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Hi guys. Can, can anyone hear me? Um If you can just pop it in the chat, please? I think we're just waiting over then we've got another moderator on now. Um So I think we should be good to get going. Um Can, can you just confirm that you can hear me? Ok, great. Um So I'll just crack on, I'll just share my slides. Can everyone see that? Um, I was hoping to be able to see the chat at the same time as presenting, um, just to make it a little bit interactive. Uh, Zen LD. Do you have any advice in terms of that? Yes. Can you hear me? Yeah. Yeah. So normally you'd have to download your slides as a PDF and then you can just use the PDF version onto meal and then you'll be able to see your chart. Oh, ok. Um That's fine. We can, we can crack on and I'll, um, I might keep it in this format then rather than a slideshow. Um, so that I can still keep an eye on the chat cos quite, quite a lot of it is a bit interactive. Um So yeah, if, if people can, uh, try and be interactive as possible, just, um, it'll work a lot better if we go through the cases. Um If people are just putting things in the chart or if, if people can unmute as well, then, then feel free. Um, but we'll just crack on like this if that's all right. Um So, yeah, this is the first session that we'll do on medical A to e emergencies. Um So in terms of what we're gonna cover today, um it will be these presentations and conditions which are taken from the UK MLA curriculum. Um So we've already had one session on respiratory emergencies, which was done by Doctor Willie Pera. That was a really, really good session. So if you guys missed that, then please watch your pack. Um It was really, really um fantastic. Um But what we're gonna focus on today is these uh these presentations and conditions that you can see here. Um And what we won't cover um which we'll do another session, session on later down the line is these things. Um So that's more kind of the, the um A LS algorithms and A CS um and a bit of gi emergencies as well. Um So, yeah, we can just crack on from there. So to start, I thought it would be useful just to go through the A to E structure. Um Just as a reminder, I'm sure everyone's very familiar with this. Um But it's just Um I think you, you guys will have kind of AK sessions as well. Uh This will be more focused on your written exams in terms of the cases that we have. Um, but it's useful to bear this in mind and even, you know, beyond thinking beyond exams before when you start working. Um, this is the structure that is really gonna lead, lead you in good stead, um, especially, you know, when you're a busy night shift. Um There's not much support around having this structure kind of nailed down is really, really important. Um So if we just talk through it, so the d um the reason I put DRS is I always used to forget in med school, it was danger response. So doctor A um I was used to forget when I first learned it to kind of shout for help every time or call for help to escalate to a senior. So I was like to put the s in just to as a kind of mental reminder to myself. Um not to forget that. And then I'm sure you're familiar with the AE structure. So we don't really need to go into depth. Um And then within that for each kind of um for each section, you can apply this look, feel this measure treat um kind of structure which is really, really good, um obviously applies slightly differently to each of the A to E components. Um But useful to bear in mind and obviously the real, real key for your Aussies as well is, is um showing that you're reassessing. So if you're doing any interventions, so if you're giving oxygen, for example, make sure later down the line, um you always say kind of, I'd like to reassess the sats um or take another set of OBS if you're giving fluids to check your BP and things like that. Um So that's just a nice little brief overview of the A to E structure. Um And like I said, this will be be more cases um for written exams but we'll every, every case will have an A to E um so we, we can talk for you guys so we can just crack on with the cases. Now. Um Does that make sense to everyone? Any anyone have any questions? You want me to go into anything in more depth? Ok. I'll just carry on. I haven't got any responses. So the first case we've got, so it's a young female. Um she's come to Ed with abdo pain vomiting and lethargy for the last couple of days. Um So can anyone just just pop any anything that comes to mind in the chat in terms of differentials um or feel free to unmute as well? Um Yeah, I I'll let you give you guys 30 seconds or so just to, to pop any, any ideas you've got in there is, is everyone able to access the chat and send messages in there. OK. If we, if we don't have anything, we can OK. There's one message. Yeah, so these are, these are good kind of differentials. So a few few ideas. So DKA appendicitis, ectopic pregnancy, um all, all very good uh good ideas, very relevant for this kind of presentation. It's very, very um kind of vague brief. So yeah, you got to keep the differentials broad. So we'll crack on with our at assessment and it should become a bit clearer what's going on. Um So on the ae um, if we read through that, so if there's anything that sticks out to you in, in this A to E or anything, you find interesting or any questions about anything, just, just, um, keep putting it in the chart and we can talk through those. Um, but for now I'll just talk through it. So the airway is patent but dry mucous membranes. So a bit of dehydration, um respirate is raised quite significantly 32. Um SAS are fine though. So, maintaining sats on room air and she's having deep labored breathing. Um So something's not right. Um If we go to see so tachycardic, hypotensive, prolonged cap refill and cold peripheries. So pretty unwell and then d alert, but drowsy and then BMS are, you know, pretty significantly raised 22.8 and no focal neurology. And then if we go to exposure, so dry skin, sweet breath odor and no rash or trauma. So does that kind of um no clear up any or rule out any differentials or, or make it point to 11 differential should be fairly obvious, I think from that assessment. Yeah, so that's right. So DK A um that's correct. So that's why I was getting at most of these will be pretty obvious. Once you see the 8080 assessment, it's more, more so we can talk through the things around them. Um, so yeah, Paul's mentioned low BP and high cap refill. So it shows dehydration. You've got the dry mucous memories as well as dry skin. So, yeah, that's correct. Is there anything else that sticks out on the, at, um, anything unusual or anything worth commenting on? Yeah. So the BM is significantly raised. Yeah. Ketotic breath. Good. Um What about the deep labored breathing? Does anyone know what that's called? Yeah. Good, Paul. So that's, that's KM breathing. Um, which is typical of, uh DK. So that's kind of these deep and fast respirations. Um, and it's quite, quite, um, pathognomonic for DK or at least metabolic acidosis. Um So that's quite a typical thing that they can throw in exams or even in osk osk stations and things to, um, to give you that clue. So, my next question is then, so once we've done this at assessment, we've kind of got our, our main differential, I'm pretty sure of the diagnosis from that, but what other investigations would we like to do at this point. Yeah. We'd wanna do an E CG. Anything else ABG? Yeah. Good. ABG. Ketones. Very important. Yeah. Yeah. So I think the main, the main thing is the ABG really? And the ketones, like you said, but the ABG is going to help us with our diagnosis the most. Um, so here we've got the investigations. So, um, I always like to split the investigations into bedside bloods and imaging. Um So by the bedside, we've done an ECG like like Paul's mentioned. Um and that's showed sinus tachycardia. So we knew that the heart rate was up. So that adds up. Um We've done some capillary ketones. Uh So that's more than three and on the urinalysis, there's ketones positive and glucose tripper positive. Um So that's all consistent with our, our top differential of DK A. Um Is anyone able to describe the ABG findings to me? Yeah, that, that's right, Paul. So you'd, you'd um place two wide ball Cannula for, for any kind of at e emergency. Um And in Os especially, that's really good to mention. Yeah, very good amelia. So m metabolic acidosis. Um So you can see that the PH is below 7.35. So it's acidotic. The bicarb is well below normal range. So normal range, lower end is normally about 22 21 22. Um So that means it's a, it's a metabolic acidosis and the partial respiratory compensation. That's really good is um you can tell that because the CO2 is lower than normal range. So that means that the body's trying to blow off CO2 to bring that ph back up to get you back to, to normal Ph rather than acidosis. Um The oxygen is OK and the base excess minus 10 um is consistent with that metabolic acidosis. And then in terms of the blood FBC shows nothing interesting. The sodium is a tiny bit low, the potassium is a bit high. Um And the urea and creatinine are uh pretty normal. Nothing to worry. And we've sent an HBA1C. Um obviously, in the longer term, that's a, that's a good practice thing to do. And on imaging chest X ray is clear, probably not really any indication for the chest X ray to be honest, but just put that in there anyway. Um So yeah, we'll talk about potassium a bit more uh when we come to the management and things, but just bear that in mind that the, the potassium is tiny raised. Um So after your investigations. So can anyone does anyone know what the diagnostic criteria are for DK? Yeah, that's really good Emelia. Um So if we move on to the next slide, we've got that here, so you need to have AAA blood glucose above 11 or a known diabetic patient. So in this case, there was no mention of any past medical history. So it sounds like it's probably the first presentation of DK A. Um but the BM was, I think, well above 11, it was in the twenties. Um phph less than 7.3. So good going acidosis bicarb less than 15. Um So again, good going metabolic acidosis ketones over three in the blood or evidence of ketosis on urinalysis. So you just need evidence of ketones on, on either of those. So capillary ketones or urinalysis and then we'll talk through the management as well. So the key with DK management is all about rehydration. So the first step is you give your first liter of normal saline over one hour and that's before you actually start any insulin. Um Does anyone know why it's rehydration rather than insulin therapy that we prioritize? Um just going back to kind of your basic physiology of things? Any ideas? Yeah. Good. Uh Good thinking. So BP, you need to, you need to get the BP up. That's along the right lines. So it's, it's from a physiological perspective. Um What's happening is you've got so much. Yeah, good thinking Paul. So you've got such a build up of your glucose um that you get something called osmotic diuresis, which is why in, in diabetes, you get that classic polyuria polydipsia, uh those kinds of symptoms because there's so much glucose that your kidneys can't um process all of that. So it's getting lost in the urine and it's dragging all the fluid with it because of osmosis. Um So actually, you're so dehydrated, you're very hypovolemic and also your kidneys aren't able to function properly. So, if you expand the uh circulatory volume, again, you're gonna bring that hypovolemia, you're gonna correct that hypovolemia and also um reperfuse the kidneys to allow it to clear the ketones, to clear the, the glucose and kind of really get it going again and bring the blood glucose down. So that's actually immediately in the, for, for the DKA side of things, the fluid resuscitation is what's really going to bring your, your blood glucose down in the very short term. Um And then you start your fixed rate insulin. So that's gonna be naught 0.1 units per kig per hour. Um Just a good, good dose to memorize co in oy it, you could easily get a, a kind of scenario where you have to be able to, to answer a question about that. Um or even in your, in your M CQ and things as well. It's a good, good one to know. Um And one of the principles is that you, so patients who are diabetic are usually on what we call ba basil bolus regimes, which you're probably familiar with. Um So that means they're on a, a long acting insulin which will be usually once a day and then usually with meal times, they'll be on short acting insulin as well. So when they come in with DKA, we want to continue the long acting insulin, but because we're switching them to fixed rate infusion of insulin, we stop the short acting that they're on. Um, and then so after you've rehydrated for that, that first hour you add your insulin and you continue your rehydration. Um and this is, this might be kind of dictated by your local guidelines. Er, so every, every trust will have a guideline in terms of what their protocol is. Once the BM is less than 14. Uh because because you've kind of rapidly corrected that hypoglycemia. Once it gets below 14, there's a risk that you, you over correct and you go, you, you induce a hypo. Um So we wanna add 10% dextrose as well. So that's one of the key principles. Um And then why have I put this about monitor potassium or add in KCL in subsequent bags? What's, what's the thinking there? Yeah. So a couple of good suggestions. Um So what Janet said, so potassium may be low will shift into cells. Um So, so what happens in DK is because you've got because you're so acidotic, um your, your blood in, in the blood, your, your body will try and compensate for that by getting rid of hydros which cause the acidosis. So the hydrin ions will shift intracellular. So hydrogen irons are gonna go from the blood into your cells to, to buffer your ph. And part of that process is in exchange for potassium So, if you remember back to our bloods, um uh bloods were here. So the potassium was a little bit raised. Um That's because of that process. So even though the potassium is raised on the bloods, the um the overall amount of potassium in the body is actually quite depleted, that's artificially raised because it's doing that job of buffering the ph by driving uh hydrogen ions into cells. Um So, so that's the process that's going on there and then abigail. Yeah, you're absolutely right. So, in insulin, if you remember to, if you remember about hyperkalemia management, um we use insulin and dextrose to drive potassium into cells. So because we're giving insulin, um it's going to drive that potassium down and actually, you're at risk of iatrogenic hypokalemia. So it's really important that we monitor the potassium um and make sure that we're giving potassium to replete those stores and also to make sure that it doesn't get low uh because of because of that process. Um And then does anyone know when we know that DK has resolved? So what kind of the next steps are? OK, we'll, we'll move on to the next slide. So it's got it on here. So the resolution is defined by these criteria. So, yeah, good. That, that's it, Amelia. So ph over 7.3 ketones less than naught 0.6 bicarb, over 15 and patients should be eating and drinking. And at that point, you can switch back to their subcut regime. So like we said, the insulin, um the kind of basal bolus regime that they're on, if they're already a known diabetic patient, um we can switch back to that. If it hasn't resolved within 24 hours, they'll, they need an endocrine review because DK is something that is very treatable in the immediate tub. Um So if it's going on, despite all this treatment, then endocrine specialists need to be involved. Um and really good practice to get the diabetic specialist nurses in which will be in, in, I think in, in all hospitals really. Um So that they can look at why they've come in with DK, why their, their diabetes is not that controlled and try to optimize their meds and their lifestyle and give them um advice and things like that and educate the patients. Um So that's DKA, I did have a slide on HHS as well, which is similar in, in kind of presentation. So it's a bit more associated with type two diabetes and it presents over days rather than kind of that more immediate presentation. So it's slightly more gradual. Um But because of that, it means that you get really severe dehydration. Um And metabolically these patients can be really, really unwell. Um So the prognosis of HHS is actually a bit worse than DKA. Um So the difference is, so you're gonna get, you're gonna still gonna get severe hyperglycemia hypovolemia as we talked about, you'll get raised osmolarity, but you won't have that, that acidosis or ketosis because the body still has endogenous insulin. Um So that's gonna prevent the breakdown of the triglycerides to your free fatty acids and the the production of ketone bodies. Um The management is quite similar in that the the real key is aggressive fluid resuscitation uh for the reasons that we alluded to before and obviously potassium monitoring for the same, same reason, insulin is um not always given. So unless there's kind of that DKA picture, so it might be a mixed picture or there's ketosis without any acidosis. Um So not quite DK but there, there are raised ketones, then we wouldn't usually give insulin and the rate is actually um half. So, oh sorry, the dose is, is half. So N 0.5 units per K per hour. Um I think there are, that's kind of a summary. There are, there are more specific guidelines on the use of insulin in the HHS with a bit more intricacies. But overall that's, those are the general general principles. Um So that's DK and HHS. Does anyone have any questions about those or um any comments, any anything they want to add? OK. So we can move on uh to our next case. So a bit of a longer brief here. So we've got a young man. He's come to Ed, he's had a, a cough for a, a week. So he's thought, let's get it checked out. He's come to Ed, he's got a history of epilepsy. Um, he's come to triage and he's lost consciousness and started seizing. He's had stiffening of the limbs and then jerking movements. It's been going on for three minutes without any signs of stopping, er, roughly. And he's got his partner with him who said that he hasn't had a seizure like this in, in years. Um, any thoughts, any comments, anything that sticks out from that, that brief? Ok. If not, we can move on. Um So a couple of things just to note of the, with this, this kind of brief, um the stiffening of the limbs followed by jerking movements um is typical of a of a tonic clonic seizure. So that's what that means. Um And if it's been going on for about three minutes, uh well, we'll, we'll go into the eem uh assessment actually. So that's your at e assessment. So, airways patent, no air obstruction, but there's some blood tinged saliva respirate is a little bit raised, maintaining SAS, no signs of respiratory distress. Heart rate is up. Blood pressure's a little bit low cap refills, slightly raised cold peripheries, G CS seven. So, so really uh unwell in that sense, unresponsive, no focal neurology. Um and blood glucose is in range and on exposure, you can see some tongue bruising and bite marks but no other injuries. Um So yeah, it could, could be encephalitis or status epilepticus that's an interesting comment. So what at what point would we say this is status epilepticus? Yeah, exactly. So what if it's gone on for five minutes or more then uh then it's defined as status? Um So that's why one of the, the really important um things to bear in mind when you see a presentation like this is always start a timer. So in an exam in an oy, if they have AAA scenario like this, um One of the key things is mention that you're gonna start a timer as well. Um So yeah, we can go on to, are there any? Well, I haven't, I haven't got an investigation slide for this because um in this scenario, you wouldn't really, there are investigations you can do, but you'd rather just, you know, you can see that the patient sees you, you'd rather just sort that out immediately and then you can send any kind of longer term investigations like Mris or eegs things that can come to a longer term diagnosis later on, but when they're in status. So, um as Nichol said, so, um a single seizure lasting over five minutes or multiple seizures within that five minutes without returning to baseline. Um So the way we manage status, so we'll give IV LORazepam. If that hasn't worked after five minutes, you can repeat another dose. Does anyone know the dose of, of LORazepam? Um And then if we're, if we can't, if we haven't got IV access yet. There are a couple of alternatives. So, Bucco Midazolam or Pr um diazePAM as well. Yeah, four mgs. So 4 mg IV LORazepam. That's good. Um If it's still ongoing up to two doses of benzo, then you can think about your second line um agents. So these are anti epileptic drugs, levetiracetam, phenytoin Valpo, I think in the acute setting, levetiracetam tends to be preferred. Um And then if it's refractory, so that's defined as over 45 minutes, we can consider G A or PHENobarbital as well. Um But you wouldn't want to wait that long to get kind of it and anesthetics involved. Um So as soon as you see that, you know, it's not responding to LORazepam, you'd start having those conversations. Um and escalating that because they're, they're gonna need some more intensive treatment. Um So Janet said, do you wait until five minutes before giving the first dose of benzo? Yes. So if it a lot of, a lot of time you'll have seizure activity which might resolve within five minutes in which case, um you, you wouldn't, you wouldn't need to give a benzo. Um So usually you, you wait for it to be stage epilepticus and then give your IV LORazepam. Um There might be exceptions to this, for example, if, if the patient is known to kind of um is, is known to have epilepsy and, and has been seizing a lot and you, you know that they, they're sometimes prolonged and things like that, then consultants might make decisions that they should give the diazePAM after a couple of minutes. But um or, or for example, if the, the airway is really um obstructed or they've got lock jaw or things like that, so there might be things in your clinical assessment that would lead you to give the, the Benzo a bit earlier, but generally you'd, you'd wait the five minutes. Um uh And, and like I just mentioned, so airway management is really, really important. So the risk here is that because the G CS is so low and they're having the seizure activity, um they can get aspiration, they can choke even on their own tongue. Um So if there's any concerns with airway, um put an airway adjunct in, make sure you're suctioning any secretions and things like that and give high flow oxygen because you wanna make sure that this patient's still able to ventilate um and call anesthetics early if there's any um worry about airway and make sure that they're in the recovery position as well, cos that is gonna prevent those issues with um aspiration and things. Um So yeah, any any questions or comments about status or does that cover everything? Cool. Let's move on to the next case. So in case three, we've got an old lady, um she's coming to Ed, she's got a two day history of fever and confusion and her family said that in the last 12 hours or so. She's been a bit more drowsy and lethargic. She's got a history of type two diabetes detention and CKD. Um, so, yeah, it's probably a bit less kind of obvious from just that, but if we move on to our ae we can start, um, thinking about differentials and, um, anything important from that assessment. So, Airways patent, there are no signs of stride or obstruction and she's, she's speaking but it's in short phrases. So maybe a little bit breathless. Um Her respirate is a little bit raised. SATS are lower end of normal. So she's managing to maintain them on re um and there's reduced breath sounds at the right base on auscultation. Um She's tachycardic and hypotensive uh prolonged cap refill time and warm peripheries. Um So seems quite unwell from those PBS G CS 13. So we know that she's confused and she's a bit drowsy, disorientated. She's got type two diabetes. So her BM is a little bit raised but not concerning in the way that we saw with those DKA or HHS type pictures. Um and then exposure everything else. She's pyrexial quite a high fever, 39.2 degrees and there's no rash. Um Anything that comes to mind there or any comments on, on any of that. Yeah, that's it. Amelia. Yeah, good. So this is, this is kind of your bond or sepsis. Um Yeah, it's, it's um the, the key with sepsis is. So Nichol said you're apsis. Um We don't know what the source is yet. Um That's something that we need to find out. So, how, how would we go about doing that and, and kind of investigating and treating the lady? Yeah. Good Paul urine culture. Anything else you'd want to do? Yeah. Blood cultures, X ray, urine culture. Yeah. Yeah, that's absolutely right. So we wanna do um a septic screen essentially. So any kind of source of infection so commonly will be urine or chest. Um But also if there's any concern about kind of um a gi infection as well, we could do a stool culture. Um If we think it could be viral, we'll do swabs a throat swab. Um And then Paul. Yeah, that's right. So start the sepsis six protocol. Does anyone know or can anyone um I'm sure you know, but can anyone put in the chat what the sepsis six is? Yeah, good amemia. So, fluids, oxygen antibiotics um is what you're gonna give and then you're gonna take the urine output blood cultures and lactate. So that's your sepsis six. really important to know that for OSC and um exams. Um Yeah, that's right. Three and three apple. Um So if we go to our investigations, so E CG again shows sinus tachycardia. We know that how raise a bit up um urinalysis. So, leucocytes, nitro nitrates 11 plus glucose, one plus. Um What do you guys take from that, that urinalysis. Is that something that you'd wanna treat or is there any other consideration that you have to think about? A bit of a leading question? Any thoughts about that, that you're in depth? So, with, with elderly patients, we don't tend to rely on you in, um, because they'll often have a picture like this, even though they are asymptomatic and don't have a uti, um, they'll often have kind of trace leucocytes or nitrates slightly positive. She's got diabetes. So she's bound to have a, you know, again, a little bit of uh of glucose in the urine. So what we really need to do to rule out a urine as a source would be send a urine M CNS. So a midstream urine for microscopy culture and sensitivities. Um Yeah, exactly. So elderly people tend to have that sort of thing on their urine dip. Anyway. Um Is anyone able to interpret that ABG for me? So just, just describe that. Um Yeah, just put it in the truck. Yeah. Good, good uh suggestion. So again, we've got acidosis. So it's slightly lower than um normal P CO2 is in range but lower end of, of normal range. Po two looks. Ok. Um The bicarb is slightly low and the lactate is high and base excess minus six. So, like Nichol said, uncompensated metabolic acidosis with elevated lactate. So lactic acidosis, which is a form of metabolic acidosis. Um uncompensated. Yes. Technically, because the, the CO2 is still in normal range just about if it was a little bit lower. Um then we could call it partially compensated. Um But that's absolutely right. And then if we run through the blood, so white cells are significantly raised. CRP is 210. Um and are OK. Bit of an AK I if we look at a baseline, creatinine is 120 here that's 210. But I sorry, electrolytes are OK. Uh But yeah, urea creatinine are raised. Um So imaging, we're going to want a chest X ray as, as someone suggested earlier. Um And this is what we've got any interpretation of that. Yeah, spot on a media. So right lower zone, you can see that um this area here, it's got some pacification. Um It fits with our ae assessment. If you remember that on auscultation, there was reduced, breath sounds at the right base. Um So it's, it's uh looks like a pneumonia in the, in that area. Um And then we've already mentioned, I think a little bit about management. So probably already mentioned these sorts of things. So, yeah, sepsis 63 and three out, we've measured that um on obviously monitor the obs the lactate and the urine output. That's kind of part of your sepsis six as well. So, if it's worsening, um we haven't mentioned, well, we mentioned yet part of the sepsis six is your broad spectrum IV antibiotics. So, if it's worsening despite all those treatments, so you're giving fluids, giving you antibiotics, you're giving oxygen, you're monitoring the patient, then um consider it input as well. Um And then treat the underlying cause. So, like we said, in this case, we've got our, we, we know it's a pneumonia. Um but if the blood cultures um come back with anything specific, um or if, for example, we've sent a, a viral swab or, or um done anything else that comes back positive. Um Then we can tailor our antibiotics and go take them from broad spectrum to a, a more narrow kind of um focused uh window. Um Does anyone know um in this case, what antibiotics would usually start considering it's a, it's a pneumonia. Um And I'll just go back to the A to e assessment for you might give you a bit of uh more guidance. Yeah. Good Nico. So, um what I was getting at with this is is uh if you look at her curb 65 score. So um she's confused. We know that the urea I think was on the next slide um is raised. So um that's, she's already scoring a too um Her respirate is high but I don't think is high enough for us to, to give us a point because it has to be over 30. Um Her BP is low and below 90/60. Um and she's over 65. So she's scoring four out of five on C 65. So she needs, um, well, from the OB S and the clinical picture as well that she needs admission to hospital, she needs IV Comox C and often we'll cover for atypicals as well. Um, does anyone know what I mean by atypicals and what we used to cover? Yeah. Good Emelia. So, so alongside our investigations, we'll send, we usually send a urinary lesion Ella and a Thrix for mycoplasma. Um, and it would usually be Clarithromycin, which is a Mac macrolide, as you said. Um, so we'd add that on as well for, for most of these kinds of patients. Um, so yeah, that's sepsis. Any, any questions or comments about that case or are we good to move on? All right, let's, let's carry on then. So case four, we've got a young man, university student. He's come to Ed, um, two day history of severe headache, fever and vomiting and the last six hours he's become quite drowsy, but he has no past medical history otherwise feeling well. Um, any thoughts, any differentials, anything that immediately comes to mind you worried about with this? Yeah, meningitis. So this is kind of your typical presentation of meningitis. So if we look at the A to e um, again, if you guys just, just pop in the chart, anything that seems a bit interesting or, um, that comes to mind. So a is patent, but he's lethargic, he's a bit slow to respond, respirate has raised a little bit. Um He's maintaining his, his sats, he's got some irregular breathing. Um, heart rate is 58 BP 14, 3/67 cap refill is slightly prolonged, three seconds and warm peripheries G CS 12. Um So pretty significantly reduced. It's got photophobia. Koenig sign if anyone can um mention what Koenig sign is in the chat as well. That'd be good. Um BM 6.4 pupils are equal but sluggishly reactive. Um He's got a high fever and he's got a typical non blanching, purpuric rash over the lower limb. Um but no other kind of signs of trauma or infection or injury. Um Anything unusual about this or anything that's caught your eyes. Yeah, very good. Nicole Cushing's tried. So, so what is Cushing's tried? And what does it indicate? Yeah, hypertension, bradycardia and irregular respirations. And, and what is that a sign of? And actually it's not just um hypertension, it's the the widened pulse pressures as well. So, um his BP is 14, 3/67. So that's a very wide gap between the systolic and diastolic. So that's uh kind of more specific um of Cushing's triad. But yeah, and as well as bradycardia, irregular respirations and yeah, exactly elevated ICP. So what do we think has happened? It's, it's meningitis. Um but he's also got a raised ICP. Why, why could that be? So, so sometimes with meningitis you can get um cerebral edema. Um just because of the inflammation in the brain and it can also happen with, with other things that affect the, the brain as well. So, um encephalitis as well. Can anyone think of any investigations that we'd want to do considering what we're thinking about in terms of diagnosis? Ok. Yeah, good suggestions. Is there anything um that would, that would stop you from doing a Lumb puncture in this case? Yeah. So the raised ICP. So, so what's the risk if you're doing a L Lumb puncture with a raised ICP? Exactly. Yeah. So coning, so brain herniation, um other reasons actually why you wouldn't um do a lumbar puncture is if, if there, if there's a rapidly evolving rash or if there's cardio respiratory involvement. So if there's, if it's a very, very severe um infection, then you would, you wouldn't do the, the um the LP as well. But yeah, in this case, it's the, the raised CP, which is a contraindication um because that risk is so high. Um But yeah, the other suggestions are very good. Um So let's have a look what we've got. So again, we've got an E CG sinus tachy. Um ABG Can anyone interpret that? For me? It's actually, it's pretty. Ok, isn't it? Um No acidosis, no alkalosis CO2 is a little bit low. Um Probably just cause he's a little bit breathless. Um aside from that lactate is a tiny bit raised as you'd expect with an infection. Um And then if we go through the blood. So again, white cells are up crp is significantly raised. Um As you'd expect with a meningitis infection, um sodium is in range, potassium is in range urea, creatinine look fine, coagulation is normal. So, again, that's important to note because if uh another contraindication for a lumbar puncture would be if there's any kind of bleeding disorder. Um And we've sent some blood cultures which is pending. Um We've got a CT head as the media suggested as well and that shows that confirms your signs of cerebral edema, which is the cause of the raised intracranial pressure. Um but no focal lesion, no hemorrhage and lumbar puncture. As we mentioned, we're, we're not gonna do it at the moment um because of those concerns. Um And then how, how are we gonna manage this patient? Yeah, I could. Amelia. Um So the antibiotic that we give is cefotaxim. Yeah. Um It seems like a bacterial infection because like I said, of the severity that they're quite ill. Um So, yeah, if we go to the management. So a lot of clues about the raised intracranial pressure aside from cushing's triad. So usually with meningitis, you'll get patients who, you know, they're photophobic. Um They'll be a little bit fatigued and kind of hiding under their, their bedsheets because of the light, but they don't tend to really have a significantly decreased gcs. Um The sluggish pupils when, when we did that at e so pupils were sluggish to react. That's wouldn't normally happen with the meningitis as well. Um I don't know if this case did have vomiting, but vomiting is another uh indication. Um And obviously we've got the uh the CT um we talked about Cushing's triad. So, as well as treating the meningitis, we need to treat the raised ICP as well. So you'd elevate the head to 30 degrees. Um Could you could consider Mannitol or hypertonic saline if it's quite severe, but that would again be a a senior decision and get neurosurgical input if needed as well. Um Again, we, we would think about the differential. So not typical for this presentation. There are reasons obviously why we thought it was meningitis, but obviously important to think about encephalitis of arachnoid hemorrhage, a viral picture as well. Um And the management is IV cefTRIAXone as um oh you said cefotaxime, but the same, same kind of class. But um I think Ketrax is the the first line um plus minus dexamethasone um and prophylaxis of close contacts. So you can either give ciprofloxacin or rifampicin, I think as well. Um So that's a bit about meningitis and raised ICP. And then I've got this slide as well in terms of when we would do a lumbar puncture, um the difference between viral fungal bacterial and tubercular um useful to know often can come up in exams in terms of giving you lumbar puncture results and asking you what the diagnosis or the management is. Um So I'll give you guys a 30 seconds to, are you elevating just the head or do we elevate the upper body? Um Good question, I think in, from my experience, it's usually um kind of the, the whole upper body. Um So you, you know, your NHS BEDS can kind of tilt upwards. It would be, it would be like that. Um Yeah, that, that's from what I've seen. So that 30 degree angle would be kind of the upper back as well. So I think that is that case done. So I think we've got one more case and then we can call it a day. So case five, 34 year old female admitted to the hospital for treatment of a soft tissue infection suddenly developed these symptoms. So, difficulty breathing, cramping, dizziness. Um and she's just started some IV flu clocks. She's got no history of asthma but no drug allergies. So, what do we think's going on? Yeah, anaphylaxis. Exactly. So if we go to our at e, that'll probably confirm what we're thinking. So, Stridor horse voice. So those are typical um, tongue swelling, unable to speak properly in full sentences. Respirate is significantly raised. Sats are starting to drop, bilateral wheeze heart rate is up. Uh hypotensive cap ref was prolonged cold, peripheries alert, but very distressed. Um, blood glucose is in range and on exposure, you can actually see a urticarial rash, swollen lips, um, but no other significant findings. So that's really typical picture of a, a true anaphylaxis. Um And often the patient is really, really distressed as, as you can imagine because everything is closing up and they, they literally just cannot breathe. Um So it's important that you just, um, try and keep them calm as you initiate the treatment as soon as, as quickly as possible as well. Um, any investigations in particular that we need to think about. Um, and also management as well as soon as we know the diagnosis, we should, we should treat this. Yeah. Really important to remove the IV. So stop whatever's, um, precipitated the anaphylaxis elevate the legs as well as, as a good thing to do. Um, how are we gonna treat the actual anaphylaxis though? Yeah. Good. I'm adrenaline 500 mcg. Yeah, exactly. Um, anything else we can think about as well alongside the adrenaline? That's, that's obviously the mainstay of treatment. Um, but there are some other little things we can give just to help, um, this patient. So, if we go to our next slide, oh, so we've got some investigations first, um, sinus tacky BM zone range, as we said before. Uh, nothing too interesting on the ABG, similar to last time. Um, lactate is a little bit up as you'd expect and bloods are still pending. Um, but we get you the management. So, like we said, Yeah, stop the precipitant I adrenaline, you given the correct dose as well. Um If needed, we can repeat that after five minutes. If there's no response, then it, that's when we call it refractory anaphylaxis. Um So for that, we'd have to treat with an adrenaline infusion, which means that they will need an it or HD U bed because they'll need uh monitoring um airway support again, similar to the status epileptic epilepticus patient. Um airway is, is really important. So if you find that the, the swelling is not coming down after you've given your adrenaline um really escalate early to itu. Um So, so that they can think about other things and airway adjuncts and opening up the airway. Um So what I was trying to allude to you earlier was that IV hydrocortisone and chlorphenamine, they are often good adjuncts. Um That can help. Um But the, the main thing is the adrenaline as you know, and then one thing we will send when we have a patient with anaplasia is tryptase. Um so that we send it at um like when it's happening at one or 21 to 2 hours and 24 hours later. Um And if that's raised at any of those points, then that confirms that it's a true anaphylaxis reaction. Um So it's just good practice to, to send that as well. Um And then, yeah, this is one thing I wanted to include as well. Something I always used to kind of learn for the exam but forget completely a, um, assume immediately after. Um, so sometimes you will get questions about this. So when, how long you need to observe patients after they've had anaphylaxis. Um, so if you just have a quick read of that, so generally it's what, as you'd expect if there's kind of a good response and they've got had complete resolution of symptoms, they already know how to use their adrenaline and they've got people at home then they can be discharged fairly quickly. So, two hours you can think about after two hours, minimum six hours, if they've needed a couple of doses or they've had a previous biopic reaction. So, it's actually not uncommon that patients who have allergies and have anaphylactic allergy allergies, um, they'll often have an anaphylaxis attack and then you'll, you'll treat them, they'll go back to normal, they'll stabilize. Um, but within about half an hour or so, it's exactly the same. It's like deja vu, they've, they're swollen up, they're wheezy, all that sort of stuff. Exactly the same again. Um, so a lot of patients will have that biphasic reaction. It's really important to note that, um, and ask the patient because they're usually aware that it's a biphasic thing. Um, so in that case, they'd need minimum six hours and then minimum 12 hours for any of these things. Um, so if it's a severe reaction with requiring more than two doses if they've got, you know, severe respiratory compromise, um, if it's kind of a slow release precipitant. So if, if it's still being absorbed, um, if it's late at night or may not be able to respond if they don't have anyone at home or, you know, they've got other issues. Um, and obviously access to care. So if they, if they don't really have emergency care on hand that can be there quickly, then you'd want to keep them in just to be on the safe side. Um So yeah, useful to know for exams, um just in case those come up. Um So that was all the cases, I've got a couple of slides on shock. Um So we'll just whizz through them because it's been over an hour already. Um So a lot of these cases had patients who had shock. Um and we often say shock, uh you know, patients in shock, but what it actually means is inadequate tissue perfusion, cellular hypoxia organ dysfunction, and then potentially death, obviously because it's like AAA severe condition and there's a few different types. So hypovolemic. So you lose your circulatory volume uh often because of hemorrhage dehydration. So rings a bell with one or two of the cases that we had. Um So you get your typical hypotension, tachycardia, dry membranes and a reduced JVP. Um And that's going to differentiate it from cardiogenic shock. So, kind of the same sort of picture apart from the raised JVP and pulmonary edema because you're gonna retain that fluid, your p your, your heart is not able to pump it out efficiently. So it's gonna go back into your lungs and, and your, your venous distension from your uh jugular. Um And obviously, that's secondary to ischemia, some mis arrhythmias, cardiomyopathies. Um So that kind of heart failure causes um and then distributive shock. So, the key differentiator with that is um the warm peripheries. So, the most common one is, is septic shock. Um So, and that's gonna be because part of that, you know, systemic inflammatory process is the release of um a lot of vasodilators. So you're gonna get really vasodilation of uh of all your vessels peripherally. So you'll have that those warm peripheries and then actually later on down the line, if it's not treated, um they'll eventually get cold peripheries uh as your, your kind of inflammatory um response um evolves. Um And then obstructive shock is a physical obstruction. So the main one we think about is pe um also tamper our attention, new authorities, hypotension, you'll get distended neck veins again because of that mechanical obstruction in, in tamponade, you'll obviously get your typical um muffled heart sounds and in pneumothorax, obviously absent breath sounds. So other, other little things that will give you clues as to what the cause of the shock is. Um I'm not, I'm not sure what, how valuable it is really to um kind of be able to differentiate them into these categories. But it's just worth having a kind of eye on just uh it could come up in exams and it's mentioned in the UK MLA curriculum. Um So just a little summary there. So these are your features, these are the signs that you're going to see on examination. Um Also renal and neuro neurological manifestations as well. Um And then management as you know, a to e approach, make sure your airway is patent, make sure they're getting oxygen, they're able to ventilate fluid resuscitation. If it's um worsening cardiogenic or distributive shock, then you can think about vasopressors and inotropes and involving the it team. Um Make sure you, you monitor their G CS treat any electrolyte derangements. Um You know, the, the DK HHS kind of things that we were talking about. So make sure their glucose is um in control and then also obviously I identify the causes and treat those as well. Um So yeah, that's uh that's it for this session. Um This is the feedback form if you guys can uh fill that out and, and let us know if there's anything you particularly enjoyed or any changes you'd like to see. Um We really appreciate that. Um If there's any questions or anything, I'm happy to take some more as well. Um Any about anything we covered. Um Just please pop, pop in the chat. Cool. Well, I hope that was useful. I can't see any questions coming in. Um So yeah, please give us the feedback and let us know what, what, what worked well, what didn't work well, what, what you'd like to see implemented in the future and that's really, really useful for us. Um But yeah, I hope you gain something from that. Thanks for your time. We'll call it a day there.