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My name is Prudence. I'm one of the um educational coordinators of so, so welcome to session two of the vascular surgery week. So today we have Dami from Aston Aston Medical School will be talking to us about carotid artery disease. So, um just want to let everyone know that um towards the end, I'll send the feedback form out in the chat. And after the completion of that, then you'll receive a cer certificate of attendance. So do please try to stay until the end and any questions just pop them in a chat and Dami will be able to answer them as well. So I'll hand over to Dami now. Hi, everyone. Um So for today, we're gonna go over two main diseases, carotid artery disease and aortic dissection. In order to cover these, we have some learning outcomes. So we're gonna talk about the anatomy of the carotid arteries and then we're gonna talk about clinical wise what the disease E is and the pathophysiology of the etc. So, if you have any questions at any time, please let me know. Um if you would like to answer questions, you can either say them in the chat or you can just speak up? I think if that's allowed. Um I don't mind. Um So my first question is just sort of, I mean, I've already said it, but does everyone know the arteries that supply the main arteries that supply the head and neck region of the body? Does anyone wanna say it in the chat or physically? What? Ok. So it's the carotid arteries. Um We're gonna focus on the common carotid first. Um And then I'll explain a bit more about the internal and external later on. So just to get our mind situated about what we're talking about, we're gonna talk and focus on the anterior triangle of the neck and in the anterior triangle of the neck, you, we can see the borders that are clearly highlighted here. So the anterior border of the stenocladum mastoid muscle is what um borders this triangle laterally. The inferior border of the mandible is what borders it superiorly and just a artificial line drawn from the middle of the neck is what borders it anti um media. So this in itself is the anterior triangle of the neck. So next, I will talk about the arteries. So we want to talk about the common carotid first. This is when the, this is the arch of the aorta. So this is you've come up from the heart, the heart is pumping oxygenated blood to the rest of the body. So this is the arch of the aorta, this bit is gonna go down and supply um blood to the lower extremities. But this is to provide blood for the head and neck. We have the brachycephalic on the right and the common crus can come straight off on the right and the subclavian. So on the right hand side, there's a bit of a little trunk here which I just talked about the brachycephalic trunk. And from that arises the common carotids and the subclavian arteries. But then on the left hand side, it just arises straight from the arch of the aorta. It doesn't have the brachiocephalic trunk beforehand. Um There's no branches or anything that it gives off in the um neck. Um and the superior edge of the cartilage uh uh um of the car well, of the thyroid cartilage. Each um common carotid artery then divides into its two terminal branches, the internal and the external carotid arteries. Does anyone know what level that is at the superior edge of the thyroid cartilage? The place where it divides into the um internal and external carotid arteries? I hope I'm not speaking too fast. Yes. Um So it's C four very easy trick to remember a lot of these bi bifurcations. It's C 4 L4. Um things like that. But for this one I'm talking about is C four and at C four, you have the um the division into the terminal branches, which is amazing. Um What else was I gonna say here. So the next thing to talk about is the internal carotid artery. So what happens is that it goes through the sheath within the neck. So the carotid sheath and there's no branches in the neck because what it does is it's, it's responsible for supplying structures within the head rather than external structures. It um it, it supplies the internal structures within the. So like the brain, the eyes, things like that. Um The branches in the brain include the autotomic artery, the posterior communicating artery, the anterior choroidal artery and the anterior cerebral artery. Um I've highlighted a little area over here and I was wondering if anyone knows what this area here is called. It's at the point, it's just at the point where the common carotid is splitting off into the internal carotid. There's a little bit of a dilation there. Does anyone know what that area is called or what resides in that area? Ok. Um OK. So that is the carotid sinus. Oh Yeah, literally b receptor design in that, in that area, the carotid sinus and that's where it helps to um flu. It looks at fluctuation, fluctuation in BP and things like that to help to control um the BP control that the body has um which is really cool. So just um what I've highlighted there and the carotid, the internal carotid end up as ultimately the middle cerebral artery, which is in the cerebrum like in the brain next up. Yeah, she's already answered. Um But I was gonna ask, what are the main re receptors that reside in the carotid sinus? So they're bors and they are the ones that um help to monitor BP. Does anyone know what type of receptors they are like? What do they check if that's a good way of posing the question? What is, what is it that they're, that they are detecting co receptors, detect a change in stimulus? So what change in the stimulus are they? Um Yes, they are detecting BP. But how did they detect BP? I think if that's if that question makes sense. Um So I think they're types of stretch receptors. So they check their mouth stretch like in the um sinus, I believe. So they would be able to detect that change in stimulus and equate that to BP changes if that makes sense and be able to control BP in that, in that way. So then we talk about the external carotid arteries. So the external carotid artery is the one that supplies the external parts of the head. Well, the neck, mainly the he the head mainly but the head and the neck. Um it gives off many branches and it has um yeah, so let's just talk about the branches that gives us first. So here we can see the superior thyroid artery is one of the ones that gives up which is down here. Then the ascending pharyngeal artery over here, the lingual artery over here, the facial artery over here, the occipital artery back here, the posterior auricular artery, the superior temporal artery and the maxillary artery. This is a better view to show what it looks like on the inside of the body. But um I honestly, the external corset is um filled with is the one that supplies mainly the head and neck structures, as I said. So, like the things like the scalp, the skin, um and areas around the neck as well and the face as well. Um There is one artery within the external carotid artery that actually um supplies intracranial structures. Does anyone know which one? It is? So, um yes, the maxillary artery is correct. The maxillary artery gives off the middle meningeal artery, which is a tiny artery. Yes, perfect, which is a tiny artery that's found on the poterium and the skull and it supplies the um levels some levels of the meninges. So it's the only one that technically supplies an intracranial structure. But um yeah, most of the external carotid artery supplies the head and neck regions on a superficial level. Um So this is about the carotid sheath and the contents. So, like I said, within the neck, the common carotid artery is first within the carotid sheath and then when the internal carotid breaks, um comes out from it, it stays within the sheath. What? However, the external artery does come out of the sheath. Um but the the sheath contains a common carotid artery like in here at this level, the internal jugular vein and the vagus nerve and it's a column of fascia and it's just like how most of the neck is divided into like multiple layers of fascia layers, right. Um This is just another fascia that has been performed around these and it's just a good, um It's just something good to know about how the the the bl blood vessels are structured within the neck. Um Next is um the clinical perspective on things. So, the main disease that we're dealing with is carotid arteries, um disease. And um it has to do with stenosis and it has to do with um the formation of atherosclerosis. Atherosclerosis is plaque, build up within the arteries and it do it technically like over time, it begins to reduce the diameter of the lumen and that can cause a risk of multiple things, a risk of embolism, a risk of stroke or ischemia like narrowing of the vessel. And that's what we're trying to um I guess limit and things like that once we know more about the disease. So the way that either present is usually asymptomatic, but it would manifest in ati a or a stroke. So when someone has ati A or they have a stroke, one of the um one good thing to look at or to rule out would be carotid artery disease to prevent it from happening again. Later on. It's classified by its va um by its severity. So there's the mild, moderate and severe columns and less than 50% reduction is mild, 50 to 69% reduction in the diameter of the carotid artery is um considered moderate and 70% is considered more than severe. Ok. So that is more about carotid artery, stenosis. It's so like stenosis of any other artery in the body. But it's just a very important artery because we know that it delivers blood to the head and the neck, which are obviously very key um key um vessels that are needed and they're vital for survival. So we need to keep a um causing that. So the first question I have here is what is the most common um cause of a carotid, bre, bre? Yeah, I mean, it's very linked to what we're learning today. So the answer is um atherosclerosis. Yes, that is the most common cause of a carotid bruit. And a carotid bruit is what we would hear on auscultation. So when we're doing our cardiovascular examination on a patient that's come in, we'll be like, oh, ok, let's listen to the carotids. First of all, we feel for them, we feel we listen to the carotids and we hear a bruise. So that's like a whooshing sound or something that sounds a bit abnormal in the neck area. I were like Oh, ok. There could be something else going on here and the most common cause of that would be atherosclerosis more than anything else. Um, which is very good. It's a good, it's a good sign to see and note that there could be something else causing the patient's ti a or stroke. So, if you were, I don't know, ever having ati a um, patient or stroke patient, um, you know, one of the checks that you could do quite quick and quite easy at the bedside is just listen for their, listen to their neck, listen to see if there's a carotid bruit. And that could point in the direction of carotid artery disease as the cause of their stroke. So the um different presentations, like I said, they have to do with TI A and stroke, those are the main ways that it um, presents. So can someone, um, tell me what stroke, um, the fast pneumonic for stroke means or what it appears as? What does that mean? Ok. So, um f is for face, does the face look? Yeah, face, arm, speech time. So it's a, it's a pneumonic that's been used to help the general public recognize stroke quite early on. Um It's obviously very, it's a crude way of, you know, um um putting it down, but it is, it has worked very well to recognize a stroke quite quickly. So, if you were looking at a patient that's having a stroke, what could they potentially present as they could have a focal, um, they could have their face slanted to one side. Um, arms, can they raise up one of their arms and not the other s do they have slurred speech? And then t means time to call 999? So, um, yeah, I just wanted to put that on there as a typical presentation for presentation for stroke. But it can be any focal neurological dysfunction that would happen to a patient. It doesn't always take the form of this form. It doesn't always take this form out. But this is one of the quickest ways to um check for it. Then you have Ati A the TI A. So they've actually changed the definition for TI A normally it will because basically you had the symptoms of a stroke but for like 24 hours. But they found that even with that, there are still patients that would have um ischemic damage from that. So they're like, ok, well, it wasn't really technically ati A, it was actually a stroke. So they've changed the definition for Ati A to be a tissue based definition, which is a transient ischem. Um a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal um ischemia without the acute infarction. So there's no actual like, I guess when you look at their brain later on, you wouldn't see any, any long term changes to the anatomy of their brain. Um, I guess that's a good way to describe it. Um, does anyone have any differentials? So, if any patient walked in with any of these symptoms or neurological defects, what are some differentials that you would give? You'd be like, oh, I don't know what's, what is happening here. What do you think? Ok. Um, so some differentials include, yeah, hypoglycemia. Bell's palsy. Yeah, seizure good. So, these are all good um, differentials. You could also have a differential, maybe it was an af that caused the emboli embolism or a stroke. Um You could call, you say that um giant arteritis or aortic valve, stenosis could be the potential causes of their presentation. So those are all different um differentials, not just carotid artery disease, but yes, I like all of the suggestions given in terms of investigations. So you have the patient right there in front of you. They've had all of these things. Um all of these presentations. What would you do or what would you like to do to check? So I've got a few just to rule out your own um differentials. You would wanna do some troponin just to make sure there's nothing going on with the heart that's causing it. Like um you would also wanna check maybe there are, you do like an E sr if you think it's giant. So arthritis as a, like you genuinely think from the history that it could be that you could also just do your normal FBC S using these LFT S. Just some, make sure that the baseline is ok. But in terms of FBC, we can look in at, we can look at things like a glucose test and check if it's hypoglycemia just as, um, prudence has said, in terms of an E CG, we would like to do an E CGI. Think it's a good idea. Yeah. Do a glucose check. Um, an E CG would be a good idea because you would like to find out if there are any um underlying um if there are any underlying cardiovascular causes. So, um in case, like I said, af is a good differential for cardio um carotid artery disease. So you could check if they have AF and potentially throwing a clot that could be a different um management step entirely. So we do an E we do an E CG just to rule out other things that we've had in our minds and it, in terms of imaging, I would like us to do an ultrasound of the neck is the quickest way or a non contrast CT as well. And a follow up if they, you saw them in clinic and they recovered, maybe it was a tia, a one follow up you could do is just a CT angiogram as well just to make sure that everything is all right in that, in that realm. Um In terms of the risk factors, I've listed all of them, they're, they're put, they're literally the same risk factors for atherosclerosis as a whole. So anywhere in the body where um you have atherosclerosis, um like P AD disease, etc, these are the same risk factors that you have there. Um So increased age, male, sex, smoking, etc all of those. Next up, we talk about the management. So like everything in medicine, you should start off with conservative surgical or like split it up into different categories. Um For the conservative management, you would want to help to manage those risk factors that they have. Um, especially if they have like, I don't know, high BP and things like that. You want to help them manage that. So manage any co comorbidities that they have as well. So, like I said, if they had a hypertension, if they had diabetes, you wanna help to make sure that those are being managed in the best way possible. You can um, also help give them like lipid lowering medications or antiplatelet medications as well. And the biggest thing that you could do after that is surgical. So, car carotid and arterectomy is the most common surgery that is done for carotid artery disease. And um there's also angioplasty and stenting. If the patient is not, if they find out that the patient cannot have car um, carotid endarterectomy, then they will do an angioplasty and stenting instead. Um, but this surgery is quite cool. It involves making an incision in the neck. So they would open up the neck, they'll open up the carotid artery and they will literally just scrape out the amount of plaque that's in there and then close it back up. That's the um, literally the surgery done, which I think is quite cool, but obviously, like anything that comes with complications, um, you have stroke, there's fa um damage to the facial nerve, damage to the glosser and you nerve damage to the recurrent laryngeal nerve and damage to the hypoglossal nerve because these are all nerves that are around that area. So when they go in, they could potentially harm those nerves. Um But yeah, those are the um complications and this is the surgery that's mainly mainly done. I think they do it uh when it's above, when it's when it's um around moderate is when they start to think about it. I'm not too sure. I think so. Um So now we're gonna talk about aortic dissection. Um So aortic dissection is a disease that occurs. Ok. Let's not talk about that. Yeah. So first question before we even start it. Um if you know anything about aortic dissection, which two layers do you think will be involved in the aortic dissection? So these are layers of the arteries. So anyone know? Yeah, intima and media is correct. So tunica intima and tunica media are the two layers that are primarily involved in an aortic dissection. So this is a better image to explain. So this is what the archery will look like. Um And then these are the different layers labeled and this is the intima, this is the lumen, this is where the blood is rushing through. Then you have the intima which is right here. And then you have the tunica media, which is the thick bit over here. So in between these two layers is where we find a a aortic dissection. So upon talking about that, what we're gonna discuss is mainly just a clinical approach, but I just went over a quick and an anatomical um prelude so that you know what we're looking at when we talk about it now. So the aortic dissection is a disease in which there is a break or a tear in the inner layers of the aorta which we've spoken about the tunica intima, the tunica externa um the tunica media. So we see that there's a little break here and then that causes blood to flow in the wrong direction or go outside of the walls of the artery. And that can number one cause a false lumen to start to appear. So we can see the progression of the forced lumen down here with quite nicely in this image, which is why I included it. So blood will then enter between the layers of the intima and the media and a FD lumen of blood is formed within the walls of the aorta. So there's now two lumens of blood. Can you see that through here as well? And this is a better view as well to show the effects that this would have. So this can then cause these the actual, the actual um lumen to become constricted. So then that would limit blood flow to the other parts of the body. Um I believe the slides are made available on the f after the feed work form has been filled out. But if I'm wrong, please um correct me. But yes, the fee for me is, yeah, after um so yeah, this is um just a good slide to show how the forced lumen sort of emerges. And you can see on the side here and I'll give you another picture as well here just to show how the effects of this end up, end up with the actual aorta or the actual lumen that we need as supplying blood to the rest of the body becoming constricted. And so you can see how this poses as a threat to the body and it poses as a threat to life in general. There are two types of um classifications and permit me to help explain this as best as I can. Um So there's a Stanford classification under the B classification, Stanford wise. It just says that type A, which is these two here, they just include the um ascending aorta before the brachiocephalic artery. And then in type B, it affects the descending aorta after the left suban artery. So over here, the descending aorta and the parts of it are affected as well. Um Then the, the ba system is type one which begins at the ascending aorta and involves at least one aortic arch if not the whole arch. Um So that is type one here. Can you see that? And then we have type two. Type two is um isolated to the a ascending aorta only. So there is no like involvement of the whole aorta, there's no involvement of like the whole aortic arch or anything. And then type three is type three and A and B. So there is the one that has, this one includes the whole of the descending aorta. But type A is the one that begins in the um a descending aorta and involves only the section above the diaphragm. And then the type um three B includes the descending aorta and it's below the level of the diaphragm. Um I hope that makes sense. So there's three, there's two ways that they classify them. And I've given you a picture that kind of shows both of them in and in, in um the same image. So this is type A type B and then type 123. So type three remember is only split by the diaphragm. So at the level where the aorta press pierces, the diaphragm um is where it goes through. And so type three A is above the diaphragm type three B is below the level of the diaphragm. So there's a lot to discuss about aortic dissection. Why does it happen? Um What are the features of it? What does a patient present as etc? So I'm just gonna try to break them down a little bit. So some of the features that suggest aortic dissection or like, you know, would hint to us that a patient might be having. It is if they have um hypertension, already hypertension is actually one of the biggest risk factors for aortic dissection. And also when they're having an aortic dissection, they can also have hypertension as well if that makes sense. So their BP will be like largely elevated differences in BP between both arms. So if you see that in one arm and the other arm, there's more than 20 mercuries of me, I'm not gonna try to say that um differences, then that is quite significant, then you check the radial pulse as well if there's a radial pulse deficit. So the radial pulse in one arm is quite decreased or absent and it doesn't match the apex beat. So that one is different. So when you're feeling the radial pulse on the other, on the person's other hand, and it's actually the same, it matches the um apex B etc, you also have um the dia if you hear a diastolic murmur, if there's a focal neurological deficit, you could say that um you could also say that if they've got a chest or abdominal pain, if they've had um a syncope or if they have hypotension because as the dissection gets worse, then obviously there's gonna be less blood. Um, one now is pooling in one region. So there could be um a potential to have hypertension as well. Clinical presentation. So when the patient comes in, if they have not had like cos these happen quite like this. Like, I think that they're one of the ones that they're literally an emergency. Like if you ever see or if you ever suspect it, um make sure you rule it out quite quickly because it's a, it's an emergency. So um when a patient comes in sometimes most of the time it's cos they've, they've already started dissecting and it's become quite bad like, yeah. So um yeah, let's just talk about the um actual presentation. So they will come in with a sudden onset severe ripping or tearing chest pain. And they say that it can be anterior if the ascending aorta is affected and it can also be posterior if the descending aorta is affected. But most of the time they, they describe a posterior one, I don't know, I think maybe descending aorta um is, is more affected. I don't know. But most of the time when I've learned about it, it would be a se a severe ripping or tearing chest pain in the back. Um The pain can obviously change location over time. But when it started, we would ask, did it start at the back? For example, um conditions that affect the connective tissue can increase your likelihood of having a dissection. So, EDS and Marfan syndrome are two main risk factors for it. So, if you have an SBA, where you have a 40 year old man with Marfan syndrome that comes to the GP with S um tearing chest pain, you should be thinking aortic dissection. This guy is gonna blow like I'm talking about an SBA scenario. It doesn't always work like that in real life. Um But yeah, in the SBA scenario, that is one of the um key risk factors that they like to use. So any issues with the connective tissues um make it easier for such a disease to occur um conditions and procedures that someone can do. So like an so like what's it called? Um Either a condition or a procedure that they've had um done to them like a uh like a surgery or something that can increase the low, the that can increase the likelihood of them having aortic dissection is a bis um aortic valve. So instead of having two, instead of having three leaflets, they have two leaflets on their aortic valve, uh coarctation of the aorta aortic valve replacement surgery and a cabbage surgery both increase the likelihood of a patient having a dissection. Um So this is my question. A man aged around 60 with a background of hypertension presents with a sudden onset tearing chest pain. What do you think is the gold standard for the potential diagnosis? So which one of these is the gold standard to check if a patient has it? Yeah. CT angio is the gold standard for aortic dissection. So, CT angiogram is the gold standard for atic dissection and for the first disease that we did was carotid um artery disease, um carotid artery disease and the main um form of investigation for that is an ultrasound quite quickly next to the bed, like you can do it very quickly. But for this, we do a CT angiogram for aortic dissection just to make sure you know the investigation for both. And so you make your, your diagnosis. So you do a um ECG and an X ray often are done to exclude any other causes and they can be normal or falsely reassuring. Um You can also do a CT angiogram which is it's the initial investigation that you perform and it can generally be be performed quite quickly. And if the patient can't tolerate a CT angio, you can also do a trans esophageal and echocardiography as well. And an MRI angiogram can be good because it can give you greater detail on, you know how to plan for the surgery and things like that, but it is it takes longer to get. So the the main gold plan is a CT angiogram, what do you think you would find is my question to you some things that we've spoken about before you can on the CT angiogram on the X ray on the ecg anything. Yeah. So you'd find an enlarged lumen, you'd find a false lumen. So on the, on the CT angiogram, you'll be able to see, obviously, it might just look bigger or it could it, or it could be that you can actually see the false lumen within the aorta. And then the second thing is in your chest X ray, you can see a widened mediastinum as well. And so that can also um elude you to think that this patient is having a dissection some of the differentials. Oh, sorry. Do you, do you, would you guys do any other blood or extra investigations just to check knowing that these are your differentials, which bloods would you like to do to rule some of these out? Yeah. Troponin for, for Angina cos it's a chest pain as well, isn't it? So one of the biggest um differentials would be is this person just having a, not just with this person having a myocardial infarction or Angina instead. So you wanna check a troponin. Do you wanna check them if they're increasing as well over the hour? Things like that decreasing. You wanna check if you could also say that card um cardiac um tamponment is another differential, a pe or myocarditis. Um is another differential for pe, you could check the d damage, you could do a well score and you could also just do investigations wise. Like I said, you would do an E CG of a chest X ray. So those are what I had to add to that management and complications. So the aortic dissection, like I said, is an emergency surgery. Like there's no, there's no, um, there's nothing you can do. Once you find out that it's there, you need to, um, alert the higher ups quite quickly so that they can put them into, see, um, to the surgery suite and, you know, do the surgery and stuff. Um, it's got a very high mortality rate and I think it's cause of they, they don't find it early enough and it's such a quick disease that once it happens it happens, like it's quite hard to stop it. So, er, unless the person gets surgery and they come in quite quickly, it's quite hard. So early detection is very, is very much key. So, always have it in the back of your mind as a differential if someone comes in with tear and chest pain and pain that they just can't explain. Just think about it, especially if they have any of the comorbidities or, um, any of the, um, of the risk factors that we saw, um, what they would need right there and then is you would need to give them some analgesia, some morphine for example, to control the pain, BP and heart rate would be controlled as well. And, um, that would involve giving them things like beta blockers. So you also need to keep them on a monitored base. So you'd need to keep them in those ones where their, their BP has been checked every other second. Um, surgical intervention, like we said, from the vascular team is needed. Um, type A, um, type BB. we've talked about the two different types. Type A can be treated with open surgery. So a midnight steno to remove the section of the aorta with the defect and um is replaced with a synthetic synthetic graft. And the aortic valve can also need replacement if it's affected in the surgery or in the procedure. Whereas type B can be treated with a thoracic a thoracic endovascular aortic repair with a catheter inserted through the femoral artery. And then it inserts a stent graft into the affected artery of the aorta um into the affected section of the descending aorta. Complicated cases may require open surgery. So remember, the type B has got to do with the involvement of the descending aorta. So that's much more difficult to reach and it's in a different, it's a lower part of the body. So they tend to go through a catheter, um ro through the femoral artery as explained just now. And um they do the TTE um procedure. Some of the point complications include myocardial infarction, you can get a stroke, you can end up being um having paraplegia, maybe just for a bit for, but also like lifelong cardio cardiac tamponade, um aortic valve regurgitation and you know, death is the worst one. So I think that is it from me. Does anyone have any questions at all from the session today? You know, it was quite a neat room. Ok. Um If no one has any question, um thank you, Dan me for that presentation that was very um helpful and also very concise. Um I'm just gonna send the feedback form out in the comment section. So hopefully everyone can see that if um everyone can please um give us some feedback that would be really helpful and that can also help you claim your certificate for today. Um So if no one has any questions, I think we can conclude it there. So thank you so much for attending. Um Next week we have um a lower gi cases session on Monday. So um please stay tuned for that and yeah, I hope everyone have the rest of their enjoy the rest of their evening. Great. Ok. The feedback link isn't working. Um Let me try to send it again. Um If it, if it doesn't work on this website, um I think afterwards you will get an email to ask you to provide feedback anyway. So you should be able to do feedback after this session and, and an email will be sent to you as well. Says thanks for feedback. Um Dami, can you try clicking onto it because it works for me? Um And yeah, when I click on it works. Yeah, let me just send it one more time. But if not, I think um if you wait for the email to come and then it should work then yeah, thanks everyone for attending and Yeah. Right. Ok. Yeah, thanks Tammy. No worries. Thank you so much. Bye guys. Bye.