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After birth, when babies start to breathe and use their lungs, these extra cells are no longer needed and are broken down. This means that the newborn baby will in fact have a relatively increased load of bilirubin to clear.
Normally, the liver can cope with this bilirubin load. If the load becomes too great, or the processes within the liver slow down, or there is some obstruction to the outflow of the bile from the liver, then bilirubin will accumulate in the blood. Eventually it will reach a level where it's deposited in the skin where it will cause the yellow colour.
Some of the bilirubin in the bile in the intestine is normally re-absorbed. If there is a significant delay in the passage of stools, then a greater amount of bilirubin will enter the circulation and add to bilirubin levels.
During pregnancy, while the baby is developing in the uterus, the liver is assisted in its functions by the placenta, including the processing of the bilirubin. At birth, the baby’s liver has to take over on its own and suddenly has to cope with the bilirubin. It normally takes a few days before the liver is fully functional. If it takes a longer period, then the bilirubin levels can become high enough to deposit out in the skin to give the yellowish colour of jaundice. Preterm babies are understandably more prone to this problem. This form of neonatal jaundice is referred to as “physiological jaundice” because it is essentially a prolongation of a normal process.
Breast milk or breastfeeding jaundice is so called because the breast milk of some mothers appears to contain factors that cause jaundice. This kind of jaundice is not harmful to the infant and is NOT a reason to stop breastfeeding.
More serious forms of jaundice are referred to as “pathological jaundice”. One very important cause is excessive breakdown of the red cells and is known as haemolytic disease of the newborn. This occurs when there is a difference (incompatibility) between the mother and her baby’s blood groups.
The most important of these causes is Rh incompatibility. The Rhesus (Rh) factor is one of the major blood group markers. In this disease the mother is Rh negative but her baby is Rh positive. The mother becomes sensitised and produces antibodies that cross through the placenta and destroy the red blood cells of the baby. The degree of haemolysis that occurs depends on the stage of the pregnancy and the amount of antibodies that cross the placenta. The liver is overwhelmed by the amount of bilirubin produced and the baby becomes jaundiced. The destruction of large numbers of red blood cells means that the baby also becomes anaemic, which adds to the problem.
This rarely happens with the first pregnancy as it usually requires two or three incompatible pregnancies for the mother to become sensitised. If the mother’s Rh factor is known after her first pregnancy, she can be given anti-D (Rh) immuno-globulin immediately after delivery to try and prevent sensitisation whenever she carries a Rh positive baby.
A second situation where there may be incompatibility between mother and baby is with the major blood groups – the ABO factors. This also leads to breakdown of the red blood cells but is usually not as severe as Rh incompatibility.
There are many other rarer causes of haemolysis. One of them is when there is a deficiency of an enzyme needed for the integrity of the red blood cells. This enzyme is known as glucose-6-phosphate dehydrogenase (G-6-PD).
If the baby has an infection resulting in hepatitis, then jaundice may appear. This happens because the inflamed liver cells are not able to process the bilirubin as efficiently as usual. They also swell up and tend to block the very small ducts in the liver that carry the processed bilirubin away to the larger bile ducts. The bilirubin accumulates and eventually leaks back into the blood stream. It is this obstructed bilirubin that accounts for most of the jaundice and hence the name “obstructive jaundice”.
In very rare instances a child may be born without functioning bile ducts. All the bilirubin processed by the liver can only escape by leaking back into the blood. This condition is known as biliary atresia and children with biliary atresia have severe obstructive jaundice.
