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something else. Oh, no, Don't tell me that. Give me. Okay. Can you all hear me? Okay. Yes, we can hear you. Fine. Can you guys see my screen as well? Okay, so I'll have to tell you when to move slide, because obviously I'm working off a separate screen. So I'm Caroline Delahanty. I'm a consultant pediatrician, and I've worked very much as a neonatologist during my career. I want to talk to you today about neonatal jaundiced. So? So I'm moving on to the second slide. So if we look at outline, I want I'm going to highlight what is neonatal jaundice? The causes of neonatal jaundice? Why? It's important. And we will talk about treatment with time. I will go on to talk about some of the other causes, So I'm on slight three now. What is neonatal jaundice? I'm showing you a picture of a jaundiced infant. Um, where we see the yellow discoloration of the skin. Next slide. Oh, no. Sorry. Same side. We all know jaundice is caused by elevated bilirubin. It's usually not clinically visible until we get serum bilirubin of greater than 100 micromoles per liter. It's very common. 60% of babies because of the immaturity of their clearance system will become jaundiced. Not all require treatment, however, um, it typically peaks for treatment between days three and five and we're going to talk about the classification of jaundiced so into physiological and pathological or biochemical classification of uncontradicted versus conjugated next slide. This slide looks rather complex of the reticuloendothelial system. But I'm going to break it down and we're going to take it step by step. So 75% of jaundice comes from the breakdown of red blood cells. The Hamal Icis of erythrocyte sets with 25% from the recirculation of bilirubin. So if we start at the top and we look at the Erythrocin sites, they in a newborn baby, one of the reasons then so susceptible for jaundice is because they've got an elevated hemoglobin with, um, they don't make their own hemoglobin for the first three months of life, so they have stored it. But those red blood cells are the wrong shape. They're not Erythrocin stick, elliptical, elliptical in shape. They are more circular and less concave and therefore they are fragile and they break. So what happens is that the globe in chain is removed, with the Alpha bond being broken. Heme is then through heme. Oxygen is the iron is removed and it's reused. Actually, it's recirculated. We create Bill Verdin, which is then further reduced by the enzyme bill Verdin, reductive into bilirubin. This is excreted into the serum where it will bind with album in or it will may remain free and it's the free bilirubin. That's our problem that can cross the blood brain barrier and be toxic to the brain and cause our acute encephalopathy and our long term damage. The placenta provides the clearance role in utero, so an in utero foetus will not become n careful. Empathic bilirubin with album in is then taken up by the liver, um, by the Patek Sinus sides, and it's like gated. And then it will be conjugated with glue. Corona Gluca ronel transfer rays into conjugated bilirubin. This is then actively excreted. Energy dependent uses a T P into the extra pathic Billary tracked into the bowel in the small bowel ville I in the brush border of the small bowel. Some of this through beating Blue Corona days will actually be recirculated, and this is an immature system in the newborn. Or some will reach the bowel, where, through bacterial decomposition, it will form Stokoe Bellingen to be excreted in the feces and create pigment in the feces. So I'm just highlighting the various sections. Don't worry, we will be going back over this. Okay, if we go on to the next slide of what causes neonatal jaundice, please for the audience and the first factor is physiological jaundice. This includes breast milk jaundice. It's innocent, but does require treatment with phototherapy to prevent that free bilirubin transferring into the brain. It's as a result of the immaturity of all these liver enzyme and bowel enzymes, and it's because of increased red blood cell turnover. I'm clicking again onto pathological jaundice on the slide. This is caused by increased Hamal icis recess disease from hemolytic disease of the newborn ab Oh, incompatibility and other red blood cell enzyme defects that I've listed here with hereditary spherocytosis, ISS and some others. They are not so important to have a knowledge of they are rare. Next slide. Oh, sorry. Click again and I show other factors of pathological jaundice. So going down the green list coolest ASUs obstructive jaundice with biliary atresia, which I will talk about the rarer choledochal cyst obstructing the pathway. And then there's other rare genetic causes, like allergy L Syndrome and cystic fibrosis. We need to think about things that could have damaged the liver and the liver's ability to metabolize in utero, such as viral infections, C M v. Herpes, rubella. We need to think about infection causing jaundice and increased red blood cell turnover. We need to think about syphilis causing damage to the liver, a creating a hepatitis, which then affects the liver's ability to work with bilirubin. Then more rarely, we've got metabolic causes and toxic causes. We will leave those. So coming back onto another slide, we see that slide again of the reticuloendothelial system, and we see you need to think about it. Is joined this uncontradicted or conjugated? Is it pre liver or post liver? Think of it the same as adults before the liver or after the liver. Okay, so coming back next, slide bras skip it and we'll go onto the slide, which is highlighted. Physiological jaundice. So physiological. Jaundiced is an elevation of unconscious gated hyperbilirubinemia in the newborn. The problem we have is because of the maturity of the enzyme systems. We have low conjugation ability because the enzymes immature and I always tell parents it takes about two weeks for this liver to mature up. Um, so that leads to us. Having decreased uptake, decrease binding, decrease excretion. We also have an immature bowel that bowel is not colonized by flora. So therefore, it's not as good at producing Stokoe Bellingen, and we re drive our entra Patek circulation. If we have a baby that is driving this more than the normal baby, who already drives this very well by having a elevated hemoglobin and abnormally shaped red blood cells. Immature shape. But if we've got a baby that's polycythemic or that's bruised, or a baby that's premature and therefore has decreased colonization of its gut flora from delayed feeding and decrease enzyme systems, all these factors will make jaundice more common with them. Okay, but again, this is all unconscious. Gated. I'm going on to the next slide, which is labeled breast milk jaundice. We don't understand it. It's very common. But what I want to highlight is that bilirubin is not necessarily a bad thing. Is a free radical scavenger. So it is neuroprotective that baby has been born through labor, which is relatively hypoxic. Process. So having a free radical scavenger for your brain to mop up free radicals is good. The important message I want to bring across is that you should not stop. Um um, breastfeeding to prove it's breast milk jaundice. She should continue to breastfeed because the benefits outweigh the jaundiced problem going on to the next slide. So again, we've got the pathological. We're back on that pathological physiological going on to the next slide of recess disease. I want to talk about hemolytic disease of the newborn. We'll need to click again to show a, um um, or an abdomen. There's a picture of an abdomen. You have a recent negative blood cell, mother, and you have a recess positive fetus sitting in the utero uterus click again to bring up something else. And I'm demonstrating that if that baby bleeds and shares some blood into the maternal circulation, we will sensitize that mother to produce antibodies against the recess positive blood cell during pregnancy. We give our mother's anti D at age 28 weeks because we accept there will have been a degree of Feto maternal sensitization because there is always some feet, um, maternal blood transfusion taking place, then at delivery. There will be further feature maternal transfusion during the delivery process and there will be further sense sensitization. So they get a further dose of anti D as preventative. They will be sensitized we mop up the sensitization. But if you have not mocked up the sensitization or if there has been more sensitization than was predicted in subsequent pregnancies, you have a mom with the ability to produce anti, uh, anti resistor antibodies and cause hemolysis in her fetus fetus. Okay, next slide onto a B o incompatibility. I just want to highlight the different blood groups. I think the important blood group for the setting of a B. O compatibility in your history here is if you have a mother who is group Oh, and a baby who is is a B or AB, because any of these the mother has anti a an anti B antibodies create. And if she has been sensitized, it creates a set in for some hemolysis, which is milder. Okay, so clicking on this slide several times, we then demonstrate a mother with a fetus in the abdomen. The baby can be a or B. The mother is Oh, and she has the ability to send anti a an anti be in a global in over into her foetus and cause this baby to be at risk of developing a B O incompatibility and jaundice. Next slide, please. Which is recess disease, hemolytic disease and the newborn. I've got a red arrow going across my R E system, and I'll be demonstrating that it's the Erythrocin sites that are driving it, So it's an unconscious gated. Next slide, please. We'll skip this slide on to the next slide if we talk about why neonatal jaundice is important, is what slide is labeled. It's important because that bilirubin can cross unbound bilirubin, crosses the blood brain barrier and will bind to brain tissue. If we click on the slide. Um, next slide. If we remember and click on it, it put, Red Arrow is going to point to the brain, demonstrating that free bilirubin going across to the brain. Next slide, please. So the clinical features of a baby that is developing encephalopathy will be that you'll have poor feeding as the starter feature. Then you'll get lethargy. The baby is more sleeping. You more sleepy. You can't rows. It feeds. Then you get abnormal posture. You get irritability, opisthotonos and eventually seizures. These are the acute clinical end, careful opathy picture. What's different about bilirubin encephalopathy is unfortunately, the bilirubin binds to the basal ganglia and thalamus, which long term gives us a child who is likely to develop athetoid, cerebral palsy, deafness, seizures and cognitive impairment. So it's really important that we do treat it. So if I go on to clinical factors, when should we worry about jaundice? We need to think about, um um, having antibodies in utero. Being high risk, We need to think about joined us within the 1st 24 of our hours. It's always pathological. You think about early onset sepsis. If you have no setting for Hamal ESIs and you must treat the bilirubin, you have to look at the serum bilirubin. I'll come onto charts that we plot on which guide us if we should treat just were phototherapy or if we need to do what we call an exchange transfusion next slide. This shows a classic bilirubin chart. They do check. They do vary around the world, actually, but these are the ones that we use in the UK. If we click on this slide, we will show that slide is label first of all, with the red circle or gestation. So the charts are gestation dependent, and that is because of the blood brain barrier being better in a more mature baby than a preterm baby. And if we click again on the slide, we highlight the phototherapy line clicking again on the slide. I'm highlighting the Red line of exchange transfusion, so we plot. I think it's also important about worrying about joined us on the next slide. We worry if the level is rapidly rising and we worry if it is prolonged. If it's greater than 14 days in term infants and greater than 21 days, which I will explain later next slide presented with the jaundice baby, you should always I should have focused on the clinical. You examine them clinically. First of all, I've talked about the lethargy, the poor feeding. Do you think they're tones abnormal? But you're then going to go on to investigate. We need to do a bilirubin. We would request a split bilirubin where we will get a measure of the conjugated and the unconjugated. The conjugated should always be less than 20%. If it's greater than 20% it implies you've got more of a liver excretion problem and it takes you down looking for different causes. We plot our level on a chart to guide us on treatment pathways. We do an antibody test, a Coombs test to see if we think the baby, um has a setting for Hamal Icis. And we also look for anemia again, looking for a Hamal Icis. And we take note of Mom's blood group and her antibody level, which will have been measured. Aunt in Italy for us. Next slide, please onto a case study because of time. I'm not going to do this interactively. Please accept my apologies. So I'm going to talk about baby. Are who is a 37 weaker who's been noticed by mother to be sleepy and poor feeding on day three common signs of jaundice. Looking through the history, which is important, we have a mum who is a positive with no antibodies identified in utero. So these are the questions you're going to be asking the mother and asking yourself and asking the case notes. There's been no prolonged rupture of membranes to set in for sepsis, and it was a normal delivery. It was a spontaneous vaginal delivery. Although the baby is sleepy, I can arouse the baby and the baby has normal tone and suck. There is no anemia, no jaundice. There is clinical jaundice, but examining the abdomen, I cannot feel pattern megaly. If I could feel how to spend a megaly, it makes me think about in utero infection, actually, and there's no evidence of skin rashes again, skin rashes. I'm thinking about low platelets in a particular rash or evidence of congenital syphilis. So again, the clinical findings are all proving reassuring here. So this baby is very likely particularly presenting Day three, a common time for the physiological jaundice that this is likely to be physiological jaundice requiring simple phototherapy. I'm showing you a phototherapy charge where I would then plot this babies by clicking on the slide. I'm highlighting the first therapy chart, and I would plot this babies bilirubin. Next slide, please. On this slide, you should be seeing pictures of babies receiving phototherapy important factors in phototherapy administration. So the light treatment, which basically what it does, is it photo? I summarizes. That's a big word. So it changes bilirubin. It breaks the bonds in bilirubin is what phototherapy does to make it water soluble so the baby can pee it out. It makes it excreta, ble and excreta ble through the kidneys. You've got lots of pictures of babies receiving phototherapy here. The important thing is that we cover their eyes so that they don't find the light intensity too much. I think it also damages the retina so their eyes are covered and then we try. We expose them if they've got light shining above. If the light is shining underneath in the billy bed down the bottom, we then make sure they're exposed on the back. They have no clothes on, and we have to make sure that they have as much skin contact with the light as possible. Next slide, please. This slide is labeled treatment of neonatal jaundice. I think the most important thing. So I'm not sure if it's coming across that prevention is so here. I am talking about treatment of Reese's hemolytic disease, the most important thing is to prevent it by giving anti D in pregnancy. If we always treat the underlying cause, we always would start with photo therapy to try to see if we can avoid exchange transfusion. We then may need to go on to intravenous immunoglobulin, which is now an evidence based practice in the management of hemolytic disease of the newborn. We can inject the baby with him in a global in to bind to its recess receptors to prevent the antibodies binding to the receptors and breaking down the red blood cells. I hope that makes sense. If that doesn't work, we then may have to go on to exchange the baby's blood, which sounds extremely invasive. But it's a practice that's been there for years. We would catheterize the umbilical vein and in small Allah quartz, we take twice the volume of the baby's blood in its whole circulation away, and we give fresh blood. So we are diluting the antibodies that that baby has received across the placenta from Mom. It is a risky procedure. You can create cardiovascular instability, obviously, which is why we do it very gently. But there is a risk of infection because you've put in central lines, electrolyte disturbance, koala coagulopathy and transfusion reaction. So we try to avoid this at all costs. Next slide, so in summary, joined us is common. Most are physiologic they don't require. Most don't require treatment. It's only a small percentage that even come to light treatment. You have increased risk in certain babies. Preterm bruising set in for Hamal ESIs and photo therapy is effective. Next slide, please. As we've still got time, I'm going to talk about prolonged jaundice. So another really important message of this lecture Bayu is drawn. Attendees requires to be seen, you have to diagnosed by exclusion that that jaundice is prolonged physiological or breast milk. You have to exclude other conditions, which we'll talk about. So the first thing you're really aiming to do is you're trying to decide. Is this pre liver or post liver? You're trying to differentiate. If it's unconscious, gated, think back to the R that particular endothelial slide, or is it conjugated? You're excluding that This baby doesn't have Hamal icis and anemia, and you want to exclude that you don't have Hillary atresia, which I will come onto hypothyroidism and you want to make sure that you have not missed an in utero infection such as syphilis or viral torch. We then have all the rarer causes, which are much further down the line. So, having examined the baby, you will then go on to doing bilirubin with a conjugation fraction. You'll do a full blood count. You'll also do a film to look for Humalog Icis. You'll do liver function tests. You'll do a thyroid function test to make sure you've not got congenital hypothyroidism, and you will consider your viral infections and do a torch and a VDRL for syphilis. I want to talk about biliary atresia. It's in Europe. It's the most common cause of childhood. Liver transplants are. I'm on to the next slide. Sorry, so this slide is highlighted. Biliary atresia, the most common cause of liver transplant in Children in Europe. It's a congenital condition. We don't fully understand it where the bio, the biliary tract becomes inflamed and you get inflammatory. Obstructive extraprostatic billary dot fibrosis taking place they present with prolonged jaundice. Untreated, they'll obviously go on to present in the first year of life with liver failure and ascites. But if you pick them up at day 10, you improve their outcome in the history you're going to ask because you're really after. Is the any evidence of obstruction of bilirubin getting into the bowel? So you're asking about stool pigmentation? And although we say pale stools, unfortunately, some of them at this stage will still have some pigment getting through. And they may be korma colored so they can be light yellow cover colors. But they shouldn't be dark. That dark green meconium should be gone, and you should be now getting what we would describe as a normal stool. You'll also get dark urine on the slide. I've highlighted a British website, the Children's Liver Foundation, Doctor or Walk. But the European Children's Liver Foundation is also a very good website, and certainly in Europe and Britain. To my knowledge, there's something called certainly in Britain. There's a yellow alert campaign highlighting to our primary care colleagues on our health visitors that a baby should not. If a baby is yellow at 10 to 14 days, they require referral to be checked. Don't assume it's the breast milk next side. Here I have a slide labeled Billary, a treasure and we have a picture of a normal gallbladder with normal docks and then on the right hand side with red arrows, I'm showing you those ducks becoming fibro those obstructed to knows where the bile cannot be excreted. Okay, next slide. I've come to questions. I'm sorry. That was a very rapid run through. Can I take any questions, please? Can you still hear me? Yes, doctor. Thank you. That was very informative and clear despite you were seeing or rushing, Um, doesn't have any questions. Anything they didn't understand, I would like to ask. Well, I guess you were clear, Doctor. You feel there was anything that you need to highlight that was important for us. I think I want to highlight the importance about breast milk jaundice. We don't understand. But the message is not to stop breastfeeding, to continue to breastfeed, um, and to be encouraging about breastfeeding because the mom will worry that she is causing the jaundice and the, you know, people keep saying, Oh, your baby's still joined us, provided the baby is thriving. I would keep going. The other thing I think it's really important to highlight is that prolonged jaundice is pathological. until proven that you have excluded things and you need to see the baby. And you need to carry out a split bilirubin to prove that this is not conjugated. This is continues to be unconscious. Gated. You need to check the baby. Thank you. We still have no questions in the chat. Um, know if anyone wants to run mute and ask you feel free since we have time. Gosh, I should have slowed down. Shouldn't. Okay, you're clear. You were clear. Formative. We have no other questions. We have a feedback form in the chat which will be beneficial for the doctor and for the CRF to continue giving lectures. So if you can please go out that feedback form. And someone has just posted a question saying Can you explain the physiology? Physiology behind breast feeding jaundice? We do. Okay, we don't understand it. I'm going to go back into some slides. I'm going to go back onto this, re highlight the slide of labeled particular endothelial system. The answer is we don't understand it. We think there is likely there's two theories. One is that there is an unidentified inhibitor in breast milk. Uh, which is unidentified that is inhibiting some of the metabolism. Two of the excretion of bilirubin. The other factor is that breast milk is when you breastfeed. You have different gut flora in your gut, so you are very predominantly lactobacillus, so you won't have some of the flora that will be driving stir kobilinsky gene production. So the fecal excretion. So we think it is therefore driving, putting an onus on driving that enterohepatic circulation and causing the breast. Uh, the joint is to keep recirculating and going through the liver and not being clearing, so it keeps the bilirubin level high, but it's not understood, understood. But we do think it's beneficial because, uh, I briefly mentioned the fact that it's a free radical scavenger. So a newborn baby has a high free radical load because it's come through a delivery, which a vaginal delivery is generating a potentially sort of hypoxic environment which that baby is able to cope with. But there will be a lot of free radical generation, and that bilirubin maybe mopping up that and therefore protecting the brain. And we we do know that breast fed babies have a higher I Q. But what we don't know is why do they have a higher i Q. And is some of that part of the free radical generation that took place that is, take free, radical mop up that is taking place. That's neuroprotective to the brain. So I I get quite crossed as a clinician. Actually, when people say, Oh, when people treat babies who have not crossed the phototherapy line Because jaundice is good for you as well as being bad for you and only treat when you cross the phototherapy line. So I appreciate that's not answered the question, but it's because we don't know the answer. Thank you. That was clear enough. Um, anybody else have any other questions? No. So thank you, Doctor, is what I can say for now. And thanks everyone for your patience. Please do fill in the form and the certificate will be posted shortly. Um, music. Grab my apologies. I honestly thought I had this all organized. I'm teaching again on Thursday. I promise I will be sorted. I am sorting it now. No problems. We understand. Thank you. We've got loads of Thank you's in the chat. Um, I'll keep the chat open for a bit longer if anyone needs to do the form and for the certificate to be posted. We also have a lecture next as well on sexual health. So please join again shortly. And Doctor, I think your work is done.