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Attles. I'm at ST George's. Uh so we'll get cracking. And so our lecture is going to be on Endocrine, um M S K and we're both editors on the Pediatric guide for this year as well. So just let me know if you can't see the slides moving. Our lecture slides are designed so that they can be printed out or scribbled on for you when you're basically cramming. So they will look really intimidating, but it's just make sure that all that knowledge is there that you need to have for your cases and your Retton's um importantly, try not to focus on absolutely absorbing everything on the slides, but just listening to what we say and hopefully that will be um what you take away and then you can build on that knowledge when um when you're revising by going through the sides in your own time has the slideshow. Just I'm just going to share the slides again. I'm sure what happened there and really important throughout this. If there's anything that you want to ask, um, just pop it in the chat and we'll, we'll go through that together. Okay. So first question is, um something I want you to write in the chat. What which of these options confirms the diagnosis of diabetes? So A is polar urea and random plasma glucose of 10.1 fast, fasting plasma glucose of 7.9 and two hour postprandial plasma glucose of 11.1 or fatigue. And HBA one C of 49 just type in the chat. Which one of the options A B or C is right? And we'll go through that if you're not sure, give it a guess. And then we can go through anyway. We got A B B good. Well done. Okay. Yeah. So the correct option is b okay. So the first topic we're covering is type one diabetes in pediatrics. It's actually the commonest type of diabetes in P S, which is kind of the opposite of what we see in adults. And, um, there is an increasing in incidents, but we think a large part of this is obviously because we're, um, living longer with some of the more chronic diseases, for instance, cystic fibrosis and the sequela to these diseases can be diabetes. Um, and then in terms of the symptoms, there's the classic triad of polyuria, polydipsia and weight loss. Um, there are also signs of DKA, which some patient's may present with. And that's kind of the thing that we don't want patient's to have because then they've probably have had undiagnosed type one diabetes for some time and come in quite uh decompensated as well. So in terms of diagnosis, most, most of the time patient's will uh just need uh often present symptomatically uh in pediatrics. So usually you'll have a symptom plus. Uh so one of the triad symptoms plus any of the following. So either your random plasma glucose or your two hour plasma glucose being more than 11.1 or a fasting plasma glucose or more than seven. Uh Generally speaking, in pediatrics, we don't use an HBO one C as part of diagnosis, but you can use it as part of your management or follow up for a patient. And in terms of especially for your paces stations, if it's a G P setting, then one of the most important things you need to say is that your patient is going to be referred to the same day, multidisciplinary team. So a specialist assessment basically at the hospital which may require admission. So the main reasons why is because your patient's are untreated type one diabetics, really high risk of becoming unwell, particularly at high risk of going to DKA. Um So they need very intense and close monitoring for the first few days and weeks following treatment from a psychological perspective, as well as from uh ensuring that the BMS are adequately controlled as part of that blood glucose monitoring at least five times a day. But in early disease, they may be doing it several even more often than that. So you get a good idea of what their control is like. The a relatively new thing although has been around for a little bit longer now is continuous glucose monitoring. So sometimes that's referred to from the brand name as the freestyle Libra. So it's something that patient's can wear on their arms or legs. Uh and it will continuously measure their glucose levels and they can read it out on an app. Um so increasingly used, But in terms of, for the NHS, uh the criteria include frequent and severe hypoglycemias, uh impaired hypoglycemic awareness and then barriers, recognizing or inability to communicate. So that's particularly in, for example, patient's who have other core mobilities or um have cognitive impairments. Uh So they're not able to communicate when they are having hypoglycemic symptoms. Then if you look in the bottom left of the slide, there are just the glucose targets that you should be aiming for as well. And then if they're not meeting those targets, then will be discussed with the endocrine team about how to tweak their um insulin regime. So, from what we've just spoken about, what are the symptoms and presenting complaints of type one diabetes. Just right at your ideas into the group chat. That's excellent. Yeah. So that is the classic triad, for sure. Lovely. Ok. All right. So the second part that we're going to be covering is the overall management of type one diabetes. Uh One thing that we want to stress is that having a diagnosis of diabetes, be that type one, type two is, is a massive lifelong and life changing diagnosis. So we um know that it's very common and increasingly common to have diabetes, but they're also any implications as a child. So we'll talk about the monitoring and the annual screenings required, but also in terms of being an adult, um life insurance costs and things like that to bear in mind. So when we make a diagnosis of diabetes, it's got to be one that we're absolutely confident we've made correctly and one that we have categorized correctly as type one and type two, we'll discuss how to do that further as well. Okay. So in terms of the overall management, education for pediatrics is key and this is a station which I could see very likely coming up as a paces station. So, um new newly diagnosed pediatric diabetes counseling, the parents about this and the need for same day admission as we've discussed already. And um educating on insulin therapy, how to administer how to test your blood glucose levels and actually also stressing the lifestyle implications as well. So the fact that um any child with diabetes, no matter how well controlled will have an increased risk of micro and macrovascular complications um compared to the average um child without diabetes. So thinking about carb counting and healthy eating is key, making sure that they have secondary care follow up. So at least four clinic appointments in the outpatient pediatric and a crime department um a year and also uh HBA one C each time they have that as well. So as we've mentioned earlier, HBA one C can only really be used for monitor in these cases, not for diagnosis. Um It's important that they're aware of the ophthalmological consequences of poorly controlled diabetes. So they should have retinopathy screening um as well as nephropathy and BP monitoring. From the age of 12 onwards, they should have thyroid disease screening as well. That's opportunistically as well as that diagnosis. And annually thereafter, they should have screening for autoimmune conditions as well. So because type one diabetes is an autoimmune condition, they often come in a constellation of other autoimmune problems like celiac disease, vitiligo and Addison's as well. And these are things that we really shouldn't be missing, especially in a child. Um And lastly also diabetic foot checks as well. Sometimes parents can become very confused because we're starting a child on insulin. And actually the blood glucose control is very good initially and that can sometimes reflect a honeymoon period. So that means that the pancreas is squeezing out, it's last bits of insulin that is able to make before it's fully destroyed through the autoimmune process. And in that time, they, their insulin requirement can be actually quite low, but inevitably that's going to increase. Um And then in terms of the insulin therapy, it's really not having to focus too much on the exact types of insulin. But just understanding that the first line is have multiple daily injections. So that's a basal bolus regimen. Um usually that involves having uh an intermediate slash a long acting insulin analog. Um And then on top of that, having the short or rapid acting insulin and uh analogs. And that is before a meal. Importantly, rather than after a meal. If patient's aren't getting along with that, there are other options as well like the mixed regimes, um as well as carb counting to, to consider and we've talked about insulin pumps to already. So I'm going to briefly talk through hypoglycemia. So it's generally as a consequence of treatment rather than inherent to the disease process itself. So we usually diagnose hypoglycemia is anything less than four millimoles. Uh um And usually people will get uh symptoms associated with it. Broadly. The symptoms are either uh neurogenic in nature. So the hypothalamus to text that you have hypoglycemia and then you get a significant sympathetic response from the body because of it. So that's going to give you sweating, clamminess, tachycardia, you're going to feel unwell essentially. And then you have your neuro hypoglycemic symptoms as well because unlike most other parts of the body, the brain basically relies on glucose. You can't use fat, for example, uh as part of his metabolism. So when you have low glucose levels, the brain basically doesn't get enough energy. So then you'll get personality change, slurred speech and when it becomes really severe, then you're going to develop coma and potentially death. Um In terms of your cutoff's, generally speaking, the diagnosis of a severe hypoglycemic episode doesn't have a value associated with it. And nowadays, usually they say any hypoglycemic episode that required third party assistance to resolve. Um So for example, if it's a kid, if they needed parents or they needed to call an ambulance because the kid became drowsy, that be considered if that uh third party assistance and therefore a severe hypoglycemic episode. In terms of treatment, generally speaking, in the community, you can give any oral, oral, short acting uh carbohydrate or glucose. So that could be um just having some food to use or snap a snack with the kid. And when it's the hypoglycemic episode is detected after 15 minutes, you need to repeat the blood glucose levels and ensure they've come above four. If they haven't, then you need to repeat your loading of your short acting carbohydrate. And you keep doing that until you're uh you're successfully treated. Once you've successfully treated the kid, then you need to give them a long acting carbohydrate. That can be anything like a sandwich, for example, that has a long acting carbonate. Um Sometimes people will be given Iron Glucagon teas in the community as well. So that's particularly useful for people who have previously had needed third party assistance. So it can be administered by somebody else. Um And then in a hospital setting, uh you can give intravenous dextrose instead. So either 10% or 20% extras. And because it's pediatrics will be as per weights of five mils per kilo. Um And nowadays, we don't use 50% extras because of uh it's higher risk. So we usually stick to only 10 and 20% in terms of your sick day rules because people can become either hyper or hypoglycemic when they're unwell. So you want to be taking your keto, your blood glucose levels every two hours and ketone testing if they're hypoglycemic or if they're particularly unwell, they should have sick day rules, agreed with endocrine or pediatric diabetic team. But generally speaking, you increase your insulin by between 10 to 20% and if they're very unwell or they're having ketones, uh persistent ketones, then they should be sent to hospital because they're either already in DKA or a really high risk of going into DKA secondary to an infection. Right. Really? Next question, what is the treatment of choice in a patient admitted in hospital with A B M of two energy CS of eight, right. Your thoughts in the chat. Yeah. Very good. Very good. So A G C s of eight, there's a pneumonic G C s of eight intubate. So that's somebody with a low G C s and um hypo as well. So that could potentially be the cause of the um the low consciousness levels anyway. And as we've said already, we really should avoid 50% dextrose. It's incredibly Vaizey irritant and has a high risk complications. Um And I am Glucagon is ideally not the first line. Okay. So the next slide looks really, really daunting. Um but when we break down the uh main management for D K A, it's um it's just a few fundamental principles and these are the things that the examiners will be looking for both in the writtens and the paces stations to make sure that you understand. So the first part is to do with actually the um the main, the diagnosis of DKA. So being confident about that. So in terms of diagnosis, it's really just in the name. So they should be diabetics or hypoglycemic. So BM of more than 11, they should be ketotic. So that can either be capillary, ketone of more than three or ketonuria of more than two and then your acidosis. So page of less than sell 0.3, but I always keep an eye out on the bicarb as well because you can diagnose it purely off a low bicarb as well. So if the bicarb is less than 15, so even if your PH is slightly more than 7.3, you can make the diagnosis purely off the bicarb. That's mainly because they may be slightly compensating and therefore the um P H maybe slightly higher and then you can use your Ph or bicarb. So the level of acidosis will give you the severity of the D K. Yeah. And in terms of the management. So if this does come up as an acute station, uh the keywords to make sure that you have put in from the get go our that diabetic ketoacidosis has um uh significant risk of um complications both through the management as well as from the disease process itself. So it must be managed in a high dependency unit, especially in pediatrics where there's 1 to 1 nursing available. Um fluid through therapy is the mainstay of the management. So it never rushed to give incident immediately. Then the first part is basically looking at um the total fluid requirement that split up into the fluid deficit and the fluid maintenance, the deficit, you will basically be able to um assess um in terms of clinical status. So, do they look very, very dry mucous membrane? Do they have hypertension tachycardia um as well? And based off of that, you can calculate whether it's 5% or likely 10% dehydration and you want to replace that over two days total. Um Then in terms of fluid maintenance, this is something you just will have to wrote, learn it's um weight dependent. So you have to have in pediatrics, a very accurate weight as well. Um And then based off of the 1st 10 kg that it's 100 mils per kilogram. Then for the next it'll be 50 mils per kilogram and every kilogram after that, it should be 20 mils per kilogram of fluid replaced um any bolus fluids that you have to give, do not count in the total. So that's for resuscitation purposes and we don't count that in the overall fluid required. Um So you'd have to replace on top of that at some point. So when the glucose level switches to less than 14, you need to um switch to 5% glucose uh rather than the normal saline because they are more likely to then switch into a hypo. Um And in terms of insulin therapy, so once you've done all the fluid management, you can then talk about IV insulin. You must always stress that the long acting insulin that the patient is on must be continued. You must discontinue any insulin pumps that they're on or any short acting insulin they have. Um and then the infusion rate of the insulin is not point not five to not 50.1 units per kilogram per hour. All right. So these are some values that you do have to wrote, learn and you have to make sure you know them very well as well. You then have to look at what the potential trigger of the D K is. So when a patient who has an established diagnosis of type one diabetes, already, some of the common things in pediatrics will be a sepsis that we've just not found the source of yet um chess infection, a dental infection. But in a newly diagnosed patient, then this may be the first presentation of their type one diabetes. Absolutely. And just remember, for example, if it's a subsystem, you need to make sure you're treating the sepsis alongside the D K. So you would advise on flu additional fluids and antibiotics as well. And then just add in terms of your fluid therapy as well. Just remember your additional potassium as well. So all but basically all patient's in DKA will have total body potassium, that's low. So even if it appears normal, you will always give, it's one of the only situations where you will always give additional potassium. Um even if it's normal and if it's raised, you'll just hold it. If the whole body uh serum potassium is low, then you might need to discuss with the senior and consider giving it a fast rate, for example, through a central line. Um And then in terms of how we monitor in DKA, given that they're very unwell. We're doing 1 to 1 nursing on these patient's, they should be managed in our high high dependency settings so that they can have uh really close monitoring. So that monitoring is in several ways. So firstly, their basic ob so heart rate, BP, temperature respirator it, we want to know what that fluid balance is. So we want to know uh we already know how much fluid we're giving. But we want to know uh basically how much urine they're passing. So we have a good idea of the output. So we know whether we're replacing uh effectively replacing fluids well, or if they're still running a significant deficit, we then want to check the D K parameters. We want to check the B M ketosis and acidosis and we want to make sure that those are resolving appropriately. The G C S is really important mainly because it can be as a direct consequence of DKA itself. As you can start having a low key CS, mainly secondary to acidosis. But you can also develop a cerebral edema because there are lots of fluid shifts that are occurring. And in the brain, um some of those fluid shifts may lead to cerebral edema and as a consequence of treatment as a consequence of correcting the D K. Um So you need to keep a close eye out for that, particularly in kids who are very young or if they're severe DKA. Um again, continuous E C G monitoring mainly because of your electrolyte abnormalities. So, um you're uh high risk of developing already having electrolyte abnormalities. Um So your continuous E C T monitoring is really important. And then once you're happy that they, they're more stable, then you might move to four hourly monitoring um after two hours. But you need to be confident that their parameters are moved in the right direction. And if not then that's the point at which you would seek further help and get the specialist in the chronology team involved. All right. So our next question is name some complications of diabetic ketoacidosis. Good. Yeah. Coma three board ocma, especially in pediatrics. Um And the challenge in pizza is that they often cannot communicate that well and sometimes their parameters will not reflect that they are also in cerebral edema. So if clinically there is something unusual going on. So personality changes, they're complaining of a headache, suddenly their G C S drops and these are all signs that you need to urgently urgently be seeking for extra, extra support. Lovely hypochelemia. Exactly. Okay. So moving on to type two diabetes now, um so in terms of type two diabetes, it's uh it's increasingly common mainly because of increasing obesity and pediatrics, but still by far less common than type one diabetes. And generally speaking, your risk factors are obesity is a massive one um than family history. So as, as we know uh type two diabetes more so in adults. But the Concord, the family concordance in type two diabetes is stronger than in type one diabetes. So there's a family history of type two diabetes significantly increases your risk of having diabetes yourself, ethnicities. So particularly if you're from uh South Asian or Asian or Afro Caribbean backgrounds, increases your risk for a given B M I. And after puberty again, once you're post puberty, you're more like an adult more likely to then develop type two diabetes. Yeah. And you'll notice that there's a significant overlap in the overall management of type two as well as type one diabetes. So I'm not going to repeat some of these. But the main stresses are that, um, type two diabetics are at an increased risk of developing other metabolic syndromes. And we have to opportunistically as well, routinely screen for these conditions that includes, um dyslipidemia. So, hypercholesterolemia, in particular, um Polycystic Ovarian syndrome, nonalcoholic fatty liver disease, as well as obstructive sleep apnea. So these are things that when they come in for their routine screening be that if foot check on retinopathy nephropathy, we really should be screening for these two at the same time. And the last thing is that um they do have an ongoing health conditions. So they are considered in the immunocompromised categories so that they would be able to get a flu vaccine and pneumococcal vaccine as well. And just to uh discuss about the diagram, the right hand side, I won't go through all of it. Um uh Just recommend going through in your own time. Essentially, it just highlights the fact that diagnosis and uh obese adolescent can be challenging when you're trying to confirm the diagnosis of diabetes. Because even if you feel type two diabetes is more, is more likely given their obesity. Type one diabetes should still be strongly with your differential just because it's far more prevalent within the pediatric community. So it just works through uh an algorithm uh in terms of how you would go about investigating and treating these patient's. All right. And the next question is what screening or monitoring does the management of type two diabetes involve? And actually also type one diabetes too? Perfect. Yeah. Monitor for micro and macro vascular complications. So that's overlap lapping for both type one and type two. And could you just expand a little bit more on what that screening would look for for your micro micro vascular complications? Yeah, I test for sure. Retinopathy screening. Yeah, use the knees for nephropathy. You also do urine a cr which is the albumin creatinine ratio. So you're checking for protein leak um secondary to their nephropathy. If that's present, then you quantify how much. Um and you then think about other medications. So things like a sin him bitters to try and help with that. Um If that's still not helping them renal referral BP monitoring. Perfect. Yep. And the other ones we've covered now, autoimmune screening for type one diabetes. Um and then metabolic syndromes that overlap with the diabetes as well for type two in particular. Next question is which of these are auto antibodies associated with type one diabetes. This will also be on that table that vivian's gone through as well for you to have a look at in your own time. A perfect. Yeah. The other two. So B is for rheumatoid arthritis. C is first surgeons. So, um, there are other ones that you just need to be aware of because they're common. Um, MCQ kind of star things. That's anti God, anti, anti I A to A, an anti I A as well. So, well, the next topic we'll move onto is precocious puberty before we move on. Any questions about diabetes at all. Perhaps if you have a thought of any, then just write it in the group chat. Perfect. So, precocious puberty is essentially when you go into puberty is developing sexual characteristics before um you should. So for boys, that's less than the age of eight and or sorry for girls, less than the age of eight, for boys, less than the age of nine. And you can broadly split it up into either organ, add a trophy independent or you could add a trophy, an independent precocious puberty. So gonadotroph independent is when uh at the level of the hypothalamus and pituitary, you're producing your gonadotroph things to stimulate puberty early. So that can be idiopathic is by far the most common cause. So essentially, there's no obvious cause found its primary, the body is just put you into puberty earlier. Um And then other than that, the main other causes are essentially all intercranial causes. Uh it could be secondary to a tumor or it could be due to a head injury. For example, in terms of treatment, generally want to start early, these kids will initially have very accelerated growth because they've gone into puberty early. But if they're uh plates fuse early, then they will ultimately often have stunted growth. So, uh if there is an underlying cause like a brain tumor, where possible, you will treat the underlying cause. Uh and then alongside that, you will give GNRH agonist. So they suppress your uh hypothalamus, pituitary gonadotroph in access and then get on top of that, you will then give th therapy. So that's growth hormone therapy. Uh The main reason being that uh if you completely suppress the access, then the told will have overall stunted growth. Still see or th therapy will just ensure that they have appropriate growth. And then you're gonna auditory of an independent precocious puberty is uh where you're not producing your gonadotroph inns at the level of the pituitary hypothalamus. But usually at the level of your gonads, for example, you're already producing sex hormones. Um So uh two bigger uh examples of acute Albright and uh congenital adrenal hyperplasia, which will go into bit more detail. But beyond those, the big other causes, essentially tumor's uh secure eating sex hormones or exogenous hormones. For example, of kids are uh taking them like contraceptive pill or testosterone gels. Uh And then in terms of treating the cause, uh if you can treat the cause, essentially, for example, if it's a tumor, again, treating the tumor either medically or surgically and if it's an exogenous hormones then to discontinue. Yeah. And the main investigations are looking at the actually at the bone age of the patient. Um and that will be usually through an X ray and then commonly the risk as well of the X ray and then looking at the hormone levels. So that's looking at the gonadotroph inns to decipher whether it's independent or dependent STV in's gone through looking at the testosterone and estrogen levels and central imaging MRI or CT brains. And obviously in pediatrics, you have to really be able to justify why a child is undergoing a CT brain because of the radiation associated with that. Um You can also think about doing hormone tests like this 17 hydroxy progesterone. That will tell you a bit more information about whether there's an enzyme deficiency I've included on the top right side, the pathway, which probably we've, we've covered some time in second year of med school, but it's just to be aware of the specific hormones. Um in congenital adrenal hyperplasia that can be deficient and this can lead to um an increase in testosterone and virilization. Um congenital adrenal hyperplasia is something which imperial focuses on quite a lot. It's actually very rare, but it's one thing that you must be aware of. Um it's a spectrum of um of severity depending on the enzyme that's actually defective. And commonly it will be the 21 hydroxylase or 11 be to hydroxylase that's deficient in females, this leads to virilization because you've got an increase in the funneling of the testosterone being produced. And in males, this can lead to precocious puberty um as well as actually salt losing crises as well. Um The main treatment is very overlapping with, um what did Ian's talked about already already in terms of treatment for test a toxic osis in females because they will, in a person who's born biologically female, they will still have a uterus and ovaries, which is why the general advice is to ensure that they're reared as a female and that they undergo um constructive surgery to basically remove the serialized genitals. Um Then there may be a need to also replace um corticosteroids, mineralocorticoid as well as the glucocorticoids as well. Um And then for the, for addressing the precocious puberty side of things, you can use G N R H agonists and growth hormone analog Z as well. Mccune Albright syndrome is a classic triad of precocious puberty as well as cafe ole spots and fibrous bone dysplasia. It's really just something where in an M C Q you need to recognize that those three have come together and you've got your diagnosis. Um apart from the kind of treatment for test a toxic osis, we've already covered, um you can use ketoconazole as well, which um classically is an antifungal, but it inhibit, it's Sarah Delia genesis as well. Um You can also use aromatase inhibitors like let result and anti androgens as well. Um So, spironolactone is uh potassium sparing diuretic but it has anti androgenic effects as well, which can be very useful. Okay. What enzyme deficiency causes congenital adrenal hyperplasia? Yeah, perfect. So this question is really just to highlight that, that's one of the enzyme enzymatic deficiencies that can lead to the condition. But there are lots of other ones as well be is to do with vitamin D activation activation and sees to do with um cholesterol synthesis. So next thing we'll talk about is delayed puberty. So it's the opposite of precocious puberty. So, in boys, the cut off is the age of 14 and in girls at the age of 13. So by far, the most common cause is constitutional delay. Um One thing that will help with that is your family history. So if either the mother or father also went into puberty late, then that's more indicative that that's what's happening for the child as well. And uh if that's not the cause, then um the main way to categorize it is your hypogonadotropic hypogonadism. So at the level of the hypothalamus pituitary, you're not producing your gonadotroph inns to stimulate puberty. Um so that can be secondary to chronic diseases. So things like celiac disease, these kind of things uh and then your hope of the llama pituitary diseases of common syndrome. So that's where you also get associated lack of smell because it's to do with the way that your nerves have not traveled appropriately during development. And then as well, your intercranial tumor's as well. You can also get at the level of the gonads. So you're hypogonadotropic hypogonadism is essentially your sex, women's. Uh your gonadotropin is being produced at the level of the pituitary, but your gonads are not responding uh for whatever reason. So that could be used to gonadal damage itself. It could also be due to Turner Syndrome, which we'll discuss a little bit more. But you end up with kind of ovarian dis genesis. So the ovaries themselves just don't functions that are not able to react to the presence of gonadotroph and, and then your steroid hormone and some deficiency means you can't convert your, um basically your uh cholesterol and your steroids into your um gonadotroph in all your sex hormones. So in boys, you can uh do pubertal staging. So things like examining the testes and using your orchid a meters to see whether the testes are small or large. Um And that will tell you whether they've gone into puberty or not. And then in girls karyotyping, the main thing we're looking for is Turner's Syndrome. And then your thyroid and sex hormone levels are basically looking for is only thyroid disease as well as part of your workups. The Turners um Friedman wise for the vast majority of people. It's just reassurance of reassuring the child as well as the parents. Um and then uh for if there is any underlying disease process like celiacs or iron deficiency, then treating that and then closely monitoring the child to see how they respond for boys. You can sometimes give uh oxandrolone or I am testosterone. So, testosterone is mainly in terms of your secondary sex characteristics. And then in girls, you can give again, you can give Eastern tile instead. Yeah, and moving on to short stature. So classically, that's a height of less than the second center aisle. So really quite short and the main differentials that you need to be aware of if this does come up as paces counseling station um is familial causes. So both parents might be very short and I think it has actually been the case before they've asked you to calculate the mid parental height. So there is a formula which we will try to attach in the size when it comes out, but just make sure that you've memorized that so that you're confident in how to do do that. Um Constitutional delay again as um similar to delayed puberty um just that they might not be um at the level that their peers are at school and that can be a massive self confidence thing, but that they will eventually, you know, catch up with them. And it's largely to do with reassurance. Again, there's um two main subcategories for short stature, which um includes dysmorphic and non dysmorphic. Dysmorphic is then split into proportionate or disproportionate short stature and proportionate, looks at more chromosome or abnormalities. So that's the like downs new nan's um degeorge Turner's as well on the bottom, right, you can see a picture of uh some of the key clinical size to look out for for Turner syndrome. The main ones I want you to be aware of our the neck webbing, cubitus valgus, which is the wide carrying angle as well as the cardiac conditions. So, bicuspid aortic valve and cooptation of the aorta as well. Um It's associated with hypothyroidism as well as ovarian dis genesis, which can translate to total infertility, infertility um in adulthood. So, disproportionate, um dysmorphic, short stature includes things like rickets. So vitamin D deficiency, skeletal dysplasia is as well as spinal problems. Then there's non dysmorphic. So that's increased weight to height ratio and that's usually endocrine causes. So problems with low thyroid function or growth hormone efficiency or cushing syndrome. Whereas the normal slash decreased weight to height ratios are things where the child has been malnourished in some way. So that can be poor absorption from celiac disease or inflammatory bowel disease or it can be due to just generally being malnourished, not having enough of um the food that they need and eating disorders as well. And then in terms of your investigations for short stature, again, bone age can be quite helpful for x rays of the wrist. Um One reason it can be helpful because it can be reassuring for example, if, if a kid is in constitutional delay and they haven't gone into puberty yet, the bone age will be younger compared to the chronological age. So you can use that to explain to the parents that, um, the child's actually has significant growth potential yet left. They haven't gone through puberty yet. They just need to close monitoring and we can review how things go and then the rest of your investigations. So you're looking IDF one G H stimulation is looking at your growth hormone thyroid function tests and then you're looking for any other um causes. So in terms of your chronic illnesses, things like celiac screening as well. Um karyotyping. So looking at your Turner syndrome, um and then any other causes, uh you might need to look at including neuro imaging to look for any hypothalamic or pituitary disease. So next question, what are some signs and symptoms of Turner syndrome? This is something that I think comes up almost every single year as an M C Q of some sort. It's much harder to include as a Paces station, I think, but I never say never in imperial. Yeah. Web net, short stature, cubitus, valgus, cardiac problems. Perfect. Exactly. There's things like lymphedema which are actually quite rare. Um as presenting complaints. It's more in the neonate when they're just born. They might have swelling of the hands and feet. Yeah. Wider space. Nipples, done a puberty. Great. Ok. Moving on now. So hypothyroidism. So, in pediatrics, it's either congenital or juvenile hypothyroidism. So, in terms of your congenital causes is generally malformation or the thyroid in some form or other. So, either maldescent or this more for genesis, um less so in the UK, but in the developing, well, your I D deficiency can also be a cause and uh you can also have TSH deficiency. So that's the secondary course. So at the level of the pituitary hypothalamus again, uh so things like tumor's can cause that. Uh and then your juvenile hypothyroidism is a little bit more like your adult hypothyroidism. So, it's an autoimmune hyper uh thyroidism instead, in terms of your presentation, your congenital hypothyroidism in the UK is generally picked up asymptomatically because it's part of your guthrie tested a heel protester or near natured have within 72 hours of birth. But if it's not picked up, for example, or if they were born abroad, generally speaking, they'll have failure to thrive through and develop they'll have learning difficulties. So, if I'm treated, they would go on to have a low IQ uh back in the previously, it was referred to as cretinism because there'd be uh they would have failure to thrive. So it'd be sure not meeting the developmental milestones. Um And they would have a low IQ then in terms of your juvenile hyperthyroidism broadly, uh do you have delayed puberty? Uh But beyond that, very similar to what you again, adults or constipation called peripheral ease, weight gain, these kinds of issues. Tens of investigations. Uh, it's, as you would expect thyroid function tests, anti TPO. So, looking for any autoantibodies to thyroid peroxide's, uh, and then your paternity home on profile, you would only really do if you're suspecting a secondary cause. Sometimes that may be from your TFTs where you might suspect that. So if you have a low thyroid, a low thyroxin, but a low TSH level that would again be suspicious. And you'd want to go on to do further uh pituitary hormone profile to see if it's a pan hyperpituitarism or if it's a more isolated issue. And then as in adults, you just replace what's missing. So you give thyroxin, this is the last topic we will cover before we have a bit of a break unless people are keen to just plow on. But there's quite a bit more in terms of muscular skeletal, also just conscious that probably mine needs a bit of arrest. Um But hypothyroidism is something that does does occur in pediatrics, but it's actually hypothyroidism that we want to stress more as the topic that we want you to be confident in recognizing and understanding that the guthrie test is looking for congenital causes and to be able to really that confidently to an examiner in paces as well as recognizing signs of this in uh M C cues for hyperthyroidism. As in adults. Some causes include transient thyroid itis as well as auto means of graves disease. And the main investigations are obviously thyroid function, looking at antibodies. So that's anti thyroid paroxy days and anti thyroid stimulating hormone. You can also consider doing ultrasounds and not take scan. So the sestamibi scan to look for any um, functional nodules, but these are really only indicated if you can feel a thyroid that is um, lumpy bumpy basically. And if there's a diffuse goi to um that's not causing much problems, then usually you just leave it alone. You can also consider doing um other tests as well. But importantly, FBC and LFTs before you initiate any treatment. Um in hyperthyroidism grace disease, you would think about propylthiouracil and carbon muscle. And for the purpose of exams, you need to recognize that a rare complication of this is agranulocytosis iss. So if a patient has come in with a sore throat feeling generally unwell, you need to recognize the need to advise them to stop the carbon muscle, have urgent blood tests done to rule out that they've had neutropenia. And if they have developed neutropenia, then they need to urgently be um seen by a specialist um to make sure that they don't become very, very unwell from this. Then um a lot of patient's will go into remission after some months, two years on carbon Azle, but they may flip back into active graves' disease again. So it's about monitoring the thyroid um symptoms as well. As the thyroid function as well. If they do do go back into Grace disease, then they can also consider things like surgery. So, a thyroidectomy or radioiodine as well, but the criteria for this is quite a bit stricter. So they need to make sure they're not around young Children. Um, and, um, all sorts of things like that. Okay. So it's time for a break. Just want to get a general consensus of whether you would prefer to carry on going or take a five minute breather. So, if there's no strong preference, let's take a five minute break. So, uh, it's, if we will restart at 7 30 uh, let's see. Let's see what they think. Yeah, cool. So we'll, we'll restart at 7 13. Okay guys. I hope that was a refreshing five minutes. Um, ready for the next part. So, first things first, the question, what are the differentials for a limping child? Just put your thoughts into the chat very good. Except that arthritis pursue fee is probably some of the main ones will transient. Sign of itis. Exactly. Gosh, I don't think you even need the next part of the lecture guys. Okay. Okay. So, uh, you've mentioned quite a few. So, um, we'll start with something that's not quite, uh, we'll give you a limping hip, but, uh, limping child. But the development dysplasia, uh, of the hip is something that is screened for, um, uh, as part of the night, the examination or is uh so neonate within 72 hours of birth should have a screening for it. And it's also then repeated at eight weeks, generally either by the health visitor or by or at the G P practice as part of the routine follow up for neonate and it's a spectrum of disease. So you can have it ranging from acetabular immaturity all the way through to frank dislocation of, of the hip. Essentially because of um during the development of the foetus and of the neonate, the um all of the hip isn't sitting appropriately uh within the curvature of the acetabular. Um Generally speaking, it affects the left hip more than the right. The thinking for this is that the neonate or the foetus, when it's inside the womb, it's left side on average lot is more commonly lying against the, towards the back of the um mother against the spine. And those compressive forces changed the shape and nature of the hip leading to the dysplasia. Uh Generally speaking affects females more often more common in breach presentations uh and in firstborns as well. Um So all kids should be checked at 72 hours and eight weeks. Uh if there's a clinical suspicion or if there are these um specific indications for uh uh ultrasound soup breech presentation at 36 weeks regardless. So whether they were delivered by C section, for example, or if they uh were delivered a normal vaginal delivery, uh with an appropriate presentation if they were breech delivery, if there's a family history of dysplasia of the hip, and if it's a multiple pregnancy, regardless of your initial assessment at birth, you will always do a six weeks check with ultrasound to have a look and assess for any dysplasia of the hip in terms of management, especially when you're closer to the mild end of the spectrum will usually resolve spontaneously within 3 to 6 weeks. So it just requires closer monitoring. Um And that may involve repeat ultrasounds and x rays to just see how the hip is developing. Um Second line would be to use the publix harness. So essentially, it fixes the hip in uh fixed abduction and external rotation. And so essentially pushes the ball of the hip uh into the socket. Um So then over time you get appropriate development of both. Uh and if uh basically reform nicely and then if needed, uh you can consider surgery with bigger casting, but um it's very rarely done and only if there's a significant malformation in the first place. And we've included a few X rays, they're mostly of the frog leg for you, which just demonstrate there's under development of the hips in each picture. And um this is something which I'd be so surprised if they ask you to interpret um in a station, but just to be aware of. So, whilst you're having a look through these notes, um but moving onto transient sign of itis. So, also known as Irritable hip syndrome, this is a really common station. So um often the trick is basically to screen for any proceeding, acute illness of the child. Usually that's a viral upper respiratory tract infection. Then that's followed by uh a painful joint. Usually the hip joint. Um and that's because the joint, the joint becomes inflamed and the synovial becomes hypertrophic as well. So the presenting signs are um an antalgic gate child may have um the hip rested in an abducted and externally rotated pa's. Um and the test that you might want to just throw in um is the positive logroll test. So you ask the child to lie down and have their legs go completely limp and you just roll it. Um And that should basically because the muscles in the legs to contract in voluntarily because it's causing pain. The main investigations are that you don't want to be missing a septic arthritis and it can be really tricky in pediatrics to get a proper history and establish these, but your main pointers will be the vital signs. So, does the child look very toxic? So, um you know, very unwell um in severe pain, mute, um do their blood reflect, uh you know, soaring crp um white blood cells are through the roof or are they just marginally off? Um And then you can consider things like x rays as well, which actually a lot of the time will be absolutely normal. Um There's an ultrasound here, it's not a routine um screening tool or investigation, but it's just to demonstrate that there is information of the Sino Veum. Um And then finally, in terms of management, the main counseling is to um explain that this is self limiting in the majority of cases and that the child requires rest. Um They require support of the hip um to avoid any strenuous exercises and to have analgesia as well too. Um In particular N says to help with the information. But obviously remember that in pediatrics, you should always avoid using aspirin because of the risk of race syndrome. There's only very um a few cases where it's okay to give aspirin and Children. So which of these are risk factors for developmental dysplasia of the hip? Perfect. All right. Very good. Okay. So, uh we'll move on now. So we'll, we'll start with Perth disease. So, Perth disease is when you get a lack of blood supply going uh to the head of the femur. So idiopathic avascular necrosis. Um And uh because of that, what happens is you get this uh loss of blood supply and then following that, you can get revascularization and re ossification. Um So the process happens like that can take up to 24 months um for it to fully resolve for when Perth disease initially presents most commonly p for Perth. So most commonly in primary school Children and maybe far more common in men did or in boys than girls associated with positive family history and a coagulopathy. Uh in terms of on your examination, uh the most significant thing would be a loss of internal rotation and abduction. Uh And uh you will do your A P and your lateral and frog leg views when you're doing your X rays and just having a look at the x rays, what you can see in both, both images but easier to see on the top one is just this destructive process of uh the head of the femur in early disease where the X rays may look more normal, but you're suspecting Perth disease. And MRI can help to make the formal diagnosis of Perth disease. And then in terms of your management options, uh non operative for younger kids with mild disease because you hope that um once you get that re the ossification, revascularization that the head of the femur uh helps and redevelops normally, uh non weight being in physiotherapy can help with that if the kid has more severe disease and uh is overweight than an osteotomy, uh may be required to an ostomy. Otta. Me just involves cutting out a small piece of bone. And the reason you do that is because it pushes the head of the femur further into the acetabulum. So that when you get that reforming process and then revascularization and ossification, um you're far more likely for the head of the femur and acetabulum to reform correctly. And now moving on to Sufi slipped up. Ephemeral epithets iss. So I used to get really confused with the two um Devens mentioned about P for primary, so primary school Children and s for secondary school Children. It just helps me think of what a likely person with Sufi might look like. Um And classically, this is somebody who's overweight. Um more likely to be uh a boy rather than a girl. Um, more likely to be, you know, around the age of 16 rather than the age of kind of primary school kids that you'd see perth's in and they might have associated other conditions like hypothyroidism as well. Um What SUFI is is basically slippage of the top part of the femur. Um and the main kind of clinical signs of this will be a limp and um a loss of internal rotation and abduction of the hip. Uh This can often present with a long history of pain in the hip, the groin and also refer to the knee as well. So in every investigation, you must also make sure to um always examine the joints above and below the the affected joint to um and then investigations, it's to have an X ray and classically, I don't think they will question you on what kind of X ray views but just be aware, lateral flow frog leg for you and a P pelvis. Um then screening for comorbidities associated with SUFIS so thorough function as well. Um And there's a few rarer things um like blood urea nitrogen, serum creatinine, which you can consider that's also to look for any associated comorbidities. But really, it's um both clinically and also from the X ray, you'll get your diagnosis. Then in terms of management, the main um mainstay will be operative and that's pin fixation you can see on the X ray here, they've had the pin fixation done in patient's who have severe cases or, or high, high risk. So anything predisposing, then the contralateral hip can also be considered to be fixated even if it's not completely transitioned into full SUFI or hasn't had it yet. Right? So which of these patient's is likely to have SUFI as opposed to Perth's? Yeah, very good. So, uh see, so 16, the um so s for Sufi, so secondary school child. So they're 16 years old and they've had their loss of internal rotation of the hip, which is a classical finding for SUFI. But you can also see that in Perth the other thing to add in terms of uh the investigations that you can do for SUFI. Generally speaking, you don't need to do your, uh you don't always need to do thyroid function and your metabolic screen. But if you're suspecting that there may be a metabolic condition going on either, usually because the kid is a lot younger than you would expect for them to have SUFI or if they're particularly short for their age, and you would consider doing this further investigations to see if there is a metabolic cause for their presentation as well. Now, Oscar Slatter is also one of the conditions which has a lot of overlapping symptoms to um osteochondritis and a bunch of the other knee problems. Um So in, in terms of MCQ S and kind of recognizing which one, it's likely to be the main things that you you have to look out for are mentions of prominence of the tibial tuberosity, tuberosity, anterior knee pain. Um and then as well as this pain on extension of the knee, um classically, these patient's are male, they're highly sporty, especially jumping kind of activities. Um and they tend to be around the 12 to 15 age range. The investigations are usually actually it's a clinical diagnosis. You can use X rays to um look at any further damage associated with this condition. So that might be that the tibial tuberosity looks obviously fragmented as in this case or irregular. Um But actually, in terms of management, the mainstay is supportive. So, NSAID to reduce the information and the pain rise. So rest ice compression elevation supporting the need with um bandaging and physiotherapy to strengthen the surrounding muscles. Um but actually a lot of it um managing expectations and counseling that unfortunately the pain can persist until the growth has fully stopped and the growth plates have fused. And then as Hannah said, you can get significant overlap in symptoms and presentation between Oscar flatter and osteochondritis desiccants. Um So osteochondritis desiccants is again a lack of blood supply, going to the subchondral bone sort of bone immediately under the cartilage that can lead to separation of the bone and the cartilage and over time that can lead to loose bodies or leave. And so uh the loose bodies are literally just pieces of bone which are sitting around or within the joint, um separate from the actual uh femur, for example. Um So you'll get me pain on activity, which is compared to Oscar flatter where you get uh new pain, which is very well localized to the tibial tuberosity. Your pain is generally poorly localized. You may have a fusion. So swelling of the joints and knee locking and giving away, which is a late sign and usually that's because of the presence of loose bodies. So the loose bodies uh inhibit or the interfere with the ability for the knee joint to move smoothly, causing the locking and the giving way. In terms of investigations, you can do your x rays as an initial views. So your weight bearing a pa and lateral. But um compared to the other x rays, something a little bit more specific for osteochondritis desiccants would be to do a not view of the um knee as well. And then your MRI of the knee is particularly helpful for people who have severe disease where you might be, for example, planning to do an operative procedure because it will give you much more detailed information about the size and nature of any loose bodies or lesions that may have formed. And in terms of your management, generally speaking, most of patient's to be monit managed non operatively. So this could be bracing to help support the knee restricted weight bearing and or physiotherapy. And then your operative management is to do arthroscopy. So it can be a form of diagnosis. So seeing what it looks like with with arthroscopy can help make your diagnosis as well as if there are any loose, loose bodies or lesions, they can be removed at that time as well as part of therapeutic treatment. Yeah. Next question, which of these cases is more likely to be Oscar Slatter as opposed to osteochondritis discounts? Yeah, perfect. Exactly. The key word is tibial tuberosity or anterior knee pain in in particular. All right. So next one is JIA A which is again, very common as well, both in the practical and the um Britain's. So um this is a condition where there's inflammation of the sign avian and thickening of it as well. There's lots of different subtypes, but the main ones I want you to be aware of our the systemic arthritis forms. So that's when patient's have constitution, also fever. Um They have multiple joints involved. This has been ongoing for at least two weeks in these patient's and there's porc articular. So that's um also known as oligoarticular um involvement. So, less than five joints, polyarticular er is more than five joints. Um and there's other subtypes site, June, Niles, psoriatic arthritis and close in spondylitis as well. The diagnosis is um mainly clinical. So the patient has to be less than 16 years old. They have to have had the symptoms for more than six weeks at least. And um, they will have classically joint pain, swelling, they'll have fever and actually, this can be kind of spikes of fevers, morning, nighttime that they might notice this. Um, they might have an antalgic gate, um, stiffness in particular because this is a type of arthritis, um, and then reduced range of motion as well. There's the classical MCQ buzzwords, so salmon colored rash, um as well in the systemic form and in the other subtypes. So the psoriatic type, there might be a psoriatic rash involved as well. The main risk factors are being for female, actually being younger. So less than six years old and having genetic predispositions, um, as well as HL A problem orf is um's in particular B 27 which we know is associated with ankylosing spondylitis and actually also a family history of auto immunity as well. And then in terms of your investigations, so bloods are a bit more useful and important in juvenile idiopathic a arthritis compared to some of the other causes we've talked about so far. So your full, full blood count will give you an idea of anemia, which can be kind of an anemia of chronic disease as well as a leukocytosis, an indication of information because this is a inflammatory process, ongoing, an autoimmune process, your ESR and CRP maybe raised, but it can also be normal. So that's useful to know because if it's normal, it doesn't, you shouldn't be falsely reassured that it's unlikely to be JIA then your antibodies. Uh I'll let you have a read through those. So your um the pattern of your auto antibodies is dependent on the type of juvenile idiopathic arthritis. The child has. Um So uh I'll just recommend you guys have a read through that in your own time. And then in terms of imaging x rays can be helpful to have a look for any kind of bony destruction or lesion's ultrasound can be used both in terms of diagnosis but also therapeutically. So, um sometimes Children may need to have cortical steroid injections as part of uh symptom control. And then MRI scan be helpful to have a look for synovial thickening or if there's any questions about a diagnosis, then in terms of management, these kids will be in a lot of uh pain and that will impact their ability to do sports and to develop. So, are not easier. So using uh nsaids or week opioids, as I said, intra-articular or if very severe and particularly for your polyarticular arthritis. Sometimes uh oral cortical steroids can be useful. Um And then uh beyond that, these kids should be managed under a specialist pediatric rheumatology team where they can consider doing extra things like your dumb odds and biologic therapies. But especially because they're in Children, I need very close monitoring if you're going to start these kinds of uh medications and then psychological support. So as with nearly any long term condition, like we were talking about the type one and type two diabetes, if you have a long term condition, which is likely to have a significant impact on the child's well being, then psychological support for both the child and uh the parents to ensure that they're developing well, they're, they're managing the condition well and it's not interfering with their social life as well as their ability to progress at school as well. And then just being aware that you can sometimes get um some uh side effects or extra articular symptoms as well. So you can get a uveitis causing visual loss and your osteo process leading to different fragility fractures as well. Yeah, and I think this in particular is a key example where you can distinguish yourself from people who you know, have passed well and who have done beyond that by talking about the psychosocial support aspects as as well beyond basically the biological and the pharmacological management's, you want to recognize or demonstrate recognition of the fact that um with these conditions, you have to take a holistic approach. Okay. So, reactive arthritis. Now, um this is a condition which is strongly associated with dysentery, which basically means bloody diarrhea. And in a lot of cases, this will be gastroenteritis secondary to shigella, um salmonella, campylobacter or sometimes also yesenia as well. There are other subtypes as well caused by sexually transmitted infections. So most commonly chlamydia, which we know is the commonest S T I anyway, um there is overlap with HLA B 27 polymorphisms as well. Um But obviously, if a child is presenting with sci associated reactive arthritis, this is a massive safeguarding um flag that needs to be raised as well. So, demonstrating understanding of that in your management plan is really important. Then in terms of diagnosis, the main risk factors that will point you towards reactive arthr itis will include being male having the HLA B 27 genotype and also a history of sci symptoms or gi upset as well. The main clinical signs are, it's actually very variable. So there is arthritis but that can be asymmetrical, that can be pony articular, it can be monoarticular as well. Um It can also involve the enthesis as well and then further investigations to help Clinton, the diagnosis can include M R rise that may show sacred Elliott up iliitis. And obviously, this can be very overlapping with um ankylosing spondylitis too. And then for diagnosing S T I S M PCRs as well. And then in terms of management plan, largely, this is supportive and um it's to explain that this is likely to be self limiting. So in the interim, having plenty of analgesia that's NSAID, in particular, as well as steroids to be considered if NSAID are not doing enough, but obviously, always try and work through the who analgesic ladder and prescribed accordingly before moving straight on to other things. And uh DeMars can also be considered. But this really is a shared care medication that um is advised by specialist teams. So, rheumatology would usually be the ones to initiate that and for rickets. So, rickets is osteo Malaysia, but in Children, so you get poor mineralization of the bone uh leading to uh weak bones and slow growth. So the most common causes vitamin D deficiency and most common cause of that being in the UK is inadequate sun exposure, particularly for people who have darker skin tones. You can be diet deplete as well in both your calcium and vitamin D, your malabsorptive conditions like celiac disease and may pre predispose you to Ricketts, uh liver disease and CKD as well. Um less commonly, you can get phosphate deficiency, which again, maybe dietary but could also be due to um renal losses. So, um basically peeing out more phosphate than you should be. Uh So in terms of your investigations, you want to do your blood to look your, uh bone profile and to have a look at your vitamin D levels, you may also need to look at your LFTs and use the knees. But if you're considering other secondary causes for why they may be having a vitamin D deficiency, urinary calcium and phosphate. Again, only really if you're considering, um, an underlying cause where you want to know if they're wasting the calcium and phosphate into the urine and not retaining it as the reason for why the um developing Ricketts and having a vitamin deficiency investigations wise, x rays of the long bones. So you expect to get this kind of bowing out of the uh long bones. So the kind of pathognomonic terms that you might see on your MCQ, the copies playing fraying and Boeing. So if you see any of those phrases, then you would automatically be thinking okay. This could be Ricketts. Then in terms of your management, it's about replacing the because the cause for the diseases that deficiencies and other vitamin D or phosphate. So it's about replacement. So usually it's vitamin D replacement or calcium replacement depending on your findings. Uh You can also advise on dietary changes for oily fish, egg yolk mushrooms can all be high in vitamin D as well. Uh Given the disease process, it can also be very painful. So in uh good pain control with nsaids initially, if uh poorly controlled, then you'll need rheumatology input to consider things like steroids and D mods, which would really only be started by a specialist in this population. Uh And what is the difference between Cody Calciferol and alpha calcid L? Ah So the ergocalciferol is plant based whereas normal cholecalciferol is not, I can't remember what actually in there is non plant based. Yep. So, um alpha calcidol is activated. This is important because if a patient has um chronic kidney disease, then they may not be able to activate um their vitamin D because they might have a deficiency in one alpha hydroxy lays. And this means that even if you give them copious amounts of Cody calciferol or it just won't do the trick because they aren't able to activate it in the first place. Okay. This is I think the last topic um that we're covering. Yes. Okay. Well done for sticking with us. This know. Okay. So in terms of your osteomyelitis, so it's fairly uncommon, but it's a very serious cause for why a child might be unwell and or having a limp. So really important to know. So most commonly it's because of human collagenous spread. So uh an infection in the blood which has gone and seeded in the meta metaphyseal region. So, in Children, the most common area for an osteomyelitis to develop is in your meta faxes. So where the growth plates are. So that's why actually it's really dangerous. And Children have an Osteomyelitis because it can damage your metaphysical plates. And therefore it can uh cause um discontinuation of growth and stunted growth in that particular uh bone and limb. Uh so the most common side. So your distal femur and proximal tibia. So essentially around the knee joint, most commonly, it's tough aureus. But um the kind of MCQ thing to be aware of is in your Children who have sickle cell, they have an increased risk of uh being secondary to salmonella. The exact cause for that is not known. Then in terms of your presentation, uh the kid will may present on wealth that he may be septic from an Osteomyelitis. So they may present uh with fevers being unwell, their basic obs maybe deranged, uh maybe hemodynamically unstable. Um And then in terms of the actual Osteomyelitis, they may have swelling, warmth and tenderness around uh the area of the infected bone, they won't be able to wait their because of the pain as well. Um And there'll be an a pseudo paralysis in terms of your investigations. Uh you want to do uh initial blood cultures. So um taking uh blood cultures to see if you can grow what the organism is because that will direct your treatment, then your other bloods including full blood count, using the CRP to monitor how the child is doing. Um X ray is really useful to have a look because at the moment or you know that this is a limping child and you have a fever, you want to make sure you're not missing out any other potential diagnosis, uh such as fractures. So that's the main benefit of X ray. It may sure you severe osteomyelitis, but it doesn't exclude Osteomyelitis. The way to confirm the presence of an Osteomyelitis is to do an MRI. The MRI will show whether the child has osteomyelitis present or not. Then in terms of your investigation, your management rather uh the mainstay is fluid and intravenous antibiotics. Uh As the child is going to be severely unwell, you will need to speak to your microbiology team. You'll be guided by them as to what antibiotics and for how long. But generally speaking for Osteomyelitis, you will have an extended course of antibiotics for several weeks. Usually, uh you might do a couple of weeks IV and then switch to oral after that. For example, you might need surgical drainage or debridement, uh an extremist. If you're not able to get on top of the infection, this may be on MRI, for example, there's a deep abscess where, you know, the infection is not going to clear unless you get in and what the abscess out. Uh And or if it's become a chronic infection. So despite your into your attempts at intravenous antibiotics, there's an inadequate response you may need to go in to remove the infection itself. Yeah, and actually overlapping with the presentation septic arthritis. So, in any limping child, you must always make sure that you have not missed a septic arthritis because the, the um complications from this can be fatal. And um, it's really hard sometimes when a child is limping because they can't give you that information. Um And you're probably dealing with a very stressed parent as well to get a coherent history. So you're working on your clinical examination as well as um what else you're picking up about their vitals? Um So in terms of the background septic arthritis is um can be secondary to osteomyelitis, basically where um where it's spread, the infection has spread beyond the joint um beyond the epithet acis as well. So what I basically want you to realize is that it's hot, swollen, tender, hard to move around um joint and um the child probably looks very unwell as well. They might actually present with pseudo paresis, which means that there, you know, not moving their limb at all. Um They will be pyrexia. Well, you'll need blood cultures, um joint aspirate. It's to make sure that you have microscopy culture and sensitivities to direct antibiotic treatment. Um ultrasounds to give you more information and x rays as well to have a look at joint destruction. Um and any other associated pathologies as well. Um As you can see, there are a bunch of other differentials that you need to consider um alongside um septic arthritis in a patient presenting with these similar symptoms. Um but the definitive management will be joint wash out in drainage. Um as well as IV antibiotics throughout that. Okay. Last question is what is the commonest organism to cause septic arthritis? Very good. Very good. Is septic arthritis more severe than osteoarthritis? Yes. So, your septic arthritis is your acute presentation of having an infection within a joint. Um, whereas your osteoarthritis is kind of a very, very uncommon in Children. Um, so your osteomyelitis, uh, that would make a lot more sense of the question. Um So I would say maybe he has a different opinion. I would say both are very, both a severe. Um It's just your treatment will be slightly different because if you have a septic arthritis, you have an infection within a joint. So you generally speaking, we want to go in and do a wash out of the joint to remove the infection, which is a lot easier to do. But both of them, uh kids can become very unwell very quickly and become uh shocked or in septic shock. I think generally speaking, septic arthritis is more common than an Osteomyelitis and you may present a little bit more acutely with a septic arthritis. Uh Yeah, and the answer was b as well. Very good. Any other questions to do with this at all? Um So this is our emails if you have any questions about this lecture or anything in general. So foundation year f pass, it's all very fresh in the minds still for both of us. So definitely drop us an email and, um, we can see where we can help as well. You're so nearly there, um, to being, uh, you know, full doctors. So just keep going. Um, and try and enjoy the ride. I definitely look back at my med school years and I think that they were so much more fun in many ways. So definitely do enjoy the, the last few years. That's great. So, yeah, if any question, I have a question. Yeah. Um So there's in terms of uh I can't really horrible feedback back here, okay. Um In terms of like paces counseling because I know that you always talked to a parent actor basically and not the child and say if you um suspect a reactive arthritis or it could be like Comedia that you want to screen for that is it would it be appropriate to ask the um parent that question? Because in real life, you wouldn't really do that you to talk to the child themselves? Probably. So from my perspective, it would uh significantly depend on the age of the child. So if the child is kind of, I would say anything from kind of 13, 14, 15 upwards, then if that's within your differential, then I would ask if the parents, I would essentially tell the parents, could you please their power? I need to just ask a few questions and if they really push, then you would just say it's standard practice for us that we ask some questions uh to the child on their own. If, if they're very concerned, you can say you have a chaperone in with them as well. Because in those situations you're uh could either be a consensual thing, particularly there a little bit older as a child. But also they're generally able to have more of a conversation with you. So you can have that conversation directly with the child. If there are a lot younger than your main concern, then is about um if there's a form of physical or sexual abuse of the child, instead, in which case, you're approach would be significantly different. I think it's difficult in a pacer station to know how to approach it. Um If you don't feel confident, it partly depends how your conversation has gone to that point. But if you don't feel confident, then I would say as part of your count your kind of discussion with the examiner, you can always say that this is part of my different and I'm concerned about this. I would discuss with the senior about what they would recommend us the next steps in terms of the history taking. Yeah. So whenever it's something to do with pediatric, safeguarding, it's never uh something that you would manage on your own. So you would always have to escalate anyway to discuss further. And actually, no matter what it is, as long as you're concerned about the safety, uh the safety of a child, then you have to make sure that you put in the necessary steps, so making sure they basically don't leave. Um And that you discuss with a senior in that time and then get back to them with a management plan. Um So you don't need to feel like you need to address or broached that topic there. But you can just say in your management plan, this is something I would discuss with a senior to proceed forwards with. The last thing I would mention is if there is a confirmed diagnosis of an S T I, then it's a little bit challenging, especially when the child is older about whether to break confidentiality or not to tell the parents again in that situation, whether the child has kind of Gillick competence or not, would be quite important to assess before breaking confidentiality. Okay. Thank you. Perfect. Is there any more questions anyone if not, then I'll stop the recording.