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Summary

This on-demand teaching session, relevant to medical professionals, will discuss acute aortic syndrome. Topics covered include pathology and classification, diagnosis and investigations, prognosis, management and complications. The session will also cover common pitfalls in clinical assessment and diagnosis. It will be led by medical professionals Harry Choi and Natasha Brahma and will be available for the next 16 weeks.
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Description

The next session in the A+E Survival Guide will cover AAA: aortic syndrome. This series is aimed at medical students and junior doctors and will cover common pathologies seen in Emergency Medicine. The sessions will include how patients may present to A+E, typical investigations and management plans for these issues. As always, the teaching will be interactive with case-based discussions and MCQs. Tune in at 6pm

Learning objectives

Learning Objectives: 1. Differentiate between acute aortic dissection, intramural hematoma, and penetrating aortic ulcer. 2. Learn the common risk factors associated with acute aortic syndromes. 3. Understand investigations and diagnostics for acute aortic syndromes. 4. Explore the various management options and their associated prognoses. 5. Identify the common pitfalls in clinical assessment and diagnosis of acute aortic syndromes.
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Mhm. Hello. Can you hear me? Ok. Ok. At six o'clock. Now I'm wondering, can anybody hear me if somebody can type in the chat? That would be great. Super. Ok. It's all set up, right? Ok, great. So my name is Harry Choi. I'm one of the, I'm another three doctor who um delivering this um sort of teaching series, a, a survival guide with my colleague, Natasha Brahma for the next sort of uh 16 weeks I believe. Um and this week's presentation is gonna be about acute aortic syndrome. Um Now I know there's AAA mix of sort of different levels in, in the um the presentation today. Um So this is kind of aimed at all levels um and feel free to stop me for questions if you have any um halfway through. Fantastic. Yeah. Uh great. Um And we will get crackin since I think we're past six o'clock now. Uh So let me see if I can get my screen up here. All right. Now, can everybody see that screen there? Forgive me. I'll be using the chat on my phone. So I might miss a few things every now again, but we can see the screen and it's moving. OK. All right. Fantastic. Let's get going then. So, as I say, um I got acute aortic syndrome, let's go. So what we're gonna cover today learning objective wise. So the basic sort of pathology and classification about acute aortic syndrome, it's various sort of subclass. Um how we approach acute aortic syndrome uh including some of what, how to make a formal diagnosis. Um What investigations are sort of surrounding that as well as the management, once you do make that diagnosis, the prognosis, um how good medical um intervention is and how good, in fact, how sur how good surgical intention is um versus one another and what the benefits of each of them are the complications of the acute optic syndrome and what can go wrong as well as common pit form when it comes to approaching clinical assessment and diagnosis. So let's get started with uh a patient. So this is Mr Stanford, obviously not his real name, but he's a gentleman who I saw in um during my foundation year in AM U. Um So now Mr Stanford was a 54 year old gentleman, um who I believe yes, had a background of asthma and psoriasis. So nothing particularly serious or nothing particularly sort of um a particular cost concern when it comes to his background. Um you know, he came in with central chest pain, um sort of worse on exertion a little bit better with rest associated with shortness of breath and dizziness. Um again, sort of worse on exertion, no loss of no loss of consciousness, no sort of syncopal episodes, no palpitations. Some nothing to suggest heart failure, no trauma. When it on systemic review, there was only some nonspecific heartburn otherwise. Well, uh um examination was largely unremarkable. Uh observations, all scoring zero heart sounds normal lungs clear. No, again, no clinical signs of heart failure. Uh No, no, his chest wasn't tender on palpation. So at this point, obviously, I'm, I'm aware that everybody sort of knows the title of the presentation. But what would you be sort of looking into or any, any ideas at this point? What kind of differentials you'd be looking at? I'll give you a couple of seconds to answer. No, I'm not sure. Ok, let's carry on then. Um So if we move to the next slide, Mr is down for a little bit more history, then uh he wasn't a smoker at all. You know, alcohol wise, it was very moderate consumption, only drinking sort of once every two weeks, uh fully independent. He was working as a full time farmer with his wife, very active lifestyle and again, nothing particularly from rock and the family history there. Um We talk in A&E uh he had his bloods done obviously with a patient coming with chest pain. Yeah, almost all of them these days will get Troon in sent. Um So his troponin came back as 29 you know, modestly raised, nothing too exciting. Uh They was a repeat um which came back as, yeah, slightly higher but nothing particularly drastic. Um And the other bu were also unremarkable using the art is all stable, um, you know, no increase in his lactate or am las all stable. Um But again, the diagnostic picture is perhaps not entirely clear here. It's sounding sort of more, you know, benign, nothing too, too exciting. Um you know, based upon that, which show you, you know, quite rightly, perhaps a and sort of a stable angina, they um you know, ordered a chest x-ray which was clear ecg showed no normal sinus rhythm, nothing to be excited about. And he was referred for cardiology review, uh started on a new anti hypertensive and the lipid profile was sent as also for completion sake. Um So, moving on to the AM U then, which is why we saw this patient. Um he was, you know, on further history and further examination uh of the of the case. Uh it transpired that he sort of had a single episode of chest pain five days before this episode that you come in. But this time uh and no previous episodes of chest pain before this rather curiously, um you know, on elaboration of his pain, you know, the whole thing, you know, Socrates on him, he described it as a sort of central gradual onset pain, perhaps the aching character with classical radiation to the back, which is obviously a concerning sign. So with that in mind, I think, you know, both myself and the consultant agree that ad should be sent at this point. And AC T Agra was requested. Now before we sort of get into what the results of that were. Um oh, so cardiology didn't fact see this patient just before uh whilst all this was going on. Um and they felt like this was also Angina. They did an inpatient e exercise tolerance test um which was negative for any endocardial ischemia they could detect and their plan was to send him home for a, you know, outpatient follow up with a coronary angiogram booked in about six weeks time. OK. So the result of that came back as showing ad diam of 2 to 217, which was, you know, well within the age adjusted range for this 54 50 or 54 year old gentleman. Um and his CT angiograms ct angiogram alta showed an aortic ulcer 10 millimeters in diameter two millimeters in depth at the start of the proximal descending aorta. Now, if you were anything like me at this point in time, I'd not even, I don't even have the idea that you could have something called an aortic ulcer. Um I was very much only aware of sort of uh sections as perhaps might be the case for many of you. Um So we discussed this one with the consultant on call at the tertiary hospital. Um and they sort of what it was a advice refer to the card team at the tertiary hospital. So now before we get into sort of what happened to Mr Stanford, from that point on, I'd like to sort of take a minute to talk about what is, you know, what this, this topic is. This presentation is called acute aortic syndrome, which is obviously, it's a little bit different from your acute aortic dissection that you normally hear about. So, can anyone tell me sort of what is the difference between acute acute aortic syndrome dissection and the ulcer perhaps we mentioned before, what is the sort of the nuances and the terminology there? Anybody have any idea? Just let me know on the chat. No, not, not quite sure. That's OK. So what we'll do is let's have a look here. So acute aortic syndrome is kind of an umbrella classification. Um I suppose it is, is an aneurysm. Uh Exactly. So I think it's it, it the aortic syndrome is like an umbrella term which refers to three distinct types of pathologies. Um So acute a dissection is the one that, you know, most of us will have heard of. Um, you know, possibly some of us will have seen. Um That's, you know, where you get that tear in the aortic into um in obviously being one of the layers of the main arteries. Um and you get that false lumen formation whereby there's blood passing from the true woman into this false lumen due to the sort of the sheer force. Now, that's, that's the reason I think probably why most of us know about that one most is that it's 70 80% of any acute aortic syndrome tend to be this presentation, acute aortic dissection possibly because it's more acute so that they, you know, typically will always present the healthcare service. Um but perhaps the other one, less less well known ones than sort of the intramural hematoma. So we don't know exactly why these happen. There's no confirmed etiology or background for, you know, the causation behind this. Um but it's widely thought to be sort of secondary to a rupture of the ves of. So, which is um you know, the blood vessels that supply the blood vessels that tiny microvasculature which um supply oxygen to the the walls of the larger vessels such as the aorta. Um and the last one, the last type then is the penetrating aortic ulcer, which is what we have in Mr Stanford's case. So, um this is where you have the in the formation of an atherosclerotic plaque um in, you know, largely involving internal inflammation and then subsequent destruction. Now, it's important to remember that all three of these types of aortic syndrome can also can all um progress and evolve into one another in, in sort of a very difficult to measure way. It's not quite, you know, we don't know whether P A progress to I mh or vice versa or, you know, both into a dissection. Um, but it is sort of being, being worth, being aware of the different presentations and sort of how the management changes. Ok. Um, I, as I say, all three conditions have similar presentations with and co so, um, risk factors, then we're talking about cardiovascular. Does anybody have any idea when it comes to this kind of problem? What are the risk factors we're looking for in history? What do you want to know? What makes you more likely to develop these kind of problems versus your, your average personal history? What do you think? So we go age. Yeah, so age is definitely one. So the older you get, obviously, the more likely you are to have these kind of um you know, cardiovascular problems uh for a multitude of reasons, smoking is a really good one. Obviously, if you smoke, then you're gonna have a very high risk of uh cardiovascular disease and hypertension is our, is our golden ticket there. Yes, family history as well. So, uh here we have it um the main three them. So hypertension um as I say is the, is the big one here. Um a lot of, you know, our population these days that a population in the UK uh have hypertension, um smoking is other can a huge problem when it comes card and uh, or this, um, is another one other, you know, less well known ones. Oh, someone's got on there on the chat here. Um, so the connect tissue disorder, certainly Marfan syndrome being the very famous one. can sort of predispose you to having these kind of problems. Um, if you can, if the connectu of your aorta isn't that much weaker, it means that you're that much more likely to have that intimal tear and then the creation of the false lumen other things, then, you know, cocaine drugs and other i other sort of illicit drugs can increase your risk um as well as hereditary val valvular diseases, um which will weaken the ro aortic root uh and aortic wall which again increase that likelihood of the, the false lumen formation. Um Any sort of systemic problems which cause vascular inflammation, any vascular vascular tis, uh autoimmune problems, you know, infection or S nasties, which will cause vasculitis such as syphilis, um or predispose you trauma, uh perhaps less likely, but again, worth bearing in mind and iatrogenic if we're doing anything that involves inserting tubes and pipes into the heart, and that's obviously gonna weaken those walls and increase your risk there as well. What's so next? So now I'll give you a bit of a spoiler. So, when it comes to presentation, um and pain, what are we particularly concerned about? How do you, how does the normal uh aortic pre aortic dissection, shall we say? How, how do these patients present? Ob, obviously we've got Mr Stanford's case where he came in with this sort of vague nonspecific radiation to the back. Any, anybody have any other ideas how his pain or how people who have a, as how their pain might present. I'll give you a few seconds, tearing pain. Yup. Good, good. Anything else? 11 out of 10? Well, yeah, I, I can't speak from experience, but I gather that, you know, according to Mr, so it wasn't indeed very painful. So, um, there was a study done on this, so the international uh registry of a dissection, I believe they did a big study looking at sort of how much, you know, how do these patients actually present. Uh And they found that, you know, pain was the number one thing. So 85% of patients who came in with the dissections had, you know, pain, the sudden sudden onset, typical chest pain now. And it's 80% of those, it, those typically anterior chest. Um how and only, you know, rather only 50% have that sort of classical textbook back or right, inter pain or radiating through. Um, the next most common one, perhaps more surprisingly was abdominal pain. Uh But it is worth bearing in mind that, you know, from everywhere, from sort of throat to neck and even to leg and arm pain, they've all been described as sort of clinical as clinical presentations of this disease. Um And the important thing to remember with this in, in particular is that when they come to you and whether wherever you are, whether it's an A&E or perhaps somewhere else in the community, um, they may well have had the pain already resolved by the time they reach your door, um, the pain itself is only going to be caused by the intima itself tearing. So if, if the intimas teared and stopped at the uh at the point that they're seeing you, they won't be having active pain, but that doesn't mean that it's not a problem. Um And again, as you as because we are in the field of medicine, uh nothing's absolute, you know, 5 to 15% of them have no pain at all. Um And coming in with other, you know, perhaps further down the timeline of their disease coming in with loss of consciousness, synco be or stroke, these are typically uh the study found to be more elderly people. Again, we know elderly people have a different perception of pain due to the fact that central system is slightly different, but that's perhaps for another day. Um So presentation, then some of the complications you can get with um aortic syndrome are, you know, the fact that it can bleed anywhere along the path of the aorta which causes a quite a variable um presentation. So, hemopericardium is definitely one of them. If you have bleeding at the aortic root and that can bleed into the pericardial sac uh and cause hemopericardium. Um These are sort of the some of the features of per clinical features of hem hem hemopericardium. Um Pulses paradox is anybody can tell me what that is. Pulse is. Paradox. Any other fallen BP with inspiration is exactly right. Um So it's a pathological uh fall in BP which is measured as being more than 10 millimeters of mercury. So, you know, most people will think you might, you might see a very small drop in the BP during inspiration just due to how the physiology of the heart and the lungs work. But if you see that drop being more than 10 millimeters of mercury, that does suggest a sort of more underlying pathology, although it is admittedly a little bit difficult to measure. Um Now, faint heart sounds another one. Obviously, if your pericardium is filled up with blood, you're gonna reduce them. You know, the heart sounds are gonna become muffled. Uh and indeed distend neck veins. And you know, if you're losing a significant amount of fluid into your pericardial sac, you will end up in hemodynamic shock. Um aortic root dilatation will cause um a wide pulse pressure due to the fact you, you know, if your aortic valve is not competent anymore, you'll sort of get that large gap in systolic and diastolic blood pressures, um and diastolic murmur for the same reason. Ok. Um true aortic lumen compression. This is essentially if you feel if the false movement becomes so large to the point where the true lumen light which carrying the blood to the rest of your body gets compressed, then you will get that systolic murmur on presentation, but again, difficult to pick up and not necessarily have the by any means. Um, and pulse deficits are more than 20 systolic. Um, again, because you're getting that, having that sort of drop in BP investigations. And can anybody tell me what investigations they'd be wanted to do? Uh, well, for an a patient who you think might have an acute aortic syndrome. Yes. So CT is a good one. CT is probably the gold standard. Um We'll get to that in just a second. So bloods are, you know, perhaps not as useful here. They largely used to rule out your differentials as, as we saw earlier, troponins are good for looking at for more acute cardiac problems. Um The I sort of international history of acute dissection looked at this as well. They looked at ECG S which is sort of a little bit of a perhaps a white elephant when it comes to um acute aortic dissection. So they found them to be completely normal, you know, normal sinus rhythm in up up to a third of cases. Um that they looked at, um, 3% of them showed a stemi, 50% showed acute ischemic training was 41 nonspecific ST wave t wave segment changes. But again, none of these are gonna be particularly helpful in sort of cementing a diagnosis though they may, if you do see some changes, they may help you sort of build towards one. Um If there's any diagnostic uncertainty, you know, a CS is always a really important differential to bear in mind. Um But again, I'm sure I, I try and I, I talk for another week uh chest x-ray in those rare cases where you'll find when you find um a hemo pericardium or he hemo uh chemo thorax perhaps um will show a wide media mon but again, you shouldn't hang your hat on that. Um So I see we should in heparin what we'll, we'll talk about management in just a second. We will get that promise. So, um bloods uh yeah. So next, let's have a look here. So, imaging. So, uh as I said, the really the gold standard here is gonna be ac uh angiogram and also that's gonna be the, you know, the best sensitivity and specificity is it's gonna be with that. Um Transthoracic echoes are good for identifying those more proximal dissections and the complications of them such as the hemopericardium and hemothorax we discussed. Um but the difficulty with transthoracic is that you get quite limited views. Now, this is sort of remedied more by the fact that you can buy a transesophageal um echocardiogram, which has, you know, a fantastic grade of 99% sensitivity and 89 specificity um due to the fact that it's very close to the AORTA. But I suppose the difficulty with the, this is that it's very, it's very, the, the availability is far less compared to a Dr Thorac sco or indeed AC T um sticking a echo down some echo probe down someone's throat is not the easiest thing to do when they're very, very unwell and it's also very operator dependent. Um So classification, does anybody know what classification we use when it comes to acute otic syndrome? I have given you a little bit of a hint in this presentation. Yeah, I think Tavis got it. So standard for classification is absolutely the right answer. Um This is the sort of easiest one I think is I find to work with a lot of sort of, you know, when you talk to sort of, they will sort of know what this is. Um So standard for classification, it's very simple. So type A is going to be involving the ascending alta and type B is everything that doesn't, everything that's beyond the ascending alta is perhaps a good mic to sort of remember it. Um There are other classifications that I think like two or three more, but uh including the deba one which sort of breaks down, breaks it into as ascending arch and also descending. But honestly, I think if you, if you know you're Stanford that's almost good enough. Um Especially given the fact that a lot of the management is based upon what standard classification, um sort of describes, you look here, then um if we look at the sort of incidence of how likely each of these types of to happen, ascending AORTA is overwhelmingly more likely than anything else. Um 70% of our of documented cases have are type A in the pa in, in the ascending aorta. Um Whereas, you know, arch and the rest of it only make up, you know, less than 50% essentially. Um It's, you know, worth bearing in mind that the ascending, what, what we'll talk about it in a little while, but ascending ter is far more serious and far more urgent. Um But as I said, we will get to that. So, some complications this, if you take away one thing from today, I'd say it's this um this big underlined, bold thing here with aortic a dissection in particular, you know, I'm not talking about intramural, he hematomas and um ulcers right now. When it comes to dissection, your mortality increases by 1 to 2% every hour after symptom onset. Uh and it's worth bearing in mind that this is after symptom onset. So this isn't the sort of, this isn't every hour from when they set foot in the clinic or in inside a ke it's from when they start experiencing the pain. So, you know, at this point, if you take it sort of pessimistically after 50 hours, they're guaranteed to be dead, which is, you know, quite con, you know, obviously quite scary if you think about it. Um, given that some patients don't necessarily present for the 1st 24 hours or for whatever reason. Um, now, obviously, we know that as, as dissections with the false lumen becoming bigger and bigger can eventually rupture, uh and they can cause a sort of a multitude of different problems as a result of that. Um which you know, I honestly, I think you can probably read fast. Uh You can probably read it faster than I can say it. Um And I won't go through it in sort of exhaustion here. Um But obviously, none of these things on the screen here are things that you want to happen and all, all quite emergent situations to be sure, um acute progressive aortic regurgitation. So if you have a dissection which extends into your aortic valve, your support the aortic root, then sort of becomes more dilated your a tic valve no longer sort of oppose correctly and no longer able to form that tight seal, you need to be able to maintain the pulse pressure. Um And you get essentially a aortic valve incompetence, um which can sort of generate a secondary heart failure, even if the dissection is managed quite well and they recover. Um You may well and patient may well still experience some heart failure um in the long term um occlusion of branch vessels. So this is a, this is an interesting one. Obviously, as you can see in the diagram on the right here, um with your false lumen getting bigger and bigger, there's a, there's the potential for it to eventually obstruct uh any offshoot vessels coming from the aorta. So, you know, there's two main mechanisms this happens um compress at either the point of origin without the dissection, progressing or the dissection does progress. Um I think again, it's a little bit difficult to sort of put the words, but I, I think the pictures do quite a nice job here. You can see the sort of true lu here uh and the false lumen getting bigger and bigger. Um And this, you can see here the false movements, getting press pushed in to the point um of the true woman and blocking it here. Whereas in this one, the, the actual false movement itself is the one that's causing the blockage. OK? And it has a very well, depending on which branch vessel you get blocked, you'll have a different different presentation, which is something a little game I've prepared today to sort of test you guys on what perhaps those presentations might be. So if we look at different branch vessel of the aorta um coronary vessels, so coronary vessels, if I blocked the coronary vessel with well with anything, but then in this case, with um a false lumen. What would my patient develop? What would you, what pathology would they then go on to develop block the coronary vessel? Let's see. Yes, exactly. So M I is the right answer a stemi or, you know, depending on the coronary vess, you might not, you might get a different type of M I might be an inferior, in fact as well, but certainly some sort of M I common carotid. Any ideas, common carotid, either one. Fantastic. So, yes, stroke is right. Um You can get any type of stroke really. Um you know, with a posterior anterior circulation, strokes. Um because again, the car, your common car, you know, supplying your entire brain, um Subclavian arteries, I won't label you on these if you, if you have an idea, what do you think? So, craving arteries is what do they supply? I know. I'm sorry, I'm testing on me. No, I'm not quite sure. So, probably um essentially a, a acute ischemia of your upper limbs. Um It's a cla artery providing supply to, to, to your arms. Essentially. Um Celiac mesenteric vessels, uh critical ischemia. Yeah, you got the critical celiac mesenteric vessels. Um We won't sort of dwell on these. This is gonna be uh your bowel ischem, acute bowel ischemia. Yeah. So ischemic bowel, which can result in all kinds of, you know, secondary problems. You can get things like, um you know, uh hemoperitoneum like bleeding into the gut and you can get heis as well as a side as a sort of offshoot of this um renal vessels. Anybody have an idea if we have renal ischemia, what might it present as? What do you think? API A G I is a good guess. It probably, you probably would definitely get an API but I think in terms of how they would present clinically, um he hematuria would probably be the first thing that you see. Um uh And then finally, our spinal vessels, um what you typically get, if you have a occlusion of your spine, the vessels would be sudden onset and painless paraplegia, obviously, very scary presentation. OK. So let's talk about how we manage all of this. So, um it, as I said before, it depends largely on what classification you're dealing with. Where is the location of the lesion? Is it ascending or is it in the descending aorta? Um If you are in the ascending aorta or type a, um this is a surgical emergency, this is the one that everybody gets worried about, you know, defin the definitive management for type A is always gonna be surgical intervention. Um cause until you sort of operate, the problem is not gonna go away no matter what medicines you use. Um Type B is a little bit more um flexible, I suppose. Uh if they, some of them can be more static and they can be managed conservatively. Uh Although that typically does still happen in the more sort of mo controlled environment such as HDU. Um but there will be cases where you need to operate, whether, you know, surgical or pa or more urgent management is necessary. Um And sort of things to think about when making that decision would be, is the lesion progressive, are they having pain refractory pain? Um Is there any evidence of organ ischemia or limb malperfusion as we discussed before any of those branch vessel occlusions? Uh And or is there a high risk of rupture? Um Now, oh, so we're gonna break this down into medical and surgical first to sort of talk about what each are involved before we talk about, you know, what, how, how successful are we at treating these? So medical management? So, the, the big thing, the, the, the the sort of crux with um aortic dissection, I suppose, or aortic syndrome is that um whilst you want them to maintain their BP to the point where they can still perfuse other organs, you want to sort of make sure that they're not so hypertensive that they're gonna pop because obviously you're working with very fragile systems here. Um Now, because of the, you know, hypertension is one of the main medical managements. Um They can be hypertensive for a number of different reasons. Hypervolemia, for example, if, as we discussed before, they're, they've dissected into the uh thorax and they're having hemothorax or hemopericardium. Um or, you know, there's simply just so much blood, the foss has progressed to the point and there's so much blood inside it uh that they've become hypovolemic. Uh The these are all reasons that they can drop their BP, um cardiogenic them. Uh in cases where pa patients are hemo pericar have hemopericardium. Um They will also typically get a cardiac tamponade. Um um and then subsequent L BS D which will essentially reduce the cardiac output. Um There's also, you know, there's also a very rare chance of getting an intra atrial septal hemorrhage um as part of the, as a part of the false lumen, um which can then cause a complete heart block but less, you know, less likely neurogenic hypertension if you, if you do get that spinal cord ischemia where we talk about the sort of painless para paraplegia, um they will also get, you know, uh you will, you'll be able to tell eventually with the painless paraplegia and sort of warm with, but preserve warm peripheries. Um That's what I'm trying to say. Uh medical management here is, I think it's everything from that. I believe that a chem website. Um So here we have, you know, again, I'm not gonna, I'm not gonna bore you by reading this out to you and um you can find this, uh you can come back later or in um on the website itself. Um But again, so that they're outlining the different kinds of beta blockers you can use to sort of maintain that, um, you know, that sweet spot when it comes to the BP, um, as well as, you know, GTN is also a good option for patients who uh beta blockers are contraindicated in. So, um, uh it's, it's a little bit sort of in disputes, I think from, based upon what I was reading, um, about the target BP, generally. Um, most sources said agree that less than 100 and 20 is what you want to be aiming for. This is gonna minimize your risk of rupture as well as and prevent the, you know, your false lumen lesion from progressing even further. Um And here we go, the IV beta blockers, you know, calcium channel blockers can be used. Uh your beta blockers are tolerated um as well as GTN. Um And you can be, and you can, you can use it sort of in conjunction with other vasodilators if necessary. If you feel like if your BP is just not, if they've got quite significant hypertension, then you're not really winning with just the beta blockers. Um Surgical management. Ok. So type A is this is gonna, as I said, this is your surgical emergency with the type A? Um It's gonna be typically open close, you know, I I'm not, I, I don't pretend to be a surgeon or have any sort of deep knowledge when it comes to surgical ma management, sort of practical side of it. Um However, based upon what my, based on what I've done for this presentation, typically open um close, close the interim tear and then eliminate the false lumen. Um limited data. There is limited dangers on sort of endovascular repair and how efficient we are at that. Yes, but I think it's an, it's an up and coming area. Uh Type B. Uh obviously again, we said before, type B is less of an emergency. Um In those 75% of uncomplicated pa patients, you can normally get away with conservative medical management. Um But again, 25% do have those complications. We talked about earlier where it's a progressive lesion, uh et cetera, et cetera. Um and they will typically get endovascular stenting with a synthetic graft. Um There is sort of ongoing trials as to sort of to sort of clarify the benefit of prop prophylactic endovascular stenting um in those patients who we know have uncomplicated disease, but then are perhaps at risk to develop complicated disease further down the line. But I think the jury is still out on that. So it's one of those things to watch this space for. Oh, good me. Um OK. Principles of management. So, painkillers, um now these patients are obviously in significant last pain, particularly during the interim dissection itself. Um we always offer sort of opioid analgesia for these patients um to help reduce that sympathetic response if the patient's not in pain they're not gonna be driving their sympathetic um reflex, which means that their BP, you'll have an easier time controlling their BP and making sure that they're not becoming hypertensive and, you know, a high risk of rupture. Um There's again, and there's no evidence that any of the relative hypertension that, that the opioids cause will re worsen the prognosis in any way. Um, hemopericardium, this um obviously with your, you know, with your typical pericardial effusion, peri pericardiocentesis, where we drain the fluid out would be something we think about. Um But in these patients, we do not do that in any circumstance. Um What the evidence has shown is that if you do this, if you do pericardiocentesis and rapidly decompress the pericardial sac that essentially promotes rapid rebleeding of the um of the dissection because you're essentially making new space for the blood to bleed into and help promote even further, even more blood loss. Um uh which is basically, yeah, pressure gradient, et cetera, et cetera, but less fancy um prognosis then. So how, as I said before, how well do we do at treating these patients? So again, it, it all comes back to the same classification as Stanford. Um where is the lesion? So, in your type, a acute aortic dissection um within 24 hours, there's a 24% mortality um which is obviously, you know, quite scary. Uh you know, within the space of the day one quarter um, of our patients don't make it if you go down a little bit further down the line of two or seven days, that's come up to 44% and then almost, almost half in two weeks. Um, that's with your medical management. You can see though that with surgical management, it's significantly better, uh, with that mortality being halved in every case. Um, it's, it's, uh, as I said before, the type A is, is a, is a surgical emergency and they do need surgical D as soon as possible in your type B A tic dissection. That's your descending or rather everything below your ascending beyond your ascending. Um That's gonna be significantly lower mortality. It's only 10% in your, in, in 30 days, obviously much better. Um The reasons that these patients die, aortic, rupture, stroke, visceral ischemia. We talked about all of these, you know, there's a, a multitude of reasons. It's, it's a, it's a really severe illness. Um And more the more reason we need to be really vigilant when it comes to picking it up. Uh Yes long. So we talked about the sort of acute tic duct section, which is obviously the really emergent stuff, but when it comes to the other, other two types of uh acute tic syndrome, uh intramural hematomas, um typically medical man medical mortality is again worse out here. So surgical management is typically recommended for you in hematoma, particularly in type A. Um But no. Notably here, you can see that in type B um type B, intramural hematoma, that is the intramural hematomas that develop in, you know, everywhere beyond the ascending or that's the arch down to the descending, down to the abdominal medical management actually does slightly better with only 14% mortality on the surgical management. 20. Um So it's worth worth bearing in mind that although surgical is also considering that there is a role for medical management here as well. So now that we've gone through all that, what happened to our Mr Stanford in the end. So, um we discussed in the cardiothoracic surgery. Um and notably that they said that posts of Clavin artery was not their, not their sort of wheelhouse and they will advise us to contact vascular for any of the if you end up, do end up funding one of these patients. Um The location again is super important to you to refer to um vascular surgery. So we discussed with them and they advised that given the patient was hemodynamically stable, they didn't want him transferred to the local tertiary hospital. Um They either advise us to, to spend all of his VT prophylaxis. Uh and IV labetalol was given uh as an infusion to help sort of. Um well, rather they would advise that we give IV labetalol to help maintain that BP target. Again, they, they gave us a BP less than 100 and 10. Um to help sort of reduce that risk of rupture. Um We uh locally and are in the regional hospital we discussed with ITU and cardio Coronary Care unit. Now, I don't if you remember, but Mrs Stanford did indeed have a backup of asthma, which obviously is a contraindication for um a beta blocker. Does anybody know why? So as a contraindication for the beta blocker, any takers? No, that's ok. So, I mean, I won't go into in detail again in this topic, but um essentially beta blockers will, can stimulate fatal Bron bronchoconstriction in asthmatics, which is why we need to avoid them. Um So instead, what we did was we gave, we gave um a Stanford GTN infusion and yeah, sort of continuous monitoring whilst he was on HPU. Um Yes, so is a happy ending to the story. Mr Stamford got stepped down to cardiology, the cardiology ward after a brief stay on HDU. Uh his BP was eventually managed to control with a sort of triple combination using um A I don't know, I don't know why it's a beta blocker there. That wasn't right. Uh It was nice with a card uh CCB and I think it was in GM as well. Ge discharged home. Um He was given a six week uh outpatient uh CT octo gram to check for some interval change and outpatient clinic follow up with um the tertiary hospital. Um And so that's the end of his story. Uh as far as I know it anyway. Um, when it comes to some pitfalls with, when it comes to approaching this diagnosis, I think the important one, I'll probably come back to another one of these presentations is that we, I don't like, we don't like to leave patients in pain. Um, pain is quite often not managed adequately. Um, although I know sometimes there's lots of doubt around sort of masking symptoms and like that, it's, it's very ra really a good idea to leave your patient in pain. Um So we, you know, it's always good to be on top of the analgesia, as I said before, opioid analgesia, that's never would worsen your prognosis, obviously when prescribed correctly. Um uh And although another one with sort of acute, given how variable it is and given how hard it is to sort of pin down, I it can be tempting to change your diagnosis due to lack of sporting signs. Your ECG might come back completely normal along with your chest x-ray and bilateral bra uh brachial BP. It might all come back normal and you might be sort of faltering on whether or not you really want to sort of go down the a as pathway, but it is sort of worth bearing in mind. These things aren't always gonna be there and that you can still be on the money even if they're even if they're not. Um Again, we sort of, we said mentioned earlier, but pain, uh, a good history when it comes to the pain and the background is really important as it, as it was with Mr Stanfield. You know, we, we, we sort of when we went back into history, the fact that he never had a previous episode before was odd. The fact that he was an active farmer working every day. Not that many cardiovascular risk history, risk factors, all very odd, all reasons to sort of raise that eyebrow and, um, look a little bit deeper. Um, again, you might find that, you know, pe once you have an echo, people might end up getting echoes for these patients. And then once it comes back clear, they might be more tempted to say, look, there's not gonna be, there's, there's nothing there. Um, it doesn't, definitely, it doesn't definitively rule out. It will only sort of pick up those very ascending, those complications of ascending dissections. If they're very severe, it might well be that it has progressed to the stage where we can think about. It might be descending problem. You don't know. And you know, just because the echo is normal doesn't mean it's not, not uh there. Uh And again, once you've actually sort of made the diagnosis or you're, you're very sort of committed the diagnosis allowing that BB to remain very high. Um, beyond what you can control whilst they're awaiting for transfer to a tertiary center is always going to be a pitfall. So in summary, then, um early diagnosis is always crucial to optimizing our patient outcomes. We mentioned before a takeaway point from today. Um your mortality goes up every by every hour by 1 to 2% from symptom onset. And obviously the earlier we pick that up, the faster we go, the faster we stop that number, right? Um Importance of history and identifying as a differential we've talked about this already. Um go into the history, get, make sure you get full pain history, make sure, you know, back to front of what all the risk factors are. Um And how many do they have um location greatly affect prognosis. We talked again our, our standard for classification A and B ascending and everything beyond that um Type A is gonna be a surgical emergency that needs to be escalated um urgently if not emergently. Um And to be aware of the complications that we talked about things like your aortic root dilatation and your branch vessel collusion um which we're all very good at. Um And these complications can occur even in your type B. Um Stanford, uh even when it's perhaps less acute, it, these complications can still occur and then progress to become more acute. So with that, um does anybody have any questions um to ask me before I, I'll leave you for today. I think going back to the chat, I think somebody mentioned about inserting heparin before going to AC T I'm guessing they mean sort of treatment dose, um treatment dose, prophylactic about to PTEII. I think it's difficult again because it, this, this is what sort of makes the whole issue very complicated in that you have two differentials. One of them being A CS, one of them being um acute tic dissection and one of them is gonna need your ma management to be um essentially uh yeah, PT prophylaxis at treatment dose. Um, or with antiplatelet therapy, which is gonna help you stop um, further progression of the A CS and one of them is gonna make that worse. Uh So it's always gonna be a difficult decision when it comes to whether you should give um, anticoagulation, et cetera, et cetera. Uh It's not a decision you should ever be making alone, I think, especially at what I'm guessing is more of a sort of low, special trainee level junior doctor level. Um, always, you know, escalate these problems first and make that decision together as part of the team. Um, but yes, it, it is, it is sort of, it is a fine line to trade, I suppose. Um Any other questions? No. Ok. Well, it's been a pleasure everybody. Um Thank you for tuning in and thank you for joining me. I'm sure I'll be seeing you again soon enough. Uh And in the meantime, um, all of you, please uh take care. Thank you very much. Oh, we got, we do have a question. Um, may I know what was the reason for doing a DD initially? So, yeah, I think the d-dimer was not, um, it's, I would say it's, it's not a part of the diagnosis of a, as, again, d-dimer are nonspecific investigations. Um, they're not going to help you come to a dinosaur. A si think more than anything else. In this case, the d-dimer was sent for, um, CT sort of, they were ruling out a possibility of DT, uh, pe. Um, again, with a sort of middle age gentleman who no other risk fact, I think came in with chest pain. Pe is another thing to consider. And again, it complicates your management a little bit more because again, you'll be giving your, um, and a graduation for it, um, which is, makes it difficult but the d-dimer I think is probably not related to this in particular. Iii I couldn't tell you if there has been a study done on d-dimer and a as, um, correlation. I would imagine that it, it wouldn't have particularly good sensitivity or specificity. Um, to be honest, um, given that it's a little bit of a different, uh, pathogenesis if that answers your question, any others before I, before I leave here for today. Ok. Well, in that case, um, I will leave you to your Wednesday evenings. Um, and thank you again, all very much for joining us and we'll see you next time you take care one extra thing, one extra thing. I'm so sorry. Um There's a feedback form that um, we've been asked to sort of fill, send it on to yourself. So if you could complete that, we'd be very, very grateful. I do appreciate it. Thank you so much. I'm gonna send it right now. Ok? All right. Thank you guys. Thank you. You take care.

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