Diseases, Disorders information

So, on to the causes of hyperbilirubinemia. I think the important thing is that you don’t really want to have a memorization of a long list. You need to think in pathophysiologic terms. One way to look at it is; increased production versus decreased clearance. Under increased production the biggest category, and probably the most common category of all, is intravascular hemolysis. I think the best way to think of all of these ways that red cells can hemolyze, is first of all you need to think of what can go wrong with a red cell, and then what are all of the components that a red cell has that may have problems. The first one obviously is autoimmune, which is often … well, not often but generally fetal/maternal incompatibility of blood type. Rh is historically the most dangerous and because of RhoGAM it is something we don’t see very much at all. ABO is now the most common problem, in terms of causing autoimmune hemolysis. Mother who is type O is the one who is most likely to have problems. You can also have minor antigens though. Antigens that at times can cause moderately high bilirubin levels. The second component of the red cell that you need to think about is the wall. The wall and structural problems, so you may see spherocytosis or elliptocytosis. Red cells also have enzymes so enzyme deficiencies can produce hyperbilirubinemia. Pyruvate kinase can present with a very impressive hyperbilirubinemia in the newborn period, as can G6PD. Hemoglobin, another component of the red cell and Hemoglobinopathies, can also present in the newborn period with jaundice.
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A very important point here is that anything that affects the beta chain isn’t going to present in the newborn period, in the first few weeks of life certainly. So sickly-cell, which affects beta chain, isn’t 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. One thing I think that you need to know is that jaundice is not going to be a presenting sign of sepsis. You aren’t going to have this well-looking kid who turns yellow and sepsis is the cause of it. It’s more that septic kids can become jaundiced. I think keeping that in mind is important. Then finally, mechanical or red blood cell destruction in things like ADM is also possible but seems to be fairly rare.
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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 doesn’t 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 and converted into bilirubin, so you may see pulmonary bleeding, GI bleeding, and in the premature baby you can even see jaundice being fairly prominent if you have a large intraventricular hemorrhage. Excess RBC load – I guess this should be more in the intravascular hemolysis – but if you see hematocrits that are up in the mid 60’s and even in the lower 60’s, that load may contribute to hyperbilirubinemia. And sometimes what we will see is that you may have a couple of these things. Cephalhematomas are common. Polycythemia is pretty common. You put those two together and you are more likely to have pretty high levels of bilirubin.
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