Just a review of some of the common pattern recognition links and association. First on your list we’ve talked about already in some detail is: if you have difficulty feeding, excess weight loss, so they have a clinical scenario for you where the baby has lost greater than 10% of their weight first week of life, think of breast feeding jaundice. If you have high reticulocyte count that strongly suggests hemolysis. Ethnicity may be a clue, so that with South East Asian or Chinese may be suggestive of alpha-thalassemia, whereas African-American, Mediterranean, and some Asians who have recently ingested fava beans or sulfa or another drug, may think of G6PD. Because it is X-linked recessive it could be suggestive of having male siblings with jaundice. Positive family history for anemia, splenectomy, spherocytosis is suggested. Also you may see something that, if it’s not in your syllabus you may want to add in, Northern European descent is linked with spherocytosis as well. Small for gestational age, hepatosplenomegaly, microcephaly all suggest TORCH infections. Neurologic symptoms with a positive urine Clinitest suggest galactosemia. And another important link with galactosemia is early onset to E. coli sepsis.
Well talk about management of indirect hyperbilirubinemia next. First thing is hydration, and I don’t’ care what the cause of indirect hyperbilirubinemia is, if you have a baby who is coming in with levels that are potentially approaching the exchange transfusion, you want to hydrate these kids. The key thing is that there is – unless they are very dehydrated or have some contraindications – the way you want to hydrate them is orally. You don’t want to give these kids IV fluids. Again, the reason you want to do that is you want to use the benefit of the enterohepatic circulation and get that stool and that bilirubin out of the gut as quickly as possible. So we’ll try to feed aggressively, bottle supplement if they are on breast feeding, and then consider even NG tube feedings if they can’t take in enough fluids. Another thing that I’ll do, a nice trick, is actually if they haven’t had a stool in awhile just give them a glycerin suppository in the hopes of increasing the stool output that you may get and get a bilirubin drop in that kind of way.
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The second is phototherapy. You aren’t probably going to get asked this on the Boards because it’s fairly controversial, not a lot of great studies recently. I think most people at this point are using different criteria for hemolytic and non-hemolytic hyperbilirubinemia. Full term babies, hemolytic, I think the goal is still to keep bilirubins less than 20. So if you have bilirubins that seem to be approaching 20, you may want to start phototherapy. With the advent of home phototherapy it often makes our life easier in terms of getting that accomplished. Non-hemolytic is .. I think people are probably willing to accept levels of 25 or even up to 29 or so without getting too alarmed. I tend to be a little more aggressive. So if you are getting bilirubins up into the 20’s even with early breast milk jaundice, I will go ahead and start phototherapy. Relatively benign intervention overall.
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The third intervention is one that we hope to avoid if at all possible, which is an exchange transfusion. Again, hemolytic, if you have levels that get much above 20 and you can’t bring them down with phototherapy, or you start phototherapy and they continue to rise, then you need to consider an exchange transfusion. If you are dealing with premature infants then you are going to need to think about using lower levels at which to do exchange transfusions. Non-hemolytic, very controversial. I think people have said that there has never been a case of kernicterus in early breast milk jaundice, and apparently there is one report recently where a level was 40 and a baby developed kernicterus. So I’m not sure we can say that absolutely, but it seems at least that kernicterus is quite unusual, if not virtually impossible in breast feeding jaundice. So because exchange transfusions have such high morbidity and really relatively high mortality rates as well, especially as we are doing them less and less often, it is probably … you really want to avoid doing an exchange transfusion for a baby who has jaundice just from late onset breast milk jaundice. Canadian viagra
Infant history: feeding history is obviously very important. Breast feeding versus bottle. It’s hard to make a diagnosis of early breast mild jaundice or late breast milk jaundice if the baby is bottle feeding. The important thing too – I’m being kind of facetious – but early breast mild jaundice, I will see kids who are admitted to the hospital with bilirubins of 23 or something like that at four or five days of age, and people are quick to jump to the diagnosis of early breast milk jaundice. You need to have data that is consistent with that. Mother should have some sense that she doesn’t have enough milk, she doesn’t feel let down, she doesn’t feel engorgement. And also you should have some objective evidence that the baby is not feeding well. So what you want to see is some moderate decrease in weight, perhaps greater than 10% in the first week of life. A baby that is thriving, feeding well, don’t jump to the diagnosis of early breast milk jaundice if they are presenting with a good feeding pattern. Vomiting history is very important and stooling pattern. Again, anything that is going to increase transit time through the gut is going to cause unconjugated hyperbilirubinemia. Generic cialis pharmacy news
Physical examination: bruising hematomas are important to look for. Hepatosplenomegaly may be suggestive of hepatitis. Plethora indicative of polycythemia, and then if you are thinking about TORCH infections, look for other signs. Baby may be small for gestational age, microcephalic, may have findings of pneumonia as well or ocular abnormalities, a bunch of different signs that you may see with congenital infection, and then I keep mentioning sepsis, signs and symptoms of sepsis should be watched for.
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Screening lab tests: if you have an indirect hyperbilirubinemia probably the most reasonable panel to get would include a CBC, a peripheral smear to look for evidence of hemolysis. Also reticulocyte count to look for evidence of hemolysis. You have to be a little bit careful. If you get it on the first day of life it’s not unusual to see fairly high reticulocyte counts because of the kind of charged up marrow with the stress of delivery. So I bet you can see reticulocyte counts in the 5-10% range in the first day or so of life, but those should drop fairly quickly in the next day or so. A type and Coombs is worth doing even if the mother is not O because you may have some of those minor antigens. And then one test that you might want to consider, if you can’t find an obvious source of hemolysis and bilirubins are getting to fairly high level, is a urinalysis. The importance of urinalysis is that you are looking for a positive Clinitest which will be seen with galactosemia. So here in California we have the newborn screening for galactosemia and that may not get back in the first few days of life, though. So you can’t be certain, in the first few days of life, that you are not dealing with galactosemia.
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Direct hyperbilirubinemia: screening tests, liver enzymes, AST, ALT, TORCH or septic workup if the diagnosis is suggestive on history and physical exam. Then a first test, in terms of looking at the liver and biliary tree, is probably an ultrasound. It’s probably the way to go. Now why all this fuss about bilirubin? Why do we worry about it? Of course the main reason we are concerned about it is kernicterus, which is staining of the basal ganglia with bilirubin. Acute symptoms – I think people are fairly familiar with the late sequelae of mental retardation, deafness and choreoathetoid CP. Again, a very important link, if they tend to mention choreoathetoid CP on the Boards they are probably thinking of kernicterus. Acute symptoms are important to know as well, and I think are not always as well known by people and those are primarily neurologic symptoms. So you’ll see lethargy, oftentimes decreased tone, often can see a very high-pitched cry and irritability, poor feeding and vomiting, GI symptoms may be present and then eventually it will lead to increased tone. You may see seizures and also opisthotonic posturing as well. Another thing to mention I think is that there is some evidence, even if we don’t have kernicterus – and it’s very rare to see kernicterus these days – that if you get bilirubins to moderately high levels, probably 20 and above, you may knock a few I.Q. points off. So my sense is that even though we tend not to worry about kernicterus that much in breast milk jaundice or breast feeding jaundice, I think I’m not completely willing to blow it off and say, “Okay, we don’t have to follow a baby with a bilirubin of 20.” I do try to intervene and keep bilirubins relatively low.
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Late breast milk jaundice, you really… 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 you’ll see at least a 2-3 point drop in 24 hours – then you can just go ahead and restart breast feeding and it seems to be absolutely safe and the jaundice will disappear after a few weeks. Discount prozac news
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. Those two are the same thing. They shouldn’t be listed separately. Intrahepatic or arteriohepatic dysplasia, Alagille syndrome, is an interesting problem. Again, one of those things that might well show up on the Board. It has a combination of facial abnormalities, with deep-set eyes, broad forehead, and this prominent or triangular-shaped chin. Also has a paucity of intrahepatic bile ducts and then also peripheral pulmonic stenosis. So it’s one of those things that if you see a cholestatic baby they have a murmur, what’s the likely one if they have these facial abnormalities; peripheral pulmonic stenosis is the cardiac lesion that you will see.
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Extrahepatic biliary problems: biliary atresia doesn’t present in the first week of life. And you would think that biliary atresia should, if they don’t have a functioning bile duct it would produce jaundice. But generally what you see is these babies present more at 3-6 weeks of age and sometimes the diagnosis can be delayed after that. Other bile duct problems: you can see choledochal cysts, also extrinsic compression of the bile duct, perhaps pancreatic in origin, and then bile ducts can all produce hypobilirubinemia.
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A couple of inborn errors that you need to be aware of. These are ones that you just have to memorize. There is no easy way of remembering these. Dubin-Johnson and Rotor’s, and then again as we mentioned before, galactosemia, tyrosinemia and then endocrine problems, hypothyroidism and hypopituitarism can all produce a direct or conjugated hyperbilirubinemia.
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So on to the evaluation of the jaundiced newborn. History, as is usual, is really a crucial factor and things that you may want to look at in the maternal history; diabetes, you may see polycythemia in infants, infections -were there any signs of infection in the first or second trimester that make you think that this mother may have had a TORCH infection? Medications, drugs that may produce hemolysis in G6PD. There is obviously a very long list that you may want to look at before you take the Boards, but the most important ones are things like sulfas or nitrofurantoin and are drugs that are fairly commonly taken by mothers, even during pregnancy. Also if you see fava beans mentioned anywhere, that link is G6PD so I’m not sure a mother would eat fava beans before delivering, but if it happens to show up in the history that would be of concern. Birth trauma; if there is a reason this baby will have a cephalhematoma. Risk factors for sepsis though, again, septic babies, jaundice is not going to be a presenting sign of sepsis. Family history is very important in jaundice. Any of the inherited causes, so things like spherocytosis or elliptocytosis, some of the conjugating or enzyme deficiencies, Gilbert’s, Crigler-Najjar, family history may be important. History of anemias, some of the hemoglobinopathies, and again, structural problems such as elliptocytosis and spherocytosis may see a positive family history. Splenectomy can be suggestive of spherocytosis. Again, spherocytosis and elliptocytosis, structural problems, are autosomal dominant so you may have a very positive family history. If there are people who have had splenectomy, think about those structural problems as a possible cause of jaundice. Then siblings with jaundice, you need to think about some of the autosomal recessive disorders.
Then the enterohepatic circulation, which we talked about briefly before, the most common cause of problems with enterohepatic circulation and reabsorbing too much bilirubin is breast-feeding jaundice – some people call it “early breast milk jaundice” – where there just isn’t enough breast milk getting in. What happens is that anything that causes slowing in passage of stool through the gut will lead to hyperbilirubinemia. Some of those things could be poor feeding, perhaps from neurologic problems, or if the baby has cleft lip and palate and is having difficulty with feeding, that could contribute. Vomiting, things like a partial obstruction, achalasia, those kind of problems could produce hyperbilirubinemia, or anything that causes decreased stooling. Meconium plugging would be an example of the things that could cause decreased stooling.
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Then on to decreased clearance. Still we are on indirect hyperbilirubinemia. Premature infants will have decreased conjugation by liver enzymes. They just don’t have enough liver enzymes around to handle the bilirubin load. In full term babies you actually can see it. In premature babies glucuronyl transferase deficiency. This is one that there’s no easy way to remember it. You just need to memorize this one. Crigler-Najjar is type I and that is autosomal recessive and has a poor prognosis, largely because the enzyme is completely absent. Type II glucuronyl transferase deficiency is by contrast autosomal dominant, generally fairly benign and in that one there is not an absolute loss of enzyme. It’s more just a deficiency of glucuronyl transferase. One more glucuronyl transferase deficiency is Gilbert’s, autosomal dominant and also fairly benign. An interesting problem, one that I’ve never seen but is kind of one they may ask about on the Boards, is Lucey-Driscoll which is a maternal gestational hormone that interferes with conjugation. Because this maternal factor is transient, the problem is going to be transient but can produce fairly high levels of bilirubin.
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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 isn’t 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 won’t 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. You should see that peaking somewhere around 3-7 days. If you see a baby that is getting dramatically jaundiced in the first day or two of life, don’t call that early breast feeding jaundice. I don’t care how well the breast feeding is going in the first day or two of life, babies are not getting a lot of breast milk. So it doesn’t matter even if breast feeding is not going well, it shouldn’t contribute to markedly high bilirubin levels. I’ve seen that mistake made a number of times where people will call bilirubin that is in the mid-teens at 36 hours of life, say “Oh, that’s breast milk jaundice.” No, it’s not.
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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. All you really need to do is supplement with formula. So you can breast feed then give formula afterwards. Whether you want to give it in a bottle or syringe is up to you. But the important thing is there is no reason to stop breast feeding.
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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