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Okay. Good morning, everyone. Um, my name is Caroline Delahanty. We've been working together for several weeks now. I was going to stick with the theme of prematurity and neonatology because I'm getting the impression that people are finding it quite interesting. So this is entitled some common neonatal problems. But I'm going to jump around topics. So let's start with hypoglycemia and low but blood sugar. We're going to talk about why it's important, but I will say it's a very controversial area. But there is evidence out there that low blood sugar can cause brain injury and poor neurodevelopmental outcome in term and preterm babies. And that can very much focus around any aspect of neurodevelopmental outcome to cognitive developmental outcome, etcetera. It can cause reduced consciousness. You can actually go into a hypoglycemic, lethargic coma. You can have apneas, and you can have seizures from low blood sugar so babies can come in fit in if they have a low sugar. The thing is, it's preventable and it's treatable and you reduce harm. And there are simple ways to prevent and treat this, you know, wherever you're working around the globe, do we need to think about normal adaptation to hypoglycemia after birth. So you cut the umbilical cord, the blood glucose, that constant feed from Mom via the presenter falls. So the baby has to respond by producing glucagon. They have a glucagon surge. They have a cat. Cool. Um, Ian Surge. They have a growth hormone surge and a cortisol surge all aimed at driving glucose homeostasis. So you glucagon will drive like the General Isis your liver stores, so you should have glycogen stored in your liver. If you are a mature enough baby, a preterm baby won't have these protective mechanisms, and we'll also have a blunt hormonal response. So Glycogenesis Isis takes place from liver stores producing glucose and lactate. You get gluconeogenesis iss from protein and fat stores, which will produce glucose. And then you get ketogenic Cicis from the breakdown of free fatty acids producing ketones as the alternative fuel which the brain can use. And that's really important. The newborn brain is adapted to use other fuels. All these things will lead to an increase in blood glucose in a well adapted baby increase in ketones and alternative fuels. They will use lactate to a certain extent, lead into adequate energy supply between feeds. Now you'll notice that I've not put a definition of low blood sugar. That's because it's so controversial. And I didn't want to put a definition in. And then you'll work in in an area working under your senior clinicians who are supervising you and say, Well, actually, I accept slightly different definitions. So in an adult, Okay, if you're diabetic, you would say that you were becoming hypoglycemic if you below. If you fall below for so we are adapted to keep our blood sugars above four in a baby. The double The World Health Organization allows 2.5 as the standard World Health Organization definition now that more recently through something called we all call it the Sugar Baby study, which took place in Oh, I'm going to say Australia and New Zealand. I'm just wondering in my head now, whether it's just New Zealand but anyway, that part of the world it took place, and basically what they showed was that we could allow in healthy term infants who were designed to fast because breast milk doesn't really come in until day three. So the human neon aid term healthy with no other factors is designed to use ketone bodies and to go into a prolonged fast in state. So there is now an acceptance in a healthy term, neonate, although you will intervene and ensure that the baby gets some express colostrum or some gluco gel that you accept less than two. But you would encourage a feed. But basically we do not routinely screen all babies for their blood glucose. That practice, which historically has been there, that if they're not feeding well to test their sugar, has now gone away unless they appear clinically unwell or if they have a risk factor. Because there will be babies with sugars of 2.2, which is less than the W H O recommendation of 2.5 who are healthy because we're not measuring their ketones and we're not measuring their lactose and they lactate. Sorry. So you have to look at how is the baby clinically behaving so which babies fail to adapt? Because I've just told you that we are accepting really what the adults would define as hypoglycemia. So we need to think about the preterm baby who has that immature hormonal response at birth. They don't get the, uh, adrenaline surge. The catecholamine surge. They have poor growth hormone levels. They have poor adaptation from the hormonal surge. They also have poor fat stores, and they don't have adequate glycogen in the liver. And they have immature enzyme pathways, and they're also diverting all their energy into the other factors that are causing them problems at birth. So any baby that's premature. Would you worry about the growth restricted babies? Because again, they won't have put down the fat and the glycogen Zara birth weight of less than 2.5 kg. Maternal diabetes Obviously, that baby has been used to a hyper insulin emmick environment. With Mom having high Um, yeah, sorry, the hyperinsulinism Right? So that baby, as a result of mum's high blood sugars, has auto regulated itself to keep itself normal glycemic by lifting its insulin levels of its own pancreatic production. That's going to take a few days to fall. We normally say that takes 72 hours to fall. So in the 1st 72 hours of life, that baby has too much insulin circulating and therefore it's going to make itself hyperglycemic. So maternal diabetes is a big risk factor. The macros. Ah, Mick, babies are always difficult because you're concerned with those really is Are they a mist? Maternal insulin missed maternal gestational diabetes. So that's why we worry about the babies that are greater than 4 kg. Because actually you think Well, if you miss maternal diabetes and therefore has this baby got hyperinsulinism and because it takes us so long to get an insulin level back, we have to assume they have and treat them as an infant of diabetic mum beta blockers. I've always struggled with this one, actually, because a lot of mums with high BP will quite often even get just one or two doses of Labetalol, a beta blocker, to control their BP as they're going into labor. And there's always this debate. Is it labour? That's put the BP up. You know, all the you know, the mom's in pain Or is this that actually you've suddenly got Mom that's got high BP so they are treated unfortunately, which then puts this baby down a pathway of having blood sugar testing and intervention. Because if you test a baby, if I go around and test every single newborn term baby on are Labour Ward. On our personal area, they have blood sugars of 2.21 point nine. But you know, it's they've got ketone bodies and because we don't actually routinely test the ketone bodies. Although sometimes we do, um, you know, they are put down this pathway of their potentially a sick baby with a lack the beta blocker. Basically, what it's doing is blocking the catecholamine response, and therefore they have impaired in adaptation. Now you can argue whether you know, if that Mom got Joseph a Beetle or two hours before delivery has it really affected that features? But anyway, it's a controversial area. The evidence isn't very good out there for it. Um, but it is in all the national and international guidelines and ill babies. Obviously, you have to worry about their ability to adapt big glucose, and we tend to run them normal glycemic. So we said quite a lot of all this premature babies less than 36 weeks have immature hormonal responses to hypoglycemia. They have poured glue, glycogen and fat stores, which predisposes them. Low birth weight are an interesting group. What is the problem again. They've got Paul glycogen and fat stores. Okay, Uh, it's a bit difficult This isn't it, because a baby born in the UK we define less than 2.5 kg is low birth weight. But around the world, you need to take in the fettle weights of your population. If you are a small race, you are going to produce small babies, and less than 2.5 will not be your definition of a low birth weight. So you need to look at the racial predisposition to fetal birth weight they do have. If they're small, they have increased heat loss and energy demands from keeping warm. And all these factors will lead to hyperglycemia. If you allow a baby to get cold because they're having to put their energy, they will use it more energy and keeping warm in running that brown adipose, those brown adipose cells into producing thermal. It's an energy dependent process, so if you're diverting energy away, you have to keep him warm, which is a basic function. You are more likely to make your brain vulnerable with using those ketone bodies, so you have to think about that. The maternal diabetes or the macros. Ah, Mick baby, who is a presumed infant of a diabetic mum. That baby has a high insulin level because Mom has been running with high sugars. Those high sugars been crossing the percenter. That placenta. The foetus responds by allowing it's pancreas to increase insulin production to compensate the high sugars to bring them to normal. And that baby ex utero has to have a time when the pancreas suddenly drops its insulin levels. So insulin prevents glucagon remember growth hormone from being produced. It's an inhibitor and all these factors, so not only does the insulin cause hypoglycemia by being too high, it also inhibits the counter balance that the baby has with the other hormonal mechanisms. Peter blockers, I've said about the fight or flight, hormonal responses to hypoglycemia, poor glycogen and fat store utilization. Because adrenaline and you know your mobilization of glucose to give you energy all leads to hypoglycemia. But I think there is. There's very few case reports. Actually, I have looked at this because I tried to challenge our management on it. There's some work that came out, but they were really babies of moms that had been on beta blockers throughout the pregnancy. So it's the mums that have essential hypertension or develop early pregnancy induced hypertension. It's not. There's not been any studies on women that have only been on beta blockers for, let's say, 1 to 2 weeks or a few days, right at the very end. But the problem is, they're all lumped together babies, right? Basically important. This is a really important group. They have increased metabolic demands, pyrexia work of breathing. They're going to use more energy. They don't feed Well, a sick baby doesn't feed. They've got lethargy. They So it's really difficult, isn't it? Is their lethargy because they're septic, or is there lethargy because they're hypoglycemic, so you have to correct it. Okay, So Anil baby absolutely has to have blood sugar check in regularly as part of their care and intervention. So the aim of screening is to identify at risk babies. We do not advocate screening every baby because you will over diagnose and over intervene and potentially stop breastfeeding being established. You want to support feed in, um, if you're monitoring, we do actually say monitor the blood glucose. If you Pam, by doing true blood glucose measurements as opposed to the stick testing that you're doing diabetes. That is very difficult because it's the true blood glucose that crosses the blood brain barrier and not necessarily the peripheral glucose, and we know that they are slightly different. But your intervene in how we intervene in simple terms that doesn't require resources is that you're going to get the mum to feed. You're going to get her to put the baby on the breast. You're going to express some claustrum, and you're going to stringent that into the baby's mouth if they cannot feed. What's cheap is also gluco gel. So your emergency hypoglycemic glucose gel that you use in people with diabetes that have hippos, that sticky glucose syrup that you put on the inside of the book buccal mucosa, easily absorbed baby doesn't need to swallow it. So put in some glucose gel on the inside of the buccal mucosa is also our so we feed. We give gluco gel if following a feed the blood sugar doesn't come up with, then give glucose gel or if it's so low. If it's say less than two, we would give glucose gel. Obviously, if the baby is sick or it isn't. Or as an infant of a diabetic and not responding. We would give intravenous glucose so they require admission and cancellation. Okay, I'm going to go on now to, as I said, I'm jumping around for the topics. I want to talk about respiratory issues that are not respiratory distress of the newborn. So lots of babies come in being to Hypnic and what you're seeing in the pictures. Or I hope what the pictures are demonstrating is I am seeing some evidence of some intercostal recessions. And then to the right hand side of the screen, I'm seeing a baby that has potentially some sternal recessions. I'm seeing that compliant chest looking as if it's caving in. If this was a dynamic image, a video, I would expect to see some nasal flaring, and I would expect to hear some grunting. The reason babies grunt is they are given themselves CPAP. They're closing their glottic this, and they are expiring, exhaling against a closed glottic. This, which takes pressure so the they're putting pressure back into their lungs by grunting, so they're giving themselves some airway pressure to open up the lungs. Also to drive fluid back into the capillary space. And obviously, in severe respiratory distress or respiratory issues, you're going to have cyanosis. We can't see that with the eye until it drops below about 85% classically like we think we can see 92 but we can't. So a baby is defined as hypoxic. The term baby. You really are looking at less than 95 in a preterm. We accept 92 because of the risk of eye damage. Um, but if they are hypoxic, they probably have SATs of 85 or below. If you see that their blue Sorry, let's talk about transient tachypnea of the newborn, which is the most common cause of respiratory distress. Okay, so it happens very commonly in term and near term babies. The reason that we even worry about babies being born at 35 36 weeks is they are. They may have to come to the neonatal unit because they may develop respiratory distress, transient time near of the newborn and need to be separated from their mother. And remember, your primary ethos is never to separate a baby and mum, if at all possible. So if you're delivered by pre labor Syrian section elective Syrian section. You increase your risk, and that's because the hormonal response of labor drives moving the the wet lungs. Remember, lungs are full of amniotic fluid. They need amniotic fluid to develop. Okay, so if you have prolonged rupture of membranes or rupture your membranes very early, for example, 17, 18 weeks, your lungs are not going to develop. So that baby, even if it goes on to deliver, is likely to die because they have poor al Viola development. So lungs are wet, and one of the processes that happens during labor that we don't fully understand is that the lungs are dried, become drier. The fluid is full pushed back into the capillary bed. So if you don't have labor, you don't do it as well. So you have inadequate clearance of lung fluid, which then makes the lungs stiff. They're less compliant. They're higher pressure because they're not aerated. The blood doesn't necessarily want to flow there as easily because it will take the path of least resistance. And remember, you have that patent foramen ovale. You have that doctors arteriosclerosis, so you have nice channels that may not immediately close for the blood to go through, as opposed to go in through high pressure lungs that haven't recruited Al Viola in and aerated and lowered the pressure. So you're gonna get respiratory distress shortly after birth. This X ray is different to an X ray of a baby with highline membrane disease. What jumps out at me when I'm looking at it? Is this fluid in the fissure? Okay, so that is excess fluid around. It's also very diffuse. Symmetrical changes in a congenital pneumoniae A or a meconium aspiration syndrome. The radiological features will be different. There are X rays coming up, but you can see that it's very diffuse, and I've got fluid in the transverse Fisher. Occasionally, you'll also get some small, uh, plural effusions as well, but they may require support. Some babies can just grunt, and if they're not hypoxic and they're not working too hard and they're able to feed, we'll leave them with their mums, saying, Oh, the granted will probably settle in the next 12 hours. We'll keep coming back to review, but if they're working hard, they can't feed or their hypoxic. They need to come across and they may require. By definition, if they have been admitted to the unit, they're going to need some resporal support. But it may be different where you work, so we would give them supplemental oxygen, put oxygen into the incubator. Some units will use head boxes around the world. They're cheap, They're just like square box. And you need less oxygen because you're only putting the oxygen around the head as opposed to around the whole body and an incubator. Sometimes we will try to give them some continuous positive airway pressure vice something called high flow or via CPAP. They very rarely require advanced respiratory support by intubation and ventilation. And if they do, you may have that diagnosis wrong. I would requestion your diagnosis. By definition, transient tachypnea of the newborn is transient. It's timescale is it should get better by 72 hours. But it camps this cyst sometimes up to five days, particularly for an infant of the diabetic, where you probably got other pathologies going on as well. Insulin, um impedes re absorption of surfactant and regeneration of surfactants, so therefore they get a sort of semi relatives fact in deficiency, which makes them slightly worse What you see in your blood gases is some mild hypoxia and hypercarbia, um, in a baby who is tiring or getting too tired and needing some pressure support, so simply treated will resolve Very. You need to be very reassuring to the family. Uh, OK, respiratory distress. We've talked about this before. The fact in deficiency of premature and occasionally term babies very rarely turn babies unless they're an insulin dependent diabetic mum. Um, signs of respiratory distress appear after birth with an oxygen requirement and the typical chest X ray changes worsens after five days. If you leave it untreated, worsens until five days. Sorry, that should see if untreated. But surfactant production then up regulates itself after Day five, and the severity is reduced, particularly in preterm mom's by giving them antenatal steroids to stimulate lung development and PSA fact int up regulation. Uh, the thing that probably is easier to jump out from the secretary. I don't know how well it's it's coming up, but basically you're not seeing any fluid in that transverse Fisher, right? I don't have a fluid line here. I look as if I've rubbed sand over this film. It's very ground glass People talk about ground as if you find finally ground glass down or finally or scattered sand across it and you should be able to pick up out some air bronch it, grams, come away from the bronch I and I can see my air Bronco grams dividing in the peri hailer region. And that is an air bronchogram, which is said to be one of the classic radiological features. Okay, so I look at this x ray, and it's very different in my baby with a respiratory distress, isn't it? I've got more solid looking, patchy areas. So what I think of here is that I've got infection. Okay, um, if this was a premature baby, equally, I could have put this fraction down the left lung and not gone into the right lung. But that's quite unusual because the right Broncos sits higher than the left, so it's easier to give that fraction replacement into the right lung, not the left. But here what I'm looking at. Let's say this is a term baby. I'm seeing patchy dense, a classification in that right lung throughout it, actually. And then also the left mid zone of the left lung. Um, I think it's affecting both the upper and the lower lobes of the left lung, actually, So I'm thinking Infection So congenital Pneumoniae a. A baby is born with pneumonia. So how did it get it? And what is the bug is what you need to be asking yourself so it can come across the percenter and have been there congenitally and be part of a congenital sepsis. And with that, we often think about cytomegalovirus, the MV We think about syphilis. We think about hysteria. We think about toxoplasmosis, and we may even think about congenital rubella and congenital in utero herpes as well. If there's been a primary herpes infection in Mom with a systemic load, as opposed to, she has herpes simplex and it's a recurrent, and she's likely she only get it Vagina Lee. So that baby is at risk during the vaginal delivery. If she gets primary herpes during the percent during the pregnancy, she is going to have a systemic hit from that. She will feel unwell, and she will allow that herpes to go across the placenta into the baby more commonly, as opposed to a congenital in utero required infection will commonly is secondary to chorioamnionitis and inhalation of infected amniotic fluid. Now Cory are Munitis usually sets up after a mom has ruptured her membranes and has prolonged rupture of membranes. I'm not an obstetrician, so I don't want to talk too much about it. But if the amniotic fluid is infected, that baby, remember, is fetal breathing. That baby breathed in the room not very much, and amniotic fluid is circulating into the baby's lungs. So unfortunately, that infected amniotic fluid is going into the lungs and will cause, um, infection. You can also pick up Group B strep and streptococcus E. Coli purpose simplex virus. If from the birth canal during delivery and give yourself a congenital pneumonia. I think we define congenital ammonia. I'm not 100% sure about this as ammonia appearing in the first five days of life, but don't quote me on that, but it doesn't have to be there on day one. It may be that you don't realize the baby's ill until day three. Early onset Group B strep is to find us less than 72 hours. The other problem that we can have with lungs, This is a picture. It's quite dramatic, actually, isn't it? Of sticky meconium, which is very sticky, very viscous. It's the contents of the fetal gut, and it's actually sterile. There's no bacteria in miconia, particularly if it happens in utero or your meconium that you produced in the 1st 48 hours is actually quite sterile because there's no bacteria there. That baby has to acquire bacteria. And remember, you want baby to acquire lactobacillus in the healthy bacteria from breast milk. So if this is aspirated into the lungs, this causes quite a problem. The meconium Aspiration syndrome. So the reason babies past meconium in utero is a hypoxic response, so they get a catecholamine surge as a result of hypoxia. And the gut responds from that, um, sympathetic response and parasympathetic response, producing the baby to have diarrhea basically, so it's the same as us. If we in fear it may affect our bowel, the flight fight, you know, flights fight, fear response. Um, again, the baby has it in response to hypoxia, and they will aspirated during their fetal breathing, but in particular if they're hypoxic. The baby is very clever, and if a hypoxic infant is born and you see them taking deep, shuttering, breathing, you know they're upper function of their brain has stopped breathing, and they're down into what we call spinal agonal last gasping. But once they get deep agonal gasping, they'll be inhaling more and more so associated with fetal hypoxia. From any reason, um, placental insufficiency called prolapse called compression preeclampsia. Anything. The reason. It's rare in prematurity. And if we see it in prematurity, we often wonder if we've got listeria around. And I don't know why that is, actually, but we think we we jump to light listeria and we change our antibiotics and give up amoxicillin as opposed to rare basic benzyl penicillin. Um, it must. It's rare in prematurity because premature, premature gut doesn't produce a lot meconium in the earliest in the early stages, in prematurity, it doesn't have that that meconium load in their gut, so we don't see it. Okay, I don't know how well this is screening, but it's a very good X ray, actually. So this is meconium aspiration. It's denser, it's fluffy. Er, isn't it? So respiratory distress was very fine. And granola. This is very dense, fluffy sort of meconium showing you that you've got meconium aspiration. You're going to have lots of problems here. Actually, the first problem you're going to have is the airway clear or is the airway blocked by that thick, sticky meconium? And you need to clear the airway. And if you clear the air way, the baby can breathe for itself. So the first thing is clear, the airway of thick, sticky meconium secretions. They can be very difficult to get up. But if you can't what we used to teach, make sure the airways patent and you've set up all the meconium to a stop them aspirating what's in the airway. But actually, now we teach. Only get the airway painted enough for you to be able to get oxygen in. They've aspirated anyway in the room and don't prolong, given them oxygen and given them ventilation support, they have a secondary surfactant deficiency. So they're al viola type one. Surfactant Producing cells do not work as well, and some of that is because their energy deplete there. A t p deplete from the hypoxia. They can have lots of problems with pulmonary hypertension, but this is getting too complicated here, but what you're really dealing with is a chemical as opposed to a bacterial process. You're dealing with a chemical pneumonitis, and you literally just have to support them. Um, the airway disease can be patchy, so sometimes we can have to ventilate them so hard we may give them a pneumothorax and the risk of pneumothorax such quite high as a result of their patchy airway disease and their ventilation perfusion mismatch. So we would intubate and ventilate meconium aspiration syndromes, actually, cause we know they're going to get worse. As the pneumonitis sets up, we give, we try to oxygenate them as well as we can, and we try to reduce the risk of pneumothorax by minimizing the lung trauma and using low pressure if we can. We tend to want to paralyze these babies. They are often big babies. They're not the preterm ones. So we completely anesthetize them as opposed for them to be awake and breathing with us. We tend to sedate them and paralyze them to take away their muscle strength so that we can gently ventilate them because otherwise we're fighting against their intercostal and their sub costal muscles. But these are what we give them surfactant replacement. It's license because we know they have a deficiency. We give them antibiotics for secondary infection. Or was there pre existing sepsis in the room, which caused them to become hypoxic, done well and develop miconia? But it's really full secondary infection, and we have to treat any other conditions that go along it. Any cardiovascular problems from the illness with inotropes any coexisting, hypoxic ischemic encephalopathy. Remember they've often been hypoxic in the room so that hypoxia could have affected the brain, the kidneys. So we have to think in a multi organ fact fashion. What I will say is ECMO, so extracorporeal membrane ISS oxygenation. If you're in an environment where you have access to this, this is actually life saving for these babies because you know meconium aspiration is going to get better. As the chemical pneumonitis, it gets improved so they have functioning lungs. At the end of the day, this is not. This is not leading to lifelong lung damage, so they can be rescued by extra corporal membranous oxygenation. They are the group that may receive ECMO. Let's go on to talk about sexist. Although all these things are slightly linked, aren't they I think. Sorry. These slides are very busy. They're not my slides. Actually, I've borrowed them. Um, So sepsis is when you've got signs of infection in the new born born. And those signs can actually be very nonspecific, right? It can be temperature instability, and it's difficult, isn't it? Because we know babies can get cold, but really, if they get like 36 4, I would accept, particularly if they'd be unwrapped or just had a bath or something like that. But certainly if you're getting anything down into the 35 or less than 36 I would be really worried and even less than in 36 1. I think. Oh, the baby should have dropped that low. I accept. 36 4, 36 3 or anything below that. I think it's getting too low. And it, as it really got a problem with its thermo regulation from sepsis, bradycardias, apneas, apneas. A pauses in breathing, which babies get. But if they're getting apneas, then that's that's wrong. And apnea is defined as a pause in breathing. Believe it or not, for 20 seconds, which sounds in credible, doesn't it? Um, but so they shouldn't have apneas. They should not be pausing their breathing. They're allowed to have shallow breathing and then go fast and have what we call periodic respiration. That is normal, where the baby will have bits when they'll breathe quickly and then they'll go shallow. But if you look at them, they're still breathing. But they're not allowed to stop. Certainly don't let them stop for more than 10 seconds. Although we set our monitors for 20 seconds, Um, particularly in prematurity. Poor tone. If you think they're floppy, they're not an active baby when you wake them. Um, obviously, if you've had a baby on a ventilator and it gets worse than you think, Oh, it's got it's now developing ventilator acquired pneumonia. It's development, sepsis, feed, intolerance or early jaundice. So the man I'm going to skip your blood test, but you may see an elevated C reactive protein C. I said. I'm going to skip it and then I go into it. You're going to look at your white blood cell count and your platelet count, and you're going to look at your sugar control. Management of infection is always supportive. And antibiotics, I appreciate times going on but we started late, so I'm going to carry on for a couple more minutes. So congenital infections. We're all living in world where actually we're probably seeing more congenital infection. We're certainly seeing more syphilis in the UK Um, so a congenital infection is when infection is spread by the blood across the placenta. So it includes congenital as CNV can Jen Mind's gone blank cytomegalovirus, toxoplasmosis, syphilis, rib, ella, varicella, chickenpox and listeria. That's why you recommend Mom's don't eat unpasteurized milk or raw eggs. Okay, it's because the risk of listeria can. Genital infections can obviously cause miscarriage, stillbirth, premature delivery If you get it in the first trimester, that's where you're going to get the real foetal teratogenesis harm. But appearances at birth can be striking and pathognomonic. Sometimes you can diagnose what infection it is from the appearance of birth. Okay, I'm not making this very interactive, but this is what we call. So this baby basically has low platelets, doesn't it? You're seeing ecchymosis ease across the baby. We call it a blueberry muffin rash. So you're seeing a lot of bruising telling you the baby's thrombocytopenia make If I felt this babies, this baby's ventilated right. There's an itchy tube through the mouth, so this baby must have a congenital pneumonia as well from that CNV. But also, if I feel the abdomen, I'm going to feel an enlarged spleen and an enlarged liver that I've tried to respond to the the Thrombocytopenia and also, but they may actually be consuming platelets as well, but they've tried to increase platelet production, so and you'll also have a hepatitis that you see on blood tests. What's showing you here is a cataract okay, that we have a white. We have a white lens, so that's classically, although it can be with any of them. The classic one is rib ella, and often you'll find that you've got a small I. The baby is small, its growth retarded, and it will have a cardiac lesion. They often have pulmonary stenosis, and they go on to have learning difficulties, actually, or just expect rem disorder and attention deficit hyperactivity disorder. So but remember, it can be eradicated if you vaccinate your mom's. So there are vaccination immunization programs to give everyone a measles mumps rubella vaccine at birth. Some countries may be given all teenage Children a rebel a vaccination. But there are vaccination programs that can prevent this. If we identify a rebel. A nonimmune mum when she comes to us presenting with her pregnancy and she has her bloods tested past that testing is rubella status after delivery. We can't vaccinate her during delivery, so it must be a live vaccine is what that's telling me. After delivery, we actually give her rib Ella to stop her being susceptible in future pregnancies. I'm gonna talk early onset sepsis. Then I'll close after early onset sepsis because it's very important, so preventing within 72 hours of birth. It's classically a group B streptococcus if we could vaccinate and there are vaccination trials in progress. But there's been vaccination trials in progress for all of my career. Um, but I think we're almost there that the Polyvalent Group B streptococcus vaccine is now in clinical trials. Okay, so if we can prevent Group B strep, we will save many lives of babies around the world. Okay, so, unfortunately, we a third of women carry Group B streptococcus in their vaginal canal as normal flora, it only causes invasive infection in the newborn period. So you know one in three babies come down a group B streptococcus environment. We don't know why some of these babies actually get infection and others don't. Why, Why the majority of the neonatal population protected we? We don't know what makes it become invasive. Um, but when it becomes invasive, it's it kills, and it kills very quickly. It's so frightening. Um, because the baby just dies within hours of you. Um, so other organisms include E. Coli s carry rich E. Coli. I probably can't say that properly. And what what you can do is be vigilant for signs of infection or if a mom has risk factors, you can think about giving them intrapartum antibiotics, but then or dull it when the baby is born. If there's been risk factors, give them antibiotics. But you will treat thousands of babies to find the one that was going to go on. So now there are various neonatal risk calculators because otherwise it's a huge resource. So a lot of people have now introduced a risk calculator where you do a calculation on, and that baby is a risk of having early onset sepsis in a baby who otherwise appears well if they appear unwell, and that can be subtle signs such as poor feeding, temperature instability, you treat okay, and then you stopped antibiotics at 36 hours. Once you've got your proved that your cultures are negative and the baby hasn't progressed in, it's clinical. Symptomatology Later onset is common after 72 hours of age. It's more common, premature or low weight babies and is usually caused by what we call nasal cold meal transmission associated with Indwelling catheters, ventilation and I've listed the bugs. I'm probably gonna stop there for questions, actually, so I'm going to stop share ing and come back any questions?