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Vascular surgery- part 1 recording

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Summary

Join us for an insightful session, hosted by a 4th year medical student from Aston Medical School, on Vascular Surgery. We will mainly discuss Abdominal Aortic Aneurysm (AAA) and Acute Limb Ischemia. Later sessions will cover Carotid Artery Disease and Aortic Dissection. Learn about the anatomy of the aorta, understand how it works and the importance of knowing its parts for good surgical practice. Our presenter will also break down complex topics like the branches of the abdominal aorta and essential anatomical levels. Towards the end, a deep dive into the clinical aspects of AAA is conducted. This content-rich webinar is a must-attend for aspiring surgeons and medical students looking to strengthen their understanding in the field.
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Description

AAA- Anatomy and clinical relevance

●   risk factors

●   What are the clinical features

●   Describe the screening programme in the UK

●   What other differentials should you consider (renal colic, IBD, IBS, GI bleed etc)

●   What are the relevant investigations (USS, CT)

●   Describe the relevant management, including the surgical options (open repair vs endovascular)

●   What are the main complications

●   Describe the identification and management of a ruptured AAA

PAD- Anatomy

●   Recognise the pulse points in the lower limb

●   Locate and describe the anatomical relationships of the great saphenous vein, fascia lata, iliotibial tract, femoral sheath and its contents, obturator nerve, sciatic nerve, femoral nerve, common peroneal nerve, tibial nerve, popliteal fossa and key vessels within and identify the main muscles and muscle groups that the nerves supply

●   Identify and side the femur, tibia and fibula

●   Recognise that the femoral artery is a branch of the external iliac which is a branch of the abdominal aorta

●   Recognise the femoral artery as the main artery of the lower limb

●   Describe the femoral triangle

●   Recognise the other vessels in the thigh that supply the lower limb and describe their course

●   Describe the course of the popliteal artery in the leg

●   Describe the arterial supply of the foot

Clinical

●   Describe the aetiology behind acute limb ischaemia

● clinical presentation of acute limb ischaemia

●   What other differentials should you consider (eg DVT, nerve compression)

●   What investigations are appropriate (bloods, ECG, doppler, CT angio)

●   What’s the appropriate management- conservative vs surgical (embolectomy, bypass, angioplasty, amputation, palliation)

●   What’s the appropriate long term management

●   What are possible complications (mortality, compartment syndrome)

Learning objectives

1. Identify and describe the anatomy and physiology of the aorta and its main sections. 2. Comprehend the critical importance of understanding the anatomy of the aorta in good surgical practice. 3. Understand the anatomical relation of the abdominal aorta with major abdominal structures and organs. 4. Discuss the clinical significance of abdominal aortic aneurysm and acute limb ischemia in vascular surgery. 5. Interpret the diagnostic modalities and management strategies for diseases related to vascular surgery such as abdominal aortic aneurysm.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Is it live now? It should be live now. So, yes. Um, hi, everybody. My name is Prudence. I'm one of the education coordinators. Welcome to SS um event. We are on week seven, I believe. And today we are on, we're talking about vascular surgery. So we have Shaha from Aston Medical School. Um He's 1/4 year student and he'll be sharing um some vascular surgery conditions to us. So I'll just hand over to Shahe now. Great. It's nice to meet you all today. So, my name is Cher Basan. I'm 1/4 year medical student from Maston. Um, for this week of the s teaching series, we'll be going over vascular surgery, um namely I'll be going over AAA so abdominal aortic aneurysm, but I'll also be going over acute limb ischemia. And then I believe on Wednesday or Thursday, my colleague would also be covering carotid artery disease and aortic dissection. So there's still, there's quite a bit to just to look over, but I'm excited to, to teach to, for you all today. I want to begin by sort of expressing my appreciation for our partners if you're someone who is quite interested in surgery. You might find these resources very useful for you. Um I myself really like to use the Teach Me platform. They've got all kinds of interesting resources with regards to studying. But if you want to have a look at the other ones too, by all means, uh sorry, quick. Hey, can you press the hide button from the bottom of, of your screen? Sure, no problem. I'll do that now. Great. I will do. Thank you. Yeah, no problem. So we're going to be, we're going to be starting off with AAA. So abdominal aortic aneurysm, here are our anatomical learning objectives. I'll just let you read that for a moment and here are our clinical learning objectives. So we've got quite a few more clinical learning objectives. So we're gonna be talking about signs, symptoms, diagnostics, investigations, management. We're gonna be covering the anatomy first and I feel like with surgery without anatomy, it's kind of like traversing a forest without a map. So you really need to know about anatomy if you want to have um for good surgical practice. When it comes to the AORTA, specifically, we have four main sections. OK? We can have a look at the image on the right four main sections, but it all, it all starts off with the left ventricle from the left ventricle. You, you get the ascending aorta and then you get the aortic arch. So it ascends and you've got the aortic arch, the aortic arch throws off various branches to the head and neck and the arms, we'll talk a little bit more about that later, once it's arched over, it'll go back down and that's the descending thoracic aorta, it ascends far enough that it starts to perforate the diaphragm at the level of T 12. Um, and once it's perforated, the diaphragm then enters the ab the abdominal cavity to become the, the abdominal aorta. You'll notice that I've um put the descending abdominal aorta in bold. And the reason is because it's uh the most relevant part of the aorta for, for this first part of our session, given that it's the AAA. So abdominal aortic aneurysm, we'll explore the abdominal aorta and just a little bit more a little later on. So I mentioned we'll be discussing the arch itself. So here's the um aortic arch. When we reach the section, I've mentioned that it throws off various arteries to the head and neck. So we start off approximately. So approximately just means closest to where it exits the left ventricle. The first proximal branch is this brachiocephalic artery, the brachycephalic artery then branches off further to give us our right common carotid artery and right, right subclavian artery, the right common carotid artery, as you may know already, um spews off, gives off various arterial blood supply to our head and neck and then our right subclavian artery. It's pre predominantly involved in um arterial supply to our arm So it's the right subclavian artery. So it would go down our right arm. But interesting to note as well that one of the branches of the right subclavian artery throws off a branch to the inferior inferior thyroid artery. So our thyroid gland, once we move past the breaker span that you can see that you've got the left common carotid. It basically does the same thing as the right common carotid. It's just like a, a aa double um pathway for arterial blood to travel up to the head. Um And you'll know perhaps from neuroanatomy that it helps to supply one of the, one of the main uh tributaries of blood to our circle of Willis. But that's amorphous for another um neuroanatomy session, which I won't be covering today. And then you've got the left Subclavian archery, which does the same thing as the right one just on the left arm. So I hope that all makes sense to you. I remember, I remember having to learn all this in my, I think the first two weeks of my er of medical school when I was in year one. So this kind of, it's, it holds a sentiment to me, it's quite valuable to me. My first piece of anatomy that I probably had to remember. So I mentioned then it then travels down the um the thorax and it sort of travels quite centrally in the thorax um in the portion of our thorax called the mediastinum and they've got different, we've got different areas of our mediastinum such as the anterior um middle, posterior and superior mediastinum. It just, it's just so happen, it just so happens to be that the aortic arch first travels up into the superior mediastinum. So the green bit and then it travels back down through the posterior mediastinum, which is the blue bit. And then you see that curve at the bottom, that's the diaphragm. And you'll notice how the um aorta perforates the diaphragm, as I mentioned at the level of T 12. OK, crossing the diaphragm. So this is another piece of anatomy that I remember having to remember. Um, the diaphragm has got a couple of quite important holes that allow important structures to pass through T 12. So the aortic hiatus is where the aorta will, will perforate through the diaphragm. But you've also got the esophageal hiatus, which is where um I believe coa 8, 1012. So T 10, this is where the esophagus perforates through the diaphragm to um continue on as a stomach. And then you've got the car opening or carve hiatus, which is where the inferior vena cava will actually drain blood up through the diaphragm to um join up with the superior vena cava. And then that will um drain blood into our right atrium. So they've got three important holes there, three important vertebral levels. And the way that I remember this, actually, I believe it was also in year 11 of my leader Nat in this told me it goes co 88, 1012, so co 88, 1012 C for car. So Vena Cava, O for oesophageal and A for aorta. So C oa 8 1012, T eight T 10 T 12. Ok. No, we're in the abdomen. This is where things get a little bit tricky, at least for me because as you can imagine the abdomen, it's full of different structures, organs, our viscera, our gut, um you know anything kidneys, our duodenum ileum, large intestines, everything really is kind of all in our abdomen. So we get our um it just so happens to be and it makes sense perhaps that the the that the abdominal aorta gives off so many branches. I mean, if you look at our image on the right, it's terrifying, really look at how many branches we we've got. Um But the main ones I really wanted to um draw your attention to are the renal arteries, the celiac arteries which will give rise to the arterial supply to our stomach. Also on the first part of our duodenum as well, the renal arteries which of course will give rise to our um arterial blood supply to our kidneys. Um I've mentioned of the superior mesenteric artery which will, which will supply blood to our um jejunum ileum up to a certain point of our transverse large codon. Then you've got some of the other ones like gonadal and iliac vessels, which we'll talk a little bit more about that later. So it's quite convoluted, quite complex. But um it doesn't make sense given that there are so many structures that, that need um perfusion. Oh, yeah, I should notice as well. I should note as well that quite a common anatomical question is at what level does the renal artery branch off from the abdominal aorta? And the answer is L1 L2. Yeah. So I also remember having to remember this um in year two, actually when I was on my renal block, um it was all the branches of the aorta, but this is the best I could find. And this is actually the method that I used when I was um when I was in year two to try to remember all of this. Um It's from this fancy youtube video that I found. So this isn't the best attempt that I've got at it. I hope this helps. You'll find that the ones in purple are the ones that are kind of in the midline. They're unpaired structures and then the ones that are paired are kind of, they're quite lateral, they're on the lateral two sides of the a of, of the abdominal aorta. So we're kind of moving on to the clinical aspects of this first part of our session now and I kind of want to take it to you guys to have a brief think about what structures we must dissect or to traverse in order to reach the aorta. And I purposefully left this question as an open question because I didn't specify whether it was the thoracic aorta or the abdominal aorta. Because ultimately, what you dissect will depend on which area of the aorta you will be um performing surgery on. For example. So if you guys want to have a think about that, now you can type your answers in the chat prune. Perfect, can even read them out to me, but just have a brief think about it for about 10 seconds or so and they will move on. So it really does depend on which area of the aorta you are trying to explore, but obviously, skin subcutaneous tissue, very important. We obviously know, well, some of that, perhaps it would be good to go over the general structure of our skin and the underlying tissue. So you've got the epi the epidermis, dermis, you've got sort of the superficial fascia, then you get sort of the deeper fascia that, that envelops our muscles. So for example, our abdominis rectus muscle will have sort of the scarp as fascia if you, if you've ever heard of that, um then we sort of get um serosal connective tissues like the peritoneum. Um If you are exploring the abdominal aorta, if you're in the thoracic A. Um Sorry if you're explore. Yeah, if you're exploring the abdominal aorta. If you're exploring the thoracic aorta, maybe you'd go down the pathway of the pleura, which is that connective tissue covering around our lungs. Um And then obviously other vascular structures that you will encounter as well. So I mentioned a renal artery. I did this on purpose cos it's one of the ones that is quite important to consider when um performing surgery on someone with an abdominal aortic aneurysm. Um And I'll explore that a little bit later. I've described the gross structure of the main parts of the aorta, but I really wanted to have a brief discussion on different layers of the aorta. So the mural anatomy. So you've got the tunica intima, which is composed of like an endothelium. I guess it allows for like slippery laminar, smooth blood throat, blood flow um as well. Um And then you've got the tunica media which is composed of smooth muscle. It's quite thick in arterial um blood vessels, but it's composed of smooth muscle and it's also composed of collagen fibers as interlaced and it gives the aorta its elasticity and its stretch stretch and its rebound. Um And then you've got the tunica externa, which is like a connective tissue covering that offers protection to the blood vessel. You'll find that in um the pathophysiology of, of an abdominal aortic aneurysm, the wall often undergoes a lot of stress inflammation, oxidation proteolysis, and that leads to the remodeling of this wall into a structure that's subpar, it just doesn't work and that can, it, it weakens the structure can lead to rupturing. So a little bit when we uh before we talk about the actual abdominal aortic aneurysm um itself, um I just wanted to discuss a brief case study just to put everything into context. So just the general points here because um I know we only have an hour or so for the session. But general points as a ripping, tearing sensation in the abdomen, quite acute onset, said two hours ago, feeling quite lightheaded, nauseous worth mentioning that they are quite old. So 75 years old, a male which is a one which I will discuss is a risk factor for something like this. Um They've got hypertension hyperlipidemia. So their cardiovascular risk factors are through the roof pretty much um socially, smoking alcohol. Um So it doesn't look like a good picture. We performed some vital examinations. So heart rate was tachycardic, respiratory rate was on the higher end of normal diaphoretic. So, sweating appearing pale as well. Um Another thing to note was diminished pulses bilaterally. So we'll talk a little bit more about why this happens. But if you think about it, um you're losing blood blood volume, effective circulating blood volume. So it won't, the pulses won't be as powerful as there's not much blood to cause that pulse in the first place. We will talk more a little bit more about that. Then a system through review, which was all normal, uh pretty much um neurologically though they are feeling quite lightheaded, which, which will make sense as I will explain a little bit later on for a situation like this. There are a number of differentials to consider. I wonder if you could have another think about this for me. Um You probably already know what the likely diagnosis is, but it's still a good practice to try to think about what other pathologies it can be pretty much. Um, so I'll give you about 10 seconds or so to just have a brief, think about what's going on. You can write your answers in the chat. If you'd like, you guys can still hear me. Right. Prudence. Yes, we can hear you. Yeah, great. All right. So, differentials, there are quite a few to consider. I remember, um, oy prepping with my friend and he goes, when we're always asked about differentials, it's good practice to try and split them up into systems to have some kind of a structure to go about the way you answer it. Um I've tried to do that at least. So urogenous, you'd consider renal colic if you don't know what that is. It's basically the ureter, the structure that collects urine or drains urine from our kidney into our bladder. Um, sometimes a stone can get lodged in there and the ureter sort of contracts to try to squeeze that stone outwards and that generates pain quite sharp, painful pain from loin to groin. Another one to consider is mesenteric ischemia. This is quite devastating if you remember all the arterial blood branch, um arterial blood uh branches to our gi tract. Um Sometimes that can get blocked whether it's an embolus or a thrombus. Typically someone with atrial fibrillation who's developed a clot in their left atrium. The clot then travels through the left ventricle, shoots off through the aortic arch down through the traffic aorta, down into the descending abdominal aorta and get lodged in one of the mesenteric arteries that leads to ischemia of all that gut. It can lead to necrosis of that gut. The, it's a very, very poor prognosis unless you can um quickly repair that um occlusion through um through laparotomy, which is when it's a surgery that you go straight through the abdomen, straight through the peritoneum, uh peritoneal um peritoneal cavity and just try to repair that, that occlusion. Then obviously gi problems as well. So pepti gos disease, all the ones that are on the slide. Msk as well. Although these typically won't really lead to lightheadedness or nausea, um You should probably consider MSK pain given the locality of the central abdominal pain and lumbar radiculopathy as well. So the spinal um nerves, some various thoracic spinal nerves like T 10 T nine, maybe even T 11. If those get impinged, it can lead to referred pain over the upper abdomen. AAA. Finally, we're here So aneurysms, well, generally speaking, it's just when the artery kind of balloons outwards. So it's supposed to be a nice linear tube, but sometimes the, the the wall can balloon outwards. And that ballooning is a weak, is a weak point in the wall of that blood vessel. They can rupture. Um The typical definition of a abdominal aortic aneurysm is the one that with a diameter from left to right is more than three centimeters. Ok. Um I know the definition is one where the abdominal aortic diameter is 1.5 times normal, which is another one but more than three centimeters is the usual definition for the aorta. At least that's what I was told by the vascular surgeon who was covering over these sides. Um Well, the problem with this is the fact that when it ruptures, ok, when it ruptures, if you imagine the aorta massive magnet blood vessel, the biggest highest magnitude arterial blood vessel in our entire body. If it ruptures, you're bleeding out quick, you're bleeding out rapidly. All that blood that's that's pumped down through the aorta is just getting lost, it's just getting lost and that is devastating. It's a really, really bad day if someone has this um the location is commonly infrarenal actually. So if you noticed, remember back to the dia the diagram where I had the, the branches of the abdominal aorta, um Typically this aneurysm occurs below the level of um below the level of the renal arteries, infrarenal infra, meaning below renal meaning renal arteries. Hi, Shahe. Um Yeah, we've got a question. Um Someone asked, can you shed some light on referred pains, please? Yeah. So referred pain is basically a term that's used when the pain it's in a location where the how can I say? So it's in a location that is you feel pain in an area that isn't directly being under attack, for example. So if you think about um the spinal nerves or let's say the thoracic spinal nerves, um though those thoracic spinal nerves are in the back, they originate from our vertebral or from our spinal column. If one of those roots gets compressed, the sensory nerve fibers that, that, that, that spinal nerve innervates um that that sensory dermatomal distribution will become quite numb. They will start to experience tingling sensation and that can sometimes manifest as pain. So it's not necessarily that the the abdomen here is under attack or that it's been burned or anything. It's the fact that a structure um like a nerve has been damaged and it sort of manifests as pain in a, in a different location. It's kind of like how you get referred pain in myocardial infarction, like M I across the left arm into the jaw as well. Um It's kind of like how you might get referred pain um from the gallbladder, let's say cholecystitis, you might get referred pain on u up until the up into the shoulder. It's just because of the innervation and the way that things innervate um that it just so happens that when certain structures in the body get damaged, um the nerve, um the nervous system manifests it as pain in a different location based on how the nervous system is structured. Does that make a little bit of sense? I hope that makes sense. Yeah. So he said, thank you. That's clear. No worries. OK. Awesome pathophysiology. I mentioned this. I always love to II love my pathophysiology when discussing all these different conditions. But remodeling is the main issue that's going on. So I mentioned oxidation proteolysis inflammation. OK? Someone with who smokes a lot, for example, someone who has high BP, it leads to um micro damages. That's just the term that I made up, but at least a damage of the wall inflammation, things like that. And that leads to weakening, gradual dilatation of that area of the aorta. I tried to illustrate that as best as I could rather simply though um through the um illustration just down the middle, how it becomes straight and then it sort of sort of starts to curve over just like that. And that's a weak point, risk factors on the right. Have a read of that. And I want you guys are telling me why is it that I did, I split these up into blue and green? Why did I do that? I'll let you think about that for a moment. I split these up into, sorry. Go ahead. Yeah. Has said green is, uh, no one is modifiable. The other is non modifiable. There you go. You hit nail on the head there. Yeah, exactly. So blue is non modifiable. You can't change this. I'm getting older. I can't change this. I'm a man, I can't change that. People with their lost and Los Marfan syndrome which are connective tissue disorders. You can't change them. It's in, it's imprinted in your DNA. If you're white Caucasian, you can't change that smoking. You can change hypertension, you can change, you know, reducing your salt intake, fluid um restriction to some regard as well. Um Cardiovascular disease relates quite a lot to hypertension. You can change that trauma to the abdomen. You can change that and obesity, you can change that signs and symptoms. The main sort of the main time or the primary time we'd get um symptoms is when the aneurysm ruptures, it's usually asymptomatic when it unruptured when it's unruptured. But you can sometimes get patient presenting with abdominal pain, generalized aching, abdominal pain in the, in the unruptured state. Um You can also feel on palpation, a expansile mass um from the aortic sac sort of pulsating with each um pulse of arterial blood flow that runs through the aorta. Um If you do get, if it's symptomatic like that, you may consider vascular surgery, um I'll talk a little bit more about the indications for when we would do vascular surgery. But unruptured is where it starts to get a bit serious. Um, you know, so ruptured is when it starts to get serious. If you imagine a rupture of the biggest vessel in our entire body, you're in big, big trouble, it's not looking good. Um, you can get, I've once again, split them up into blue and green the best as I could. Um, but I wonder if you guys can tell me why I decided to do this again. Why? What's special about green? That I, um, what's special about green? What's special about blue? I tried to do this the best I could. There may be a few inaccuracies but for the, but for the most part, um, so no one's put anything in the chat so far, but I think green is symptom and blue is signs. Yeah, I try my best to sort of split it up into signs and symptoms. Ok. Um, there may be a few inaccuracies. Um, but I've tried my best but essentially symptoms are what the patient tells you they're experiencing and signs are what the doctor finds out about the patient. So the patient doesn't know that they're hypotensive. The doctor finds it about them. The patient doesn't really know that they're tachycardic. That's something that the doctor finds out on examination. For example, sometimes a patient doesn't know that they've got a pulsating abdominal mass, but if on a gi peripheral vascular examination, you'll find out that they have an expansile mass. That's more of a sign. I would want you guys to just double check that though key investigations for a Oh, I also want to mention actually that the consultant who was checking over my slides, he made an interesting point about anterior ruptures and posterior ruptures and how anterior rupturing of the abdominal aortic aneurysm usually leads to instant death as opposed to a posterior, which you can work with ever so slightly. And my understanding is that when you bleed into the posterior abdominal cavity, it's quite a rigid structure. So as you do get bleeding, you soon enough have back log of blood that's pressing back on the aorta and stopping it from bleeding out further. But when it comes to the anterior abdominal aorta, if you think about it that it's bleeding, it's bleeding into the abdominal cavity, it's bleeding into the peritoneal cavity. If you've ever seen people with ascites, all that blood, all all that fluid in their peritoneal cavity, it can get massive. So if you think about it, anterior rupturing, all that blood starts to bleed and bleed and bleed and there seems to be no limit with when it stops. So eventually the patient just lose their, loses their effect of circulating body. They become hypertensive very quickly and it sudden death is what the surgery, the vascular surgeon um told me it usually happens with these key investigations, have a brief think about this. For me, I'll try not to spend too long. So ultrasound is the main one, but we can also opt for, um, CT angiogram. So ultrasound is mainly for screening CT angiogram for if you want to investigate the aneurysm further, it's very helpful for if you want to perform surgery, you can see on these, um, CT angiographies below. Um, what I mean by the aneurysm. Yeah, you can also see see that white circle, that really white circle, that's the contrast agent being used, it shows up really nicely. And if you can see around that blue, that white circle, you get this like this crescent darkening around it. That's an intramural thrombus. So it's kind of like blood clotting within the um within the aneurysmal sac. And my understanding is that it's because the blood flow within this area, it's not as laminar, it's quite turbulent. It's, it's relatively stagnant, for example. And then it just builds up and it clots over time screening. So men are screened at 65 years old. Once the reason why men are not women is because, well, women are not at increased risk of this at AAA, they can still get it, but they're not at increased risk. It's kind of the same reason why you get women being screened for breast cancer. But men are not, it's because men are not at increased risk. It is another illustration interpreting our diameter. So we actually use this ultrasound to, in er, to um inform what we should do next. So, aneurysms that are less than three centimeters aren't presumed to be normal. So nothing really happened in the long term. But as the, the bigger it gets the, um, the more urgent things get. So, aneurysms more than 5.5 centimeters often lead to vascular surgery referrals very urgently because there's a really serious risk of them rupturing and then things in between. So two months, scanning, two months, scanning three months. So this is quite a common, I believe quite a common question. Actually, in exams, I know I was tested on this once. So management for an uncomplicated, so unruptured um AAA so you like to put it up into lifestyle and surgical lifestyle includes, you know, don't smoke weight loss, diet exercise. You know, these are all risk factors I mentioned before. Um managing your BP, your diabetes, your hyperlipidemia statins. Interesting one. Actually, um statins are usually good statins if you're 10% risk of cardiovascular disease, if your few risk of cardiovascular disease is more than 10%. Um we usually, we usually start off with 20 mg of atorvastatin. But if you have a uh previous history of cardiovascular disease, you might want to move up to 18 mg elective repair as well. So for someone who's got an aneurysm, that's more than 5.5 centimeters that's growing by more than a centimeter a year or that's causing symptoms straight for elective repair. Generally speaking, and they've got two options. You've got open repair and then they've got endovascular repair. I'll talk a little bit more about these. This is open repair. So open, it's just because the nature of it is quite open, it's not really a discrete hole through which we enter the um aorta, it's straight down the middle, down the hatch. Um Usually what we do is we incise through the abdomen, we clamp the aorta above and below. Um And then we take out the aneurysmal sac in its place. We sew on a synthetic sort of tube that will act as a lumen, then you will um uh close the clamps and then um close up the incisions as well. Um I wanted to mention why it's important to consider the renal arteries because you can see the renal arteries here actually. And you can imagine that if some people um get clamped above the site of the renal arteries and if that's the case, what happens when you're reducing arterial perfusion to the kidneys and that can lead to AK I. So it's very important to consider these structures. If you have accidentally hit one of these structures when you're perform, when you're incising and trying to remove the aneurysmal site, it's not good news. Then you've got endovascular repair, endo meaning means inside. So it's more hidden, it's more discrete. Um And essentially you enter through the femoral artery, you put a catheter in a sort of a guide wire that will guide a sort of AAA piece of equipment that um helps to place a tube down into the uh into the aorta. So you, you go through the femoral, then you um insert the stent like structure through this guide wide tube. Um And you can see over here that the stent like structure covers the aneurysm quite nicely. Um It's hollow so it allows blood to flow through the stent as well. Obviously, then the catheter, the guidewire removed and then the incision is closed. OK. So you've got open repair, then you've got, um then you've got um endovascular test. So this is a big, big problem, ok. Ruptured aneurysms are quite a big, big problem, as I mentioned already, but as with all emergencies, ABCD E airway breathing circulation, disability exposure, um as well and everything else. Um There is a concept of permissive hypotension. So it's the point where you um you don't want to reduce BP so much. Um Well, you want to reduce BP, but you um see the issue is that when you have that much bleeding, your BP will reduce quite drastically, but you don't want to reduce it so much that you threaten the perfusion of other organs. Ok? Um You want to raise the BP so that you do increase this perfusion. But if you raise it so high, then you might encourage further bleeding. So there's kind of like a balance that needs to be had. Ok? If a patient is unstable, you opt straight for surgery and if a patient is stable, then you'll do a CT angiogram just to investigate the issue further. Ok. Complications are as follows. I am aware I'm actually running beyond what I was hoping for. So I'll try and be as quick as I can, but you can read them as on the slide endo leak is something that I wanted to mention. Actually, um it's basically when um typical of uh endovascular repair where you sort of the stent doesn't quite exclude the aneurysmal sac from the lumen of the aorta. So you do get sort of blood that sort starts to flow into the aneurysmal sac. So continued blood flow into the aneurysmal sac. Ok? And that can lead to the proliferation of symptoms and indeed can lead to rupturing in the future. OK. I mentioned a renal hyperperfusion due to clamping general surgical risks like bleeding, infection, venous, stronger embolisms as well. Um We're in de de de as well. So all these different things. All right, if I'm going too fast, please let me know. II just have to hurry up because uh I'm kind of running out of a little bit out of time. So, peripheral arterial disease, we're now on to the next stage. I wanted to talk about acute limb ischemia actually here are our learning objectives. Ok. So we'll cover the anatomy of the different blood vessels, the nerve supply, so on and so forth. So, I mean, we, we left off at the abdominal aorta, the abdominal aorta then branches off to form our common iliac vessels. Common iliac vessels, each branch off to form internal and, and external iliac um blood vessels. Ok. These structures, they help to um perfuse arterial blood to pelvic structures. But the external iliac typically is for perfusion down on legs. Ok. The level of bifurcation, by the way, the so and to me would be a good idea to talk about this. But level of aortic bifurcation down into the common iliac cos at the level of t uh at the level of, you know, actually you tell me, do I, does anyone know what the level of the aortic bifurcation into the common iliac is? Who knows this? Someone, someone tell me any idea. L4, LL 4 L4. Yes, that's right. It's L for, yeah. OK. Quite a lot to cover. Really. Anatomy is anatomy. I mean, I always just find that if you stare at images of anatomy soon enough, it will come to your mind. But we can see that the um main thing is the, where I, where the femoral artery originates from the external iliac artery. Ok. So the external iliac artery branches off to form the femoral artery, femoral artery then helps to supply um our leg. Ok. Um There's a, a ligament that runs from our anterior superior iliac spine to our um roughly around the pubic sympus. But actually our pubic tubercle, it's called the inguinal ligament. And you'll find that the femoral artery is kind of in the middle between the two. So that's the place where we palpate for our febrile polls. You'll notice the femoral artery gives off various profunda branches, so deep branches of the femoral artery, um and they just help with perfusion of the leg as well. Further down, you do get the popularity of artery arising, but we'll talk a little bit more about that later. So femoral artery, it then descends down our anterior thigh really. And then it spins around our humerus to form the popliteal artery. Ok. Do you see the artery pop artery? So you've got femoral artery up here, turns around the femur, ok. Sorry, not the humerus. I mentioned the humerus. It, the femur, sorry, humerus is up here. By the way, femur turns around the femur and it forms a pop artery. The artery then help um branches off to form the posterior tibial artery, anterior tibial artery, um common peroneal artery, I believe is another one of them as well. So, um yeah, of the peroneal artery generally, just all this anatomy. So you just, you just have to learn it really. There's no easy way to go about it. Um But the main point is that it all starts off really with the, with the femoral popliteal, then it gives off various branches such as the um perennial artery and then the anterior and posterior tibial arteries. Ok? I wanted to make um make note of the dorsalis. Um the various pulse points I already mentioned the femoral pulse, which is sort of in the middle between the anterior superior iliac spine and the pubic tubercle popliteal is where you do get that. You see that popliteal artery, it's behind the knee and you'll need to the patient to flex their knee if, if you wanna feel this notoriously difficult to feel it. But I think you do have to press quite firmly to have a feel or any chance to feel it. And then further down the anterior tibial artery, which is a branch of the popliteal artery travels down sort of the um what can I say? The medial malleolus just behind the medial malleolus um to form the um or rather the posterior tibial artery forms the posterior tibial pulse. Ok. And then the anterior tibial artery, it moves over the dorsum of our foot, which is like the top surface of our foot. And that's when we get the dorsalis pedis pulse. Ok. So we've covered the femoral pulse, popliteal pulse, then the posterior tibial pulse. Ok. And then also the um um the dorsalis pedis artery pulse, the dorsum of the third. There you go. There you go. Femoral triangle, important structure. Ok. Um, a lot of different structures, but the way I remember is navy pants. So, femoral artery is kind of where your pants are. Pretty much navy pants are nerve artery vein from natural to medial. It's a nerve artery vein. Ok. Um, so you have the, um, the femoral nerve, then you've got the uh femoral artery, then you've got the femoral vein as well. Um You've also had some lymph nodes as well. So, um, sort of, I imagine would be like inguinal lymph nodes. But I'm not sure if that's, that's entirely correct, but you do get lymph nodes. Ok. Great saphenous vein, by the way, perforates through the fascia lata, which is like a, uh like a membrane around the um upper leg. Um, the greater sahan vein pers through that structure and joins up with our femoral vein and then that helps to drain vein, drain blood or venous blood out of the leg. Ok. It's important. It's an important, um, piece of anatomy, the femoral triangle. I remember when I was in A&E once I snuck into A&E. Um, and I actually, one of the doctors was asked to do a femoral nerve block, which is when you sort of block the nervous transmission through the femoral nerve, I suppose for pain relief or something along those lines. Um, it's the place where you feel the pulse. Um, it's the place to which you can guide various. Um, I, um, med um, treatment, um guide various treatments such as if you're gonna um do cardiac catheterization. Um things like that, even we even discussed the endovascular repair. So that's where you place the catheter and the guidewire as well. OK. And then other pathologies too. So, femoral triangle is where you'd spot the femoral hernias as well. You do get some um if a tumor forms, it can compress the femoral nerve at this point. So, so there's quite a lot going on general structure of the femoral triangle. OK. So I'm afraid you're just going to have to learn this essentially. But um I suppose the best image, uh the one that I'll take from this slide is the top right image. So you've got the in inguinal ligament, which is from the aci to the pubic tubercle, the sartorius, which is like a diagonal muscle that goes right down. Then the abductor longus muscle, which is kind of like medial towards the groin area. And that forms like the triangle and the outer lining of the triangle. OK. Um I'll try and speed up. I know there's a lot of anatomy, but I'll try and speed up. The main point is I wanted to discuss the boundaries of the femoral triangle. There is a table in the, in the latest slides. It's just another piece of anatomy. Really. We can see the femoral vein, you can see the artery, the femoral canal, which is like an empty space where you've got lymph nodes. OK. You can also see the inguinal ligament which forms the sort of anterior border of this structure as well. OK. Then the fascia lata was like covering around the femoral triangle. I mentioned how this was the place where the greatest aus perforates through and joins up with the femoral no, a femoral vein. It just forms the um the roof or the covering over the femoral triangle. OK? And we can see the inguinal ligament up top. Here's a table to briefly summarize the borders of the um of the femoral triangle. I mentioned the inguinal ligament from the top, the sartorius, which was that diagonal muscle going down the abductive lus, which obviously was that medial muscle. I mentioned a roof which was the covering, that's the fascia lata and the underlying muscle underneath. So if I go back, if you have a look here, the underlying muscles underneath, you've got the abductor. Um you've got um sort of the aucta magnus brevis muscles, all these muscles, they help to form the, the the floor of the femoral triangle. OK. Pectineus said, and IOS muscle as well, sorry. So many muscles, it hard to you get confused sometimes. OK. Here's some bonus anatomy, probably not that much related, but it's in the learning objectives. And I wanted to summarize that the proximal lower limb can be summarized into three compartments, the anterior compartment in blue, the medial compartment in green, posterior compartment in red Um each of these has a very, has a primary nerve that helps to innervate the structure. So the anterior compartment is more for the femoral nerve, medial compartment is for the obturator nerve. And the posterior compartment is a sciatic nerve. We'll talk a little bit more about the sciatic nerve. Ok. Um um Yeah, these muscle groups, they group because they help with certain primary functions of the lower limb. So I imagine the anterior compartment would help with, would help with knee extension. The medial compartment would help with knee abduction. The posterior compartment would help with knee flexion as well. So they've kind of got their own big groups of these big groups of compartments have their big groups of motor functions and the big groups of nerves, sciatic nerve just mentioned very briefly. It's uh is a branch from the sacral plexus. OK. The biggest of the branches of the sacral plexus. Um very important when it comes to nerve innervation down the leg. Ok. We've got the femoral nerve of course, which, which does its own thing. I mean, we've got the lateral femoral cutaneous nerve branch as well, which has its own thing. But the sciatic nerve is the big nerve when it comes to leg innervation. Here's another sort of compartmental studies of the leg. But this time we will be discussing the lower leg. So we've got four main compartments this time. As opposed to three, you can appreciate this slide in your own time. But the main thing that I wanted to, to um discuss was that the leg is split up into these compartments. Each of these compartments has their own primary nerve and each of these compartments has a primary set of functions and it does. Ok. Um We'll talk a little bit more about compartment syndrome a little bit later on. But when the pressure in these compartments increases, so when the intra compartmental pressure increases so much that it starts to block blood flow, um it starts to squeeze the arteries in that compartment so much so that it starts to restrict blood flow down. Um distal to that um occlusion, it can lead to acute limb ischemia. Ok. So like trauma, accidents can lead to too much bleeding within the compartment. Presses on the arteries can lead to compartment syndrome. Does that make sense? I'm going to have to go a bit quicker than this because I am I am actually running out of time pretty much, but I'll continue going. I believe fasting prudence, I think fasting, I think is broken now, right? Something like like like like that. If someone can just confirm with 20 I think it's if is my group now, we'll see. Well, if you're breaking your fast, go ahead. Um and you can leave if, if you want to, but it'd be great if you stick along. Um I'm just gonna continue this entire the rest of the slide we've discussed the Femoral triangle, OK, which is one of the big sort of neurovascular bundles, I should say of the lower limb. The other big collection of the big neurovascular collection is the uh Popliteal fossa. OK. And the Popliteal fossa also has its arrangement. So kind of like how the femoral triangle has got its navy pants arrangement. So nerve artery vein from natural to media, the popliteal fossa has its own arrangement Um from nerve vein, artery lateral to immediately. OK. Um I sometimes do grappling or B JJ and there's something in B JJ called popping your knee. It's when someone twists your leg so much that your anterior cruciate ligaments tear into two. It's extremely painful and it's quite, it's not very good when it happens. But I remember this popliteal because it's right behind the knee. So I remember it as never pop your knee. So never N va nerve vein artery, never pop your knee. And then of course, I remembered uh Navy pants, Soor Triangle. Navy pants, a nerve artery vein all natural to medial. OK. Another little detail is that um the artery is the deepest of these structures and it makes sense because um all that blood really and all that perfusion that responsibility to perfuse all that blood down, the lower limb is quite important. So I feel like it's deep just so it's protected a little bit more. It's just God's creation really? OK. Clinical learning objections. Th this is the last bit of our session. Um I'll try and get this over and done with before we conclude the session. Really? Ok. So we've got another case study. 65 year old male. The name is irrelevant, but I remember putting it in and I forgot to take it out. But they've also got a prolific history of cardiovascular disease. So, hypertension hyperlipidemia, um, they've got sudden onset of pain in the lower leg, right lower leg, um, they woke up this morning with severe pain. The, it feels cold to the touch, it feels numb. So there's some kind of paraesthesia issue going on here and they've got an inability to move their toes. So not good, really, really not good. Um Systems review all seems normal medications are on statins. Presumably they've got previous, uh or previous cage. So previous, probably previous M I probably or um, so that's bypass graft. So, um some kind of coronary artery disease and that's, that's led to them having statins. Um, and aspirin too, which helps with cardiovascular health. These are the vitals. Main ones to notice are um, two out of five, right leg, uh right lower leg, um, muscle power. So you remember the MRC muscle power scale, you've got, I can't remember where, where it starts off as I think it's one where there's nothing at all. Two where there's fasciculations, three where it's movement with uh without gravity for where it's against something like that. It's the muscle power scale that you guys will have to read up about. I always forget this quite uh classic in Aussies. Um But it's two out of five, which is not good. Um I think that's slightly above fasciculations. I might be wrong. I might be wrong. You guys are gonna have to read up about that. But essentially the muscle, the, the motor power in the right lower extremity is not good. That's the main point here. Um They've got reduced sensation to light touch, pinprick sensations poor, OK. Um Vascular, in terms of vascular examination, they've got poor absent, dorsalis, pedis pulses, posterior tibial pulses are also absent. We spoke about these pulses earlier. But if you get um proximal occlusion of arterial blood flow, you're not having any blood flow down distally through these arterial branches. So you do not feel the pulse at that point. Ok. Could be the refill time. More than two, more than three seconds. It should be less than three seconds. Ok. Cool to the touch. Most likely diagnosis. Would you guys tell me, give me one, give me, you know, just have a think about it. I know I'm running out of time, but we'll have a think about it. What a differential shall we consider in the case of a classic unilateral sudden onset of lower limb pain? What differentials would we consider over here? I mean, we given that it's on the 10 really? But given that it's a key in the scheme. Yeah. Um What other differentials should be considered in this situation? I'll let you guys have a think about that if you want to put it in the chart. Go ahead. So Ashok has mentioned renal damage due to occlusion. Sorry, say that, say say that again. So he said renal damage due to occlusion but he's not too sure. Just a guess reason damage, renal damage due to occlusion. The kidneys. Oh, interesting. I mean, I'm no expert at vascular surgery, but that's an a renal damage due to occlusion. Huh? Oh. What, what's being occluded? Like the kidney like AK I? Is that what you're talking about? So personally, I think the shouts either like compartment syndrome or acutely ischemia? Sure. Ok. Fine. Yeah. Yeah. Yeah, of course. Yes, it does acute limb ischemia, compartment syndrome. Good options. Um Here are what we consider. Ok. Um I'm interested in what he mentioned. He said renal due to occlusion. Yeah. So he said potentially the renal artery might be occluded. Oh, but given that it's lower limb sudden onset weakness. Um What makes you think it's renal occlusion? Surely it, it is more likely or more likely to be something vascular in the leg rather than the renal artery. I wonder if they can explain why, why they think that way. It's an interesting idea and I, and I will move on. I mean, I'm not an expert, I'm, I'm still a student. So maybe I'm missing something dead obvious. So here are some differentials. OK. So arterial thrombosis, deep vein, throm thrombosis sciatica radiculopathy. Again, I mentioned the referred pain. Typically, if you're gonna get lower limb weakness, the radiculopathy or the spinal nerve typically will be something like L4 L5 or something like that. L4 L5, possibly L3. You might talk about S one, you know, something like white like that. But with radiculopathy, would, would you find absent pulses? Probably not. That's the only thing compartment syndrome. Yes, prudence. You're right with that one compartment syndrome. Um I'll talk a little bit more about compon syndrome later. If I do get time slightly running out of time though acute liver ischemia, this main most likely diagnosis. All right, sudden reduction in limb perfusion, acute, acute for a reason, limb it's affecting limb ischemia, not much oxygen becomes ischemic can become necrotic if it's not being treated quick enough. Ok. Um limb viability is compromised. Ok. As I mentioned, can become necrotic if not treated soon enough. Typical exam questions are like, what are the six ps of acute limb ischemia? Like there are on, there are on the slide really. But if you have a look at that image, you can, you can just look at how almost it looks s it looks pall that blue sign of nose almost doesn't look good. I'd imagine this patient would have some degree of paresthesia, pain at rest, pulseless as well. Um Compared to the right, the patient's right foot, left foot rather, it seems well perfused. Florid red seems nicely well perfused. But the left one seems in deep trouble. The three main patterns of acute limb of peripheral arterial disease that acute limb ischemia falls under. We've got sort of intermittent claudication, which is when the pain is reproducible. It comes on when they're walking around, they're using those muscles, increasing the metabolic demand of those leg muscles or those compartment muscular groups then leads to lactate build up. And that manifests as pain, critical limb ischemia, which is like a very end stage um version of of, of um peripheral arterial disease where there's been a chronic damage over time. It's not necessarily acute, it's chronic, but it's been chronic. It's been there for such a long time that now you start to get ulcer formation. You know, it's been chronic enough for ulcer formation, arterial ulcer formation, so on and so forth. Um eventual damage. Um at this point, uh necrosis as well. And then acute limb ischemia, which is when um you get very sudden from all right to very bad, very, very suddenly. Ok. So we can expect ischemia, sudden onset necrosis um and things can get a very bad turn. Um if not treated well, I suppose with critical limb ischemia, chronic limb ischemia because it's chronic, you have that time to try to make adjustments in management and try to prevent the development of further complications, but with acute limb ischemia because it's so sudden, there wasn't really much of a chance to get rid of it or there wasn't really much of a chance to, um, prevent the event from happening in the first place. Ok. Uh I am aware that we are at 630. Um, I'll continue to keep on going. I apologize for going over time. Risk factors. Ok. As on the left etiology to embolism. So if someone's got maybe a far fetched, but let's say they've got a clot from the heart that's gone down or let's say they've got a thrombus that's broken off and uh it um the thrombus turns because it's broken off, that piece turns into an embolus and then it blocks artery arteries further down. That's uh another cause for um per acute limb ischemia compartment syndrome. We mentioned trauma, for example, compartment syndrome. If you remember um with trauma, for example, you get bleeding into the compartments, it leads to very high intracompartmental pressure. All right. And that can sort of squeeze the neurovascular structures in the compartments can restrict arterial blood supply down the leg. Ok. Compartment syndrome. Very important. Typically, what they do is I believe it's a fas a fasciotomy. They might do a fasciotomy to try to relieve the pressure um as a temporary measure. Um But yeah, that's all I remember from Component Syndrome, some hemostatic measures as well. Diagnosis had been diagnosed something like this. So examination we mentioned this patient has gotten uh the absent pulses. Ok. Not good at all. Ok. Um We need some investigation. So U not A US or yeah, it is A US but ultrasound arterial Doppler. Ok. So you wanna have a look for if there is any blood flowing through? Ok. What's the blood looking like? Um Is there a signal that's being picked up to suggest that there is at least some patency of blood. What degree of patency is there? What's the severity looking like? A BPI? Which is when you measure the BP on the affected limb and and um ankle brachial. So ankle pressure, compare it to your brachial pressure, pressure on the same side. Ok. Um And that will give you a reading to give you a measure of how BP in your ankle compares to the brachial, sort of how things should um as a comparison. And we use that to interpret how severe of the stenosis is, what severity of the stenosis is going on? Right? And that table is down at the bottom left. We can see someone with naught 0.9 to 1.3 a value of that. So if you put it in the, in terms of the numeracy, it would be ankle pressure over the arm pressure or brachial pressure if you put that in, it's a systolic pressure, by the way, not the diastolic. If you put that in, you get and interpret the value. You can use a table like this naught 0.9 to 1.3 is normal. The worst, the acute limb ischemia is the um the lower the value you all right makes sense though. Because ankle, if there's lower limb ischemia, acute limb ischemia of the lower limb, you're restricting blood flow to the lower leg. So your BP on the on the ankle is not gonna be very high. So the top number, the numer the numerate is not gonna be very big, but the top number the brachial is gonna be normal or big, for example. So small number on top of a big number leads to small number. So small value leads to a severe arterial blood, um s severe peripheral arterial disease. All right, here's our management job. Try and this is just a brief one slided summary. All right, we've got ABCD. Of course, every emergency ABCD if you're in an OSK scenario and you've got an emergency ABCD at airway, non rebs 15 L. If they've got CO PD, you might want to be a bit careful IV access, you give IV Heparin. This is the anticoagulation of choice. OK. Heparin, what does it do? It's a thrombin. Um It's a thrombin deactivator, I guess. Is that the term deactivator factor two factor 10. Ok. It stops clot formation. Ok. If, if it is indeed an A clot, the VT E and embry, it could help to um reduce that clot. All right, the surgeon, he goes to me that what you do is you give a bonus like, so how many units, um, um, he described to me you'd give a certain number of units at one go and then you'd follow that up with an infusion over time. Ok. Vascular surgery, vascular review is needed. Pain relief is gonna be painful. Ok. Pain is one of the six PS. All right. So you have IV uh opioids. Um P So you can still hear me right? Yes, I can actually we have a question about the A BPI. Yes. Yes. So um someone's asked how, how do ABP reading thresholds help differentiate venous arterial and mixed etiology, vascular ulcers? Oh, that's an interesting question. 00, damn. Sorry about that. Sorry. Could you repeat the, well, that's not good. Could you repeat the question again for me, please? Yeah. So um someone's asked how do ABP readings help differentiate venous arterial and mixed etiology? Vascular ulcers? Sure. So I feel um message. 00, no, no good. So um I um this is a good question. I'm not entirely sure if I know the answer. Maybe it's because I'm under pressure. Um Maybe I might know this answer if I was a bit more calm. But I think if it's an arterial etiology, we'd be thinking more about it being on the lower end of the scale. So we'd be thinking more about, um, the ABP measurement being quite low as far as venous. Huh? What can I say about venous? Oh, really? Testing me here. Yeah. Um, if, if I might add to this. Yeah. Yeah. I think ABPI is for arterial only and venous. It doesn't really take into account of venous insufficiency. Yeah. So, I believe it's just arterial. That's what I was thinking at one point. Yeah. Um, I hope that's true. Cos I feel like I read a lot and sometimes I read so much that it makes me doubt my answer a lot, but I feel like you might be right. Prudence. You know what? Er, so who asked that question? So it's doctor a addy, huh? Interesting. I'll have to read up about that actually, to be honest, it's a good question. Yeah. Mm. That's good. Um, hm, I'll read up about that. I'm sorry, I don't have an answer for you. Um, but I think it'll be good for me to read up about that to see what's going on. But Prudence, I think your answer kind of makes sense. Um, yeah, that cos it's mainly a BPI, it's mainly arterial that you're gonna, it's a reflection of the arterial system rather than the venous system. Um, interesting question. Interesting question. Ok. Well, we'll, we'll move on. I'm sorry, I'm sorry, I don't have a clear cut answer for you. Um, but we'll move on. I'll, I'll have to read up about that um I mentioned the opioids. Ok. Um Sometimes if it's a very low severity, um, acute limb ischemia, we might opt for just heparin alone. Um The other fit scale is a scale that's used to, to classify the severity of um, of an acute limb ischemia by the way. Um, if the heparin does not help in this scenario, we may, we may then want to move on to surgery and the surgery options. Surgical options are as follows. Ok, so you've got endovascular thrombolysis, which is when you literally lies the blood clot with um sort of thrombolytic drugs. I imagine things like alter places, streptokinase. I wonder if that's more for myocardial infarction as opposed to peripheral arterial disease but sort of thrombolytic thrombolytics, endarterectomy, which is when you literally remove the, um the causative atherosclerotic plaques that's causing the issue, surgical thrombectomy as well, which is when you remove by the surgery, the thrombus that's causing the issue bypass surgery, which is when you sort of bridge over the occluded portion. Uh I'm not sure exactly what they would use for that bridging. Um I know they use a saphenous vein a lot for like cabbage, for example, or the mam mam mammilla, what's mammillary vein or something like that for the, uh that's another option, but I'm not entirely sure about the logistics for that angioplasty, which is when you open up the um vein using a stenting amputation straight up for if it's necrotic and there's no life left. Um Then you'd go for amputation, long term management as well. So, lifestyle, we've, we've mentioned the risk factors, antiplatelets. So the clopidogrel, aspirin, things like that. OK. Um And then you've got the anticoagulations of warfarin, right? So we mentioned Heparin which II guess falls under this as well. Um Then the management of comorbidities or um predisposing conditions that would put you at increased risk of something like this from happening. So, atrial fibrillation, you get stagnation of blood in the atrium can lead to clot formation, hypertension, diabetes, obesity, prescribe a statin given that this is a, a major peripheral vascular event, you bump up straight to atorvastatin 18 mg as opposed to 20 then because of issues of movement, mobility, motor, you may want to consider a multidisciplinary action with physiotherapy occupational therapy, things like that. Ok. Does that make sense? Here are the surgical options? The three of those actually endarterectomy on the left, the thrombolysis in the middle balloon angioplasty. OK. I imagine they would um catheterize through the femoral and go back down through the lake to try to reach these areas of a collusion. OK. There you go guys. Well, that was an experience for me. I appreciate you all for listening in. Um If there are, if there are any questions I would appreciate if you just let me know, I try to, I try my best to answer them as best as I can. Um If I can't, then I'll let you know, I'll be honest with you. But um yeah, any feedback as well would be phenomenal. This is a very new experience for me. So please give me some feedback about how I can improve. Was I too fast? Was I too slow? Just let me know. I need to know. Ok, thank you very much, everybody. Great. So I don't think we have any more questions, but yes, please, everyone. If you, I'll just send out the feedback form again. So we will really appreciate if you can fill in the feedback form and then upon completion of that, you will receive a certificate of attendance. So I if we don't have any questions, I think we can rock up here. Great. So thank you for your help for the presentation. It was really helpful and different pneumonics as well. So definitely you mean like they never pop your knee? Was that the one that you probably never heard of that before? I've heard of the knee? Yeah. II kind of made that up on the whim. II II made that one up on the whim. I thought how, what's the best way for me to remember this? Because I always forget it. And I, yeah, that's the way I remembered it. Yeah, that's great. Yeah. So yeah, if there aren't any further questions, we will II recognize some names here. Actually, you are in the audience. I really want to thank you guys for coming in. Just provide some feedback to me as well. That would be great and um stick into the next uh the next session by my colleague on Wednesday. Prudence. Is that Wednesday? Yeah, Wednesday 6 p.m. Yeah, Wednesday 6 p.m. So carotid artery disease and aortic dissection. Thanks guys. I appreciate that. Yeah, great. Thank you guys and enjoy your fast, your well earned. Oh, yeah, I haven't even broken it yet, which is terrible. Great. Ok, thank you, everyone. No. Should I leave? Should I leave or should I stick around for longer? Um I don't think we have any more questions. I'll just end the call, I think. Ok, sounds good. All right, perfect. Great. Thank you. Thanks Sha. Ok. No worries. Mhm. No worries. I can see some comments for me. See you.