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Hi, everyone. My name is Go Pick a suffragette and I'm one of the FC Rose currently placed at Craigavon Area Hospital. And today I will be doing a new neonatology revision lecture. Um So basically at my main aim is to cover some of the basic topics that are required for your finals as well as your fourth year exams. With respect to neonatology. It's a very broad subject. So I've tried to break down into simple language for your own revision. Um So without further to do, let's get started. Um So next slide, please. So the topic that we're gonna be covering is first of all new newborn baby check and resuscitation, um causes of low birth weight. And are you g are a bit about neonatal screening, uh neonatal hypoglycemia, neonatal respiratory conditions and new little jaundice. Next I please. Okay. So first of all, uh newborn baby check, now this is quite not commonly asked in your office keys, but it's important for you to know. Um So first of all, whenever you're doing an examination, we're going to be starting with general inspection. So looking at head to toe, first of all, inspecting the infant for any clinical signs, um suggest suggesting any signs of pathology, looking at the skin color for any rashes, any signs of Palo cyanosis or signs of jaundice looking for any bruising. Um and also, you know, neonate if they usually um start to cry. So looking for any week cry or any Latorre gee or poor feeding, etcetera, uh feeling for the tone. So you can usually assess the tone by gently moving the new bonds, uh limbs passively, or you can even check the tone by holding the new bond. And if there any signs of hypotonia, you must be thinking about hypoglycemia or even sepsis head. So you can, so usually what I like to do with newborn baby check is to, is to do a full head to toe examination. So, um this usually would involve first of all, with respect to head, uh measuring the head circumference and usually take three uh you know, readings and you would record the highest. And the next thing would be to inspect the shape of the head and check for any abnormalities such as skiffle hematoma or cap, it's Axid a knee. Um and you have to palpal eight palpate each and every quadrant of the head. And then you will also be palpating the anteria and posterior fontanel and you will be checking for any signs of dehydration by feeling for any sunken fontanel or if it feels flat, it's usually normal. If it's sunken, it's um you know, or bulging, it could be abnormal, um looking at the skin. So this would be something that you would have already inspected generally. So, inspect the skin for any color abnormalities, um looking for any bruising lacerations or even any birthmarks because birthmarks also must be um you know, written in the red book. Um And then again, from head, we're going to go down to face. So again, with respect to face, you can start with the eyes. So looking for any signs of dysmorphic features such as up slanting palpa gray, um looking for any epic until folds um and also looking for any brush field spots and that can be um you know, characteristic of Down Syndrome. Um And then you will also be looking for the red reflex and this can be done either with an ophthalmoscope or it can also be done with a pinpoint like a torch. Um And if there is absence of red reflex, then this can be sign of congenital cataract. Um again, going down from the nose, looking at the uh going down from the eyes, looking at the nose. Um So looking at the size and the symmetry of the nose, flattened nose can be characteristic of Down Syndrome. Um The next thing is looking at the mouth. So looking inside the mouth for any signs of any visible abnormalities, obstruction, feeling the soft and the hard palate um for any um you know, signs of and feeling if there's any signs of cleft lip or cleft palate. Um um The next thing would be um looking at the yost looking again for any signs of structural abnormalities, any skin tags, any bruising, um and also any signs of low set years, which could be a type of dysmorphic features. Um Next slide, please. So again, going down from the head face yours and we're gonna go down to the neck and the clavicle. So we're going to be feeling for the clavicle for the formation of the clavicle or if it's absent or present. Uh and then usually like to go down to the chest. So we're going to be looking at the chest signs for any respiratory distress signs for any in drawing of the muscles, tachypnea, uh you know, record the respiratory rate, look for a feel for the central CRT, listen to the chest, listen to the lung fields, listen to the heart sounds for any added heart sounds. Um And then usually you could and then you can go to the arms and look and the hands. So first of all, look at the length of the arms, they should be equal uh looking at the fingers. So the number of fingers must be counted and they should be equal as well. Looking at the palmer creases. So if there's a single palm, a crease, again, that's characteristic of Dawn syndrome. Um and then going down to the abdomen. So, feel for the abdomen. Again, look, inspection, palpation and uh ostentation. So, inspect the abdomen for any bulging, any distention, look at the umbilical stump as well for any signs of infection or redness or swelling. Um And then feel for the abdomen, feel the abdomen as well for any signs of distension guarding, etcetera. Um And then we will also be um uh listening to the bowel sounds as well. Um And, and listening for any abnormal bowel sounds such as stink, ling or absent bowel sounds. Um The next thing is of course, genitalia. So when we go down, uh for males, we have to look at the penis and retract the foreskin and check for any signs of hypospadias or check for the position of the urethral meatus. And for females, we need to look at um you know, we need to look at any uh signs of fused labia and usually you can even assess the anus as well for the patency at the same time. Um After that, going to the lower limbs again, looking at the length of the, of the legs if they're symmetrical and equal in length and if there is no discrepancy. Um after that, you could also do the Barlow and portal Lonnie's um test and that is basically done to deduce any kind of D D H or developmental displacing of the hip. So, um Barlow is basically internal rotation and pushing down of the, of the leg and that is basically Barlow is bad. So that's something that I used to think about. Um Barlow is dislocation of the hip joint. And Ortolani is basically relocating the hip joint. And if there are signs of um D D H, usually when you do the Ortolani maneuver, the click sound or the relocation would not be present because there is some dislocation. So that is why you have to do both the maneuvers at the same time to check for any signs of D D H. Um The next thing is of course to feel for the femoral pulse um and looking for the rate the rhythm and the volume. Um and then uh counting the number of toes as well. After that, you can um you know, just lift the baby up and feel for the back and spine for any signs of abnormalities. And then you can end this with checking the reflexes. So usually there are three types of reflexes you need to check. So one is the palm a grasp the uh routing reflex or the suckling reflex and moral reflex as well, which is basically you hold, hold the baby onto the table and you just um look if you know whether their feet are touching the ground um and they are able to stabilize. Yeah. Oh, sorry. Next slide, please. Okay. So, uh this is basically I've just, I've just put in a slide talking about newborn resuscitation. Um It's uh it's just a red, I feel like the red part is the most important part that you need to know as a medical student or as an F one. Um So first of all, um starting with the birth itself, try, we have to try and delay core clamping if possible. And that is just to make sure that there's enough oxygen and enough nutrients that are being supplied to the baby. And as much as as we can, we want to try and supply the oxygen and nutrients. So we will try to delay court clamping. Um Second, as soon as that is, you know, as soon as the cord is clammed, the second thing that we need to do is dry and wrap the baby and make sure that the baby is warm and try to keep them warm and stimulate them by rubbing quite aggressively usually. Um And as and as you do that after you do that, the main thing is to assess the baby and this is usually using the Apgar score. So you'll be assessing the color, the tone breathing and the heart rate. Um And after that, once you've done all these two steps, the the main, the to the main two other steps are of ABC. So airway and breathing. So usually make sure you ensure an open airway and for preterm, you should usually consider CPAP and if the baby is not breathing or gasping instead of giving um you know, um like breathing with oxygen mask, we usually don't give that first. We give them Aaron Flay shin breaths and we usually give five inflation's. Now, this is usually seen, I think mostly you might see these questions in your M C Q s and they might ask you a question, regard, newborn resuscitation, and they might give you all these options. But the first and foremost that you must do is of course dry wrap and keep the baby warm. And then you have to make sure that you can proceed to assess the baby and keep the airway open. And whenever you're trying to um if the baby's not breathing, the first step is not use oxygen, it is to give air inflation, um sorry, uh inflation using air rather than oxygen. Okay. Uh Next slide, please. Okay. So the next thing that I would like to talk about is um preet um um sorry, a low birth weight and the causes of low birth weight. So uh the main issue that the two main causes of low birth weight in the units are preterm delivery and fetal growth restriction. So, preterm delivery in turn can cause, of course, it can cause pre maturity and the conditions associated with prematurity. For example, new needle respiratory distress syndrome, necrotizing enterocolitis, which I will be talking about um infection and parliamentary hyperplasia. Fetal growth restriction. F G R is a very important positive factor of um low birth weight and usually it is down to the maternal risk factors, they're very easy to remember. So all the things that are quite bad. So smoking, alcohol, poor nutrition, severe anemia, hypertension, which can cause pre eclampsia, diabetes, torch infection. So that is toxoplasmosis rubella site, omega the virus and herpes um and hepatitis infection as well. Some of the fetal risk factors include chromosomal abnormalities and inherited disorders and multiple pregnancies. For example, twin pregnancy or triplet pregnancy. Um One of the babies are, they are at a risk of F G R and so that in turn can cause low birth weight. And the reason why low birth weight is important is, as we mentioned, you know, it is a serious risk factor for respiratory distress syndrome as well as um neonatal sepsis. So that is why it's important to understand the causes of low birth weight and what can be done. Uh You know, if you encounter them next slide, please. So this is just a small slide. Um regarding neonatal blood spot screening, I think queens usually likes to ask one of one question from this um every year. Um I think one of the questions we got was regarding cystic fibrosis and like when cystic fibrosis is usually detected and that is during the heel prick test or the neonatal blood spot screening. And that is done between 5 to 9 days of life. The main conditions that you need to be aware of is sickle cell disease, cystic fibrosis phenylketonuria, homocystinuria and congenital hip pa divert is um, these are the five main conditions they usually like to ask and they might just ask, you know, um, is this condition usually screened or um, you know, what is the name of the screening process, etcetera? And it's something, it's a good thing that if you're, you know, if you're given a patient, if you're given a neonate in your Rosky station, it's something that you can talk about to the parent as well. Next slide, please. All right. So I hope you guys don't have any questions regarding that. Um But the next thing that I'm going to talk about is neonatal respiratory diseases. So, these are the two main ones that are quite important and that you need to know um uh with respect to your finals. So, the first one is respiratory distress syndrome and the second one is transient tachypnea of the newborn. So, next slide, please. Um All right. So respiratory distress syndrome is a condition which is usually seen in premature infants and this is usually caused you to surfactant deficiency. Now, now, usually lungs, um babies usually have their lungs mature um after 30 weeks of gestation and premature infants. Now, prematurity can be divided into extreme prematurity, mild to moderate prematurity. This is usually seen in new units who are at extreme premature condition, for example, less than 30 less than 28 to 30 weeks of gestation. And in that case, usually, the lungs are not at all developed. And a particular chemical called the sulfa acting, which is produced in the lungs is also not produced and surfactant essential because it reduces the self essential in the lungs which allows the lungs to work and allows the baby to breathe properly and prevents atelectasis or lung collapse. Um So, if the surfactant is deficient, then of course, there's a risk of the baby's lungs to not work properly and the lung will collapse. And as a result, the baby becomes hypoxic tack apneic and can go into respiratory failure. Um One of the main predisposing factors as we talked about was prematurity and there is factors for prematurity is what we talked about in the previous slide. Um Other, other predisposing factors include C section, cesarean section, hypoxia, and maternal diabetes as well. Now, imaging usually you're not expected to know how to read um unical X ray, but it's important to know what the X ray might entail, which, which you can probably, you know, if you see ground glass appearance and you see um you know, the stem white um consistent with the respiratory distress syndrome, you know what you're getting at. So the imaging is usually um it's described as a ground glass appearance as you can see on the right um and so poorly aerated. So usually you won't be able to see the lung markets properly because the lung has collapsed because of low uh affected. Um the main prevention, of course, you know, uh this is mainly seen, you know, you might read this an obscene Gynie but um you can't prevent this. So uh the the easiest way to prevent it is of course to delay preterm. But um and that can be done using to politics, giving Erythromycin, etcetera, but also by giving antenatal steroids to maternal cortical steroids, two doses, 12 hours apart is usually given for any mother um undergoing premature delivery. Um And of course, once the baby is born, it's very important that we prevent hypoxia by optimizing post resource scam. The main treatment for these um new needs is of course the fact and replacement and this is done in the neonatal ICU and you will also be giving oxygen and CPAP to make sure that the airways are open through positive ventilation. Next slide, please. Um Sorry. Um Sorry, do you mind going to the previous slide? Sorry. Um Just um okay, that's fine. Um So just one thing regarding um um respiratory distress syndrome, other complications that you need to know. So as we talked about hypoxia is the main thing, but pneumothorax is another thing and infection um as well as um uh parliamentary hemorrhage as well. Now talking about transient tachypnea of the newborn. So this is another condition which is commonly seen in new units. What at term. So that's an important differential if you're getting confused as to which type of respiratory distress, you know what respiratory condition does the neonate have? So, transient tachypnea is seen in units who are born at term. And the main cause of transient tachypnea is usually one of the main predisposing factor is C section. Now, usually there is formation of some fetal lung fluid. So the babies that the lungs, they produce some fluid that will allow the work of, you know, the allow the work of breathing and basically functioning of the lungs. And this fluid is USJ removed during labor and during the mechanical contraction of the of the muscles and of the movement and the passage of the baby through the vagina during vaginal delivery. And as a result of fetal lung fluid is removed during that mechanical contraction. But in babies who are born through C section, that um you know, benefit is gone, that's not there because that mechanical push or the mechanical contraction that adrenaline rush is not seen in C section. And as it is out, the fetal lung fluid is still present in the lungs and it doesn't get removed. And this can present with signs of to cope mia hypoxia, overinflated chest because of the presence of fluid. But as the name suggests, it's transient. So it usually settles within 24 to 48 hours. And the uh the, the X ray kind of looks like a pulmonary edema X ray that you might see in an adult. So it's easy to understand um, it's quite a heavy lung or a wet lung is what they like to call. And as you can see by the white arrow, I don't know if you can see my arrow, but there's a white arrow here and you can see the line going to, that's basically a bit of the horizontal fissure and that is white on the next raise fluid, quite consistent with the fluid that is not removed, um, in this, in this baby and that can cause the tachypnea. Um You don't, there's not much management that's quite supportive. Um And it's usually resolved without any added support. But the most important thing to remember is that we need to differentiate between a congenital cardiac disease and transient tachypnea because the presentation is quite similar to cardiac failure. So it's important to differentiate between cardiac failure and trans transient tachypnea. And this can be done through E C G echo um taking bloods. And it's also important to do a septic screen if necessary. If you think that the fluid and the tachypnea or the hypoxia can be due to something else. Um The main treatment is to prevent um transient tachypnea. Yeah, next like please. So a bit about neonatal hypoglycemia. So, um hypoglycemia is very common after birth and the main when usually we tend to get worried when the hypoglycemia or the glucose levels go below 2.6. Um or if the uh if the baby is symptomatic. So that's when we usually worry and that's when we have to start treating them. Now, sometimes, uh you know, some of the main causes a physiological hypoglycemia can be due to dehydration. So a lot of new needs, a lot of babies when they're born, they are at a risk of dehydration. And that can cause hypoglycemia and that is usually asymptomatic and this can be, you know, treated by encouraging normal and frequent feeding. Um But features of symptomatic hypoglycemia include jitteriness, weakness, ballo week, cry, having tachypnea, poor feeding and the worst thing could happen is seizures or even the BP can get into coma. Uh The main risk factors for hypoglycemia is of course preterm delivery, maternal diabetes mellitus because the baby is exposed to too much glucose when inside the mother's womb, the baby produces a lot of insulin. So once the baby is out of the mother's womb, and once it is not exposed to as much of glucose as it was exposed to. Um you know, in the mother's womb, um you know, the insulin tends to drive hypoglycemia because of the amount of insulin that's present. Um, hypothermia is another cause of hypoglycemia. And another another important thing to rule out if, if a neonate has hypoglycemia is neonatal sepsis to do a sepsis screen. And if you suspect to do um sepsis six protocol, if they're symptomatic, um you need to admit them to the neonatal ICU and administer 10% of Dextros. Thank you. Uh next slide, please. All right. Okay. So the next thing, the last topic that I'm going to talk about is neonatal jaundice. So um I think with respect to neonatal jaundice, I kind of found, you know, I found it easier to uh segregate into these four topics when learning about jaundice in general. So, first of all, uh pathophysiology of jaundice, uh difference between unconscious gated versus conjugated bilirubin because that is important to important to know when you are reading the blood results. Um conditions associated with neonatal jaundice and complications again, needed. Get a question regarding complications of jaundice in our finals. Now, whenever you're examining a baby or a neonate that has jaundice, there are three important points to keep in mind. First of all, check if the baby's well or unwell uh by taking a proper history and doing a head to examination. Um Another thing is check. When did the jaundice appear? So, when did the baby start um showing these symptoms? Was it within 24 hours of delivery? If that's the case, it is a pathological or is the jaundice persistent beyond 14 days? And that is also pathological. Um And then, and the other one is to understand between conjugated and uncomplicated bilirubin and to check which is higher or which is lower because that can help you identify if it's prehepatic hepatic or posthepatic jaundice. Next slide, please. So just, you know, basic understanding of pathophysiology I'm going to try doing it to a medical student level rather than a consultant level. So, um first of all erythrocyte sor your red blood cells, they get broken down by macrophages in the spleen and bone marrow. Um uh sorry, and that is broken down into him and Billy Ruben. Um So the Billy Ruben then gets transported to the level where it because Billy Ruben is insoluble in water. It cannot be transported to the small intestine or it cannot be excreted out through urine. Therefore, it has to be converted to a soluble form where it is soluble in water. And that is through conjugation and that conjugation is done in the liver. So once the Billy Ruben reaches the liver, it is, it undergoes a process called conjugation. So all the bilirubin that is present before the liver are called uncontradicted bilirubin. And once it, you know, is present in the liver and you know, passes through the bile duct, it becomes conjugated bilirubin. And that is, that's important to understand that you will know um you know the cause if something out the other is higher than the other, you can know the cause of jaundice. And once it becomes uh conjugated bilirubin, it then goes to the bile duct and from the bile duct, it goes the small intestine where it becomes, it is excreted a circle. Billon in the, in the stools and it is then reabsorbed in the large intestine into the bloodstream where it goes to the kidneys where it is excreted as urobilin in the urine. All right. So this is the basic fizzy path of uh pathophysiology of Billy Ruben at its pathway. Now, prehepatic jaundice is usually seen because of excess breakdown of red blood cells. Hepatic is usually due to conjugation issues and posthepatic is due to obstruction to bile flow. All right. Now, these are, these are the blood tests that are usually associated with jaundice. So that's uncomplicated. Bilirubin is also called indirect bilirubin. If you may have seen during LFTs, conjugated bilirubin is also called direct and total bilirubin is basically the some of direct and indirect. Okay. So if you know this, then all the other things are quite easy to understand regarding the initial jaundice. Okay, next slide, please. Um Okay. So first of all, let's talk about uncomplicated bilirubinemia. So, if there is an isolated rise in uncomplicated Billy Ruben, um then you can think about is it a benign rice or is it a pathological rice? So, benign causes, as I mentioned is usually more than 24 hours. So if it's between 24 to 14, 24 hours to 14 days, that is usually where you see benign conditions. The two most important benign causes of rise and unconscious gated bilirubin, our physiological. So usually, um you know, babies when they are born, they have extremely high levels of hemoglobin and red blood cells to combat the stress and of course, to get enough oxygen and nutrients into their body because you know, um they're just born, so they have very, very high levels of hemoglobin. So as a result, if high levels of hemoglobin, there's going to be high levels of breakdown of hemoglobin and therefore high levels of bilirubin as such. So this is usually physiological and if there are any, if there's presence of jaundice in a baby more than 24 hours, this is usually a diagnosis of exclusion, but this is something that you can keep in mind. And in this case, as I mentioned, the conjugated component will be low because conjugation only happens from liver and thereafter, but this is usually before the liver. All right. The other one is breast milk, jaundice of breast milk is a high, very high risk factor of causing jaundice in uh units. And again, this usually persist until 2 to 3 weeks. If you get an Oscar station regarding breast milk jaundice, this is sometimes something that you can probably um tell the parent that it can maybe reassure them, saying that this can still persist until 2 to 3 weeks. Usually as I mentioned in this case, conjugation or conjugated component or the direct bilirubin is quite low. All right. So, next slide, please. Okay. So now where the issue comes is when the, when there is rise in uncomplicated bilirubin and it is within 24 hours. That is when it's an issue. So the two main important differentials that we need to rule out our sepsis and D I C as well as hemolysis, talking about hemolysis, I'll just give a very basic understanding of races incompatibility. So usually a mother that is Reese's negative if she becomes pregnant with a baby who's racist positive because the Reese's positive has the races because the baby whose races positive that babies, red blood cells has the racist antigen. And the Reese's negative mother doesn't have races antigen, but the Reese's negative mother will produce anti racist antibodies. So the anti racist antibodies usually don't target the baby's red blood cells during the first birth, but they usually kept in the immune system, they kept as a memory um you know, by the body to defend the mother's body um from future sensitivity sensitization. Now, if the mother gets pregnant again and during the second pregnancy, um the babies again, Reese is positive that I e um you know, the baby has recess antigens on the red blood cells. Um the mother's anterior society bodies gets triggered and they try to fight it off because um the reasons antigen um is basically their enemy. They try to fight it off and the fighting is done through him all icis. So the antibodies um direct there uh you know, um their fight against the Reese's Antigen by breaking down the red blood cells process called Hamal icis. And that is why it's known as humility, disease of the newborn and breaking down of these red blood cells can cause anemia, severe anemia because the red blood cells are broken down and there's not enough red blood cells for the baby to have any oxygen or nutrients. And this can in turn cause a condition called hydrops, be Dallas where there is severe anemia and that is extremely high output cardiac failure because the heart is unable to compensate for the severe anemia. And this can cause pleural effusion and societies. And this is a very critical condition for the child. So this is just the basic understanding and the reason why this is connected with unconjugated bilirubinemia is, as I mentioned, um you know, um this is hemolysis. So it happens before it reaches the liver. Therefore, these high levels of unconscious hated blade of anemia. The other thing that you need to rule out is sepsis. So, one of the main courses of neonatal sepsis is of course um maternal G B S. So um um maternal group B streptococcus infection. So, sepsis immune, it's quite similar to what you might see in, in adults. The signs of poor feeding, lethargy, tachypnea, hypertension shock if you suspect unit with sepsis. Um you know, of course, do your A B C D E do an urgent sepsis screen. Um do a sepsis six protocol that is give three, take three blood cultures, lactate um urine output um and give three. So give broad spectrum antibiotics. Usually for neonate, you must give it within one hour. Um and you need to give oxygen and fluids. All right. Of course, this is all done by your seniors, but this is something that you need to think about, you need to know about. Um And another course of neonatal sepsis is equal I and UTI as well. Um So, um usually a lumbar puncture can also be performed if you suspect any signs of meningitis. Um So that's, that's a bit of basics of sepsis and D I C. So, these are the two main conditions you need to think about if a baby presents with pathological jaundice within 24 hours. Next slide, please. Ok. So, lastly, we're gonna talk about conjugated bilirubinemia, so high conjugated bilirubin. So this is usually seen as I mentioned, either hepatic cause the posthepatic courses if it is posthepatic courses, um you will be able to see the baby presents with pale stools and dark urine. Um This is what we got for our fourth years last year in our Osti, we had to take a history from a mother who was um you know, who presented with a baby who had prolonged jaundice. Um And um kind of showed us some pale stools and we had to identify, you know, the management plan. Um So the main important differential for prolonged jaundice more than 14 days and bail stools and dark urine is biliary atresia, uh biliary Tricia is a type of condition, whether it's obliteration or discontinuity with the extrahepatic biliary system and usually seen presenting with jaundice extending beyond 14 days. And you will also have the baby presenting with poor appetite and growth. And um and in this case, the total bilirubin might be normal, but there conjugated bilirubin is extremely high. There's an isolated rice and conjugated bilirubin. And that can be one of the features of ability Patricia which you can think about if you see. Um in the question, um again, you know, investigations are quite similar to what you would do for any other type of jaundice. So taking your full blood count, you and a CRP LFTs do a coagulation screen, blood cultures, blood BM, that's glucose lactate and top screen as I talked about before. And you would also do a hepatitis screen as well. Scan. The main scan is ultrasound, scan of the biliary tree and liver and treatment. Again, this is something you kind of need to know. So it's called in layman's terms, it's called Kasai procedure. But Queens could also give you as um Hip Ato Poteau Antrostomy. So you kind of have to know that for your exam. Um Otherwise it's just called Kasai procedure, but most probably they might give you uh the surgical name, not the Lehman name. Um So your next slide, please. All right. So not treating neonatal jaundice. So, the reason why it's important for us to treat um neonatal jaundice is because of the complications associated with it. So, one of the most important complications you need to be aware of is Karnik Tris. So connect this is basically when because that is very high levels of bilirubin in the blood. Um it can um the bilirubin is usually able to uh cross the blood brain barrier and it can directly cause damage the central nervous system. And this can, this can present with unresponsive baby baby in coma, um poor feeding, lethargy, hypotonia. Um And if this is not treated, then this can lead to a permanent damage to the central nervous system in including cerebral policy, learning disability and deafness. So that is why it's very important that if, whether it's physiological, whether it's pathological, it's very important for the baby to be treated for the jaundice to be treated as soon as possible. Um So there are two types, there are two different mechanisms of treating jaundice. Um First of all, phototherapy, so, phototherapy is something that you need to know about and also know how to explain phototherapy in layman terms and basic language when you're speaking to the parent because that is something that they usually like to test as well in your house keys. Um So basically, phototherapy is where as you can see on the picture in, in the, in the right, the baby is kept in an incubator or in a kind of yeah, in an incubator. Um And um um blue light is usually shown on to the baby's skin and this blue light usually converts unconscious gated billy Ruben into isomers that are easily excreted in the, in the urine or in the stools. And therefore it kind of bypasses the conjugation. And it's easy for the bilirubin to be excreted instead of going all the way to the liver and then getting excreted. So, um it's usually, you know, this, this box is called an incubator or a light box. And either you can have a double phototherapy or a single photo therapy depending on the severity. Uh This chart is quite important to know about because they basically any, any child who is being treated for jaundice, their serum bilirubin levels are measured um quite frequently, usually every four hours when they started the treatment. Um and then, um you know, less frequently. Um And for example, in this case, if the baby was 72 hours old that I eat three days old and their serum bilirubin was 300 that means it is, you know, about the phototherapy line and therefore they require phototherapy. So it's kind of a way to assess the severity of the disease, but also to understand whether you need to be giving phototherapy for this baby. Um And also to check for the disease progression as you, you know, uh just write all the uh sorry, I I and you can also identify disease progression um on the chart as well. Sorry. Um So yeah, so that's, that's, that's uh that, so can I uh next, next slide, please? Okay. So um I just have four cases that you know, that we can just discuss basically. Um So the first case is um you are Astrid review on our old unit on the delivery suite. Uh, they were born, we're elective C section. Maternal antenatal history is for gestational diabetes. A he'll break test shows that the baby's blood glucose is 2.2. And what is the next step in management? In this case, I'm kind of going to give the answer, but you can pause. Um So in this case, um because if you think about it, the baby's blood glucose is 2.2, but the baby is not showing any signs of um um any, any signs, any, any symptoms. Um It's usually that we would have to just be observed and you would encourage early feeding. But if the baby showed signs of that means the answer would be e if the baby showed signs of um um jitteriness, any, any poor feeding lethargy, um you know, signs of tachycardia, um uh signs of tuck apnea or any signs of seizures, then they are symptomatic and they then have to be admitted to the ICU. So the answer would be um next please. So case to a six day old baby is met it to the neonatal ICU after having difficulty breathing in the last 24 hours. She was born at 39 weeks, gestation weighing 2 kg with no complications during pregnancy. Her mother had an episode of tonsillitis that resolved spontaneously on examination. There is nasal flaring and the baby is using accessory muscles to breathe. She is tachycardic and tack up, nick and looks fatigued. What is the most important factor that has likely contributed to the development? So this is basically a case of neonatal sepsis. So you can see straight off the bat, the baby is six years old and is admitted to the N I C O N E baby was admitted the in ICU, they must be extremely severe uh in condition. So they have difficulty breathing. The gestation is fine, 39 weeks, that's normal, but they have extremely low birth weight. There. Just 2 kg, her mother had an episode of tonsillitis, trans colitis, not usually caused by group B strep. So um usually group A. So that wouldn't be the reason and on examination that is nasal flaring and the baby is using accessory muscles to breathe. So you already know that this patient, this baby is having respiratory distress and having all um signs of respiratory distress such as nasal flaring and using accessory muscles. They look tachycardic and tuck apneic. So we already know that this patient is in um sepsis. Okay. So what is the most likely contributing factor? The most likely contributing factor would be her birth weight because she no birth weight, as I mentioned before is a very important risk factor for new needle sepsis. Looking at the others, her sex wouldn't be a contributing factor. This type of bacterial infection, as I mentioned, it's not group B strep number of gestations she was delivered at 39. She was not premature. So the answer is her birth weight. Next slide, please. Sorry, that's the wrong answer. It is her birth weight. It's not the it's actually a I forgot to change the answer. Um So the yes, this one is the third case. So a two hour old baby is reviewed for increased work of breathing. Um He was born two hours ago. We are elective C section at 39 weeks. The pregnancy was uncomplicated. Currently, he has respiratory rate of 75 oxygen saturation of 95 there is nasal flaring, visible chest X ray shows hyperinflated lungs and a line of fluid in the horizontal official. So we already know what it is. Um So given the most likely diagnosis, what is the most appropriate management? Um So this is transient accompany of newborn because if you see hyperinflation and line of fluid, you already know it's a wet lung and this patient is born at term. So you're not not a risk of prematurity or respiratory distress syndrome. Um So most likely would be um supportive care. All right, because as I mentioned, it's transient. So it would resolve within 24 to 48 hours. Next slide, please. It's the last case. So the last case, 15 day old baby presents to the E D with his mother. His mother states he has not been feeding or drinking well, for the last two days, she believes he is not gaining much weight and his stools have been more pale than usual on examination. You know, the baby is visibly jaundice and has hepatomegaly, your team conducts a newborn jaundice screen, which is basically just all the bloods and LFT and sepsis screen and doing a full liver screen with one of the differentials being biliary atresia. What finding would support this diagnosis? Would it be age of presentation? I don't think so because, well, it could be 15 day old, but that wouldn't be the most pertinent raised bile acids and A L T that would probably give you a more of hepatic picture, raise level of unconscious hated that would give you a prehepatic picture. This they're trying to, you know, the main differential is biliary atresia. That is the most, more, more that would be more of posthepatic picture. Poor feeding and drinking could be one race level of conjugated, be due to poor feeding and drinking is not specific to biliary atresia. It could be due to anything else. It could even be due to sepsis. It could just be physiological as well, maybe just issues with suckling. But the main, the main differential like, you know, the main uh uh the answer is basically raised level of conjugated grade Ruben because conjugated bilirubin will be high in posthepatic or hepatic jaundice. Uh Biliary, a Tricia's posthepatic jaundice. And as a result because there's an obstruction in the ability tract because of the obliteration of the ability tract. Therefore, these high levels of conjugated bilirubin. So yes. So that's, that's all, that's the end of my presentation. Thank you so much to everyone who watched that. And if you have any questions, um I can share my email address and then you guys can ask me any questions. Um If not, um Thank you so much for watching and all the best for your exams. Thank you. Thank you so much Koepka. So, um that's an event for today and if you have any questions as go pick a mentioned, you can email her or you can send a message on our Instagram uh Facebook page and we'll try to get back as soon as possible. Thank you. And we also will be providing feedback forms for you to fill in. Um But before that, we'll make the recording available to you so that you can receive her feedback and it will be much appreciated if you guys can fill it up. Thank you so much and have a lovely day. Thank you.