Jaundice in newborn babies are a common occurrence and is evident as a yellowish discoloration of the skin, mouth and whites of the eye (sclera). In babies, the discoloration of the sclera is often more prominent than it is in jaundiced adults. Jaundice is due to an elevated level of bilirubin in the blood (hyperbilirubinemia).
Neonatal jaundice that is not pathological may be due to physiologic jaundice, breastfeeding jaundice or breast milk jaundice. Jaundice in newborn babies that may be due to pathological causes includes non-hemolytic jaundice in a condition like Gilbert’s syndrome or hemolytic jaundice as a result of erythroblastosis fetalis.
Bilirubin in Babies
Bilirubin from the fetus is managed by the mother’s liver but once the baby is born, the newborn’s body has to rely on its own mechanisms for the conjugation of bilirubin. Comparatively, a baby lives in a state of hypoxia within the mother’s uterus – this means that there is a low oxygen availability compared to oxygen acquired through respiration (breathing). In order to cope, the fetus produces and maintains a higher volume of red blood cells (erythrocytes), which is over 4 million cells per cubic millimeter. Once the baby is born and breathing, the body no long requires these red blood cells and begins to break down the excess cells.
The rush of bilirubin released as a result of hemoglobin metabolism coupled with the immature liver’s inability to conjugate bilirubin efficiently often results in jaundice in the newborn. Other factors that contribute to the high levels of bilirubin include diminished hepatic flow and an almost sterile gut lacking the natural intestinal flora (bacteria) that is required to further break down bilirubin in the gut. This is known as physiologic jaundice. It starts about 2 to 4 days after life and often passes on its own with no need for medical intervention.
Jaundice in the Breastfed Baby
This type of jaundice is often associated with physiologic jaundice but is a result of a lower blood plasma volume in the baby. This increases the concentration of bilirubin in the blood but subsides once the baby is feeding for a period of time. It is often complicated by a low breast milk supply as the mother’s breast tissue begins to produce milk in the first few days of the baby’s life. Breastfeeding jaundice subsides as the blood plasma volume increases.
Breast Milk Jaundice
This type of jaundice occurs in a breastfeeding baby as a result of the mother’s progesterone impairing the conjugation of bile. Pregnane-3-alpha 20 beta-diol is a metabolite of progesterone and passes through the breast milk into the baby’s body. It inhibits the enzyme glucuronyl transferase which is necessary for the conjugation of free bilirubin with glucuronic acid. Breast milk jaundice starts about 4 to 7 days after birth and resolves spontaneously with no need for medical treatment.
A type of hemolytic jaundice seen in newborns is known as erythroblastosis fetalis. It arises when a baby inherits Rh-positive red blood cells from the father while the mother is Rh-negative. The process begins in the fetus and antibodies produced in the mother’s body crosses the placental barrier where it destroys the baby’s red blood cells. In erythroblastosis fetalis, the baby is often born jaundiced.
Non-Hemolytic Jaundice in a Newborn
Certain inherited disorders may affect the genes responsible for glucuronyl transferase. This enzyme is necessary for the conjugation of bilirubin. In Crigler-Najar syndrome type 1, there is a deficiency or absence of glucuronyl transferase, while in Gilbert syndrome, there is an underactivity of glucuronyl transferase either due to a quantitative or qualitative deficiency. Both these conditions may only be detected weeks after the baby is born as it may be initially misdiagnosed as physiologic, breastfeeding and breast milk jaundice.