Collapse - To admit or not to admit?

SPEAKER_02 0:11

Hello and welcome to a new episode of Home of Medicine Podcast in association with the Royal College for Physicians Edinburgh. My name is Ben Lovell, I'm a consultant in Acute Medicine, and I'm here with my podcast host.

SPEAKER_01 0:24

Hi, I'm Dr. Amy Beveridge, a consultant in acute and general medicine in the UK.

SPEAKER_02 0:29

So, Amy, it's my turn and I've got a case for you. Are you ready?

SPEAKER_01 0:32

Okay, absolutely.

SPEAKER_02 0:34

Okay. Emergency department, you're on the take. New referral from E.D. 42-year-old man collapsed whilst out jogging. Apparently, according to bystanders, he just hit the ground, lost consciousness for less than a minute, and recovered spontaneously and seemed a bit groggy. But by the time the paramedics arrived, he was oriented and alert, although he did look quite pale and clammy. And he told the paramedics he'd been a bit ill with a flu-like illness for a couple of days, but is otherwise in very good health. And he was transferred into the ED, where he was found to be slightly hypotensive at 95 over 60, heart rate 110 regular, ephebrile, normal saturations, normal respiratory rate. Initial reactions, please.

SPEAKER_01 1:33

My initial reaction is why has this gentleman been brought to hospital? He was going for a run, he's clearly had a vasorvagle, he probably hadn't eaten breakfast. And I'm happy to give him a cup of tea and a coke and send him home. However, that is not the right thing. So that's, you know, some that's my type one thinking at play there. But my type two thinking is going 42-year-old man, collapse whilst jogging, loss of consciousness, could it be vasovagal? Did he have a low blood sugar? Could it be a cardiac arrhythmia? Exercise induced cardiac arrhythmia. Did he have a flu-like illness? Has he gone out to exercise too soon and just felt very weak and unwell? Other things that cause sudden loss of consciousness, I'm thinking really serious. Could this be a pulmonary embolism? Could this be a hemorrhage, brain hemorrhage? That's where my brain is at the moment.

SPEAKER_02 2:31

Um fine. You've named I think three systems there, um, neural, cardio, and respiratory, which is absolutely fine. And then we'll we'll we'll home in as the story uh progresses. Um for me, I don't like exertional syncope. I it it makes I don't like it in my bones, it makes me nervous. Uh people who are standing around all day and their blood, blood all pools to their legs, and then they're the vasovagolas for me when they get us. But I don't like people who who are uh lose consciousness when exertion, it makes me anxious for cardiac problems, especially when they're a bit tacky afterwards. Although the spontaneous recovery very quickly, the lack of a post dictal phase, it sounds like, um, and uh looking pale and clammy, that does that could be you know that could be vagal, couldn't it? But um I I I thought it smelt a bit cardiac. Although, what do I mean by cardiac by smells cardiac? You mentioned arrhythmias.

SPEAKER_01 3:30

Um smells cardiac. Um I guess I'm thinking, is this an electrical problem in the heart? Is this a structural problem in the heart? Is it a flow problem with the heart? So electrical problem, I'd be thinking, is it an arrhythmia? So have we got a problem with the AV node, the SA node? Have we got a bundle branch block? Have we got one of those weird syndromes, regardless syndrome that you know you occasionally see? Um, then I'm thinking, is this a structural abnormality of the heart? So is he known to have a dilated cardiomyopathy? Is he known to have a structural abnormality from birth that hasn't been picked up, although it is quite late, I guess, for that? Has he got left ventricular outflow tract obstruction, which can also contribute to these types of symptoms, particularly on exercise and exertion? And the final one is this a blood flow. So is this um, you know, a coronary uh artery blockage that would indicate to myocardial infarction? Potentially. So that's where my thought process is going at the moment. As well as that, you can also have things like infections and toxins that may be affecting the heart, but that's more like an indirect effect on the heart than a direct.

SPEAKER_02 4:45

Yeah, I agree. And thinking about just going through what you've mentioned, um, arrhythmias, um, why would a 42-year-old suddenly have what kind of arrhythmia would make would fail you in your tracks when you're jogging your 42? It'll be something super fast or super slow. A super fast one, which we all would would fear the most, would be VT. So did he have an episode of ventricular tachycardia and down he went, um, just a de novo. Um, if he had a bit of AF fibrillation or flutter, in my experience, that doesn't cause syncope very rarely in in younger people who are able to compensate for it because um going up to a rate of 140, 150, 160, even if he had a burst of SVT, which can go up sort of 180, 190, just in my experience, tends not to make people suddenly lose consciousness. They tend to just compensate, okay. But VT, absolutely.

SPEAKER_03 5:36

Yeah.

SPEAKER_02 5:37

Or did he go too slow? So did he go too slow and have a braddy episode? Did um he have an AV nodal block, like you say? So his uh sinus node is firing away and his ventricles don't know what's going on and they just don't pump enough, or did he have a sinus node problem and he just wasn't generating a rapid enough heartbeat for it for any particular reason? So, yeah, arhythmogenic collapse would be something I'd be really worried about. And you mentioned flow as well, left ventricular outflow obstruction. Um, I do think about exertional syncope. I think of HOCUM, so hyperobstructive um um uh uh LV OT uh block. And usually, I mean, uh people can present later in life. People who've got familial HOCM, so hyperobstructive cardiomyopathy, they they can usually get picked up in screening when they're children because they had a relative, because there are screening programs, but sporadic hocum can present in your 40s, 50s, 60s when you've developed enough anterior systolic motion of the mitral valve or or that horrible asymmetrical and hypergrophy they get, which blocks the LVOT. And maybe it just big hit critical narrowness and and then down he went when he just tried to mount a good blood pressure to support him running. So yeah, it's either two same thoughts. PE I think is a good thought. P does I've seen P present with syncope quite a few times, yeah.

SPEAKER_01 6:56

Yeah, yeah. And it's not something years ago when somebody had syncope. PE wasn't in my mind. And now anybody who comes with syncope, I'm like, is this a PE? Why isn't it a PE? Uh I've seen quite a few actually, so it's always at the forefront of my mind, absolutely. I've was he a new exerciser or is he always exercised?

SPEAKER_02 7:16

I'll tell you, but first I want to know why you're asking.

SPEAKER_01 7:19

Well, if he's I'd be more worried if he was an an is if he's always exercised, because um if he's always exercised, it means that his body's probably used to it um exertion and it would make Hokum and L VOT a bit less likely because as we discussed before, you tend to pick that up earlier. But if he's a new exerciser, then I'd be like, okay, well, actually, I've seen this happen before. Somebody's gone to the gym, they've gone wild, and they haven't exercised for 25 years.

SPEAKER_02 7:52

Um and I guess he'd never run before, and if he tries running for the first time, it could unmask for example, which he'd never know to this before because he's never had never put his heart under that much strain purpose before. That would be an interesting thought. Okay. Uh he actually was a regular jogger. It was something he quite fit and active person. So we talked about cardio and we talked about respiratory things, and then you briefly mentioned did something happen intracranially. I guess so. I guess I least prefer that because why did he recover?

SPEAKER_01 8:22

Uh at the speed. Yeah.

SPEAKER_02 8:25

If he'd had a hemorrhage, for example, he should still be quite unwell if it was enough to knock his GCS down a few points. All right then. So that's your initial reaction. I was just interested to hear. Um, and I wrote down um smells cardiac, arrhythmia versus obstruction. So we had dissimilar sort of mind lines there. Um, his history was that this has never happened before. Um, and when I said to him, Um, did you did you get any warning? Did you get chest pain, palpitations thinking about um an arrhythmia? He says, No, no warning, just he was running, and then the next thing he's coming around on the floor. Um, and that's never happened before. Usually very fit and well, an active guy with actually no past medical history and no regular medications on board, um, and socially um exercised a lot. It was a non-smoker, very little alcohol. So I um I thought that was interesting.

SPEAKER_01 9:18

Um could it have been a seizure?

SPEAKER_02 9:23

Okay.

SPEAKER_01 9:24

I think the recovery's too quick.

SPEAKER_02 9:26

Yeah, he didn't seem to have a post dictator according to the witness history, but um exercise induced seizure. I mean, yeah, I think I have seen that before. Um, and it isn't completely off the table. I whenever I'd see patients, I uh a lot of people I see on the ECU, the enhanced care unit, which is our area of AMU, you've come in with collapse, with transient loss of consciousness, or a T lock, as they the kids call it. I often do say to them on my ward round, so what we're going to do, we always try to work out is um when people lose consciousness, is is it head or heart? Head or heart? And they're the two main things. And of course that's not quite true because then we just be always mentioned P just then. But we're trying to work out something happened in your brain or something happened in your heart. And that's how I frame it for patients. Got quite a nice way of understanding um why I'm doing the test that I'm doing. So um, yeah, I saw him in ED, and now I need to make not only a diagnosis but a plan. So what would you like to do next?

SPEAKER_01 10:26

Okay, so I'd like to do a clinical examination. So heart sounds.

SPEAKER_02 10:31

Great. Heart sounds, no murmurs.

SPEAKER_01 10:34

Okay.

SPEAKER_02 10:35

Um, no radioradial and no radiophemoral delay. Do you remember the murmur you get for Hokum? I remember learning it for paces.

SPEAKER_01 10:44

You're gonna know this and I'm not. Is it a pan-systolic murmur?

SPEAKER_02 10:48

Yes, it's systolic. But do you remember how you accentuated and and everything like that? No, you don't.

SPEAKER_01 10:55

No, I shouldn't.

SPEAKER_02 10:56

You must have done this when we were reading Game Freddy for paces.

SPEAKER_01 10:59

Absolutely, it was a long time ago when I did paces.

SPEAKER_02 11:01

So it's a systolic murmur, harsh systolic murmur. Harsh systolic murmur increases when they do valva. Yes. Because it increases the Venus return. And also increases on standing up and is quieter on lying down. And I remember being taught on a paces course that was saying, so if you think someone's got Hokum, you make them squat on the floor. Yes.

SPEAKER_01 11:24

I remember.

SPEAKER_02 11:25

You listen to their murmur, and then you get them to stand up with your stethoscope still in situ and listen. I'll s never in my life have I done that big front of real quick.

SPEAKER_00 11:35

So it hurts me.

SPEAKER_02 11:37

Yeah. I know. And I'd have to squat with them, wouldn't I? So that's off the table. But this made me, I'm gonna go, oh god, that's an old flash uh back uh memory there from the past. So anywho didn't have a murmur. So that's Okay. So she had uh chest is out, chest was clear, chest was clear, no pedal edema. Um he had a blood a blood pressure of 110 over 70.

SPEAKER_00 12:03

Did you do it on both arms, the blood pressure?

SPEAKER_02 12:05

I didn't. Why what are you thinking? Co octation of the iota or something? I did not, I confess. Um I did uh a heart rate, which was 80 and regular, um, and his stats were 97, 90 under men, he was afer with a normal respiratory rate. It's not a very revealing examination, actually.

SPEAKER_00 12:32

Rookie dokor what do you want what do you want? I want an ECG.

SPEAKER_02 12:41

Okay, good. So heart or head, heart or head. Let's look at the heart for first of all.

SPEAKER_01 12:46

Let's let's look at the heart, yeah.

SPEAKER_02 12:48

Yeah, but sinus. Sinus tacky at the time of recording, about 102, so not a great tacky, with some very non-specific T-wave flattening in the lateral leads.

SPEAKER_00 13:02

Okay.

SPEAKER_01 13:04

Uh oh. Doesn't really tell me much, I guess. Maybe a bit of schemier, possibly, pre-I don't know. It's not it's not very specific.

SPEAKER_02 13:14

Exactly.

SPEAKER_01 13:15

Um, I'd certainly want to have a a little more of a look into the heart potentially. Has he had any previous ECGs? It doesn't sound like he has. No, but no, I'd probably want to put him on a monitor um at this point because with these arrhythmias, sometimes they can obviously um click, you know, go into arrhythmia and come out of the arrhythmia. So that might be an idea. Because he was hypotensive as well, wasn't he?

SPEAKER_02 13:39

On the scene, yeah. Yeah.

SPEAKER_01 13:45

Glucose?

SPEAKER_02 13:47

Okay, glucose was normal.

SPEAKER_01 13:49

Okay, blood tests, so full blood count, usenes, LFs.

SPEAKER_02 13:53

Full blood count was normal across the board.

SPEAKER_01 13:55

Yeah.

SPEAKER_02 13:55

Um urea, uh, creatinine, sodium, potassium, normal, normal, normal, normal. CRP, four. Any blood tests you might get. CK? CK was 4,100. Wow. Our upper limit of normal is 500. So it was up. But let's just contextualize this. He was jogging.

SPEAKER_01 14:26

I wonder if my CK goes up that much.

SPEAKER_02 14:28

It will. Have you never had people? Oh, well, because I work in London, so we get some people who come in after the London Marathon, and their CKs blow your mind and make your head stand on end. They're like five figures. Um, but it that's a normal finding after after you dull marathon. So I bet yours does grow up a little bit.

SPEAKER_01 14:45

Oh, okay. Okay.

SPEAKER_02 14:46

So I've got eyeball, what's the highest CK you've ever seen?

SPEAKER_01 14:50

Oh, like 150,000.

SPEAKER_02 14:52

Okay. I once saw 500,000. But the diagnosis, it was a patient with polymycitis. So that is inflammatory and rather sort of muscle distraction. Well, it was inflammatory muscle destruction. Gosh. I remember that very clearly. I was like, I've got a patient with a CK of half a million, and they went to ITU. I was an SHO in neurology at the time, and they were accepted at ITU for ventilatory support. And I can't remember why, but for some reason, me and the Reds, the neurology regs, were going with the patient as they were being wheeled by the porters from the neurology war to ITU. And I just remember it's one of those things that stay in your memory forever. The neurology reg said to me, Ben, out of the patient's ears, if he arrests on the way to ITU, we just run. Okay, don't stop and do CPR. We just run to ITU and push as fast as we can. And I stuck with me because I remember thinking to myself, oh my gosh, this is the most terrifying thing anyone's ever said to me. Do you think that's gonna happen? But also it was it was quite exciting but terrifying. Anyway, that memory stuck in my mind that half a million CK. Anyway, you're about to say something really intelligent about this man's blood results, I could tell.

SPEAKER_01 15:57

Hi, and likely. Um, would you do a troponin?

SPEAKER_02 16:01

Would I? Well, someone had already done one.

SPEAKER_01 16:05

Okay.

SPEAKER_02 16:06

So we're still going heads or heart, and we're now we we we we want to admit him to telemetry bed, right? Because we're looking for arrhythmia. Shall we look for myonecrosis? Shall we look for heart muscle damage? Got an elevated CK, which we say, oh, maybe this is running, but of course you get a CK release with myonecrosis as well. So his troponin was 88-0 and the upper limit of normal for us is 14.1.4.

SPEAKER_01 16:28

Oh, right. So it is high.

SPEAKER_02 16:30

Yeah.

SPEAKER_01 16:30

Okay. Did you do a calcium-magnesium level?

SPEAKER_02 16:34

We didn't do a magnesium, but did have a calcium which was normal.

SPEAKER_01 16:37

Okay.

SPEAKER_02 16:38

What are you thinking of there?

SPEAKER_01 16:40

No, I was thinking of calcium because some calcium abdominalities can cause cardiac arrhythmia. Is easy hypocalcemic or hypercalcemic? And I was just thinking, has it become really, really hypocalcemic gone into Sardopois, VF, and then collapsed?

SPEAKER_02 16:53

Oh, that's a good point, actually. And I should have mentioned when I mentioned talked about his ECG that he had a normal QT, normal QTT.

SPEAKER_01 16:59

Okay, excellent. Okay. And then magnesium, again, low magnesium levels can contribute towards cardiac arrhythmias. Um I'm I'm stuck, Ben. If I'm being honest, I'm we've got our routine blood test, we've done a glucose, we've done usenies, LFTs, magnesium, calcium, ck, trop T. Ooh, would you do a D-dimer?

SPEAKER_02 17:26

No, I did it. I actually didn't do one. Okay. Because you're thinking about P. Why would you I'm not hate D-dimers? Why did you sound so excited about it?

SPEAKER_01 17:36

Yes, I just wondered whether you'd done one or not. No, I I wouldn't I wouldn't have done a D-dimer in this gentleman, to be honest.

SPEAKER_02 17:41

Um I I didn't do a D-dimer because I thought that I thought the pretest probability was was low. Maybe I should have done because of course if you'd had a massive P that would have caused heart strain and that would have caused that cytroponin rise as well, wouldn't it? So maybe in respect a D-dimer would in this instance have been useful. Um in at this point, I'm not gonna ask you for a diagnosis, which is fine, but what's your plan?

SPEAKER_01 18:06

Now, I've got two, I've got like two things on my shoulders. One's going discharge and uh discharge, watch and wait, consider a 48-hour 72 hour halt monitor. Um that's my one brain, and my other brain is but why is the drop high? Why is the CK high? This is odd, he's got some T-Wave flattening. So I think in reality, I'm gonna admit, I'm gonna put him on a monitor, yeah. I'm going to keep an eye on his ECG, I'm gonna get routine, I'm gonna get some 12 lead ECGs as well. Yeah, I'm probably gonna have a chat to the cardiology reg and say, look, can I just run this past due? I'm struggling to really get to grips with what's going on here. Do I scan his head? I'm gonna scan his head then.

SPEAKER_02 19:02

Okay. So your plan as the post-tech warner, to be clear, is uh admit to a telemetry bed for monitoring, yeah, two, discuss with cardio, three, CT head.

SPEAKER_00 19:12

That's my plan.

SPEAKER_03 19:14

Okay.

SPEAKER_02 19:15

Um I admitted him. I always I admit unexplained T Logs. I do, I just do for for telemetry, which is an investigation, by the way. No test. Um, and I don't admit all T logs if I can explain it. For example, if someone has a line standing blood pressure and there's a drop and they had a postural um transition and I think they're safe, I'll discharge them. Um if someone has, I don't know, um uh uh an episode in keeping with a non-epileptic uh event, then I won't admit them for T log. But unexplained T logs, I do because I just worry about cardiac arrhythmias and I want to make sure they don't have anything that I could unmask on an overnight monitoring. That's that's that's the uh the truth there. So I admitted him. The troponin I couldn't quite explain. No, he doesn't have a textbook history for an ACS, right? He didn't say he didn't have chest pain, he just went down. But I was a bit worried that there had been some kind of atypical presentation of some kind of acute corony syndrome. His ECG is not normal, his troponin's not normal. So from that, I made a decision to treat him empirically overnight with ACS treatment, which is aspirin, clopidogryl and fondaparinux, put him on a monitored bed, cardiology review in the morning, and I requested an echo because I want to structurally look at the heart. Um, I know from experience cardiology like to have an echo when they review patients. Um, the echo request I made was any um transit loss of consciousness in a healthy young man on exertion, query structural abnormalities, and also elevated troponin with lateral T-wave um depression, query regional wall motion abnormalities. Did he have an infarct? Has he lost? Has he got a regional wall motion problem now? He's got like a hypokinetic lateral wall or something that might indicate uh an ischemic, an infarct. So I admitted him for for those things. Um and uh oh, and I said, and let's repeat his troponin. You know, trends are interesting. Yeah, absolutely. Troponins, you know, they they can travel in different directions. So so that was my plan. Um and in the morning I came in. The uh doctor who'd been um attending overnight said he had a little bit of the patient had a little bit of intermittent but very non-severe chest tightness at rest, which they treated with some GTN. Um and they did some serial ECGs overnight, and his uh he had some very new mild ST depression laterally. So and they repeated his uh his troponin, and it went from 80 to 7649. Wow. Um, which is obviously a high and um then he had his. Echo and it showed he had globally reduced ejection, globally reduced LV function with an ejection fraction of 40%. And there was no regional wall motion abnormality to indicate he'd knocked out a wall within infarcting the territory. It was globally the LV looked sluggish. So a massive four-digit Chapone number, new finding of LV uh dysfunction with global um reduction in motion um in a healthy young patient. This pushed a new diagnosis to the top of my differential now. Oh, with a preceding two-day viral illness.

SPEAKER_00 22:43

Pericarditis?

SPEAKER_02 22:45

Pericarditis.

SPEAKER_00 22:47

Myocarditis. Yes.

SPEAKER_02 22:50

I've choked in my own language, my own words there. I said this has got to be myocarditis, viral myocarditis. He's um whenever you see a trop rise in the thousands, to me, I don't you don't see that with an infarct. You see that when the whole myocardium is inflamed and it's releasing um troponin. So whenever I see troponin north of a thousands, that's me, that always makes you go, ooh, could this be an inflammatory process? It says my um um myocarditis. Um and that would also explain his uh reduced LV function, it would explain the troponin. Um, it probably would explain his T lock. If he had an ejection fraction of 40% and he was pushing himself or pushing himself, he just did not create enough of a cardiac output to produce his pain and down he went, lights go out. Myocarditis tends not to hurt because there are the nosoceptors in the heart are primarily in the pericardium and uh coronary vessels. I mean, they uh the myocardium does have some pain receptors, but they tend to mostly detect ischemia rather than inflammation. So the fact he was having some pain now, I thought probably the pericardium is involved as well. So I pushed it all together and I said likely viral myopericarditis. Um and I thought that fitted together very nicely. And of course, if you want to diagnose this, you've got to do a cardiac MRI. Did you do one? Yeah. He went for a CMR and the CMR confirmed the diagnosis of viral uh of myopericarditis.

SPEAKER_01 24:19

And did you try and isolate the virus that it caused it?

SPEAKER_02 24:23

I didn't, and I did say to a cardiologist, do you routinely screen for Sacky virus? So he says, honest, we don't. It doesn't change anything for the patient. There's no role for immunosuppression or or antiviral treatment. So actually, whilst it might be intriguing to know the core virus, it actually doesn't matter for the patient trajectory.

SPEAKER_01 24:43

Okay. So when you first started talking about this case, I'll show you because I have written it. I don't need to think I'm just totally making things up.

SPEAKER_02 24:50

Oh, it's like on countdown where they share their answers with someone else.

SPEAKER_01 24:53

I've got I've written COVID.

SPEAKER_02 24:55

Oh yeah, you did. Is that how you think? Show me that bit of paper again. That is crazy. Well, you just write things in random patches of the paper. You don't go left to right or top to bottom. This is a representation of your mind. What a fascinating insight.

SPEAKER_01 25:12

Nobody wants to be my mice. But it's it's weird because my desk is the same and my office and everything, and that's I know where everything is, but yeah, so I I initially thought could this be COVID uh virus, and then because I had a similar episode and I did something passed out running, but I had COVID. Um anyway. So this gentleman then had a viral myopericarditis.

SPEAKER_02 25:41

Yes.

SPEAKER_01 25:41

What was the management plan and follow-up for this gentleman?

SPEAKER_02 25:45

I'm glad you asked. So um viral uh myocarditis, they do like to keep them as an inpatient until the trop starts to fall. Because a rising trop puts them more at risk for fulminant myocarditis, myonecrosis, fatal arrhythmias such as VT, which is much more likely when you've got structural um problems with the myocardium or scar. Um, so they we you keep them in until their trop turns the corner and starts to fall again. And in the acute phase, there's actually really good evidence for beta blockers and ACE inhibitors or ARBs, but anything that blocks um uh angiotensin girls, just like with normal heart failure, it helps protect the patient from cardiac remodeling and promotes the healing process. So you start them on something like ramapril and a bit of bisoprolol, uh, and that actually is vastly improves their prognosis. So that we started on both as medications for him. There's really important you have to avoid NSAIDs, which is sort of counterintuitive because you imagine if there's inflammation, NSAIDs are the exact right thing to give, a bit of ibuprofen or a bit of um neproxin or something like that. But in fact, NSAIDs have been shown A, to be ineffective for the inflammation of the heart muscle, and B, can actually increase the area of the myocarditis and increase mortality. So you don't go near them. I thought that was a really interesting learning point for me because common sense says, oh, inflammation, let's switch that off with an anti-inflammatory drug. Um, and with the pain, because I suspected there was pericardial involvement, there's really good evidence for culturesine.

unknown 27:16

Yes.

SPEAKER_02 27:19

Yes. And my little applause.

SPEAKER_01 27:23

Anybody would think we've been doing these podcasts together for a few years, man.

SPEAKER_02 27:27

The culture scene doesn't really have much evidence for myocarditis, but it's very good for the pericardium and it prevents recurrent pericarditis down the line. And actually, you have to be on cultural for three months, which is a long time. And you have to tell the patient don't stop taking it just because you feel better. It's a bit like what we say with antibiotics, finish the course. Because even though the pain's gone, it um helps your prognosis that you don't develop a future pericarditis. So you take three months of colchicine if there is pericardial involvement as well.

SPEAKER_01 27:56

And do you give 500 micrograms a day of that of colchicine?

SPEAKER_02 27:59

B D. B D. BD. The commonest side effect that people really struggle with with colchicine, as you know, is diarrhea. Um so you warn them about that, but most people get away with it. Um, and actually the prognosis is good with that therapy. Most patients have either a full or a partial clinical recovery and can stop beta blockade and angiotensin blockade further down.

SPEAKER_01 28:20

Just a random piece of uh history, but colchicine is one of the oldest medications ever that we've used. Yeah. And it comes from the autumn crocus. So, you know, so around this time of year, in fact, although it's very warm, you're probably not going to see them yet. But you have like um they're small little crocuses that pop up, they've got like beautiful purple um flowers, and on the inside they've got the orange stems, and that's actually where you get saffron from, is also from the same plant. So you get saffron and colchicine from the same plant. Isn't that crazy? And um colchicine was originally used as a purgative, so it didn't matter what you had wrong with you. This is thousands of years ago, you would get colchicine because it would it would purge. So you'd either vomit or you would um have pastaces.

SPEAKER_02 29:09

Um or you would improve from my viral pericarditis.

SPEAKER_01 29:13

Exactly. And also it it the way that it works, because it's um, yes, it is anti-inflammatory, but it also works on the cell cycle itself. So um going back to DNA replication, um, is that it does actually affect DNA replication and therefore reduces inflammation.

SPEAKER_02 29:28

Brilliant. I love that. A little fact of the day.

SPEAKER_01 29:31

Random fact of the day, yeah.

SPEAKER_02 29:32

Yeah.

SPEAKER_01 29:33

So I thought that was a nice really close, yeah.

SPEAKER_02 29:35

Head versus heart. It's nice to have a little bit of CPD about myocarditis. And I do see it sort of once or twice a year. Um, and this was a patient who actually, although had a slightly atypical presentation, all his results were very typical for this particular condition.

SPEAKER_01 29:51

Thank you so much, Fen. That was a really, really interesting case and actually highlights the beauty again of acute and general medicine. You know, you've got a gentleman, 42-year-old, collapse, the CK and the raised trop T, you know, where do we go from there? Actually, when you listen to the history, when you take the history, the hit the diagnosis is almost there, isn't it? Um when you put with the ECG and the troponin, you can go, okay, yeah, absolutely. Brilliant. So my key takeaways are viral myopericarditis, use an ACE inhibitor, use a beta blocker, and cultural C.

SPEAKER_02 30:30

There you go. Thank you. Thank you. I hope you enjoyed that. I hope people listening at home enjoyed that as well. Um, that is the end of another episode of Home of Medicine Podcast. We love doing this podcast and we love it when we get feedback. So please do uh send us a message. Our emails are very findable. Um, and you uh are very welcome to recommend this podcast to anyone else you think might enjoy it as well. Um, we're not super um experts in podcasting algorithms, but we are told that the more sort of ratings we get and comments we get, the higher the podcast comes when people look for good medical podcasts. And we just want to reach more and more people. Um and we do this for the love of it. So please do uh pass this on to acquaintances who may get something out of it. And please do leave us a review uh or a comment wherever you're listening to this if you have the time. Thank you so much, and thank you again, Amy.

SPEAKER_01 31:24

Thank you very much. Thanks for listening. Goodbye.