal circulatory anatomy, blood is largely shunted past the liver, and this decreased hepatic circulation limits the capacity of the fetal liver to convert bilirubin to its watersoluble state. With the circulatory changes that occur after birth with the clamping of the cord, hepatic circulation is dramatically increased; the newborn's still-maturing liver then assumes responsibility for bilirubin metabolism, converting lipidsoluble unconjugated bilirubin to water-soluble conjugated bilirubin which can then be excreted. Bilirubin only becomes sufficiently water soluble to enter the bile following hepatic conjugation with glucuronic acid. Once converted to this watersoluble conjugated state, bilirubin passes to the gut. In the gut, it is hydrolyzed by bacteria and converted to urobilinogen, which is oxidized to stercobilin. Stercobilin is what gives feces its characteristic brown color (Blackburn, 2007). Meconium is rich in ready-for-excretion bilirubin. Therefore, babies who stool early and often develop less hyperbilirubinemia. The newborn produces up to 8 to 10 mg/kg/day of bilirubin, more than twice as much as adults do (Blackburn, 2007). This increased bilirubin production is primarily due to a greater circulating red blood cell volume per kilogram. As a physiological adaptation to the relatively oxygen-poor intrauterine environment, the fetus produces comparatively more red blood cells than the newborn does. Fetal hemoglobin and hematocrit levels are significantly higher than infant hemoglobin levels, with cord blood laboratory hematocrit values normally ranging from 43% to 63%, and hemoglobin values normally ranging from 14–20 g/dL (Fanaroff & Martin, 2002). Moreover, neonatal red blood cells
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normally have shorter life spans (80–100 days in term babies and 60–80 days in preterm babies) than do adult red blood cells (120 days; Blackburn, 2007). This comparatively higher fetal red blood cell count becomes unnecessary after birth in the oxygen-richer extrauterine environment, and an expected physiologic catabolism of unnecessary red blood cells occurs. The result is that the healthy newborn has higher bilirubin levels than one would see at any other point in the life span. It is as normal a finding as the twice-as-fast-as-adult's heart and respiratory rates we see in newborns (Maisels, 2006). Visible physiological jaundice is seen in most newborns (AAP, 2004). This phenomenon has been variably described as benign or beneficial. Bilirubin is a potent antioxidant which helps protect the baby from oxidative stress and celldamaging free radicals (Sedlak & Snyder, 2004). Gartner and Herschel (2001) note that the higher range of bilirubin levels in breast-fed infants may be protective because of antioxidant effects. Anthropologically speaking, Thibo (1999) questions why hyperbilirubinemia would be so common in the early days of life unless it conferred some biological advantage. Still, it is the balance of conjugation and elimination of bilirubin that are important. Biliary conversion of bilirubin to its ready-to-excrete form is part of the equation, but the baby must then actually excrete it. Water-soluble bilirubin in the gut is unstable and can be hydrolyzed by the relatively alkaline environment of the intestinal tract and recycled back to the circulation. Absorbed across gut mucosa, this bilirubin is returned to the bloodstream and the portal venous system once again, a process called enterohepatic circulation (Steffansrud, 2004). Hence, the bilirubin reenters the baby's body rather than being excreted and contributes to the load on the neonatal liver once again. Specific enzymes, for example, beta-glucuronidase (Ratnavel & Ives, 2005) or increased amounts of certain fatty acids (Blackburn, 2007) are thought to contribute to prolonging this gutback-to-bloodstream recycling of bilirubin in enterohepatic circulation. Breast milk is rich in beta-glucuronidase; routine infant formula is not (Gourley, Zhanhai, Kreamer, & Kosorok, 2005). The presence of gut flora will minimize enterohepatic circulation as certain intestinal bacteria will change bilirubin to less absorbable forms such as stercobilinogen, but the neonate's gut is sterile at birth and flora are minimal until feeding is
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established. Again, this indicates the need to start breast-feeding as soon as the baby wants to, which for healthy unsedated term babies, is generally in the first hour of life. Bilirubin levels physiologically rise and fall in relation to gestational age, age in hours/days after birth, type of feeding, race (Maisels, 2006), and even altitude. Asian babies overall demonstrate higher bilirubin levels in the first week of life than Caucasian or African American babies (Blackburn, 2007). Babies born at higher altitudes develop higher levels of bilirubin than babies born at sea level; the mechanism is possibly related to elevated hematocrits and hypoxemia at high altitude (Leibson, Brown, & Thibodeau, 1989). The system portrays harmonious and delicate balance between production of and elimination of bilirubin and is an example of the fascinating physiology of the baby's adaptation to extrauterine life. Astute nursing care nurtures mother–baby psychophysiology and strives to appreciate and protect this delicate balance.
Pathological Hyperbilirubinemia and Risk for Kernicterus Pathological imbalance in bilirubin metabolism is of concern. Pathological imbalance, and attendant hyperbilirubinemia and risk of kernicterus, can occur with (a) excess production of bilirubin, (b) insufficient biliary conversion or elimination of bilirubin, (c) irregular binding of bilirubin to albumin in the bloodstream, and/or (d) altered permeability of the blood–brain barrier to bilirubin (Blackburn, 2007; Cohen, 2006; Wennberg et al., 2006). Any factor that increases the catabolism of red blood cells increases bilirubin levels beyond what is physiologically expected. Such excessive destruction of red blood cells can be secondary to hemolytic disease (Rh or ABO incompatibility), prematurity, polycythemia, red blood cell abnormalities, sepsis, excessive blood loss such as in cephalohematoma or other birth injuries, or G6PD deficiency (an X-linked enzyme deficiency). Jaundice related to excessive destruction of red blood cells is called hemolytic jaundice. Any factor which inhibits biliary conversion or elimination of bilirubin also increases bilirubin levels beyond what is physiologically expected. Decreased elimination can be secondary to inadequate stooling, prematurity/hepatic immaturity, intestinal obstruction, or liver disease such as biliary atresia or neonatal hepatitis.
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Any factor which alters the binding capacity or affinity between albumin and bilirubin in the bloodstream can potentially accentuate bilirubin levels. Most bilirubin in the bloodstream is normally bound to albumin—1 gram of albumin binds 8.5 mg to 10 mg of bilirubin (Blackburn, 2007). However, as bilirubin levels rise, the availability of albumin to bind with bilirubin is challenged, particularly in the preterm baby, because of lower albumin concentration, decreased albumin binding capacity, and/or decreased affinity of albumin for bilirubin. The role of this free bilirubin—bilirubin in the bloodstream unbound to albumin—is not well understood, and as AAP (2004) notes, more study is necessary to understand the role of albumin binding in bilirubin neurotoxicity. Recently, Wennberg et al. (2006) stated that albumin binding varies considerably among newborns; it is lower in sick infants and may increase with postnatal age, and the effective concentration of albumin can be reduced by drugs such as sulfonimides that bind to the same locus on bilirubin. Although measurement of free bilirubin may be useful in better identification of jaundiced infants at risk for kernicterus (Wennberg et al., 2006), there is presently no method available for this measurement in serum or plasma (McDonagh & Maisels, 2006). In the meantime, medical guidelines (AAP, 2004; CPS, 2007) for intervention strategies for treatment of hyperbilirubinemia with phototherapy or exchange transfusion remain based on total serum bilirubin levels. Wennberg et al. (2006) also explain that the blood–brain barrier is involved in the risk for kernicterus disruptions in the blood–brain barrier allows bilirubin to move more rapidly into brain tissue. Bilirubin uptake by the brain may involve comorbid factors such as acidosis, dehydration, and infection. More study is clearly needed to understand the basic processes of neuronal toxicity (Bhutani & Johnson, 2006).
(2000) note that significant improvements in preterm birthrates require population health initiatives toward reducing poverty, reducing women's addictions, and ending the epidemic of domestic violence that so many women endure.
PRIMARY PREVENTION OF BREAST-FEEDING-RELATED HYPERBILIRUBINEMIA
Promote Safe Physiological Birth for Babies
Population Health Initiatives to Decrease Preterm Birthrate All other things being equal, the premature baby is more at risk for severe hyperbilirubinemia as the liver, gut, and feeding behaviors are immature. Prematurity rates have not significantly declined in recent decades. Heamon, Sprague, and Stewart
Avoid Iatrogenic Prematurity Buus-Frank (2005) aptly describes near-term babies, many born by elective induction of labor or by elective cesarian days or weeks before term, as “great imposters.” They may fall within normal term weight, some are large for gestational age (LGA) or macrosomic, and many do not face the major respiratory problems of tiny preemies that may keep them in hospital longer. Some may be “estimated” to be at or near term. Bhutani and Johnson (2006) note that clinical practitioners commonly have not recognized late prematurity (34 to 37 weeks) as a risk factor for hazardous hyperbilirubinemia. By not completing all of their third trimester development, these babies are more likely to be challenged in establishing breastfeeding and face prolonged or exaggerated jaundice accompanied by an escalated risk of kernicterus (Sarici et al., 2004). Steffansrud (2004) notes that near-term infants should be considered a separate class from term infants. Breast-feeding difficulty related to decreased energy reserves and more immature hepatic function place these infants at special risk for the development of significantly elevated serum bilirubin levels. In a retrospective review of the Pilot Kernicterus Registry of U.S. births 1992–2003, Bhutani and Johnson (2006) found that breast-fed LGA late preterm babies were disproportionally represented among those who developed kernicterus compared with babies who were term or appropriate for gestational age. Typically these babies were discharged as per routine within 48 hours of age but with insufficient lactation support and delayed follow-up.
Keeping normal birth normal would do much to prevent the risk factors which can lead to hyperbilirubinemia. Vacuum extraction or forceps birth and pitocin induction are risk factors associated with severe hyperbilirubinemia (Bhutani & Johnson, 2006). Use of labor medications and birth by cesarean section impact negatively on baby breastfeeding behavior (Dewey, Nommsen-Rivers, Heinig, & Cohen, 2003; Shealy, Li, Benton-Davis, & Grummer-Strawm, 2005). Rates of elective
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induction of labor and cesarian sections have escalated in recent years (Health Canada, 2003) to the point where true physiologic birth is an increasingly rare event in North American hospitals. Babies whose mothers received intrapartum analgesia had less frequent massage-like hand movements, made fewer hand-to-mouth movements, fewer licking movements, suckled less, and cried more than babies whose mothers who used nonpharmacological pain relief (Ransjo-Arvidson et al., 2001). Women who had epidurals (Torvaldsen, Roberts, Simpson, Thompson, & Ellwood, 2006) or intrapartum fentanyl (Jordan, Emery, Bradshaw, Watkins, & Friswell, 2005) are more likely to stop breast-feeding. Medicated babies may be less behaviorally organized, less able to coordinate latch and suckling behaviors and, therefore, require extra support to establish breast-feeding (Jordan, 2006). In the current birth environment in most North American hospitals, babies frequently require extra support to deal with the “side effects” of common obstetric interventions in the early days of breast-feeding.
Establish Early, Regular, and Sustained Breast-feeding Much of what has been termed breast-feeding jaundice—the significant jaundice that breast-fed babies develop in the first week of life—might more appropriately be termed not-enough-breastmilk jaundice. Doing so might remove the subtle suggestion that the mother inadvertently caused the jaundice by breast-feeding and the baby now requires artificial food (formula), technological wizardry (phototherapy), and highly skilled infant care specialists to take over where her body failed her baby. The solution is not to stop breast-feeding but to understand and honor mother–baby psychophysiology and remedy root problems. As a form of primary prevention, AAP (2004) states that clinicians should advise mothers to nurse their infants at least 8 to 12 times per day for the first several days. Poor caloric intake and/or dehydration associated with inadequate breastfeeding contribute to the development of hyperbilirubinemia. Babies who are effectively transferring adequate amounts of milk rarely develop severe hyperbilirubinemia (AAP, 2004) unless there is another underlying pathology. Breast-feed Within First Hour of Life This time period is a critically sensitive time when mothers' increased oxytocin levels contri-
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butes toward increased milk ejection and promotes maternal nurturing reflex (Matthiesen, RansjoArvidson, Nissen, & Uvnas-Moberg, 2001), and most infants are awake with strong feeding cues (Klaus & Klaus, 1998). Although this first feeding and skin-to-skin contact has less to do with baby's nutrition than nurturing mother to baby interaction, early feeding begins to establish gut flora and helps initiate a cascade of events which promote maternal confidence and infant satiation. Clearly strides have been made toward supporting this initial breastfeeding from days when mothers and babies were routinely separated after birth. But the practice remains particularly challenged among the approximately 30% of North American babies today who are born in an operating room. Feed Baby Early, Feed Baby Often Frequent nursing, beginning in the first hour of life, stimulates maternal breast milk production and neonatal gastrointestinal motility (Biancuzzo, 1999; Blackburn, 2007). Infants fed in the first 1 to 3 hours after birth were found to pass meconium sooner than infants fed after 4 hours (Boyer & Vidyasagar, 1987). Yamauchi and Yamauchi (1990) found bilirubin levels to be lower among babies who were fed more than 8 to 9 times in 24 hours. Blackburn (2007) reports that the neonatal intestines may contain 100 mg to 200 mg of bilirubin; half of this is unconjugated bilirubin and equals 5 to 10 times the daily bilirubin production rate that one expects from heme catabolism in healthy term newborns. Any delay in passage of meconium increases the likelihood that conjugated water-soluble bilirubin will be returned to the circulation. Appropriate Monitoring of the Breast-fed Newborn It is essential that babies' feeding behavior, hydration status, voiding and stooling patterns, and weight changes be observed to either affirm normalcy or identify problems early. If frequency is insufficient or if milk transfer is not occurring, skilled breast-feeding support includes finding alternative methods of maternal expression/neonatal ingestion of breast milk. Teaching mothers how to manually express or pump milk, droplet-feed, finger-feed, or cup-feed expressed milk are acceptable methods of feeding breast milk to babies who are reluctant to nurse in the early days of life. According to CPS (2007), exclusively breast-fed infants experience their maximum
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weight loss by Day 3 and lose, on average, 6% to 8% of their birth weight. Infants who lose more than 10% of their birth weight fall outside of normal physiological expectations and must be carefully evaluated.
Feeding Breast-fed Term Infants With Jaundice The current position statements of AAP (2004) and CPS (2007) state that breast-feeding is not contraindicated in the presence of hyperbilirubinemia and should be continued. Regardless of the cause of jaundice, breast is best, formula feeding involves health risks, and all infants require surveillance that they are meeting normal developmental indicators. Feeding Babies With Early-onset Jaundice A literature review by Shoemaker and Ellis (2003) found no studies demonstrating that cessation of breast-feeding in jaundiced term infants improves clinical outcomes. Whether they require phototherapy or not, continuing breast-feeding in jaundiced babies is not associated with adverse outcomes. Tan (1998) found that exclusively breast-fed infants had slower responses to phototherapy in the first 24 hours of phototherapy than babies who were formula fed or who received supplementation with formula, but there were no significant differences in the total length of phototherapy required by the different groups. Martinez, Maisels, and Otheguy (1989) conducted a randomized clinical trial involving 125 jaundiced (total serum bilirubin z17 mg/dL) breast-fed infants comparing four treatment approaches: (a) continue breast-feeding and observe; (b) discontinue breast-feeding and substitute formula; (c) discontinue breast-feeding, substitute formula, and administer phototherapy; and (d) continue breast-feeding and administer phototherapy. Martinez et al. (1989) did not find a clinically significant difference in serum bilirubin reduction to normal levels at 48 hours between breast-fed and bottle-fed groups undergoing phototherapy or between breast-fed and bottlefed groups who did not have phototherapy. Phototherapy was beneficial, and breast-feeding can be continued during phototherapy. Feeding Babies With Not-Enough-Breast-feeding Jaundice There is no evidence that a trial of formula may solve the problem—the objective is to get more
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breast milk into baby and treat jaundice with phototherapy according to medical guidelines. However, if lactation has been understimulated, little expressed milk is available and a baby is clearly underhydrated, losing weight, and jaundiced, supplementation with formula is appropriate. AAP (2004) does not recommend supplementation with dextrose water which may temporarily satiate the infant but lead to inadequate caloric intake, which increases bilirubin levels. However, mothers can be encouraged to concurrently stimulate breasts with pumping, thereby enhancing milk production and reducing required formula supplementation. Spatz and Goldschmidt (2006) recommend double pumping breasts with a hospital-grade electric pump if milk transfer is not occurring and encouraging mother–baby skin-to-skin contact. We have seen mothers transform feelings of sorrow and inadequacy to joy and renewed confidence in their nurturing abilities as they visualize the increase in milk production after even 1 day of regular pumping. However, reversing discouragement usually takes skilled support by caregivers who honor lactation psychophysiology and “walk the talk” of believing in women's inherent capability of breast-feeding. Feeding Babies With Breast Milk Jaundice Breast milk jaundice is prolonged jaundice in babies who are otherwise thriving. Although other possible pathologies must be ruled out, babies with breast milk jaundice can continue to breast-feed. According to Thilo (1999), it is not known to result in bilirubin encephalopathy. CONCLUSION Breast-feeding is a fundamental step in life span health promotion. The evidence in favor of promoting exclusive breast-feeding is overwhelming, but translating research into practice has not been without barriers. In some cultures, inexperienced mothers receive support from experienced grandmothers, but such resources are frequently unavailable to modern women whose own mothers and grandmothers bottle-fed their babies. In North America, nurses usually advise new mothers about infant feeding, but not all nurses have sufficient expertise and not all maternity units are adequately staffed. Not-enough-breast-feeding jaundice and breastfeeding failure associated with jaundice are largely preventable through a systems-based approach
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(Bhutani, Johnson, Shwoebel & Gennaro, 2006) to ensure that all babies receive skilled lactation support and appropriate surveillance. Breast-fed babies save health care dollars (Ball and Wright, 1999), but we must first invest in saving breast-
feeding. The time to establish breast-feeding is perinatally and in the early postpartum, and we generally only have this one chance to get it right— for the benefit of the baby for a lifetime and, by extension, all of society.
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