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Metabolic acidosis is often a clue. Again, you’ve got a set of electrolytes already on the chart before you’ve been consulted. So you can calculate the anion gap and see if this child has metabolic acidosis. If they have acidosis with a normal anion gap then you can look at other causes; GI, renal losses of bicarb, congenital renal hyperplasia. If the anion gap is increased, look at something very simple like glucose, which we know is already on the chart. If the child is hyperglycemic and ketonuric then you’ve made a very simple diagnosis of a very common disease, diabetes. Can newborns have diabetes? Of course they can. If the glucose is normal then have a look at the ammonia, and if the ammonia is near normal then you may be dealing with a organic aciduria. But bear in mind that this term is spread throughout the entire algorithm here. But if the ammonia is high, then you may be dealing with a urea cycle disorder. If the anion gap is elevated and you have hypoglycemia and a normal ammonia then there are still many different categories you can deal with. Or if you have a slight hyperammonemia then have look at the urine and see if there are ketones present. If there are no ketones present then you may have a defect in fatty acid oxidation, such as MCAD, medium chain acyl-CoA dehydrogenase deficiency, which is not as uncommon as we used to think. So this is just a general algorithm that helps you categorize what might be going on, and it’s all done with very simple lab tests that come back within a matter or hours.
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Hyperammonemia. There are many causes of hyperammonemia. It may have to do with immaturity of the hepatic enzymes. But it goes away. It doesn’t mean that it might not need to be treated before it goes away. Urea cycle disorders certainly scare us all to death and have, on occasion, really ruined a weekend for me. Organic acidemias can lead to a slight increase in ammonia. There is this phenomenon called Reye’s syndrome, and it’s probably a significant proportion of kids with Reye’s syndrome who actually have undiagnosed metabolic disease. Urea cycle disorders usually present in the neonatal period, but they can present in infancy and occasionally there is juvenile onset in a mild form. So there’s that rare case report of the college student who binges at the pizza party and goes into hyperammonemic coma because there was too much pepperoni on the pizza. But those are reportable cases. Pheromone cologne for men to attract women. The symptoms are usually nonspecific, but can often lead to coma. In the newborn period, another one of the nonspecific symptoms, is hyperthermia.
Normally there is zero homocystine in the plasma. So this is easy to make the diagnosis, as long as the sample gets to the lab properly. It has to be placed on ice and has to be spun down within an hour or two. Because this is an unstable compound and if you let it sit out on the lab bench or you stick it in the mailbox you are not going to see this. This peak here is methionine. It’s normally high because of the metabolic block, and then when you treat with betaine it goes even higher.
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Metabolic diseases of the newborn. We are talking about 1:10,000, 1:100,000. So individually all these disorders are rare, but you put them all together and they are a formidable enemy and have to be dealt with, and suspected. The symptoms are non-specific because babies only do so many things. Bear in mind that if you delay the diagnosis in some of these disorders you may have allowed to occur irreversible damage. So it is paramount to diagnose these disorders as soon as possible because you may be able to do something about them. When do we suspect an acute metabolic disease in infancy? First of all, gather a little family history. You may possibly generate a family history where there have been some neonatal deaths. These kids usually appear healthy in the immediate newborn period but then may gradually develop symptoms over the first week or so of life. They may become anorectic, they may start vomiting, they may have lethargy. This can progress, in some conditions, all the way to coma in the matter of a few days. They may seizures, they may have funny odors, they may have ketones in their urine, they may have altered acid/base status, such as metabolic acidosis.
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So let’s look at the common tests because you may have some clues there as to what might be going on. For example, you can look at a CBC. If the child has neutropenia or thrombocytopenia this might be a clue that the child has methylmalonic aciduria, or propionic aciduria. If the child is spilling ketones, or not spilling ketones, that may lead you down a certain pathway, which I’ll show you in a minute. Look at their glucose. If they are hypoglycemic then they may have a defect in beta oxidation, or they may have a glycogen storage disease. So these are all very simple, very cheap, readily available tests and please don’t forget ammonia, because that is very useful and you would hate to miss an infant with hyperammonemia.
Phenylketonuria is the most common amino acid disorder. The screening test is very simply measuring phenylalanine from a blood spot on a newborn screening card from a heel stick. There’s a prerequisite. Children have to have taken in protein in the form of formula for at least 24 hours. If not, you’ll have a false negative. And in these days of early discharge from the hospital where kids barely get a little glucose to suck on, it’s very important to bring them back in the first few days of life to their primary care provider to get an adequate specimen, meeting the prerequisite. The diagnostic test is to do a quantitative plasma amino acid profile so that you can actually quantitate the amount of phenylalanine that’s there. You are all familiar with the clinical features; mental retardation, you can also see autism and seizures. The treatment is the lifetime, preferable, treatment of low phenylalanine in the diet. Just like the diabetics who count calories, these folks have to count grams of phenylalanine, grams of protein as well. The lifetime diet is optimal for yet another reason. High phenylalanine is teratogenic. Half of PKU patients are going to be female, and like most females, they like to grow up and have families and if they go off diet – although it may not harm them very much – this can lead to birth defects in the unborn child, even though the child does not have PKU. If the mother’s PKU, the phenylalanine, the phenylketones, the phenyl lactate across the placenta, are neurotoxic and can also cause some somatic disorders as well such as congenital heart disease. It’s very difficult to control pregnant mothers with PKU because the fetus is growing rapidly, you have to make sure you provide the fetus with enough protein, enough phenylalanine, but not too much. So we usually hospitalize these moms for a week or two to get them on diet. Hopefully they have been on diet before they got pregnant, because as you realize the first six weeks of gestation are the most critical in terms of neurologic development.
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Homocystinuria is very uncommon, compared to PKU, and the screening test in those states that do it is not to measure homocystine, because it’s a little difficult – because it’s an unstable compound – they actually measure methionine. The diagnostic test is to do a complete plasma amino acid profile. I’ll stress again, nobody gets urine amino acids anymore. The only thing you get from urine is organic acids. So don’t waste our time getting urine amino acids. In differential diagnosis of pediatric stroke, you have to make sure that homocystinuria is in your differential.
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How do we treat these kids? For the most part we don’t really treat them with dietary restriction of protein or methionine anymore. But rather we supplement them with either folate or pyridoxine or betaine. Betaine recycles homocystine and methylates it back to methionine, and methionine is non-toxic. And certainly low-dose aspirin for any coagulation.
Biochemical disorders are caused by genetically determined defects, usually in an enzyme, although sometimes they are in receptors or other parts of the pathway. Unfortunately sometimes the body makes toxic substances. In the case of PKU, the body makes phenylactate and phenylpyruvate, which are neurotoxins. So it has decreased phenylalanine a little bit but it has made some toxic substances in the meantime. This is not good. So these are alternative so-called salvage pathways which are often not such a good idea.
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How do inborn errors present? They present a number of different ways. They can present acutely as metabolic disease of the newborn. This is when you have a child that looks like he has sepsis. You give him antibiotics and he does not get better. They can be progressive disorders which present with gradual organomegaly, loss of milestones. They can present chronically with failure to thrive or mental retardation. They can even be late or benign, such as hypercholesterolemia which does not present in childhood or adolescence but usually in adulthood.
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There are so many metabolic diseases but in most states in the United States only three are screened for in the newborn period. These are PKU, galactosemia, and hypothyroidism. Why just those three? Why don’t we screen for pipecolic aciduria? Well, they are very rare. That’s one reason. Another reason is that there is not a darn thing you can do about it, and the third reason is there is no cheap screening test. So these are the principles that we have to deal with. First of all, it must be a serious disease. It has to be preventable or treatable. You have to do something about it. We could screen all newborns for Huntington’s disease but don’t because there is nothing we can do about it. Lastly, the methods for screening must be practical, cheap, available to the population. You have to be able to teach state employees how to run these things, who sometimes have trouble licking a stamp. And you must understand the inheritance and the pathogenesis so you can explain it to families when you do ascertain cases. There has to be a high benefit-to-cost ratio, so all these tests are relatively cheap. They cost pennies to do, and there must be a very high sensitivity and specificity. You don’t want to miss cases. You’d rather have false positives than false negatives. Screening for PKU, galactosemia and hypothyroidism meet all these criteria and there are very few others that do. There are some states that have PET screening programs for someone’s favorite disease. There is someone in that state has a grant to cover the cost of the screening. So the state of Virginia can screen for MCAD and a few other interesting metabolic diseases, but most states don’t have the funds to do so.
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The third one here is a high peak and this one can be due to a couple of different things. Again, you see this peak falls outside of the box. Moderate levels are generally due to things like thinning of the tympanic membrane. So a child who has had recurrent infections may have thinning of the tympanic membrane and you may see moderate levels. The other thing, though, that can cause a very high peak is ossicular disarticulation and there you may see curves that literally go off the map. I guess I forgot to put the slide in, but there should be one where there is a completely flat line for the audiogram and this is one which I bet you will come up upon on the Boards. And there are two possibilities for explanation of when you have a flat line in the tympanometry test. One is that – and most commonly – it is a middle ear effusion so you have that fluid there and basically it’s pushing against that tympanic membrane and it just won’t move. The other possibility though is that you can have a perforation. So if you have a perforation in that tympanic membrane, when the pressure is put in it’s going to go right through that tympanic membrane and isn’t going to move it at all. So all you are going to see in a tympanometry test with a perforations is a very flat line. The key to the differentiation of these two is looking at the ear canal volume. And what you are going to see is, if there is a middle ear effusion, you are going to have an normal ear canal volume, 1 cc or so. Whereas if you have a perforation ear canal volume is going to go up and it’s going to be abnormal. Because what it’s seeing is this huge ear canal because that perforation makes it seem like the ear canal volume is going to be quite high. So you may see ear canal volumes of 3 cc or something like that. So that’s where the ear canal volume comes in and is very very important when you are trying to differentiate a perforation from a simple middle ear effusion.
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Okay, on to audiologic evaluations. I think the trick here – I’m going to cheat, it’s really not cheating but – if you look at the tympanometry first I think it can suggest a little bit of where the pathology may lie. So here we have a curve that’s shifted to the left, which means negative pressure. Cialis professional online. The left ear is completely normal. And looking at the legend here, the air conduction on the right is circles, X is left ear and what you see here is essentially the air conduction is shifted down slightly. So this is just a right sided mild eustachian tube dysfunction with a retracted ear drum that’s just not going to function quite as well in terms of hearing. The second one, you see a flat line here. Most likely it’s going to be a middle ear effusion. I don’t think we have the ear canal volume. Let’s assume it’s normal. This time the X’s air conduction on the left side is shifted down slightly. So this is consistent with a middle ear effusion on the left side interfering with air conduction and on this one, and on the previous one, the brackets you’ll notice are for bone conduction. Those are completely normal. Remember that I said, with conductive hearing loss you are going to see abnormal air conduction, normal bone conduction. I hope this is getting through but you may have to review this afterwards later because it can be a little bit confusing.
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Finally, we have one where the tympanic membranes are completely normal on tympanometry. They move very nicely, the pressures are normal. But here you see profound hearing loss bilaterally on both sides and you see both air conduction loss and with the brackets you also see that bone conduction is abnormal and it is much worse at the higher threshold. So this is a fairly classic audiogram for sensorineural hearing loss.
A very brief word about speech audiometry. A couple of things that will be tested on, which is more advanced than the pure tone audiometry, one is something that is called the “Speech Reception Threshold” or SRT. That is defined as the lowest sound intensity in decibels at which a child can identify selected words in 50% of the trials. So give them a list of words and they can identify what those words are 50% of the time. In comparison you have the speech discrimination score where you have a percent of words on a standardized list that are correctly identified if presented at a sound level 25-40 decibels above the speech reception threshold. Kind of complicated, pretty unlikely to show up on the test but might be worth kind of noting. One fact worth remembering about these though, is that looking at speech discrimination scores, if you look at these in sensorineural hearing loss, they tend to be lower than conductive loss. So kids with hearing loss due to conductive problems actually probably can pick up speech better than if there is sensorineural hearing loss.
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On to tympanometry. In tympanometry what you are trying to assess is two things, essentially. One is mobility of the tympanic membrane and second is indirectly you are trying to measure the pressure, or estimate the pressure, in the middle ear. There are three key things that you want to look at when you are looking at audiometry. And that is, the peak of the curve. So the three things that you are looking at is the peak of the curve – so how high does this get? And the vertical axis here is compliant which is essentially looking at how much volume of air is displaced at different pressures. So a tympanometry machine is applying different pressures and measuring how much air is displaced and essentially gives you a sense of how well, indirectly, the tympanic membrane is moving. So the peak is the height in the compliance. Canadian viagra at discount pharmacy shop. The location along this pressure curve where the peak occurs – so here the peak is at zero – is completely normal. Also a key thing to look at is you may see this peak shifted to the left if there’s negative pressure in the eardrum or to the right if there’s positive pressure in the eardrum. And the third thing, which is a nice little trick as well, is to look at ear canal volume. Here it’s 1 cc which is normal. Kids can have ear canal volumes anywhere from 0.2 to 2.00 ml. So this is a normal curve. The peak falls within this box below this line, above this line so the mobility is normal. The pressure is normal, the peak falls at zero and the ear canal volume is normal at 1 cc.
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Next one, what you see here is the peak height or the height of the peak is normal so the eardrum can move normally but the problem is that the peak is coming out at the left of this box at negative 200. So what that means is that while there is normal mobility there is negative pressure behind that middle ear, or behind that tympanic membrane within the middle ear and that is consistent with eustachian tube dysfunction and a retracted eardrum.
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