Breast milk jaundice Breastfeeding jaundice
characterized by indirect
hyperbilirubinemia in an manifests in the first 3 days
otherwise healthy of life, peaks by 5-15 days
breastfeed newborn that of life, disappears by week
develops after the first four 3 of life, and is caused by
Onset to seven days of life and insufficient production or
persists no longer than intake of breast milk.
physiologic jaundice and may reoccur during the
has no other identifiable breast feeding period
cause
Newborns may not receive
optimal milk intake, which
leads to elevated bilirubin
levels due to increased
Unknown but probably due reabsorption of bilirubin in
to B-glucuronidase in the intestines. Inadequate
Pathophysiology breast milk which increases milk intake also delays the
enterohepatic circulation passage of meconium,
which contains large
amounts of bilirubin that is
then transferred into the
infant’s circulation.
The exact etiology of breast
milk jaundice has not been
determined. Most of the
proposed etiologies
involve the factors
present in the human
breast milk itself while
other hypotheses suggest
1. Difficulty breastfeeding
potential genetic
2. Insufficient milk
mutations present in the
production
affected neonates
Etiology 1. Glucuronidase has also
3. improper latching
4. supplemented with other
been found in some
substitutes that interfere
breast milk
with breastfeeding.
2. Decreased UGT1A1
activity may be
associated with
prolonged
hyperbilirubinemia in
breast milk jaundice
3. The G211A mutation in
exon 1 is most common
Incidence 0.5–2% of breastfed infants 10% of breastfed infants
characterized by indirect
hyperbilirubinemia in an manifests in the first 3 days
otherwise healthy of life, peaks by 5-15 days
breastfeed newborn that of life, disappears by week
develops after the first four 3 of life, and is caused by
Onset to seven days of life and insufficient production or
persists no longer than intake of breast milk.
physiologic jaundice and may reoccur during the
has no other identifiable breast feeding period
cause
Newborns may not receive
optimal milk intake, which
leads to elevated bilirubin
levels due to increased
Unknown but probably due reabsorption of bilirubin in
to B-glucuronidase in the intestines. Inadequate
Pathophysiology breast milk which increases milk intake also delays the
enterohepatic circulation passage of meconium,
which contains large
amounts of bilirubin that is
then transferred into the
infant’s circulation.
The exact etiology of breast
milk jaundice has not been
determined. Most of the
proposed etiologies
involve the factors
present in the human
breast milk itself while
other hypotheses suggest
1. Difficulty breastfeeding
potential genetic
2. Insufficient milk
mutations present in the
production
affected neonates
Etiology 1. Glucuronidase has also
3. improper latching
4. supplemented with other
been found in some
substitutes that interfere
breast milk
with breastfeeding.
2. Decreased UGT1A1
activity may be
associated with
prolonged
hyperbilirubinemia in
breast milk jaundice
3. The G211A mutation in
exon 1 is most common
Incidence 0.5–2% of breastfed infants 10% of breastfed infants
