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Jaundice in the Newborn

Jaundice in the newborn. Bilirubin is derived from hemoglobin. One gm of hemoglobin will produce 34 mg of bilirubin, so what you can see here is that you donít need a heck of a lot of hemolysis going on to produce fair amounts of bilirubin. It enters the circulation in the unconjugated form.

Then is transported to the liver where it is conjugated, excreted into the bile duct and then into the small intestine. One thing which is absolutely crucial for you to understand when thinking about jaundice in the newborn is the enterohepatic circulation where bilirubin is reabsorbed from the gut and the key thing is that it is reabsorbed in the unconjugated form. So that anything that produces a slowing of passage of stool through the GI tract will produce an unconjugated hyperbilirubinemia.

So why are bilirubin levels higher in newborns? A number of different reasons. Obviously there is large red blood cell load, not unusual to see hematocrits of 60 or 65. There is also a shorter red blood cell life span. There is a fair amount of hematopoietic tissue, which is being degraded. The liver is immature and especially in premature babies.

A very important point here is that anything that affects the beta chain isnít going to present in the newborn period, in the first few weeks of life certainly. So sickly-cell, which affects beta chain, isnít going to show up in the first few weeks of life with jaundice. That is because there is plenty of fetal hemoglobin around and so these children really will not be symptomatic early on because of that fetal hemoglobin. Sepsis should be on your list as causing intravascular hemolysis.

So on to other forms of increased production: extravascular hemolysis. So rather than having the blood cells breaking down inside the vessels we have breakdown of blood outside the vessels. Things like hematomas, cephalhematomas, can commonly cause increased bilirubins. Bruising doesnít tend to be as much of a problem in full term babies. They seem to be able to handle that bilirubin a little bit better, but certainly premature babies, if they are fairly bruised, can get quite jaundiced just from the bruising. Hemorrhage also. If you bleed into any closed space that hemoglobin is going to be reabsorbed.

Inborn errors of metabolism, galactosemia, tyrosinemia, can interfere with clearance and the important thing here is they may start as an unconjugated hyperbilirubinemia but can become conjugated. So they will show up on both your differential diagnosis, both for indirect hyperbilirubinemia and direct hyperbilirubinemia. There are endocrinologic problems, hypothyroidism, hypopituitarism, these two can present in the conjugated form as well. Then late-onset breast milk jaundice, in contrast to the breast-feeding jaundice, this isnít a problem with the amount of breast milk that is there. It seems that there is an intrinsic factor in the breast milk that causes hyperbilirubinemia and again is not related to adequacy of nutrition. Generally what you will see with this late breast milk jaundice is it wonít present in the first week of life, it will present more in the second or third week of life. Another thing to note about the early breast feeding jaundice is the timing.

Just a word about management of early breast feeding jaundice and later breast milk jaundice. The important thing is that there is absolutely no reason to stop breast feeding. As a matter of fact you want to kind of continue to encourage breast feeding unless they have tremendously high levels, and you want to make sure you are getting in as much as possible.

Late breast milk jaundice, you reallyÖ all you need to do is make sure there is no hemolysis. And generally what we do  is just stop breast feeding for 24 hours and if the bilirubin drops - usually youíll see at least a 2-3 point drop in 24 hours. On the direct hyperbilirubinemia, fortunately the list for direct for hyperbilirubinemia is a shorter risk. Number one cause is hepatitis. A bunch of different infections that you may see. But certainly TORCH infections all can present with hepatitis. Also there is idiopathic or giant cell hepatitis as well as sepsis that can cause a direct hyperbilirubinemia. Second is cholestasis. There is a slight error on this slide. Under intrahepatic you see arteriohepatic dysplasia and the Alagille syndrome.