eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Breast Milk Jaundice

Author: Prashant G Deshpande, MD, Consulting Staff, Department of Pediatrics, Hope Children's Hospital
Contributor Information and Disclosures

Updated: Oct 3, 2008

Introduction

Background

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 week of life and is caused by insufficient production or intake of breast milk.

Pathophysiology

The etiology of breast milk jaundice is not clearly understood, but the following factors have been suggested to play a role:

  • An unusual metabolite of progesterone (pregnane-3-alpha 20 beta-diol), a substance in the breast milk that inhibits uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase
  • Increased concentrations of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase
  • Increased enterohepatic circulation of bilirubin due to (1) increased content of beta glucuronidase activity in breast milk and, therefore, the intestines of the breastfed neonate and (2) delayed establishment of enteric flora in breastfed infants
  • Defects in uridine diphosphate-glucuronyl transferase (UGT1A1) activity in infants who are homozygous or heterozygous for variant Gilbert syndrome promoter polymorphism

Please see Jaundice, Neonatal for an in-depth review of the pathophysiology of hyperbilirubinemia.

Frequency

United States

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.

International

International frequency is not extensively reported but is thought to be similar to that in the United States.

Mortality/Morbidity

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. Another group of breastfed infants who may be at risk of complications are borderline premature infants (36-37 weeks' gestational age) who are poorly nursing.

Race

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

No sex predilection is known.

Age

Breast milk jaundice manifests after the first 4-7 days of life and can persist for 3-12 weeks.

Clinical

History

  • 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.
  • In clinical practice, differentiating between physiologic jaundice from breast milk jaundice is important so that the duration of hyperbilirubinemia can be predicted. Identifying the infants who become dehydrated secondary to inadequate breastfeeding is also important. These babies need to be identified early and given breastfeeding support and formula supplementation as necessary. Depending on serum bilirubin concentration, neonates with hyperbilirubinemia may become sleepy and feed poorly.

Physical

  • 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.
  • Neurologic examination, including neonatal reflexes, should be normal, although the infant may be sleepy. Muscle tone and reflexes (eg, Moro reflex, grasp, rooting) should be normal.
  • Evaluate hydration status by an assessment of the percentage of birth weight that may have been lost, observation of mucous membranes, fontanelle, and skin turgor.

Causes

  • Supplementation of breastfeeding with dextrose 5% in water (D5W) can actually increase the prevalence or degree of jaundice.
  • 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.
  • Defects in uridine diphosphate-glucuronyl transferase (UGT1A1) activity may be associated with prolonged hyperbilirubinemia in breast milk jaundice. One or more components in breast milk may trigger such mutations.1 This may be comparable to some patients with Gilbert syndrome.

More on Breast Milk Jaundice

Overview: Breast Milk Jaundice
Differential Diagnoses & Workup: Breast Milk Jaundice
Treatment & Medication: Breast Milk Jaundice
Follow-up: Breast Milk Jaundice
References
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References

  1. Maruo Y, Nishizawa K, Sato H, Sawa H, Shimada M. Prolonged unconjugated hyperbilirubinemia associated with breast milk and mutations of the bilirubin uridine diphosphate- glucuronosyltransferase gene. Pediatrics. Nov 2000;106(5):E59. [Medline]. [Full Text].

  2. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. Jul 2004;114(1):297-316. [Medline].

  3. van Dommelen P, van Wouwe JP, Breuning-Boers JM, van Buuren S, Verkerk PH. Reference chart for relative weight change to detect hypernatraemic dehydration. Arch Dis Child. Jun 2007;92(6):490-4. [Medline].

  4. Gourley GR, Li Z, Kreamer BL. A Controlled, Randomized, Double-Blind Trial of Prophylaxis Against Jaundice Among Breastfed Newborns. Pediatrics. 116:385 - 391. [Medline].

  5. Bhutani VK, Johnson L, Sivieri EM. Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics. Jan 1999;103(1):6-14. [Medline].

  6. Fontaine P. The first month of life. In: Handbook of Pregnancy and Perinatal Care in Family Practice. Hanley & Belfus; 1995:396-429.

  7. Gartner LM, Herschel M. Jaundice and breastfeeding. Pediatr Clin North Am. Apr 2001;48(2):389-99. [Medline].

  8. Grunebaum E, Amir J, Merlob P, et al. Breast mild jaundice: natural history, familial incidence and late neurodevelopmental outcome of the infant. Eur J Pediatr. Feb 1991;150(4):267-70. [Medline].

  9. Hamosh M, Bitman J. Human milk in disease: lipid composition. Lipids. Nov 1992;27(11):848-57. [Medline].

  10. Johnson LH, Bhutani VK, Brown AK. System-based approach to management of neonatal jaundice and prevention of kernicterus. J Pediatr. Apr 2002;140(4):396-403. [Medline].

  11. Lovejoy FH Jr, Robertson WO, Woolf AD. Poison centers, poison prevention, and the pediatrician. Pediatrics. Aug 1994;94(2 Pt 1):220-4. [Medline].

  12. Maisels MJ, Newman TB. Kernicterus in otherwise healthy, breast-fed term newborns. Pediatrics. Oct 1995;96(4 Pt 1):730-3. [Medline].

  13. Martinez JC, Maisels MJ, Otheguy L, et al. Hyperbilirubinemia in the breast-fed newborn: a controlled trial of four interventions. Pediatrics. Feb 1993;91(2):470-3. [Medline].

  14. Schneider AP 2nd. Breast milk jaundice in the newborn. A real entity. JAMA. Jun 20 1986;255(23):3270-4. [Medline].

  15. Yamauchi Y, Yamanouchi I. Breast-feeding frequency during the first 24 hours after birth in full-term neonates. Pediatrics. Aug 1990;86(2):171-5. [Medline].

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Further Reading

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Keywords

breast milk jaundice, jaundice, neonatal jaundice, indirect bilirubin, bilirubin, breastfeeding, physiologic jaundice, uridine diphosphoglucuronic acid, UDPGA, UDPGA glucuronyl transferase, unconjugated bilirubin pigment, conjugated bilirubin, hyperbilirubinemia, clinical jaundice, cholestatic jaundice, bilirubin level, pathologic jaundice, phototherapy, breast milk, breastfeeding-associated jaundice, Gilbert syndrome, kernicterus

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Contributor Information and Disclosures

Author

Prashant G Deshpande, MD, Consulting Staff, Department of Pediatrics, Hope Children's Hospital
Prashant G Deshpande, MD is a member of the following medical societies: American Academy of Pediatrics and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Oussama Itani, MD, FAAP, FACN, Clinical Associate Professor of Pediatrics and Human Development, Michigan State University; Medical Director, Department of Neonatology, Borgess Medical Center
Oussama Itani, MD, FAAP, FACN is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Brian S Carter, MD, FAAP, Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Co-director, Pediatric Advance Comfort Team, Monroe Carell Jr Children's Hospital at Vanderbilt
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, National Hospice and Palliative Care Organization, and National Perinatal Association
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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