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Hi, everyone. Welcome to today's session. I'm Rashida. I'm one of the social media leads at S This is our very last session of our 15 week teaching series. And today we are joined by Shater who is 1/5 year medical student at Cambridge. We will be releasing the slides and the recording soon after the session. And if you have any questions during the session, please feel free to put them in the chat. And without any further ado I would pass it on the shelter to take us through pediatric cardio thoracic surgery. Hi, Roen, thanks. Um So as we said earlier, we're gonna go through congenital heart diseases, uh which is a big part of sort of pediatric surgery and specialist cardiovascular medicine. Um And before we start going through the clinical aspects of it, I think it's really important to go through the embryology of cardiovascular development. Uh but I don't want to bore you with the details. Um So cardiac development starts around week three of feri life with the cardiac crescent forming from the mesoderm. So that's um far left top of the screen um at number one. And then during that first um week of development. So week three of uh cardiovascular development, then you start forming the linear heart tube um as you fold uh the embryo. So if you remember from embryology, for those who have done it, um the embryo goes through lateral folding processes very early on um forming that shrimp like structure. And during that time, um you have linear folding of the heart tube and then you push the cardiac crescent and the linear heart tube down into the thorax. Um And after you've formed the linear heart tube, then you go through looping processes uh which is a very complex and intricate process where that linear structure then starts bulging out and looping in multiple directions and a um axes. Um And then it's all numbered. So if you follow the numbers, um so we're now looping in the middle, on the right side. Um If you go to the nu numbers four, so right ventricle and left ventricle. So at the very top of that linear tube, you've got the outflow tracts. Um And in the middle, you form the ventricles. So they actually start as the superior chambers and then they come down to form the inferior chambers being the ventricles. Um And then if you go to number five, so just towards the right side, next to the left ventricle, you start forming um the sorry number seven, the atria with the atrial septum. Um And because the ventricles are being pushed down the atria, then loop backwards and up and start forming um the superior chambers. And then you have to form the atrial septum, which I'll go through the details of in a moment. Um And then when with all of that, because you initially start with a linear heart tube that has no structures and no septum in the middle, there are no valves forming. Um So you have to form the valves as extra structures coming into those chambers. Um The outflow tracts of um the heart and the cardiovascular system. So mainly thinking the pulmonary trunk and the aorta come from the aortic arch. So that doesn't actually come from the cardiac crescent, but from structures that form very early on um closer to the cardiac crescent. Um but we won't go through the details of it. And then within all of that, you also form the coronary arteries. So that's a very quick overview of what happens during cardiovascular development. Um And then we have our patients. So um Children present with a plethora of things um when it comes to cardiovascular development. Um and congenital heart diseases, there are two main ways of picking them up. It's either your clinical features um that they present with or picking them up during intrauterine life. Um And if you don't pick up something during intrauterine life, one of the main features that a child would present with if they have a congenital heart disease is a heart murmur. So you auscultate a child the same way you auscultate. Um an adult over there, you will take pulmonic areas with a trichopi and mitral areas and the left sternal border. Um But it's worth remembering that if you cult um and hear a murmur, that doesn't mean that it's pathological. So a lot of kids can come in um with a murmur, um which can be concerning for you as a clinician. But if you follow the seven Ss rule, um then you're probably hearing an innocent murmur. So if it's a short um murmur and a soft murmur, that's hard on systole um with neuro associated symptoms. So it's symptomless. Um and all of your special tests are normal. So your echo, your E CG your chest X rays and it has variability on position. So standing and sitting. Um and if you hear it over the left sternal edge, then it's probably an innocent murmur. So just because you're hearing a murmur in a child, it doesn't mean that they've got a congenital heart disease. Um It can just be an innocent murmur, that's part of normal development and it will usually just um disappear by later teenage years. And then we go, sorry. Yeah. So then we go through congenital heart diseases and the way I like thinking about them is uh looking at how the child presents. So are they presenting cyanotic or are they ayano? Say the color is completely normal? Um and there are different ways that people look at this. Um I think with an AYO, you can then split it into having a left to right shunt. So we know that our blood flow normally um in the postnatal in sorry, the neonatal period um should be separated. There shouldn't be any shunting between them. But if the child is having a left to right shunt, then that's indicative of uh specific conditions, namely a patent doxy arteriosis, an atrial septal defect or a ventricular septal defect. Um But if there is an outflow obstruction, then that is probably um due to pulmonary stenosis, aortic stenosis or ation of the aorta. So that's your acyanotic child. Um But if the child presents very early on with synosis, then you're thinking more of the tetralogy of fallot tricuspid atresia transposition of the great arteries and truncus arteries. Um obviously, with the ayo conditions, you, you can also get SINOS later down the line. But as a first presentation, it's more likely for the child to be ayo with these conditions than cyanotic with the other ones. So that's the classification. Um and then just going through the different conditions. So, patent ductus arteriosus. So if you remember from um what I've said during intra uterine life during the cardiovascular development, there's a lot of that um looping and folding of the embryo to form the cardiovascular system. But with that comes um a lot of shunts that are required to maintain a healthy embryo and a healthy fetus during intra uterine life. And one of the main things that you need is a ductus arteriosis. Um And that's basically a connection between the aorta and the pulmonary arteries where in uterine life, um the pulmonary, any blood flowing through the pulmonary artery is bypassing the lungs and going straight into the aorta. Um I just think in utero, the child is um covered up with amniotic fluid um and therefore, is unable to breathe and the lungs are not fully developed. Um So you need to bypass the lungs and all of the oxygenated blood is coming from um the inferior vena cava um through the right atrium and the right ventricle up into the pulmonary artery. So you're bypassing um all of your pulmonary circulation with the ductus artery aces with the very first few breaths of life, you're supposed to shut down that ductus um with the increased pressure um in the lungs. Um unfortunately, in some Children that duct, for whatever reason remains open. Uh and there are different causes for it. So it can be a genetic cause um with underlying syndromes or just an isolated condition, but it could also indicate uh maternal infection and namely rubella and the child would present with shortness of breath. So, so uh difficulty feeding for weight gain, uh lower respiratory tract infections and the sort of feature that is the main thing that you should think of. Um in patent ductus arteries is, is a continuous Crescenta Deressa murmur. So it's continuous. So you hear a after S one and after S two as well. And the reason for the continuation is blood flow is flowing through the ductus, um, throughout systole and diastole. So it's not dependent on the contraction of the heart muscles. Um, and then investigations. So if you are suspecting, um, a PDA, you should have, you should have the child have an echo with Doppler studies and the Doppler studies just allow you to see where the blood is flowing and in what direction. And you should also have a chest X ray done for the child just to rule out any um hypertrophy of the muscles. So, complications, if the duct remains open, then you're predisposing the child to heart failure and something called Ice Mangers syndrome. Um Ice Mangers syndrome is basically when there is long standing left to right shunt which causes pulmonary hypertension. So think about all of the blood that's coming out of the aorta into the ductus and then into the pulmonary arteries build up of volume and therefore, pressure causes pulmonary hypertension and with the pulmonary hypertension, then you've got downstream effects on the right ventricle. So the right ventricle then hypertrophy in order to try and maintain that build up and pressure and volume um down the line with that build up of pressure um in the pulmonary circulation and right ventricular hypertrophy, you actually switch up that shunt. So instead of it being a left, sorry, a right to left shunt, um you form a right to left shunt um and the blood starts flowing back into the aorta rather than down into the pulmonary artery. Um and management of the patent ductus arteriosis can be conservative. So, if the child um is asymptomatic, is having no complications and is under the age of one, so you've just randomly picked up this crescendo, decrescendo murmur. Um then you just manage it conservatively and you just leave them be and hope that by age one, when you reassess, then they would have closed it off physiologically. Um If they start developing symptoms or if you're concerned about having complications, then you could give them indomethacin. Um And indomethacin is a prostaglandin inhibitor. And if you remember from physiology, uh prostaglandins allow you to basically say prostaglandins allow you to vasoconstrict uh giving a prostaglandin inhibitor. Sorry. It all the way around say prostaglandins al allow you to vaso dilate giving a prostaglandin inhibitor, then shuts off that ductus. So you're trying to manage it um medically with minimum interventions, but sometimes the duct is too big. You've got other concerns and you can't wait um due to complications or really severe features and presentation of the child. So you go into a surgical uh management where you either go through a transcatheter um or surgical closure. So a transcatheter is just um going through the veins and arteries and trying not to open up their chest and have open heart surgery. So that's a patent ductus arteriosis and the other ayo um condition that's known to have a left to right shunt um is an atrial septal defect. So I said I'll go through a bit of the embryology of um the atrial septum. So if you remember, you've got the atria which form a sort of one big chamber and then you have to split it into a left and right chambers. Um And you've got the connection open between them. What happens um is you've got a bit of tissue that starts growing down, which is called the septum premium. Um So that's in red N A. So septum premium then starts coming down to try and close off that chamber. But the moment it starts um growing too far down into the ACC. So these are the endocardial cushions that then form the valves. Um You start having regression of certain parts of the septum premium to form um an opening in it. So that opening is the ostium um Secundum. And then another sort of bit of tissue then starts growing down as well. So you've got two tissues coming together trying to close off. Um And then you've got sort of an S shaped flow between them. Um So an atrial septal defect can present as either osteum premium or ostium secundum based on which one of them remains open. Um But with both of them, you get an ejection systolic murmur. So every time you have, um, systole, then you can hear the murmur and then you also hear splitting of S two very early on in the S two cycle. Um And then the child can also present with dyspnea, just think about the amount of oxygenated blood and deoxygenated blood that's sort of mixing up together. Um, and also the amount of um, a sort of work of breathing and walk of contraction that the child has to go through in order to compensate. Um, the interesting thing about a SDS is that they can present in adulthood. So you can grow completely normally, um, well into your fifties and sixties and then present with pulmonary hypertension or right heart failure or a stroke or sometimes just af so atrial flutter or atrial fibrillation. Um And at that point, further investigations then show that you've got a congenital heart disease, namely an atrial septal defect. Um So you investigate for them with an echo and an E CG. And if for those who have done sort of clinical placements and have looked at AC DS, um when you get a V one M shaped QR S complex and a W shaped QR S complex, um in V six, then you're thinking of a right bundle branch block. Um So with both types of a SDS, you get a right bundle branch block uh with an ostium premium you get left, um, um, left axis deviation and with an osteum secundum, you get right, um, axis deviation. So that's the way to differentiate them on ECG S. Um But obviously you shouldn't really rely on ECG S on their own to make the diagnosis um of what subtype of a that you're looking at. Um, and then management, you can again leave it conservatively if it's small and asymptomatic and hope that the child is gonna sort of sort themselves out. Um Or you can go through the surgical route again the same way as you do it in a PDA, either transcatheter if it's a simple ASD or complete open surgical closure. Um if it's a complicated one with multiple sort of tissues coming up and down um in adults, if they're presenting at that point, because there is an increased risk of stroke in af then you have to add aspirin warfarin and OA um basically a stroke prophylaxis. So that's a SDS. And then the last type um of a left to right ventricular shunt um causing acyanotic congenital heart disease is a PSD. Uh So that's a ventricular septal defect. Um and it's caused as an isolated defect sometimes, but it could also be a part of an underlying genetic condition and with the same um sort of mechanisms that we discussed uh where APD can be caused by rubella infections um during intra uterine life. A PSD could also be associated with congenital infections. Um, a child would present either very early on to a 20 week scan. Um, you can pick a VSD up but they could also go unnoticed up until birth. Um, and into sort of neonatal life where they present with failure to thrive um, or heart failure, er, and features of heart failure such as hepatomegaly, er, tachypnea, tachycardia or pallor. Um, but they could also have a pansystolic murmur and the interesting thing about uh VSD murmurs um is the bigger, er, the defect is sort of the quieter, the murmur and the smaller the defect is the louder the murmur. So it's um sort of an inverse relationship of how much you can hear of the murmur and how big um the defect actually is and then you investigate it the same way you investigate everything, um an echo, um you could add an A Doppler, an E CG and a chest X ray uh and complications. So with A VSD, you could have aortic regurgitation. Um So that's when the aortic valve becomes um quite weak and then you get backflow into the left ventricle. Um You can also have an infective endocarditis, right heart failure and again, ice mangas syndrome, same way you'd have it in a PDA. And the management for A VSD is again, with everything you're gonna get bored of it at the end of this. Um conservatively, you manage their nutrition, you manage their heart failure. Uh but most of the time with V SDS, you have to go through surgical um correction to try and close off that septum. So that's left to right. Sh and Ayo. And then I'm gonna jump into the cyanotic causes of congenital heart diseases. Um And we're gonna look at tetralogy of fall. So, um tetralogy of fallot um is one of the main causes of cyanotic um presentations in a child and it's a combination of four different things um as it says in the name, etcetera. So it's a ventricular septal defect with an overriding aorta, a pulmonary valve that's stenosed and a right ventricular hypertrophy. Um So I'm gonna explain them er separately. So, an ventricular septal defect that ventricular septum, as we said, with a simple V ST um hasn't closed off properly for whatever reason. So that's open and overriding aorta with the AORTA isn't only covering the left ventricle, but it's also peeking into the right ventricle. So it's taking up more of the space. Um a pulmonary valve that's steno. So just a tighter um outflow tract into the pulmonary um um artery and then right ventricular hypertrophy because of uh the pulmonary stenosis, you get a thickening of the right ventricle. So it's just downstream effects of trying to compensate for these changes. Um And the risk factors, again, congenital infection with rubella um can predispose the child to develop the Trelegy of fall increase maternal age. So you're namely thinking anyone over the age of 40 alcohol consumption during pregnancy and maternal diabetes, mellitus are risk factors for this condition. Um And features sinois is the main one clubbing because of that heart failure and um sort of increased work of the heart poor feeding and failure to thrive. Um And in an ejection systolic murmur um and something called tet spells. Um and tet spells are what's described as sudden cyanotic phases when the child um is either feeding or crying. Uh So they suddenly become all blue. Um And then it takes a while for them to self recover and every time they go through feeding or crying sort of fit, they get a tet spell um investigations, you do an echo and a chest X ray. And if you look at the right hand side of the screen, if I can convince you that that's a chest X ray of a child with the Trelegy of fall. Um And if I can convince you that it looks like a boot, um So basically a boot shaped heart on a chest X ray is what we describe uh a sort of a, a key presentation for to tr of fall and from a management side, um you have to give a prostaglandin infusion. So with um PDA with a patent ducts, arteriosis, you give indomethacin, which is a prostaglandin inhibitor to try and close it off with um the Trelegy of fallot. You're actually depending on those ducts to remain open uh you don't want them to close off naturally. So you give prostaglandin infusion to keep everything opened up until you intervene with a total surgical repair. Um without surgical repair, the prognosis is quite poor. Um And basically, you're encouraging the parents to go through a prostaglandin infusion sort of process and then the surgical repair to try and save the child. Um with the Trelegy of fallot, um the clinical severity and the features of it is dependent on how stenosis, the pulmonary um valves. So the more stenosed it is the more cyanotic uh the child becomes and the more sort of downstream effects um of this condition. So that's the Trelegy of follow up. And then another condition is transposition of the great arteries. And that's basically um due to inability of the septum between the uh sort of greater outflow tracts to spiral during development. So, normally in the second picture. So on the left hand side, you can see what um it would look like in transposition of the great arteries in the middle. So or the right picture, um you see what normally should happen. So within the aortic arch, um you should uh you should form the aorta, you should form the pulmonary trunk and then they should spiral around each other so that your pulmonary trunk is going to the right side of the heart and the aorta is opening up into the left side of the heart, but failure to spiral means that the aorta basically remains on the right side of the heart. So it's transposed to the right and the pulmonary artery remains on the left side of the heart. So it's transposed to the left hand side. Um, and the risk factors for a a namely maternal diabetes, mellitus. Um And the child again presents with sinuses, tachypnea, a loud single SS two and prominent right ventricular impulse. Um So you notice these symptoms very early on, um, usually a few hours after birth. Um, and investigations for it, you do an echocardiogram and a chest X ray and again another chest X ray. But this time, um if I can convince you that it doesn't look like a boot, it actually looks like an egg hanging on a thread. Um So they call it an egg on side, um, or an egg on string chest X ray. Um And that's your sign that you look for on a chest X ray for a child with transposition of the great arteries. Uh and managements again, prostaglandins and surgery. So you give them prostaglandins to try and keep that ductus arteriosis open because without it, um it's only deoxygenated blood going back into the um systemic circulation. Um So it's a closed loop. So you keep whatever duct you've got open and then intervene with surgery to try and put them back in the right place. Um And then another condition is coarctation of the aorta. So that's basically, when you have congenital narrowing of the descending aorta. Um and it's associated with male sex, but also Turner syndrome. Um and those who don't know, Turner syndrome is an exo condition. So it's actually um genetically female. Um, they just lack the other X chromosome. So it's quite interesting that you see it in males but also females with Down Syndrome. And unfortunately, I've not been able to explain this myself and I can't find any proper explanations for it. Um It's also associated with a bicuspid aortic valve. So, the aortic valve is usually um a tricuspid one. So a bicuspid aortic valve is associated with ation of the aorta um and neurofibromatosis, which is a genetic condition with multiple features um systemically around the body. And one of them would be um coarctation of the aorta. Um And features for it would be heart failure in infancy and if you somehow manage to miss it and it's not stenosed enough. Um So that descending aorta hasn't stenosed tight enough for you to pick it up in infancy. It can present as hypertension in adulthood. Um You also get radiofemoral delay. So, because it's in the de it's um the sort of narrowing is in the descending part of the aorta, your upper limbs are receiving blood completely normally. Um So there is some radiofemoral delay between the radial arteries and the femoral arteries when your um palpating for a pulse. Um you get a mid systolic murmur, um and secondary to that decreased flow um into the lower parts of the body. You get underdevelopment of the limbs and mainly the lower limbs and and organ hypoperfusion. Um So they can present with failure of specific um sort of end organs. Um So you're thinking um kidneys, for example, or um liver. So those are the features of the condition and then investigations, you try and do a CT angiography. Um So on the right hand side of the screen, now you can see um the aortic arch coming up nicely and then where the white arrows are, that's where the sort of narrowing is happening. Um And then the aorta then extends down management is symp symptom dependent. So again, because that narrowing could be so um sort of minimal that you only pick it up in adulthood, nothing should happen. Um Unless it's indicated by the features that the child is coming up with. Um And if it's too severe, uh and it requires surgical repair, then you go through surgical repair. Uh And it depends on the degree of the stenosis basically. So you either give sort of a balloon angioplasty where you try and expand it, sort of an expanding balloon into the vessel itself or you do um open surgical repair and try and put a stent in and complications. The main one is recurrence. Um So even though you could treat it during childhood, um that stenosis and narrowing can then recur later on in life and you have to treat it. Um And then another condition is hyperplastic left heart. Um So with the hyperplastic left heart, that's um basically a presentation where there is severe underdevelopment of the left side of the heart associated with um genetic, sorry, that should say genetic mutations. Um but also other syndromes. Um So the main two genetic conditions that we're thinking of and II don't think anyone is expected as a medical student or junior doctor sort to sort of blurb those out. But for those who are interested, um GJ A one and hand one mutations, um you usually see a hyperplastic left heart syndrome, um Patau syndrome and Edwards syndrome and those two are sort of your classic clinical school um syndromes that you should be aware of with the details. So if you presented with these two, then think hyperplastic left heart um as a presenting feature and child comes in sinus in respiratory distress, there's history of poor feeding. Um and if there's sinus, you're giving them oxygen, there is no response to oxygen because there's not much cardiac output going um through to the body just because the the volume of your left ventricle is so small. Um and they get weak peripheral pulses again because of the reduced um cardiac output. And then they could also come um quite de um sort of towards the end of life and end of presentation. So, in a cardiogenic shock and they could present um literally dead. Um, depending on the degree of how hyperplastic, um, the left side of the heart is investigations for it would include, um, diagnosis prenatally. So that's on your anomaly, um, ultrasound scans. And an echocardiogram would also pick up the degree um of um, sort of on the development of the left ventricle mainly, um, management prostaglandin. So keep any shunts open, um, keep it all mixed up, that's better than sort of stopping everything from mixing up. Um And then you go through surgical repair, which um if you're trying to treat it, it could be a three stage repair, but it could also just be palliative to try and decrease the symptoms and sort of extend life and make it um as sort of painless as possible for the child. Um And then the last two symptom um syndromes that I wanted to go through of diseases, um is an atrioventricular septal defect and tricuspid atresia. So if you go through the atrioventricular septal defect, it's basically having an ASD and a BSD. So there is basically complete blood mixing, everything is going in all direction. Um And there are no valves and in tricuspid atresia, um this complete lack of the tricuspid valve. Um And with that, if you follow, uh basically the arrows, you get right atrium to left atrium flow and then everything goes basically through the septum, the VSD hole, um goes up into the aorta and then goes into the pulmonary trunk. Um So everything is mixed up everywhere, but there is no flow between the right atrium and the right ventricle. And the reason I've put them both together there is because um on ECG they present basically the same. Um So they present with left axis deviation. So it's a positive um sort of uh positive QR S complex in lead one and then a negative one and lead two and then another negative one and aVF which is your classic sign of left axis deviation. So, child with an ECG presenting with um LD, then you're thinking either atrial ventricular septal defect or tricuspid atresia. Um And then last but not least, although we talked about all of these syndromes are sort of um sorry conditions are separate conditions. Um Sometimes it's worth thinking about this is sort of what the child is presenting um as just the complete picture. So, is it just there are cardiovascular um features and cardiovascular symptoms that you're concerned about or is there more to the child that we are missing? Um So you have to think of any syndromic uh features that the child might be presenting with. So, fetal alcohol syndrome is associated with a SDS and V SDS, Trisomy 21. So Down syndrome is associated with A VSD ASD or VSD Turner syndrome, um which we touched upon coarctation of the aorta or a bicuspid aortic valve. So that's all linked um Noonan syndrome, uh pulmonary stenosis asd hypertrophic cardiomyopathy with Noonan Syndrome. Just think about any developmental delays. Um Do they have t of the eye? Does the child have undescended testes? There's a whole load of pictures that you should be thinking of if you pick someone up with pulmonary stenosis, for example, and then Williams syndrome uh with a supravalvular aortic stenosis. So, unlike a coarctation of the aorta, that narrowing is actually happening right above the valve or with aortic um right above the aortic valve. Um and then you could also get peripheral pulmonary stenosis. Um and with Marfan syndrome, so, hypermobility um and mitral valve prolapse is sort of a key feature, tall child, very long limbs. Um So don't miss the overall picture of the child. So that's all of the info I wanted to go through. Um We've got a few questions that we can go through and they sort of covered one of like the main topics that we went through today. Um So we treated you and her about the pool, I suppose I'll just wait a couple of minutes for everyone to respond. Thank you. We have a 5050 split between B and E B and E. OK. Interesting. Um Is anyone sort of brave enough to give me sort of why they think they thought um it was B or E? OK. Don't. Right. So what, so writing that question I would have gone with C so upper left sternal edge if you just go. So I'm gonna go back. It's probably not the best idea to go all the way back, but upper left sternal edge, you're thinking pulmonic area. Um So I think it's more of sort of a pulmonary stenosis picture. So it is most likely going to be um a child with Noonan syndrome um presenting with pulmonary valve incompetence, which is sort of a pulmonary stenosis side of things. Um So that's this one. And then question two, we have 50% saying B and then 25% with A and 25 with D OK. So I would go with the 50% who say it's B. Um So as we said on the last slide where we discussed individual conditions, um when you say when you see a left axis deviation on ecg um it's either an atrioventricular septal defect or tricuspid atresia. So it's that um positive deflection in V one with negative deflections. Oh sorry in lead one. And then pos negative deflections in lead two and AV F um say trichopi atresia or a complete AV canal which is an ST um and then question three, we have majority going with C OK. Yeah. So Sinois with a murmur, one of the things that you should think of the main one should be tetralogy of fallot and the degree of pulmonary stenosis, as we said, is associated with the degree um of clinical severity and cyanosis of the child. So see and then question four, we have only 20, we have three responses but majority are going with Williams Syndrome guys. All your responses are anonymous. So don't be hard to answer the questions. I can't see anything and honestly, no judgment. Some of these questions are quite mean. Um which is this one? Um So valvular aortic stenosis and a three year old boy with learning difficulties. Um To be honest, if you don't know the association, it's quite difficult to figure this one out. Cos I haven't really put any specific details that would make you differentiate between the syndromes. Um But yeah, see with P Williams syndrome with the supravalve aortic stenosis. Um and then question five, we have split between AD and E AD and E OK. Um So the way I'd figure this one out is using the other sort of noncardiac presentations of the child first. So we've got a 15 year old girl, um short stature um with primary amenorrhea. So she hasn't started her period yet. Um and a wide neck um in exam world, a wide neck means down syndrome if it's a sort of an older girl um who's presenting with primary amenorrhea. So here you're thinking Pri um Turner syndrome and we said that it's associated with um coarctation of the aorta. So that would be a um and then question six majority go with a Yeah, exactly. So this is um you're called to the postnatal ward. Um an infant born eight hours ago, suddenly turned blue, which is basically a telltale sign that there has been. So the duct closure process is now happening. And therefore the child is becoming um symptomatic because there is duct closure, which means that this congenital heart disease, whatever is going on is a duct dependent um condition. And therefore, you're mainly thinking transposition of the great arteries uh because it's such a sort of sudden presentation, it's so quickly happening. Um So it's likely TGA and therefore you have to give them prostaglandin to prevent further duct closure. Um So a is a type of prostaglandin. Um And just to say, fury and nasogastric tube insertion um are sensible suggestions, but they won't be your initial management. They are things that you should do later on if the child then develops heart failure and you should actually avoid ibuprofen. Um because it's a, it acts basically as a duct, it promotes duct closure. So it's like a prostaglandin inhibitor um and give him oxygen. But the main thing is keep that duct tape with a prostaglandin. Um And then question seven, we have majority going but d fatigue with endocarditis. Yeah, exactly. So with A VSD and a pansystolic murmur, um infective endocarditis is sort of one of the main complications. Um And just if anyone is confused, um it's pulmonary hypertension that could develop a not essential hypertension and the rest are not associated with VSD. Um And then question eight. So we've got 10 questions. So we're almost there. I OK, we have one response so far. So if I really can respond to this, it would be really great. It's fine. Um So this is basically your knowledge of uh antenatal care and linking it with um congenital heart diseases and sort of postnatal um complications. So, the fetus has been picked up on antenatal scans to have um a large PDA. Um So we know that the mum is asking about indomethacin, which is a prostaglandin inhibitor to try and shut that dot off, which is that medical management for PDA. Um So if we go through um the options indomethacin given to the mother is actually very useless. So it won't do anything to the child. So what you do is wait for the baby to be born. Um You don't give it right after delivery, you wait for a little bit. Um So you have, you do that echo, you do any chest X rays and ECG S that you have to do just to try and rule out any other conditions that also present with a PDA, um that might um be duct dependent. And therefore, once you've ruled everything out and you know that it's an isolated PDA, you give um the indomethacin um afterwards and then question nine. I might just sh shall I go through the more people wanting to answer first? I think we'll give them a couple of minutes to answer this and then you can come through it. We have majority going with e with a OK. So, um with coarctation of the aorta, if we go back to the first sort of few slides where I discussed, if it's acyanotic or cyanotic, it's actually an acyanotic condition. Um And you don't really get a drop in oxygen saturations from a pre to face ductal measurement. Um It's only that narrowing um in the descending aorta so that you sh you shouldn't really have um oxygen drop. It's mainly that pressure and flow difference. So it's not a um it doesn't present with hypertension in the legs. Um There's just less blood flowing through. Um So the pulses are weaker. Um And then if we look at C which is and lactic acidosis. So we said that with the low um blood flow to end organs, you get end organ damage and therefore hyperperfusion and with hypoperfusion, you get renal failure and lactic acidosis. Um So the answer is actually c um and it's not the commonest form of congenital heart defect. Um and it's associated with Turners rather than Down Syndrome. And then last but not least, see, we have a split between C and E OK. So if we go through it quickly, so it's a four year old girl. Um So you're quite young. Um it's presenting with a productive cough and wheeze. So you've got sort of a, an infectious process going on. Um, there's a systolic murmur, um, and the second intercostal space lateral to the left sternal edge, it's got an intensity of 1/6. Um And that just means that it's quite a soft murmur. Um So anyone with no sort of cardiology training should be able to hear it. Um It's not audible when she lies flat. So there is a discrepancy between that standing sitting. Uh So it varies with position. Um So there's quite a lot of ss so it's a systolic soft murmur. Um And there are no other sort of cardiac symptoms that you're concerned about. Um And it's positional, so it's most likely going to be an innocent murmur. Um And I've just added the seven essays for Innocent Murmurs um on the right hand side of the screen, um, obviously really important to rule out anything else. Um Innocent murmurs usually become worse when someone is unwell. So if there are coral symptoms that cough wheeze um a viral infection or a bacterial one, and they then get better when the child has recovered and gone back to sort of normal. So that's everything for me today. Thank you so much for listening. Um And yeah, if anyone has any questions, I'm happy to stick around for a little bit longer and answer them. Thank you, Shelter. I think that was an amazing end to our teaching series. A massive thank you to you guys. As well for joining us today. And especially those of you who have been joining us since the beginning, we really, really appreciate all your support and hopefully we'll see you guys next year for, uh, next teaching series I have so I have put in the feedback form in the chart. 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