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Breastmilk Jaundice
Breastmilk Jaundice
Arias first described breast milk jaundice (BMJ) in 1963. Breast milk jaundice is a type of
neonatal jaundice associated with breastfeeding. It is characterized by indirect
hyperbilirubinemia in a breastfed newborn that develops after the first 4-7 days of life,
persists longer than physiologic jaundice, and has no other identifiable cause. It should be
differentiated from breastfeeding jaundice, which manifests in the first 3 days of life and is
caused by insufficient production or intake of breast milk.
Pathophysiology
Jaundice occurs in 50-70% of newborns. Moderate jaundice (bilirubin level >12 mg/dL)
develops in 4% of bottle-fed newborns, compared to 14% of breastfed newborns. Severe
jaundice (bilirubin level >15 mg/dL) occurs in 0.3% of bottle-fed newborns, compared to
2% of breastfed newborns. A strong familial predisposition is also suggested by the
recurrence of breast milk jaundice in siblings. In the exclusively breast fed infant, the
incidence during the first 2-3 weeks has been reported to be 36%.[5]
International
International frequency is not extensively reported but is thought to be similar to that in the
United States.
Mortality/Morbidity
The prognosis is excellent, although jaundice in breastfed infants may persist for as long as
12 weeks.
Breast milk jaundice in otherwise healthy full-term infants rarely causes kernicterus
(bilirubin encephalopathy). Case reports suggest that some breastfed infants who suffer
from prolonged periods of inadequate breast milk intake and whose bilirubin levels
exceeded 25 mg/dL may be at risk of kernicterus. Kernicterus (bilirubin encephalopathy) is
a preventable cause of cerebral palsy. Another group of breastfed infants who may be at risk
of complications is late preterm infants who are nursing poorly.
Whether racial differences are observed in breast milk jaundice is unclear, although an
increased prevalence of physiologic jaundice is observed in babies of Chinese, Japanese,
Korean, and Native American descent.
Sex
Breast milk jaundice manifests after the first 4-7 days of life and can persist for 3-12 weeks.
History
Aspects of history may include the following:
Physiologic jaundice usually manifests after the first 24 hours of life. This can be
accentuated by breastfeeding, which, in the first few days of life, may be associated
with suboptimal milk and suboptimal caloric intake, especially if milk production is
delayed. This is known as breastfeeding jaundice. Jaundice that manifests before the
first 24 hours of life should always be considered pathologic until proven otherwise.
In this situation, a full diagnostic workup with emphasis on infection and hemolysis
should be undertaken.
True breast milk jaundice (BMJ) manifests after the first 4-7 days of life. A second
peak in serum bilirubin level is noted by age 14 days.
Physical
The following physical findings may be noted:
Clinical jaundice is usually first noticed in the sclera and the face. Then it
progresses caudally to reach the abdomen and extremities. Gentle pressure on the
skin helps to reveal the extent of jaundice, especially in darker-skinned babies;
however, clinical observation is not an accurate measure of the severity of the
hyperbilirubinemia.
A rough correlation is observed between blood levels and the extent of jaundice
(face, approximately 5 mg/dL; mid abdomen, approximately 15 mg/dL; soles, 20
mg/dL). Therefore, clinical decisions should always be based on serum levels of
bilirubin. Skin should have normal perfusion and turgor and show no petechiae.
Causes
The following causes may be noted:
Delayed milk production and poor feeding lead to decreased caloric intake,
dehydration, and increased enterohepatic circulation, resulting in higher serum
bilirubin concentration.
The biochemical cause of breast milk jaundice remains under investigation. Some
research reported that lipoprotein lipase, found in some breast milk, produces
nonesterified long-chain fatty acids, which competitively inhibit glucuronyl
transferase conjugating activity.
Glucuronidase has also been found in some breast milk, which results in jaundice.
A 2011 study has shown that neonates with nucleotide 211GA or AA variation in
UGT1A1 genotypes had higher peak serum bilirubin levels than those with GG.
This effect was more pronounced in the exclusively breast fed infants compared
with exclusively or partially formula fed neonates.[10]
The organic anion transporters (OATPs) are a family of multispecific pumps that
mediate the Na- independent uptake of bile salts and broad range of organic
compounds. In humans, 3 liver-specific OATPs have been identified: OATP-A,
OATP-2, and OATP-8. Unconjugated bilirubin is transported in the liver by OATP2. A genetic polymorphism for OATP-2 (also known as OATP-C) at nucleotide 388
has been shown to correlate with 3-fold increased risk for development of neonatal
jaundice (peak serum bilirubin level of 20 mg/dL) when adjusted for covariates.[11, 12]
When the combination of the OATP-2 gene polymorphism with the variant
UGT1A1 gene at nucleotide 211 further increased the risk to 22-fold (95% CI, 5.588). When these genetic variants were combined with breast milk feeding, the risk
for marked neonatal hyperbilirubinemia increased further to 88-fold (95%CI, 12.5642.5).
Diagnostic Considerations
Important considerations
Large cephalhematoma
Hypothyroidism
Sepsis
Gilbert syndrome
Early galactosemia
Differential Diagnoses
Anemia, Acute
Hypothyroidism
Neonatal Jaundice
Neonatal Sepsis
Polycythemia
Laboratory Studies
Breast milk jaundice (BMJ) is a diagnosis of exclusion. Note the following:
Detailed history and physical examination showing that the infant is thriving and
that lactation is well established are key elements to diagnosis. Breastfed babies
should have 3-4 transitional stools and 6-7 wet diapers per day and should have
regained birth weight by the end of the second week of life or demonstrate a weight
gain of 1 oz/d.
Measure total serum bilirubin concentration in neonates who have jaundice that has
progressed from the face to the chest and in neonates at risk for hemolytic disease of
the newborn.
Consider obtaining the tests discussed below if serum bilirubin levels are greater than 12
mg/dL (170 mol/L). A total serum bilirubin concentration that rises faster than 5 mg/dL/d
(85 mol/L/d) or jaundice before 24 hours of life suggests pathologic jaundice.
A level of conjugated bilirubin greater than 2 mg/dL (34 mol/L) suggests cholestasis,
biliary atresia, or sepsis (see Neonatal Jaundice).
CBC count with reticulocyte count findings are as follows:
Sepsis (WBC count, < 5 K/mL or >20 K/mL) with immature to total neutrophil ratio
greater than 0.2
Coombs test, as well as an elution test for antibodies against A or B, to evaluate for
immune mediated hemolysis
Pallor, hepatosplenomegaly
Rapid increase in serum bilirubin level after 24-48 hours (G-6-PD deficiency)
Blood culture
WBC differential
Platelet count
Poor feeding
Vomiting
Lethargy
Temperature instability
Apnea
Tachypnea
Signs of cholestatic jaundice that suggest the need to rule out biliary atresia or other causes
of cholestasis include the following:
Light-colored stools
The follow-up includes the state newborn screen for galactosemia and hypothyroidism.
Medical Care
Treatment recommendations in this section apply only to healthy term infants with no signs
of pathologic jaundice and are based on the severity of hyperbilirubinemia. In preterm,
anemic, or ill infants and those with early (< 24 h) or severe jaundice (>25 mg/dL or 430
mol/L), different treatment protocols should be pursued (see Neonatal Jaundice).
For healthy term infants with breast milk or breastfeeding jaundice and with bilirubin levels
of 12 mg/dL (170 mol/L) to 17 mg/dL, the following options are acceptable:
Increase breastfeeding to 8-12 times per day and recheck the serum bilirubin level
in 12-24 hours. The mother should be reassured about the relatively benign nature
of breast milk jaundice (BMJ). This recommendation assumes that effective
breastfeeding is occurring, including milk production, effective latching, and
effective sucking with resultant letdown of milk. Breastfeeding can also be
supported with manual or electric pumps and the pumped milk given as a
supplement to the baby.
For infants with serum bilirubin levels from 17-25 mg/dL (294-430 mol/L), add
phototherapy to any of the previously stated treatment options. The reader is referred to the
Fiberoptic phototherapy can often be safely administered at home, which may allow
for improved infant-maternal bonding.
Phototherapy can be discontinued when serum bilirubin levels drop to less than 15
mg/dL (260 mol/L).
Average bilirubin level rebound has been shown to be less than 1 mg/dL (17
mol/L); therefore, rechecking the level after discontinuation of phototherapy is not
necessary unless hyperbilirubinemia is due to a hemolytic process.
Consultations
The following consultations may be indicated:
Diet
Continue breastfeeding, if possible, and increase frequency of feeding to 8-12 times per
day. Depending on maternal preference, breastfeeding can be supplemented or replaced by
formula at the same frequency. Supplementation with dextrose solution is not
recommended because it may decrease caloric intake and milk production and may
consequently delay the drop in serum bilirubin concentration. Breastfeeding can also be
supplemented by pumped breast milk.
Activity
No restrictions are necessary. Encourage parents to remove the child from the warmer or
infant crib for feeding and bonding. Fiberoptic blankets allow holding and breastfeeding
without interruption in treatment.
(< 20 mg/dL) and is not rapidly rising, home phototherapy is an option to consider as long
as thorough outpatient follow-up (home visiting nursing assessment or office check-up and
bilirubin level monitoring) are feasible.
Weight monitoring is very important in breastfed infants to avoid prolonged and severe
jaundice, as well as to avoid hypernatremic dehydration. The general standard states that
loss of 10% of birth weight is considered to be significant.
A reference chart for relative weight change to detect hypernatremic dehydration has been
proposed.[15]
Transfer
Transfer infants with pathologic jaundice or bilirubin levels greater than 20 mg/dL to a
center capable of performing exchange transfusions.
Deterrence/Prevention
Keys to deterrence and prevention include the following:
Infants who nursed more than 8 times during the first 24 hours had earlier
meconium passage, reduced maximum weight loss, increased breast milk intake on
days 3 and 5, and lower serum bilirubin levels and significantly lower incidence of
severe hyperbilirubinemia (>15 mg/dL) on day 6.
In a recent double-blind controlled study, beta-glucuronidase inhibition with Laspartic acid and enzymatically hydrolyzed casein in exclusively breastfed babies
resulted in reduction in peak serum bilirubin level by 70% in first week of life.[17]
Recent studies suggest that combining clinical risk factors with predischarge
measurement of TSB or TcB levels improves the accuracy of risk assessment for
subsequent hyperbilirubinemia.[19] The factors most predictive included predischarge
TSB or TcB levels above 75th percentile, lower gestational age, and exclusive
breastfeeding.[20]
Newborns who are exclusively breastfed and who have elevated predischarge TcB
or TSB levels do not qualify for discharge before 48 hours and should be evaluated
for phototherapy in 24 hours. Newborns with TcB and TSB levels in the highintermediate range and newborns who were born at less than 38 weeks' gestation
should undergo repeat TSB and TcB measurement within 24 hours of discharge or
should receive follow-up within 2 days.[21]
Patient Education
Provide excellent breastfeeding education. Refer to a lactation consultant or La Leche
League.
For patient education resources, see the Pregnancy and Reproduction Center, as well as
Breastfeeding.