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Uh, hello. We'll just give everyone a few minutes to, to join. If someone can let me know if they can hear me in the chat. That would be great. Mhm. Oh, the truck? Can you hear me? Oh, I still meet it somehow. Ok. Well, I think I'm un metered so we'll, we'll kick off. Um, this is just past six o'clock now. Anyway. So my name is doctor, um, a bit of background about myself is that, um, I'm a UK graduate. I've been working in pediatrics and neonatal medicine for about a year and a half now. Um, and so, um, it'd be great if you guys could put in the chat if what grade you are at the moment and kind of, um, what your experience is in terms of it and to give me an idea of kind of where to pitch this. Um, but if not, we'll just kick off and like I said, I'll try like this, um, as possible and check the chat, but if you have any questions at all, just, um, put them in the chat and I'll do my best to answer them as we go along. Um, so jaundice um is a yellowing discoloration of the skin due to an elevated plasma bilirubin. Um It's particularly prevalent topic in neonatal medicine as it's quite common. Um And then another period, around 60% of 10 babies and 80% of pre term babies have been jaundice in the first week of life. This isn't to say that kind of 60% of babies need treatment and 803 time babies need treatment, but it will become visible in around over half of babies that are born um at term. So it's an important topic. Most neonatal jaundice is mild and transient. So, like I said, most jaundice does not require any treatment. Um however, untreated, high levels of bilirubin can lead to encephalopathy, seizures and sometimes death. Those surviving have advanced features can develop features connect to us and we'll jump into this a bit later in the presentation. So we're gonna go back all the way to very beginning. So um the radio physiology of jaundice and understand this to really submit our knowledge moving forward. So, over 80% of a bilirubin comes from the breakdown of hemoglobin. 20% coming down from myoglobin and kind of cytos which we weren't really looking into too much for the purpose of our presentation. So 80% of it is coming from hemoglobin, which is broken down into heme and globin molecules, globins and further broken down into amino acids and then recycled. So they were left to kind of he molecules which are then catalyzed by he oxygenase to biliverdin and iron, the iron is then recycled within the body. So our father bin, which is then reduced to create unconjugated bilirubin. So we've gone from hemoglobin to he molecules, he molecules to Billy Verdon, Verdon to unconjugated Bill Rubin. Fabulous. So uh un contrary to bilirubin then binds to albumin and this is transported to the liver where it's conjugated by Yeah. And we call it UDP. I'll let you guys try and pronounce it yourselves. I think it's urine diphosphate, glucotransferase. Essentially, this is the only enzyme I actually want you to remember and part of this process because it's the only one that's really clinically relevant for this presentation. Um So unconjugated bit by the admin and is conjugated in the liver by UDP. Pus. Bilirubin is then excreted in the Judean into bile and converted into il and sterilon. Sorry, excreted in the feces, approximately 20% of the Ubelin is then reabsorbed into the hepatic circulation and further oxidized into was excreted in the urine. So to go back for that, once more, very quickly, we've got a hemoglobin breakdown to heme, he gone to and, and it reduced by to create unconjugated and that binds to albumin which got into the liver that's conjugated by our important enzyme UDP. Um Billy Rubin is then excreted into duodenum into bile converts into lin and stable and excreted in the feces and around 20% of that is reabsorbed into the intrahepatic circulation of fox dies into lin, which is created in urine. So why the nes get jaundiced more than the rest of the population? So this comes from a number of kind of physiological reasons. But neonates have a relatively high amount of hemoglobin due to their relatively hypoxic environment in the uterus. So if you consider it like this, when its are in the uterus, um all the blood supply comes from the placenta and the umbilical vein and umbilical arteries. Um So they move from this environment which is relatively oxygen depleted inside the uterus to a relatively um oxygen surplus environments when they're born. Um And this stimulates the breakdown of um some of the hemoglobin. This coupled along with the fact that hemoglobin, um fetal hemoglobin has a shorter half life than the other hemoglobin. And so remember, fetal hemoglobin is produced in order to move the oxygen association curve so that you can take oxygen molecules from maternal blood supplies. So the fetal hemoglobin have a shorter halflife anyway. And so you have an increase of hemolysis at first. Um This associated along with kind of delayed cord clamping. So when babies are born, what we try and do is to give them at least two minutes of delayed cord clamping. Um So leaving them attached to the placental cord um in order to make sure they have as much um red cell mass um causing that in order to um increase the iron stores, which really beneficial for, for newborn babies and for neonates in general and be preventing um anemia. Ongoing. As we know that breast milk doesn't have a very good iron content in it. And it's a common problem. We see and, and kind of later um in infants life. So we see quite a lot of anemia um related to this. So best practice is for today, Ging. However, that can increase of red cell mass, increasing hemoglobin increase in bilirubin. We also see GT, which is our all important enzyme we mentioned earlier. So it's the enzyme that conjugates uh unconjugated bilirubin, bilirubin. Um and this activity is reduced in the unit. So it's approximately only 1% of the output capacity. So as this is responsible for conjugation, we have a reduced amount of conjugation and reduced excretion of jaundice and bin. So this is kind of involved in conditions like Gilberts and C AJ and which we'll come on to a little bit later. So all of this leads to um an increased amount of hemoglobin that I've mentioned so far. So increased amounts of hemoglobin and increased amounts of red cell mass, which is breaking down faster, due to shorter half lives and then being conjugated, slower due to decreased UGT activity and excreted slower due to uh intrahepatic circulation. So we have an increased intrahepatic circulation in neonates. So as we mentioned before, around 20% um was reabsorbed back into the system to be reconverted and excreted in the urine. Um So we have that, that's increased in it. And therefore we have more, we have been in the system for a longer period of time. So that Euro, Euro. Oh sorry, that Euro um when it's reabsorbed is gonna be more present in the circulation. So it take longer for to excrete at all. Um So we're having increased production, reduced clearance and an increased intrahepatic circulation. So that's all kind of physiological things that happen and an explanation of why we see jaundice so much more in units. So first, we'll, we'll talk about is physiological jaundice and then we'll move on to kind of pathological jaundice uh um cause of jaundice afterwards. So, physiological jaundice presents after the first day of life. So it's never been the 1st 24 hours of life. That's a really important point to make whenever we're thinking about jaundice, thinking about it in terms of kind of hours since birth. And so, if it's within the 1st 24 hours, we know that's absolutely pathological and we need to be considering different causes of jaundice. Um So, like I mentioned, physiological jaundice is present after the first day of life. Um and generally peaks around day four to day five, we got a slightly delayed peak. Um And in preterm around day 78 and there is generally no underlying cause. Um it can persist up to 10 weeks in some breastfed babies, but generally resolves up to around two weeks of life. Um Breastfed babies are most common. Um it but more common in breastfed babies and this is kind of uh the to be due to increased glucose in breast milk. So, therefore, increasing that intrahepatic circulation again. Um and as we said, increase in the intrahepatic circulation needs to increase jaundice levels and increase bilirubin in the system due to raised amounts of Elgin. So another point to make is that sometimes we can also see physiological or pathological jaundice exacerbated by reduced intake, which has the effect of reducing action and therefore increasing enterohepatic circulation of bilirubin. So if your gut is not moving through nicely, then we're gonna get more increased absorption of that bilirubin that's already there. And so we can see that happen sometimes in pathological jaundice, we're kind of considering the same free faction factors that I've mentioned there. So we're still considering causes that led to increased production, reduced clearance and increase in intrahepatic circulation. And it's a really good way to think about our pathological cause of jaundice. I kind of separate this out so that when we're in a clinical scenario, we can kind of piece together what's going on and what our course courses of jaundice are. So for increased production, um most commonly, we'll find that we have uh he disease of the newborn. So our A bo and rhesus incompatibilities um we have disorders such as G six PD and hers, we can see it more of infections. Um So thinking about um D IC and torch infections in particular, um and we can see in polycythemia vera. So um increased HB in the first place, reduced clearance, like I mentioned, um Reja and Gilbert syndrome. So that's to do with our UDP, which we'll again, we'll go into shortly. Um We can see it in some inborn errors of metabolism. We can see ANB atresia bile duct stenosis and called Donal cysts. So these are all kind of causes of obstructive causes of jaundice. You can see in Roar syndrome and J Johnson syndrome, um which is a disorder of kind of um the movement or jaundice around the body. Again, I'll go into this a little bit more and we can see in hypothyroidism. So we can see that um he fights in to reduce gut movement, which also can cross our final point, which is increased intrahepatic circulation. So we can see that in Pinal stenosis and we can see it in large or small bowel obstructions as well. So before we go for it in a bit more detail, uh some people like to think about it in terms of um correlating it to how old the baby is. And as I mentioned, kind of, we've got our early pathological causes. So early causes, you're often thinking about hemolytic causes um such as Pes and I cap and infections. Again, often more likely linked to congenital infections. At that point in time, you've got your intermediate courses kind of day two to day 14, for which most of them are often are physiological. But we always keep in mind again, things like sepsis, hemolysis, jaw polyphem, excessive bruising around birth is not one that often overlooked. Um, drugs needing conjugation for excretion, um and kind of TPN which can also cause uh cholestasis as well. Um Again, more specific scenarios there. Um But if we're thinking about um kind of go back to bruising, we can see things like cephalohematomas um which can cause raised amounts of hemolysis. Um And then some drugs can also cause um increased amounts of um in the system due to competition for conjugation and excretion as well. And then finally, we kind of prolonged jaundice or day 14 onwards jaundiced um typically kind of associated with biliary tree abnormalities, infections in inborn errors of metabolism as well. Um So we'll first talk about kind of hemolytic causes. Um so any condition which causes hemolysis, the breakdown of hemoglobin, um which spoke about it produces hemoglobin molecules which is then converted into B burden and then he oxidase converts this into bilirubin um which is conjugated by our lovely enzyme GT again, so we have um lots of different causes of this. So, a in capacity which I should mention first here. So maternal blood group is different than neonatal blood group causing an alloimmune hemolytic anemia. So that's an alloimmune hemolytic anemia. So, for example, if a maternal blood group is O and the fetal blood group is either A B OA B, this can lead to maternal I GG cells, IgG cells causing the placenta. So, immunoglobulins, IgG can cross the placenta. Um not to be confused of IGA, which is given in breast milk because IgG cells can cross the placenta hemolysis um of the fet cell, red blood cells in an A bo incompatibility. We see um ao incompatibilities percent often less severe than et incompatibility. And this is because rhesus antigens are often expressed a lot more than A bo antigens are. So similarly, here, rhesus incompatibility occurs when a rhesus negative mother has a rhesus positive fetus. And again, we have IgG antibodies which are developed which can cross the placenta bar causing red cell hemolysis. Again, this requires a sensi sensitizing event. So that's usually a previous pregnancy. Oh and a fetal meatal hemorrhage. So, in our histories, we often need to concern ourselves with things like trauma, traumatic events and bleeding events, which may have caused, I think sensitization reactions where um NTD isn't given. Um but fortunately, most um mothers that are at risk. So most obesus negative mothers will have anti D um during the pregnancy as well. So we see this a lot less now than it previously. It has been seen. Um Well, just move on to kind of some of the enzyme defects and um some of the some membrane defects here but essentially um red cell membrane defects, cytosis and elliptocytosis. So, what we have here is we have misshapen blood cells um in terms of spherocytes which um then conjugate together as they go through the circulation and increased risk of hemolysis. So, this increased risk of hemolysis obviously causes a further breakdown of hemoglobin and increased levels of jaundice. Um We don't always see this presenting at birth and it can present later and can have just a physiological jaundice at Beth which isn't picked up. Um but it can contribute to this um particularly in kind of of red cell membrane defects. Um such as um sickle cell anemia, we can see a similar presentation as well um of enzyme defects um such as G six PD. Um So G six PD is an excellent recessive condition and it's kind of often in exam questions will be associated with your Mediterranean origin patients. And it's often what we see in terms of kind of epidemiology of the patients as well. Um So it's the most common cause of severe neonatal jaundice in the entire world, which is why I've kind of included it in this presentation. Obviously, it's less common in the UK due to a reduction, reduced Mediterranean um population here, but it's the most common cause in the world of severe neonatal jaundice. So, hemolysis is seen with situations of oxidative stress or classically again in your exam questions, ingestion of things like fava beans. Um So that's why we kind of get this presentation of birth. Um after a period of stress often um which can cause jaundice pyruvate kinase deficiency sometimes leads to a uh insufficient ATP production in red blood cells and can cause kind of rigid red blood cells which subsequently hemolyze. Um this is a lot less common than G six PD. So when I'm thinking about enzyme defects, we usually test for G six PD defect first and then takes for a pyruvate kinase um course after this. Um So we'll move on from here, we take out, we'll move on to um Cr and Gilbert's. So as I mentioned before, we really drilling home the point, but um UDP is that enzyme we talked about earlier, which helps conjugate unconjugated in the lever to conjugate bilirubin. So Gilbert's, we see a reduced um activity of UDP, it usually presents in adolescents. So we don't usually see it related to neonatal jaundice. Um but it's important to kind of consider this because it helps us understand click and J as well. So we usually see it in recurrent jaundice in in the context of kind of intercurrent illnesses um due to a reduction in UDP. Uh charity R as we said, is responsible for conjugating bilirubin and and kind of re jar is a, you can think of it as an extension of this almost. So instead of having reduced activity of UDP, we have an inactive or profound reduction in UDP. Um So this will often present with an unconjugated hyperbilirubinemia in the neonatal period. So unconjugated because we're not having that UDP activity to conjugate our bilirubin. So the mainstay of treatment in creatin jaw is kind of phototherapy um and liver transplantation, which would be the only kind of curative treatment available. Um So, usually required by kind of quaternary services or at least tertiary services from liver transplant centers to kind of treat these patients. And then we can speak about kind of obstructive jaundice. So causes of of of jaundice, again, we can break down further. So, um bilary atresia is the most common cause of neonatal liver disease. Um and it results from an inability to pass bile from the liver to the extrahepatic bilary system and thus excrete by the kind of small bowel onwards from there. So this sense as a mixed jaundice, typically in the first couple of weeks of life and commonly, you'll find that in kind of SBA questions and in clinical scenarios, you'll have a baby with white stools and dark urine due to the lack of excretes, dec VG and urobilin. So a baby with kind of white stools and dark urine, we're considering bilary atresia until proven otherwise. So again, we have a delayed clearance of bilirubin leading to our increased levels of jaundice in the in, in kind of obstructive jaundice in this picture treatment um is initially with a port oh Pours toy um which kind of touches the porta hepatis, which is the transverse fissure to a loop of the small intestine. Um but patients can sometimes require a transplantation if there's kind of persistent failure to thrive or ongoing cirrhosis of the liver. Um bile duct stenosis is a rarely congenital and more often kind of related to um surgical or post surgical changes. So we don't usually see it in the in it, but it's something that might come up. Um And again, similar to kind of ocal cysts, choc cysts are kind of rare causes of obstructive jaundice. Um But again, it needs to be kind of considered in different groups. So um these present more in kind of Chinese and Japanese origins and ethnicities. Um studies assist the common bile duct and lead to obstruction of the bile ducts and retention of bile which leads to scarring and cirrhosis. Um and raise my remaining system. Um Again, the mainstay of treatment is, is for surgery. Um It's just important to kind of understand um whether you'll be treating these patients as neonates or later on what what's kind of happened and what her initial problems were. So next, we can kind of move on to the sorts of transport and storage which I slightly alluded to earlier. Um So we have Roar Syndrome and Jin Johnson syndrome. So, um Rotor syndrome is an autosomal recessive condition, which causes defects in two genes resulting in the um resulting in um proteins for transport and storage of bilirubin being ineffective. So, we have um reduction in activity of transport capacity of bile and decreased storage capacity of hepatocytes. Um as a result of the two genes that are abnormal in this case. So this causes a mixed hyperbilirubinemia usually present in the neonatal period. Dubin Johnson syndrome again, is a very similar condition. So, um difficult to kind of differentiate um on, on simple tests alone. Uh Again, it's caused by a defect in a um multidrug resistant protein. I don't think particularly you need to remember the name of that unless you're thinking about sitting your um college of pediatric exams. Um but in case you are, it's multidrug resistant protein two um which leads to the effect of transport of bilirubin. Um So in uh ba questions, again, we'll commonly find that J and Johnson syndrome has a black pigmentation of the liver. Um And um a little tip that I was told to kind of help. Remember, remember this is that um between the drop between the rock Johnson and DJ um has black tattoos and that's how I've kind of remembered that and I pass on the little tip for you guys. Um So these are disorders of transport and storage. So Roar syndrome and J Johnson syndrome. So they're both mixed hyperbilirubinemias. So, um in all babies, we should approach um jaundice with a clinical assessment in a global manner, with consideration every aspect of your examination, but in particular, um what we want to know about is kind of previous pregnancies. And again, that's alluding to um previous sensitization events. So whether given an d previously um maternal blood groups, again, hemolytic events that age in kind of days and hours, because obviously, again, this depends on kind of where we're thinking about it. Is this pathological, is this physiological jaundice, any family history in terms of um any hemolytic problems I've had in the past other babies that they've had that required to go on to um phototherapy or um have further treatments. Um They're weight changes. So this kind of really feeds into, um is this baby putting on weight, have they lost over kind of 12% of their birth weight? Um because we kind of expect up to around 12% by on day five or we accept that. Um But around that point in time, they should be starting to put their weight back on. Um So if they're not doing that and we're kind of persisting, is this baby feeding? Well, that moves on to that as well. And what are their bowel habits like? And again, we're looking for kind of signs of, of white stools and, and darkened urine and stuff like that as well. Um Obviously a clinical assessment, we're looking at jaundice. So jaundice is first visible in the sclera. Um followed by kind of a caudal approach. So face downwards and then the feet finally, um initial kind of symptoms of hyperbilirubinemia can be lethargy. Um We can see hypertonia and a decreased suck. It's really important. We do require a thorough and neuro exam on, on babies that are planing with jaundice and later presentations. We can kind of see hypotonia and irritability. Um And obviously, we can see kind of seizures and further neurological changes. But hopefully, we won't be seeing babies at this point in time. Um, in terms of investigations, we've got a number of investigations, we can do, not, all of them are relevant at all points in time. So it's important to understand the justification for selecting each investigation. So, um we have our serum bilirubin. So this is um really important for kind of um understanding how high the bilirubin level is. So once we've seen jaundice in a neonate, it's kind of near enough impossible to look at the baby and think they look like jaundice and give an accurate number to that. Um So we need to plot uh serum bilirubin, which I'll move on to in a little bit. Um, in order to determine the significance of their values, um for blood count, it's important for looking at the, the HB and seeing if it's rapidly dropping, we might be thinking about a, a hemolysis. Um and the kind of reticular site count to see, are you producing um, a lot of red blood cells at the same time as well. Um split bilirubin. So looking at the conjugated um value and comparing it to unconjugated amounts of bilirubin. And as we've mentioned, some presentations can have a raised amount of conjugated or unconjugated hyperemia. So that really kind of helps narrow down um what we're looking at, we're looking at blood groups. So we're looking at maternal and baby blood groups um to see if we, we'd be likely to have a AB or Rs in compatibility and we can kind of support this by looking at a that testing or Cums testing, um which can give us a positive or negative results. Um but we can still have um autoimmune um hemolysis. Despite this as well, we can look at blood films um for evidence of any hemoglobin or kind of protein electrophoresis and stuff like that as well. Um And then if we're thinking about things like infection, we can look at CRP S blood cultures and CSF S. Um And obviously, we can look at different um causes of, of different signs of infection in specific infections as well. So we can think about cranial ultrasounds for some of our torch infections as well. And then uh finally, um looking more towards kind of prolonged cause of jaundice um with kind of urine cultures and T FT S for um hypothyroidism and urine infections um for um prolonged jaundice. So, move on to treatment. Now, um So, phototherapy is the mainstay of treatment. Um So this works by the geometric photo is summarizing of the unconjugated bilirubinemia from AZ to an E isomer. So I don't know if I remember it's from chemistry, but we have kind of two forms of isomers of molecules and it essentially flips the image from AZ to an E um which makes the bilirubin water soluble in this case, um making it excretable about having to undergo conjugation basically. Um So, ideally for this to be effective, we need to have a large surface area exposed to lights for as long as possible. Um So, whilst working on the wards, you might be asked kind of a number of questions regarding um phototherapy from parents and stuff and it'll often be your responsibility to kind of speak to parents about what the light therapy does and and what the important parts of it are. Um So my usual um kind of speak is around the longer kind of you leave on the day, the more chance the baby has for um what time the light has to um make it so that the jaundice levels can go down. So baby can wean it out and pull it out? Um Common questions again would be kind of regarding is it gonna affect my baby's eyes? Because we put little eye masks on all the babies. And the answer is, although we're kind of cautious around um putting eye masks on babies and protecting baby's eyes. Um There's actually no evidence to suggest that um, phototherapy causes any damage to baby's eyes. Um We're just very cautious, that's all pharmacological treatments. Um can include kind of um intravenous immunoglobulins, pates, um or phenobarb which we rarely, rarely see. Um more commonly we kind of see exchange transfusion. So exchange transfusion is performed in severe hyperb hyperbilirubinemia um to prevent connect. Uh and it kind of involves replacing the a of blood with donor blood. Um But obviously, there's a lot of risks with this and we have a raised level of morbidity and mortality. Um And so it is done in an ICU setting in specialist centers only. Um So, tertiary neonatal units often will have um spots for exchange transfusion um and then treating the underlying cause um in instances of kind of inborn errors of metabolism and hyperthyroidism or gonorrhea, atresia will result in um improvement and resolution of your jaundice. So I mentioned kind of here um our phototherapy and our graphs. So and stability in terms of um using those values to kind of determine treatment. So I've just put on evidence of um the graph, the graph that you'll see across the country using the UK here. So um if you search on Google nice um jaundice treatment chart, it'll come up as the first link that comes up. Um And on the website, we'll link you to a Excel document which will come up with the best treatment chart essentially. Um It's really important that we, when we're plotting this, we're considering um the time of birth. So, um we need to be quite specific about the time of birth and putting that as point day 0.0 and moving counting forwards from then. Um because obviously within our first kind of four days, um we have a an increase slant here for our therapy treatment line. Um So we don't want to unnecessarily treat any baby that can kind of take away from their moms. And we'd like to form a good, good uh attachment during that period of time. It's really important. Um But equally, we wanna make sure that we're not close to like change infusion line at any point in time. So any value that's above the photo line, we obviously start phototherapy on. Um And we usually continue this from anywhere between 6 to 12 hours before doing another repeat level like this kind of depends on where you are in relation to the exchange transfusion line. Um So if you were quite close to the exchange transfusion line, you'd be thinking about repeating this after kind of six hours of photo therapy to make sure you're not sneaking above that range. Um But if you're kind of quite low and you're quite close to photo therapy line, you might be thinking about doing this kind of 8 to 10 hours or so after your after your starting off therapy um just to, to see, give him a bit longer to that um Bilirubin to come down. Bye once we've um started photo therapy. Um and we've got a, a second value so you can repeat sample at kind of your 8 to 10 hours for normal case. Um What we need to see happen is for the repeat values to be 50 below the phototherapy line. So making sure that when you're doing your repeat value with at least 50 below the FF line before we're stopping treatment. Um And at that point, we kind of do a, a rebound bilirubin, which is what you'll hear it referred to. And that's a period of after we've stopped the lights. So after that second test has shown that we're at least 50 below, we'll wait a further 8 to 12 hours before doing another sample to ensure that that's not kind of rapidly rising again. And so the baby's able to clear that jaundice on their own afterwards. Um And it's not just the phototherapy, but I'm solely responsible for clearing that that um bilirubin. Um So again, just to quickly go over that again. So any value that's about therapy line, we treat, treat it for usually between eight and 12 hours um before repeating it, if that repeat is 50 below the line, then we can stop phototherapy. Um And if we're stopping photo therapy, we do another value 8 to 12 hours after that to make sure the baby is kind of clearing that on their own. Fabulous. Um, some helpful tips and tips. Um, if you search Bili, so bi li A PP, um, in, um, certainly in the, er, Apple Store. I'm not sure about the Android store. Um, but that's a really helpful app. It's really simple to use and it kind of plots the jaundice level for you using the charts that we've just seen, um, and tells you exactly when to repeat the level as well. Um So really useful to do, but obviously you shouldn't replace you being able to use the charts as well. Um And again, to go through, just going through again what I said there regarding kind of rebound for therapy and when to take levels. So we've got a couple of short cases here. Um just to kind of solidify a few things there that we've spoken about. Um So a 39 week old female baby is born via normal vaginal delivery and it is noted to be drawn this uh eight hours of life. There's no prolonged work for membranes, no maternal GPS and no maternal sepsis. She is otherwise feeding well, passing wet and dirty nappies, a parial with normal ce operations and no signs of distress. Her mother is G two P two and has a big group of O positive which of the following set of investigations is most appropriate. And I've got a little pole I can put in for this as well. So that should have popped up. Now, I'll give everyone a minute or so to, to think of your answers in the poll and try and put an answer in. OK. OK. Um So in this case, um where we have kind of no features of sepsis. So we're looking for kind of two risk factors for the sepsis or any clinical signs um of sepsis. Um Our most likely cause of jaundice is most likely to be hemolysis than infection. Um So option number two, looking at bilirubin FBC that and a blood group is most important here. Um And kind of following this. Um You might depend uh on doing a full film on family history and further investigations if the first therapy were, wasn't quite proving the jaundice at that point in time. Um So that's great. Well, the one um case number two, we have a 35 week old baby's born normal vaginal delivery on the labor ward. At 845 the midwives informed me that the baby is born in good condition and required nervous gestation at birth. There's no GBS in pregnancy and no maternal sepsis, membranes ruptured at half one in the morning. Um So that's just over 18 hours beforehand. There is no family history of notes and at 36 out of life, the baby now appears to be jaundiced. What is the most likely cause? So, again, we've got a little hole for us to do. Ok. And I'll give everyone kind of a minute to read that through again and to give out on the poll. Ok. Um So in the second case, what we actually have here is two risk factors for um sepsis. So we have prolonged membranes of a premature baby as you have um membranes ruptured for over 18 hours um in a baby less than 37 weeks. And we have a spontaneous, premature um premature birth. Um So, spontaneous rupture membranes um in a premature baby. Um So there's two risk factors for sepsis. So our most likely cause is kind of infection at this point and you would hope that this baby had been screened for sepsis um at birth or shortly afterwards. Um Case three is a um a bit of a longer case. So we have a patient, Billy Andrews um who is four weeks old um was born at 39 weeks. So gestational age is now 43 weeks um with a birth weight of 3.2 kg on the 20 percentile. Um the male and have an otherwise unremarkable prenatal and perinatal history. They present with a um oh that says female apologies for that sent to the assessment unit with concerns about prolonged jaundice and report that the baby's skin and eyes have been progressively yellow for the last week. So another poll for us guys to do um where would be the most concerning part of the baby to see evidence of jaundice. Ok. So great. So um soles of the feet would be the most concerning parts of the baby's feet. Oh um concerning part of the baby sea jaundice, as we've mentioned, um it kind of presents CFO quality, so top down. Um So sores and feet would be the last place that we would expect to see it. Um So in fair for you, um we have visible jaundice of the skin and sclera, a pa megaly of two centimeters below the liver edge, um below the costal margins, acomic stools seen in the nappy. So that's white stool seen in the nappy and dark urine. So parents are for in the baby's urine is quite dark but otherwise the examination is normal observations. Her temperature is 37.5. Her heart rate is 140. Her rest rate is 30. Her BP is stable, um 80/50 sar to 98% in room air. Our initial investigations show a serum bilirubin of 430 a conjugated bilirubin of 273. Uh ast um above the reference range of 120 at 110 and ap of 400 all above the reference range. So which investigation is likely to be diagnostic for this patient? I just close to the pole, I just give you 30 seconds. I appreciate it pretty close to an hour. Now it's a great, yeah. Um shown is most likely to be uh kind of diagnostic in this patient. Um So uh most likely diagnosis is probably going to be a um an obstructive um hyperemia. So, of those most likely to be a um atresia. So what is the most appropriate initial management of this patient? And then we got final hole here. So the most appropriate um initial management of this patient would be a precise procedure. Um So fontan and bolic to struts um both to do with the heart. Um although liver transplantation may be at the the final point and most appropriate initial one is the procedure. Um And then just to to go over, finally, um some last key points that we've mentioned for the presentation. Jaundice is a result of the breakdown of red blood cells. It is common and often transient presentation in the innate and there's lots of physiological reasons for this as we've gone through kind of our increased uh hemolysis today. Um excretion and increased enterohepatic circulation. Physicalness never cares. In the 1st 24 hours of life. Most jaundice is managed to therapy and take the time to plot this carefully on the chart. And pathological jaundice can be broken down into, again, increased production, decreased clearance and increased hen hepatic circulation. Any questions at all, pop and chat for me to see. Um I'm happy to answer anything you guys might have. Um And if not, I will send out the feedback forms for now. And as soon as I remember how to send them out. Uh mhm. There we go. Um So that should apologies that that should now um the feedback forward to the chat now. Thank you very much and I'll stay in the chat for 5, 10 minutes to make sure that no one has got any other questions you want to ask.