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Um, hello everyone. So my name is Manish. I'm an F one. I'm currently in Hull, uh, which wasn't my first choice, but it's actually all right. So, uh, um, that's that for everyone who's looking forward to apply this year, uh I'll be taking you through vascular like kind of high yield for finals and uh, paces as well. Um, a lot of what I'll talk about is based off this really good book called, um, all you need to know about vascular surgery by the Vascular Society, Great Britain and Ireland, just great read. So, follow that link and uh, if you're interested in vascular, you can look through that as well. Um So what we'll do is we'll go through the conditions that will be for written and then go through the pace, examination kind of signs that you'll do how to do an ABPI and things. And then also just a note on the procedures so that when people say, oh yeah, you go, they go for open surgery or oh yeah, they go for an like a, um, angioplasty, like what that actually means. So these are the conditions that I'll go through, I'll be focusing more on like the high yield stuff and I'll kind of explain the, the things that I didn't understand when I was a student just so that it's more relevant to you guys. Um, and I think with this, you should really just be able to go into finals and then get a pretty solid mark and ba like, I'm pretty sure I've covered everything. Um, there's a few questions to begin and we'll go through the answers at the end. And so I'll just give you some time to read the questions, think of what you'd answer. And then at the end of the talk, we'll go through them. I mean, to be fair, there's actually not a lot of you. So maybe we'll just go through them at the end. Oh, ok. So we'll start off with arterial conditions. So we'll go through AAAS first. Um So essentially there's three main presentations to A AAA. And by far the most common is asymptomatic, which is picked up instantly or via screening. Um Think about symptomatic AAAS. They usually have a tender pulse mass in their abdomen and they'll have lower back or abdominal pain. A lot of the time it's actually nonspecific and then the worst one is rupture and they will be hemo dynamically unstable and they'll have back pain. Ok. Um Some of the questions, they might be kind of unclear where what it is at first, but always think about the AORTA. All right. Um in exams. So essentially in terms of things you need to know, basically, like most aaas are infrarenal, which just means they're a bit easier to treat. And there's also thoracic aortic aneurysms, but that won't really be covered. And they're pretty rare in terms of the risk factors you need. No. Um, it's the standard atherosclerosis, vasculopathic picture. So, diabetes, hypertension, smoking, hyperlipidemia, but also things like connective tissue disorders, European origin and a family or personal history of aneurysms is also a risk factor in terms of screening. Now, this this probably will come in, come up in questions. I'm pretty sure it did last year. Essentially. What you need to know is that males on their 65th birthday are invited for an aortic ultrasound scan. And then what happens from that scan is like dictated by the size. So that's what an ultrasound of the aorta looks like. And then they can measure the actual uh diameter of the aorta. Um Essentially, if it's under three centimeters, uh we don't really need to do anything at all if it's uh they're also good like um windows. So it's 3 to 4.54 0.5 to 5.5 and above 5.5. So 3 to 4.5 they just need 12 monthly ultrasound. Follow up 4.5 to 5.5 they'll need a three month follow up scan and then if it's always 4.5 to 5.5 you'll just have to carry on scanning and then if it's over 5.5 they need a vascular referral. And then in terms of the management that we would do for these as well, um If it's just 12 monthly follow up scans, we'd just be thinking about conservative management. So that's smoking, cessation, weight loss and exercise and alcohol cessation and medical management would be optimizing the BP. A statin which would usually be 80 mgs atorva statin and antiplatelets. So for AORTA is AAA is usage aspirin. And then the actual surgical intervention that a vascular surgeon would do is open surgery where they open up the aorta, they, they do a midline laparotomy. It's quite invasive or they can do something called an evar, which is an endovascular aneurysm repair where they go in through the femoral artery and then they do like a massive stent of the aorta. Um So it, it's very minimally minimally invasive also intervention, uh indications that you need to be aware of. It's not just if it's over 5.5. Um it's if the uh the aorta is over 4.4 centimeters and it's growing uh uh by over one centimeter a year. So if it's got more than one centimeter, yearly growth, it needs to be operated on because it's high risk of rupture, any symptomatic AAA should be um operated on and obviously, if there's a rupture and needs an operation. So this is just a bit of an explanation about those operations. So, open surgery, we can see, they, they literally expose the whole aorta and then they sew in a graft. Whereas endovascular, they don't actually open anything up. They just go in through the femoral and put in a covered stent so that it kind, the aneurysm doesn't really have any blood flow into it. And so that's what an open surgery looks like. And then that's what evar looks like. Uh in terms of what to choose, I'm pretty sure this did come up in one of the exams. So basically, what you need to know is it would most likely be open. There are some contraindications for an open surgery like a hostile abdomen. So like if they're, if they're peritonitic and they've got sepsis, um if there's specific anesthetic risks and also some patient specific factors, uh which basically means if they're like really old and frail, you just do an evar. Um But the nice guidelines basically do say open and less contraindicated. So most likely the answer will be open. Now, if we're looking at this scan, um what this is looking at is it's a CT angio of uh the abdomen and observant people or maybe not. So observant people might see the structure kind of anteriorly in the middle. So this is the aorta. Ok. Um That whole oval bit is the aorta and then you can see like a more apa pacifying area within the aorta and that's the actual patent lumen. So the bit between the red and the orange is all thrombus. So that's clotted blood. Ok. And you might also see this, which you can appreciate maybe which um is blood and you can see the kidneys here and we know that the kidneys are retroperitoneal. So this is a retroperitoneal, ruptured AAA and it, and it's important to make the distinction between retroperitoneal and peritoneal because if you've got an anterior rupture that goes directly into the peritoneal and you're essentially as good as dead, like most people with that will die at the scene because there's, there's nothing to stop the blood, the whole abdomen can just fill with blood. Whereas in retroperitoneal, it's a relatively small space. So it can actually tamper out itself and it can clot and provide a stable enough wall for the opening of the aorta for it to not bleed catastrophically. So, what we see with a presentation for ruptured aorta is uh a triad of hemodynamic instability back or abdo pain and a pulsatile mass. Ok. Um Other things that can be present as well, loin to groin or scrotal pain, hematuria and also collapse common misdiagnoses. And it's important because they're very easy to miss renal colic, perforated viscous and diverticulitis. This could very easily come up on the acute station in cases as well. So be aware if, if it's an elderly person, especially if they're a man and you're suspecting one of those three diagnoses. Remember to think about a ruptured AAA um, in terms of investigations that we do. So, first of all, you need to do some blood. So you'd most likely do an AVG or VBG just immediately because you can do point of care testing. So you can look at the lactate and the hemoglobin immediately, you then do FBC, you definitely do a group and say in cross match because they're probably going to need units and probably go to theater and then use these and coag the other stuff not as important, but you probably do it anyway. In terms of an ed, what they do is um they could do a point of care ultrasound scan or they can do a CT Angio. So a CT Angio would be the gold standard and it's the best to kind of look at what's actually going on and it can determine whether the patient is feasible for evar as well. Whereas point of care ultrasound is really fast, readily available, but it is a bit unreliable. It's not 100% reliable at ruling out ruptures in terms of the management. I've, I've put three things that we'll explore a bit more in the next slide. So first of all, the 30 minute rule, so if you suspect to rup to AAA, the patient should be assessed, scanned and sent to theater in under 30 minutes, then permissive hypotension. So essentially, we aim for the systolic to be a bit low because the higher the BP, the higher the likelihood that the pressure will overwhelm over kind of power the tampon that's present and then it will just rebleed. So we want to keep that tamponade retroperitoneal like in place so that it doesn't, uh the patient doesn't rebleed. And then again, when we choose between open and evar, it's conventional to do open, uh because you can clamp the aorta that's um like proximately on top of the bleed. So you can just kind of stop, stop any bleeding. But you can also use evar if you really need to. Um but it's not as good as completely stopping the bleed, but you can use like a balloon in the in the artery, then you can think about hemorrhagic shock. So there's four classes and what you can know is that um only in grade three shock, does the BP reduce? So they might just be a bit tacky and anxious, but they could actually be actively bleeding with up to 1.5 L of blood loss. So that's also something to be aware of. Now, I think that's covered the important stuff of A AAA uh if we move on to aortic dissection now. So, um what you need to know is the Stanford classification. So type A and type B and that determines management. So um what you look at with presentation again, aortic dissection is a very easy to miss diagnosis and you've got to actively think about it, which is why, again, it could come up on the acute stage of cases. What you've got to think about is they'll have chest pain, but it might just not be typical of an mi it might be, it will be severe, but it will probably be tearing in nature, radiate to the back and it can have all these other symptoms including perfusion problems. So, if there's a dissection, then the blood vessels that are coming off the aorta where the dissections is will be compromised. So they may have paresthesia to whatever arm or leg, paralysis, headache, neck pain, also radiation to the arms and legs if they've got a dissection that involves the, you know, femorals or the brachial. Uh and then also mesenteric ischemia can uh present a radiation of pain to the abdomen. And that's the same thing where the dissection has progressed all the way to the uh you know, sma and whatnot on a classical sign on, on, on the examination is ABP discrepancy. So, um that's the thing to be aware of, but there's other things that can be present. So, absent or weak pulses and signs of a tampon or a fusion like uh you know, on ecg you might see pulse paradoxus. Um you can have aortic regurge or an E junction systolic murmur depending on the nature of the uh dissection. And then also it can have three different kinds of shock, which is a bit annoying. But because the uh uh the blood supply to the spinal cord can be affected, you can get neurogenic shock as well. The risk factor is important to know, obviously, hypertension, the uh actual question might, might say, you know, they were weightlifting or they were taking drugs when this occurred. And that's because abrupt increase in BP can precipitate the dissection. And then the things that you should know like connective tissue disorders and congenital abnormalities also increase the risk. So the investigations that we want to do uh bedside, you do BP and ECG bloods D dime is actually very useful because it's very sensitive. Um So it's useful to rule out a dissection if you don't think it is and you just kind of want to do a blood test, you do amylase as well because radiation to the back can be pancreatitis and then you do troponin because it, it might present like a heart attack group and saving cross match and the VBG for the same reasons as before with the AAA. And in terms of imaging that you do, you'd, you'd basically do at, at E or a CT angiogram. So um to e transesophageal um echocardiogram, and those two can assess the aorta very well and look for a dissection and also on a chest X ray, you might, you might look for widened media. So this is CT angio and you can see that where the dissection is because you can see a false lumen and a real lumen with a, a bit of probably intima that's separating the two. The management important thing to know is that the troponin ecg might make it look like it's an mi but it's not. And if you treat for an ante, for example, where you're going on the parox, then you're anticoagulated someone with a dissection and that can exacerbate the dissection because again, the false lumen, the blood in it can just clot and then it basically tamponades, the entry point and it's basically just doesn't matter that much anticoagulation can then make that worse if it's type A. So type A is when it's um proximal to the arch, uh then they need cardiothoracic because they are high risk of the, the uh dissection going into the pericardial um back and then causing a tampon which will kill the patient. Type B is a bit less severe. So it's distal to the arch. And essentially what can just happen is you just manage them with beta blockers and then you just surveil the uh the dissection of lifelong. And then if, if the blood is clotted, it doesn't matter too much. Uh But if in certain circumstances, you can do ATR which is a thoracic endovascular um aortic repair and it's basically just putting a stent in, it's um that can be done as well. Now, if we think about peripheral vascular disease. This is another big topic in vascular. This will definitely come up. Uh what it is is atherosclerosis in the arteries which causes a stenosis, which is a narrowing, um which then reduces the ability to perfuse distal organs and limbs. And the risk factor is vascular paths and diabetes. So it's just the standard vascular stuff. All of it is basically just smoking, diabetes, bad diet, etc, etc. The two chronic presentations of PVD are claudication and critical limb ischemia. And the way I think about that is claudication is just stable angina of the leg. And critical limb ischemia is unstable angina of the leg. So intimate and claudication when you're at exercising, the leg is not getting enough blood. So it starts cramping and then when you stop, it relieves critical ischemia is the pains at rest. It disrupts your sleep and you need to hang your foot off the side of the bed. So that gravity allows the blood to kind of, it's easier for the blood to flow down the leg. On examination with claudication, it might be normal, but the pulses might be difficult. And the ABPI which we'll talk about later, which is the ankle brachial pressure index will probably be under 0.9. Whereas with critical limb ischemia, it will definitely be under 0.9 but it might even be under 0.5 which we class it as severe. You might also see arterial ulceration and skin changes with critical limb ischemia. This is the Rutherford staging. So you don't need to know it, but it's useful to kind of to characterize physical in ischemia. And you can see that it's a continuum from asymptomatic to tissue loss. And um that's just how it progresses over time if it's untreated important differentials to consider a spinal stenosis compartment syndrome and sciatica. So, spinal stenosis um is basically it comes up in exams, lumbar flexion reduces the pain. So if they sit forward, then this cramping claudication like pain goes away. Um Compartment syndrome will be more like derma, derma to tingling and numbness and they'll also have muscle weakness and also it'll probably be a bit more obvious um in the history if it's in a question and then sciatica, it will be dermatomal again, more likely pain, shooting pain in nature. And lumbar flexion is the main exacerbation. Whereas with intermittent claudication, it's more like exercise rather than flexion. And another little niche thing to know is Lari syndrome. So essentially you get an occlusion of where the aorta turns into the eye ax. And so I've put a circle around it there. You can see that this is a CT angio. So that, that bit should be white and it's gray because of the thrombus. Um and that presents with a triad of Buttock cola impotence and absent femoral pulses. And um what, what the concept here to know is that with uh PVD the pain occurs distal to the stenosis because distally is what's impacted with regards to the blood supply. So even with Lari syndrome, the stenosis is at the aorta, but it's the buttocks which are getting claudication. Uh Yeah. So then the management that we think of with PVD for chronic PVD is again the standard conservative stuff. Then medical, we'd think about clopidogrel, uh A statin again and then optimizing diabe diabetes and hypertension medication. And if they've got thrombotic or embolic events, which is more like acute limb ischemia, which we'll talk about. Uh then you'd think about anticoagulation as well. Things you can do for symptomatic relief in hospital, you can give iloprost as an infusion and then you can also give nasty dose furry oxalate, which basically, I think it's just like a bit like uh nitrate, but I think that's come up in exams before. So just be aware of that um that drug and then the interventional stuff we can do is um angioplasty, which is basically just a stent and open. There are a few open options. So, endarterectomy, which is when you've cut into the artery and you remove the actual um atherosclerosis, there's bypass where the atherosclerosis stays and you basically just with a vein or a graft, you kind of just go go what you bypass it. So you do anastomosis proximal to it, which will supply blood and then anastomosis is distal to the block and then the tube will give a collateral supply rather than just having to rely on the rubbish artery. And then if it's too late, you can also do an amputation where the tissue is dead, it's useless. So you just cut off if we think about acute limb ischemia. Now, you've all heard of the six ps. So, uh pain, pulseless paralysis, para we called pa and uh uh uh uh paralysis, sorry and paresthesia. So, um those are the six. But what you've actually got to think about is the six will only ever present simultaneously if it's an embolic uh ischemic er ischemic lim. So, if it's thrombotic, the distinction is if it's thrombotic, you've got someone with critical limb ischemia chronically. And then at this point, either there's been a thrombus on the atherosclerosis or the the atherosclerosis is just built up too much. So, um there will be a small trickle of blood that's getting to the leg and therefore, you may not have all six signs, but you'll definitely have some of the six, right? Um Whereas with embolic, it's, there's been like with af they have a thrombus which is in the heart and then it's spat off into the leg that will just occlude the whole supply and they'll get all six simultaneously. Ok? Um So just be aware, sometimes they might not have all six, but it will be a a acute limb ischemia. And you can see in this image at the top of a real patient. This is um the left leg is the ischemic limb. It's not actually got pa it's actually got a bit of like rubber, but you can see that the toe is very, very blue and the cap refill will be nonexistent and that is an ischemic limb. Ok. So then what we do with that is medically, I mean, it's a medical emergency. You need to call the vascular surgeons, but medically what you can do is you can give high flow oxygen. Um you can give them anticoagulation, so you can give them low molecular weight heparin, but usually just stick on a heparin infusion. So that isn't low molecular weight heparin. That's um it's just a constant infusion of heparin. Uh and it requires a lot of monitoring. So you need to do like hourly A PTT ratios and every time you change the dose, you've got to do another A PTT ratio. So it's a bit of af uh but uh that's what you do. And then surgically, if it's embolic in nature, you can do an embolectomy where you interventional radiology or a osteo surgeon with interventional skills will go in through the femoral, put a wire past the embolism, blow up a balloon and then drag it out thrombolysis where they'll, they'll take a catheter again from the femoral to, to exactly where the block is and then release some thrombo thrombolytic agent directly into the clot. And then there's bypass as well. And then thrombotic, you can do thrombolysis, but you can also do angioplasties where you stick a stent in as well. Uh If the tissue is dead and we can't do anything about it, then you just amputate uh whatever is unsalvageable. And sometimes when you reperfuse the limb, there's a lot of oxidative stress that happens and they can actually get compartment syndrome and you'd have to do a fa fasciotomy for that for carotid artery stenosis. Um The thing that the way this links into the UK MA syllabus is that for vascular, you need to know about the causes of amaurosis. Folks, few gaps and strokes and with vascular that will be carotid artery stenosis. So essentially, you get a atherosclerotic plaque in the carotid. Uh if you remember, plaques usually occur at bifurcations because of the uh turbulent flow of a, of a bifurcation. So that's where things are deposited. So you'll get it at a bifurcation from the common carotid to the internal and the external. And you can see pretty beautifully with this. And this is a fluoroscopy. You can see the uh the stenosis really well. So the presentation of that a lot of them will be asymptomatic and the way they present is strokes, tia s and aortic flux, which is just ati a of of vision essentially. So any person with a stroke, um query getting a, a scan of their carotids, um A lot of them will just have small little clots thrown off. So it will be more like tia in terms of risk factors. Again, vascular part. So that will be everything. Um, with the examination, you'll hear, you might hear some bruits and also you might see some neurological neurology. So again, they'll present as a stroke investigations. So what you do is a duplex, ultrasound or a CT angiogram and you can do an MRA, which is a, um, an MRI angiogram, but usually they're a bit of af to organize and it's just easier to do a CT angiogram. Um if people don't know what a duplex is as well, it's basically you have a duplex and a Doppler are used interchangeably a lot, but you get an ultrasound and you get the visual aspect, which is one, a duplex is like two things. So you get the visual aspect of a normal ultrasound and then you get the Doppler imaging of like a probe. So you combine those two and you can, you can um see the blood flow on the actual screen, which is a duplex in terms of management. So again, there'd be the usual medical stuff, but usually with a symptomatic carotid artery stenosis, they would do some intervention. So they can do a stent where they again access through the femorals, get the stent guidewire all the way to the, the stenosis and then they would insert a, a balloon, expanding, expanding stent, which then makes the internal carotid patent again or they would do a carotid endarterectomy where they cut into the neck, they get the carotid, they cut it open and they remove the plaque. If it's asymptomatic, you can also consider those two interventions if they're high stroke risk. And they've got a stenosis which is bigger than 60%. Now, another big one. DVT. OK. So this will definitely come up. So you need to know this stuff. Um The way it will present is a throbbing, like unilateral leg pain, swelling, reddening of the skin, they'll have probably have risk factors or provocation. It might present already as a pe and occasionally it can also be asymptomatic. Um What you'll see on examination is edema, redness, so swollen, red limb warmth, it will be tender and you might also see distension of the superficial veins as well because the deep vein is blocked. So the blood, the blood has to go back to the superficial veins instead. Um Differentials you can consider trauma um because red, painful swelling, you know, that sounds like septic arthritis or, or like a fracture to me, uh venous insufficiency. So that's more just like superficial venous insufficiency rather than deep. They might just have edema for whatever reason or cellulitis. And remember S Triad was thinking of the etiology of a DVT. So, um if you think about that, you can cover most of the bases. Um You need to know how to like use a well score I wouldn't say you need to know every component of the well score. They, they probably give that to you, but you need to have an understanding about it. So when you look at risk factors for DVT, there's a lot. So this is from nice, you can see that, you know, history of DVT cancer, old age, male, overweight on OCP, things like that are important risk factors. But what we can do instead is we can just do a two level well score where we, we memorize or we have a list of the important things like active cancer. Um recent immobility, localized tenderness along the venous system and calf swelling. And then what you can do is you can add up the points and then uh depending on what the well score is, we can think is the DVT likely or is, is it unlikely? So, um I think it would be mean for a question to not give you the actual uh uh components of a well score. So just be aware of some of the risk factors, but you don't have to memorize this. Um So if we go through uh the actual well score, we dichotomise into whether it was zero or one or whether it was two or above. So if it was zero or one, what we'd do is that they're in A&E uh we're thinking about a DVT. So we've done a well score 01. Now we do a four hour D dimer. Ok. Um, and if the D dimer can't be done within four hours, we just anticoagulate them and then we just do the D dime as fast as possible if the D dimer is positive. So it's high, then within four hours we then want to do an ultrasound Doppler, which is, uh, basically just the duplex. Ok. So you, then that would be a scan of the deep vein venous systems to uh to see if there's blood flow or if there's a clot in there. OK. We can't get the ultrasound in four hours. We get it within 24 hours and we just anticoagulate them if we haven't already. OK? If the D dimer is negative and the well score is zero or one, we can be pretty confident that there's no DVT and we can stop the anticoagulation if we started it. OK. So now let's think about the, the Doppler. If the Doppler comes back positive, then we would just, we would begin anticoagulation if we haven't already or we would just continue it. And if it's negative, then again, we just stop the anticoagulation if we started it. Now, if the, the well score is two or above, we would just jump straight to a da Doppler, we wouldn't do the D dimer. But if we can't get a Doppler within four hours, then we wouldn't do ad dimer. We'd then give anticoagulation as well. And then we'd just get the the Doppler as soon as possible and then it's just the, essentially the same now. So if, if the Doppler is positive, we just anticoagulate and if it's negative we'd stop anticoagulation if we started it. Uh So you might be able to see that you can think of the well score being over two, which is jumping straight to the Doppler. Um And what we do with anticoagulation is it's now a doac so we do Apixaban or Rivaroxaban. And if it's a provoked DVT, it'd be for three months. And if it was unprovoked, we'd do it for six months. Ok. Now, let's talk about venous insufficiency. So this is a spectrum. Again, you don't need to know these clinical stages, but it's just, it's a good way to think about it. So it starts off as nothing. And then the important thing is varicose veins. Um venous skin changes and venous alteration. But if they have varicose veins, they can progress to having a venous ulcers. It's a spectrum. Ok? And if they have, if you have leg telangiectasia, you may then as well progress to varicose veins. OK? And what that looks like in practice is uh you can see images there so you can see that um if we look at C two, we can see varicose veins. And if we look at C four, we can see the skin changes quite well. So, um venous insufficiency is essentially there's pressure in the venous system which is, which is high for whatever reason. And then that essentially causes. So for example, it can be immobility if I'm immobile, my calves aren't doing that pumping, which is helping blood flow go back up the leg. So then the blood pools in the, the foot and the pressure increases in the foot. If the pressure increases to a high level, it can kind of exceed the arteriolar pressure. And at that point, there's no, there's nothing that the blood can do but kind of like filter out of the capillaries. And that's why you get deposition of hemosiderin, which is kind of like iron deposits from the blood and you also get edema because liquid is having to kind of uh leach out of the vein. Ok. Um And then all of that irritation because that leaching out is irritable can then progress to an ulcer as well eventually. Um And yeah, we can see, I've just explained that essentially, if you've got venous congestion and you've got reduced pumping of the, the, the blood back of the vein, you'll get dilatation of the vein, it will fail and it'll get leakage of fluids. Now, if we look at management of varicose veins, um they're quite common. So some stents are quite stringent with what they, what with what they'll take and what they won't. So the criteria are nice for a referral is if they're symptomatic. So if they're painful or like really itchy, if there are skin changes, which indicates more severe venous insufficiency if there's superficial vein, thrombosis, which is the same as thrombophlebitis. And then if there's ulceration, if we look at what we can do. So, first of all, you map the veins with a duplex so that you can see what's going on with like where the veins are and then, uh, and what, what's, what's torturous, what's a varicose vein and what's fine. And there are three options. So there's uh ablation where you go into the vein with a little with a and it's like a catheter with a guidewire and it has a little like device on the end of it. So that goes into the vein and then you can turn it on. So it's either a laser or it's radio frequency and it basically just destroys the vein from the inside and you can pull that as it's on and then that will kind of close the vein. So that's that first image. OK. Foam sclerotherapy is used more for spider veins. So telangiectasia and it's literally just foam that gets injected into the center of the vein of the telangiectasia. And it's really cool to watch. You can just see the vein fills with foam and it just disrupts and then surgically, you can also ligate the vein, strip it and evolve it. So that's different words for basically like ripping the vein out, um it off and just destroying it surgically. OK. Um And then what we can do for venous insufficiency is the mainstay of treatment if we're not doing any surgery is give Stockings. So that's like Ted Stockings, graduated stockings. And it's important though, you can only give the stocking if the arterial status is good. So you need to do an AV P and determine that there's good blood flow down the foot because otherwise the stocking will increase the pressure in the foot even more and it will reduce blood supply. And then conservatively, you can do weight loss, avoid extended sitting or standing because that's one of the main uh provoke provoking causes of uh of insufficiency and also just light exercise. And just to be aware if they've got a bleeding varicosity, that's technically, they need to see vascular like as a sort of an emergency. So if that's in question, they've got a bleeding VIAS and it's not stopping. They need a vascular admission actually. So superficial thrombophlebitis. So that's the same as superficial vein thrombosis. Um I checked that on night because I wasn't sure. But yeah, they're, they're exactly the same thing. Um What it is is it's inflammation of a superficial vein that's associated with venous thrombosis and it's usually the Great Suen vein or the lesser Sufa vein in the leg. And you can see in this image that's the Great Suen vein which is irritated and you can actually almost see like the cord of it. Ok. Um uh They can just happen spontaneously, but they can happen due to trauma and also similar risk factors for DVT, similar uh for venous stasis or venous stasis can cause it. Ok. Um, cannulation can also cause thrombophlebitis as well just to be aware of and autoimmune conditions can too. Um, the treatment is just nsaids and worn, compress and again, stockings, if there's no arterial or um, the way it will present is pain and itching and it will be a localized swelling. Um On examination, you'll feel it as a firm cord. Um and there'll be erythema, it'll be tender and it's usually a tender eryth erythema cord that's located on a varicosity. So on a varicose vein. Ok. And then there are the relevant differentials. So we've done the main arterial and venous uh diseases now. So, like vascular is not many uh diseases, but it's just like you just got to know them quite well. So now this is an important one for paces for acute uh pace station and just for uh written in general diabetic foot syndrome, which is surrounding diabetic ulcers. Ok. So the the, the three factors that cause diabetic foot syndrome are peripheral vascular disease, neuropathy and a precipitant. Ok. So, um poor perfusion means that the tissues don't heal very well. Ok. Easy neuropathy means that there is de facto loss of protection, protective sensation. So they can just hurt themselves easier, but also they've got less appropriate section of their foot. They don't know how to keep it in a good position. So you can get foot deformity, you can get Charcot's foot, for example. Ok? And, and then a precipitant. So that might be macro Truma. So that's standing on a nail or, you know, standing on glass. They just won't feel it, ok? Or microtrauma. So they're just putting pressure on abnormal pressure points in their foot which aren't designed to take pressure. Um, or they're just, you know, they're lying in the hospital bed and their foot is just jammed against the, the backstop of the bed and they don't feel that there's loads of pressure on their foot. Ok. That's just screaming for an ulcer to, to happen. Ok. So as a con continue of what the ulcer can be, ok? Um It can be neuropathic in nature. It could be ischemic in nature and it can have a combination of the two, right? Um And the thing is with diabetic foot ulcers is it's a really high risk sepsis and also osteomyelitis and it has an extension necrosis and gangrene. Ok. So you've got to be really aware of these patients because they'll have horrible um infections that can just kill them, right? So any diabetic foot ulcer, if you're concerned about it, you do you. So, so basically any diabetic foot ulcer for you just X ray and this came up in, in exams. Um an MRI is also warranted, ok. Um If there's any sign concerning for osteomyelitis or the X ray isn't conclusive that it's not osteomyelitis. You just MRI because it's really important to rule out. And then what we do for management is you do, uh, a referral within 24 hours to the diabetic foot ulcer VT and you, they'll do mechanical offloading. So they'll try and make sure that there's not pressure on the pressure points and then you'll debride the wound and potentially amputate if they're at high risk. Ok? Um That leads well on to gangrene. So there's two types, there's dry and wet. Ok. So if we use diabetic feet as an example, an ischemic ulcer um can progress to dry gangrene because this is an arterial problem really well, demarcated death of the tissue and it's dry. So bacteria can't survive. Whereas if it's um more like a neuropathic ulcer and it gets infected, it will be wet gangrene. So, um basically, there is a bit of, there is blood supply and that means that the tissue is moist and then the cause of the cell death is more to do with like bacteria invading. And then these are the people that will get septic and you'll have a hard time treating. So this is a summary of the ulcers. So I'll just give you a second to uh screenshot this. This is all you need to know about them. Um I didn't put any pictures which I apologize for, but um essentially the way to differentiate the three is that arterial, a distal severe pain and they are well defined, punched out deep lesions. Ok. Uh The severe pain will be the important thing there in the, in the question, um in venous, they're shallow and irregular and they're in the gator region. So that's the medial aspect of the calf and the ankle. Ok. So that's like the gator there. You can always imagine them rubbing together and they're like fluffy, shallow, they can be achy. Um But like they're pretty easy to differentiate between an arterial. And if they're in the gator region, you can't go wrong just guessing at the venous and a neuropathic, they'll have a callus, they can be kind of hard to differentiated from arterial, but the pain is the real thing and they won't be painful. Um But they'll also have a callus whereas an arterial probably won't. And then the, the other stuff I'll just leave for you to go through in your own time. It's, it's pretty obvious though, arterial things you do an ABPI and an angio, ok? Venous things, you do a duplex of the veins and then neuropathic, you kind of need to do a bit of both, but because it's most like diabetes, you need to do those X ray and MRI. Ok? Um Now if we go into the bit more niche things which might come up, which you probably just like, don't know because it's literally a niche to, to revise um thoracic outlet outlet syndrome. So essentially um this diagram bottom right is really good. You can see that the subclavian vein, subclavian artery and then the brachial plexus come out in a very narrow area um of the chest. Ok. And with the first rib and the clavicle, they can be compressed quite easily, especially due to posture because of the muscles. Um and anatomical variations and essentially, depending on what is compressed, you can have three different types of tos thoracic outlet syndrome. You have neurological, you have arterial and penis. Ok? And they just present as lesions to the area. So a neurological um to will present as like pain, paresthesia, weakness and it will be weird dermatomes which which won't really align well to a single vein but probably to a nerve root. Ok. Arterial will be claudication, ischemia, weak pulse because the the artery is not spine and blood and the veins will be signs of not being able to drain. So, swelling of the arm and cyanosis as well. And then there's something that I can't pronounce Paget schroter syndrome, which is a DVT of the subclavian due to tos because of that compression causes stasis, which then causes a clot. Ok. Um An important etiology is something called a cervical rib, which as you can see in the X ray at the top and it's like a congenital like abnormality where they just have an extra rib that comes from the cervical vertebra and then that, that just is high risk for causing more kind of obstruction of the outlet. Ok. So surgical options are just removing the first or the cervical rib. Um And then you've got some specific things that you can do for um a specific kind of etiology. So if it's neurological, you most likely just do physio um trying to try to reduce some inflammation. If it's arterial, you can also, if, if the artery is in a terrible spot, you can reconstruct with like grafts and things that's quite niche. And then if it's venous, you might also want to anticoagulate, you might want to thromb um and also compress the arm so that there's more of a pressure to drive um draining through that compression of the subclavian. I hope that makes sense. Ok. Um The Subclavian Steal Syndrome, this is like, I found this quite hard to understand what you need to know for Subclavian Steal syndrome is that um the vertebral arteries come from the subclavian vein and they are like one of the only arteries that joins back together at the midline, which means that there's a left to right circulation, potentially. So, Subclavian Steal syndrome is when you get stenosis or blockage of the subclavian artery. Ok. But it the blockage is before the vertebral artery comes off it. Ok. So you've now got no flow in that side from the aorta to the um to the arm. Ok? Because uh the subclavian goes down to the arm here. So because it's before the vertebral artery and because the vertebral artery joins up with the other vertebral artery. On the other side, it means that there's actually potentially cholesterol flow. So if you, I don't know if you can see my mouse, but you can see um with the other vertebra artery, blood can go up and then blood can reverse down the ipsilateral affected vertebral artery and it can have backwards blood flow, then that will supply the subclavian artery and then supply the arm as well. So really strange what happens is when someone uses their arm, they get really strange neurological symptoms, they might faint when they use their arm, they might get neurology like stroke like symptoms when they use their arm and they might also get claudication of their arm because it's not getting much blood blood flow. Ok. Um But that's the pathophysiology of Subclavian Steal syndrome. And again, like most of vascular, what you'd do is you'd image the, the vessel. So you do an ultrasound or you do a CT angio and then like vascular, you give, you give a, an antiplatelet and you give a statin and then you can intervene. So you can do an angioplasty. So you can shove a stent into the occlusion and then open it up so that we've got a patent artery now or you can bypass it where you um do an anastomosis proximal and distal to the obstruction and the blood flow can, can kind of bypass it. Ok. And then lymphedema is technically a vascular condition. Um Basically, it's a problem with the lymphatic system. So you can differentiate it into primary and secondary. Ok. So, um primary is congenital lymphatic malformation. So it just can't drain back. And then secondary is often due to radiotherapy or resection for cancer where they take the lymph node, the, the lymph system out and now the lymph has nowhere to go and remember what is it? It's like 1 mL per like something per, per day or per hour that the lymph drains. And if, if that doesn't drain, then that would be there's a stockpiling of lymph in the affected lymph that just won't ever go away and it'll be one ml per day or whatever it is. So, there's not actually a lot that can be done for lymphedema. But if you look at nice guidelines, there are some things in certain situations. Ok. So breast surgery is very common. Lymph node clearance is very common. Ok. So this is a very common cause of lymphedema. So what you can do during axillary lymph node clearance. So they do the breast surgery, they take out the cancer and then they might choose to take the uh sentinel lymph node and then do some axillary node clearance. If that's positive, then they could also, when they're doing that, do a really like intricate tiny anastomosis from the lymphatic system into the venous system. So that's a really delicate, complicated surgery. But that is actually um something that can be done based on nice guidelines and then liposuction has limited utility, but it may have some utility. Um, but there needs to be more evidence about around that before anything definitive. That's all you really need to know about lymphedema. It's quite unfortunate like there's not a lot that can be done. It can be really debilitating. Um So we'll go through the questions now. OK. Um I rushed through a bit, but what I tried to do is like, I assume a lot of people watch this on recordings. I've tried to just have a high yield so you can screenshot the slides, you can just stick it in your, in your notes. So, um, we'll go through these questions, I'll give like a minute for each question and then we'll go through them and then I've got the exam to go through and then we'll talk about uh the surgery really quick and then we'll be done. Perfect. Uh If there's also any questions in the chart, just like shout the app. So, OK, just in the interest of time, I don't want to keep you all. So we'll go to the answer. So I'll just, I was going through the answer. So, so the correct answer is four and the reasoning behind this, if anyone got it wrong at all is because the aneurysm is above four centimeters and it's grown by more than a centimeter in the last year. So that's a high risk of rupture because it's growing too fast. So you need to refer them for surgical intervention. Question two, I'll, I'll, I'll just do like 30 seconds and then we'll, uh, all right. So the answer to this is CTA Autom because it looks like it's an M, but there's a few signs that point towards a potential dissection. And we'd want to rule out the dissection before uh starting on any definitive treatment these days, you can get an A, a CT or done really, really fast. So, um that's the reason why you do that if you gave Fondaparinux. So even if you gave Aspirin, it might just precipitate a massive er increase in size of the dissection. Uh questions, three has any four questions. OK. The answer to this is af because this seems like an embolic acute ischemia, it, the pulse isn't sinus for them. So, um yeah, and last question, but I shouldn't say I should say uh like, OK, the answer is three months of Apixaban because this is a provoked DVT. So uh now let's move on to the examination. So um the vascular examination is really fast to do. Um and there are certain things that you can do to kind of stand out. So I'd say some of the things that I'm talking about, you don't have to do them to get a, a pretty good mark. But if you want to kind of like get the best and those are the things to consider. The way I would do. The vascular exam is inspection, extremities, pulses and then special tests. Ok. And um you've got three minutes and usually it will be an upper or lower exam. Um and there's no real kind of distinction between two, like most in real life, you just, you would just do the whole thing, but like in imperial, you do it. OK. Um The patient is the same as breast and so there's probably no signs not OK. But there's good things that you can mention, which shows the examiner that you know what you're talking about. The choice whether to go proximal to distal or distal to proximal is yours. But if you do distal to proximal and you feel the distal pulse, you can be confident that the neck, the proximal, the pulse proximal to it. Is that so you're confident with your pulses, I would suggest doing distal to proximal and then you can do extremities with it. So it's just easier to forget. OK. Um So if we go through, I'll go through it properly in detail. But if we just look at it, do the inspection, you're looking for specific signs for arterial venous or diabetic pathology and then you're looking for surgical signs as well like scars, OK. In extremities, you're feeling for the temperature and you're assessing the cup refill. OK. Try and remember those um the pulse is what you try and do is you try and um in the upper limb especially you need to comment on the rate, rhythm, character and volume, which we'll talk about. Now, you also might need to do certain, you know, radiofemoral delay, radio, radial delay, feeling the symmetry between the legs. OK? And then I put sensation special tests because I like to group things. And so if I think a special tests are OK, then more than one thing. So I sensation, oh I've got to do burgers as well and then to complete you'd offer BP and um A BPI as well. So um looking at inspection first. So if we look at the right hand side, this is the flow of what I'd do. So I'd come into, I'd come into the room or I'd be asked to perform the vas exam. I'd look around the room, look for mobility. A look for crutches look for like, I don't know a prosthetic limb. Uh like somewhere, look for a wheelchair. Yeah. And then look at the patient, see if there's any obvious the body habitus and if there's obvious um amputations, OK? If you then go on to the leg exam, look at the leg like it sounds obvious, but it's easy to forget like under the leg as well. You know, a lot of varicose veins are on the, the, the posterior side of the calf, right. And some scars are actually quite hard to see. And then unfortunately, er, if, if you're trying to gun for top marks, stick your gloves on and actually, like, look between the toes because a lot of ulcers, a lot of um, like, er, ischemia can present between the toes and you don't, you don't really see it and count the toes because certain toe amputations, you look at the toe, the feet and you won't, you won't think about an amputation. But when you count the toes, oh wow, there's actually a digit. Ok. And then while you're at the feet or the hands, just feel for temperature, assess cap refill as well. Really important. The arterial signs that you'll see mostly in the leg will be mobility aids, amputations, ulcers. You can see livedo reticularis, which is the mussing of the skin from uh um ischemia. And also you can see pallor or rub. And the reason you see rubor in a limb, which is not getting a lot of blood is that the capillaries lose their tone and they can like leak uh blood. So it can look like a deep red uh which we saw in that image before. Actually, in terms of venous status, look for varicosities. Um look for edema, look for this lipodermatosclerosis, which is when you get this um thickening of the skin. Um this darkening of the skin um and just they just look swollen they don't look nice. Ok. And that will be bilateral, the hemosiderin deposit. That's the darkening with the lipodermatosclerosis. And then look for a, a goiter ulcer or a healed gait ulcer in diabetes. You'll see amputations, foot deformity and ulcer. And then in, uh, in the upper limb, what you can see, there's much less to see in the upper limb. Um, but you'll see the stent like things like in a pulmonary or cardio exam. It's just the same thing, but also swelling. Ok. And then in terms of surgery finds what you'll see is in the neck, you'll see a carotid and autotomy scar. You can see a midline laparotomy for an aorta, you'll see a great. So this vein harvest, um which is medial side, whole length of leg, femoral cut down for certain femoral procedures, which is at the groin, popliteal cut down, which might just be a scar around the knee and then femoral access, which might again groin scars. So if we look at these four pictures at the top, we've got a great toe amputation. Then in the middle left, we've got a carotid endarterectomy scar. We've got on the right, we've got uh sclerosis and a bit of swelling it looks like and maybe some hemato deposits. And then here on the bottom, we can see, I don't know if you see them on mouse, but you can appreciate a great saphenous vein scar. Oops, there we go. In terms of pulses in the lower limb. You've got to do all of those. Basically. What if it's red, I'm gonna go through, hard to find it. Um, if it's in a bracket you don't necessarily need to do it, but you can do it if you want. Right. So, I'll go through most of the leg, the leg pulses because they're quite hard and I'll go through the brachial as well. And that's the order I would do it in as well. I would just go distal to proximal. And if possible, I'd feel both at the same time and if not possible, I'd use both my hands so that the examiner can see why I'm not measuring both of them at the same time because I need both of my hands to go. Um Then in terms of the extra pulse, things we need to do when in the lower limb, we offer radio femoral delay. OK? And in the upper limb, we do radio radial delay and then we need to auscultate for bruit. So carotid aorta and renal for the upper limb. And then you, you can do popliteal, but you don't really need to. But you can um if you're trying to do everything popliteal, femoral aorta and renal and again, you're just listening to the pulse trying to hear like a which would indicate turbulent flow. Um And then with commenting on the pulse, OK. You can't, you can, I guess you can in the lower limb, comment on the character and volume of the pulse with the femorals. OK. And then you can comment on the rate and rhythm just in general as well. But usually what we do is in the upper limbs, we measure the radial and the carotid and that'll give us rate and rhythm from radial and character and volume for the carotid. And then in lower limb, you want to compare both sides to see if one side is exceptionally weak compared to the other in terms of pedal pulses. And let's go through it. So dorsal pedis, we can see in green from the diagram of the art art arterial supply that it runs in the ridge between the 1st and 2nd metatarsal. So on surface anatomy, we're gonna look for that ridge between the 1st and 2nd toe and we're just gonna feel from distal to proximal with length with like the length of our fingers in the ridge and we're just gonna like try and relax. You can close your eyes and make it easier and you just feel with like slowly through that ridge and then you should be able to find a pulse. My recommendation of practice is just do it on yourself because they're hard enough on yourself. To be honest with the posterior tibial, you can, what you need to do is you need to find the medial malleolus. OK. And that's an easy bony structure to find. Then what you do is you find the posterior inferior border. So you basically find the bit that's lowest and furthest back. OK. Um So essentially that top diagram, the border of that uh red box that's touching the bone, that would be the body you're looking for. And you can see that the artery runs a bit lower and a bit further behind there. So then you move one centimeter down and one centimeter back from that bony landmark. And it will be in a bit of a like a fossa like a bit of a dip in the, in the foot between the calone tendon and the bone. And it will be there. It's one centimeter down and one centimeter back from the medial aioli like it is. And um since I learned that I've been able to feel most so that, that, that's a, a tip that I'd say is good in terms of our leg pulses. Now, um with the femoral pulse, what we do is you can see on this uh diagram of the femoral triangle where it is. And you can see actually that the inguinal ligament sits just on top of the um the vascular bundle. So what you do is you find the inguinal ligament by finding the ace in the pubic tubercle. And then you draw a line between the two in the midpoint of that line, you move one centimeter down from that and you've got your pulse and you can see from the diagram that there's actually not a lot of, of muscle that's in the way for you feeling that pulse. So if you find that inguinal ligament surface anatomy, you just move a bit further down, you'll be able to feel it. Ok. And again, I just say practice on yourself. Um I'm trying to remember if we had to do it or if we just offered it, I think we, we did, we did have to do it. So uh practice and then Popliteal um for, for this, it's just hope and pray. Basically what you do is you find the Popliteal fossa and you go to the inferior kind of half of it. So the half of it that's on the tibia and you just dig your, your, your fingers, both, both hands, fingers, all four just into the fossa and you, you do it like start lightly and press firmer and then you just do that until you can find it. Don't be afraid to report that you can't feel the pulse because it's common to not be able to feel the pulse unless you're a vascular red. So, um but, but also it probably will be palpable because it's a normal person. And then in the arm, people find the brachial artery, heart, the brachial artery. If you look at this diagram, like the anatomical diagram, it runs just under the bicep, right on the medial side. So, and it actually runs under the bicep on the medial side for the whole arm. So you can feel the brachial artery up the whole of the upper arm. Um, once you find it. Ok. So, what I would do is I would, I would get the patient to tense if I need to or if they've got some good muscle bulk, you don't need tense and then you just, you feel for the bicep and you just feel for where it ends, which you can feel. Um And, and uh it, you'll feel like bone under the bicep. OK? And then you just hug that line until you get to the, the elbow crease or the antecubital fossa. So you start under the bicep and you go closer and closer to the antecubital fossa. And if you ask them to tend, you can feel the bicep tendon and if you go under the bicep tendon, um that's where the racial artery will be and it definitely will be there. You can see the A Viagra, it's once you kind of find the bicep, it should be easy. And if you want to, you can then track it all the way up to the arm into the axilla because that's how it goes. So, yeah, uh that is the point where I put the circles, which is where you'll be able to most easily find the brachial artery. And this is technically a central artery. So you can comment on the character and volume of it. Uh And then in terms of special tests, you need to see the gross sensation. So just go to the extremity and test the sensation. Um And then obviously, if they can't feel just come proximal and test the dermatomes to see if it's glove and stocking or if it's um, uh like a derma term, but again, there probably won't be anything. Uh You can offer burgers test. What you do is you get them to lie flat and raise the legs slowly. Um You get them up to 45 degrees and you keep it there for 1 to 2 minutes. If the leg goes like all the color flushes away and the leg becomes pale, that's positive. And if it's positive, you know the angle at which this occurred. Ok. And that's berger's angle. So the, the smaller the angle, the worse the the like stenosis is right. Um Once you've done that, you then hang the leg off the bed. So you get them to sit up and hang their legs down and you'll see the leg will go from white to blue because um that's the hypoxic blood and then it will turn red and that's because of reactive hyperemia and it might become itchy like tingly and stuff. Uh and, and yeah, that would show reactive hyperemia, which would also indicate peripheral vascular disease. And then to complete the examination, you'd offer a cardio exam, a neuro exam, an ABP the bloods that we talked about before. And the imaging. So you can't go wrong with an ultrasound Doppler and uh you know, CT angio if indicated, right. And now if we actually talk about what an A BPI is ankle brachial pressure index, so it's basically the pressure in the ankle divided by the pressure, pressure in the brachial artery. And if you think about it, the ankle is lower than the brachial artery. So it should be higher. Ok. So, um a normal BP is naught 0.9 to 1.2. And the way you do an A BPI is you can do it just palpation because you're just feeling for the systolic BP. But it's best to do it with a Doppler probe. And that is just like, um, you can see a picture in the bo in the bottom, right? Oh. And it's just, it's just like a little probe and it makes a noise and it goes like when you hear when it's on an artery. So what you need is a BP cuff, a Doppler probe and some ultrasound gel. And you'd locate the pulse based on your surface anatomy to find all palpations to find where it is. You stick the Doppler on it. I think the best is to go 45 degrees from the, from the artery and you'd, you'd hear that whoosh. Ok. You then attach the cuff. So either to the, you'd do it to the ankle and to the arm like normal Ok. And then, um, so the way I would do it is I would first do you need to do both sides, left and right. So first I do left side and I would, um attach the BP cuff to the left ankle. I'd locate the posterior tibial and the dorsal pedis pulses. And then I would inflate the cuff until there's no audible pulse for the Doppler or I can't feel a pulse. Ok. I'd then slowly release the pressure while looking at the dial. And then when I start hearing the Doppler make arterial, uh uh you know, read arterial pulsation, that's my systolic BP. Ok. I'd make a note of that. I'd then do that for the posterior tibial and the dorsalis pedis and then I'd know which one's higher. Ok. I'd then do it for the brachial. And then my left SBA BPI is the highest of the foot pulses divided by the brachial. Ok. And I'd do that for the right as well. It's actually really easy. Um It's just most people haven't been told how to do it. And then the way to interpret it is normal is 0.9 to 1.2. If it's really high over 1.2 there's probably calcification of the arteries which is making them less compliant, which is less, making them less likely to be able to stretch and accommodate for the pressure. So it increases. Ok. And then if it's under nine then you've got to think about peripheral artery disease. And if it's under five, it's severe peripheral artery disease and that's it. So now, literally two slides left all of these like interventional surgeries, you don't really know what they are. You just hear the names. So all interventional surgeries for vascular, they gain access through the groin. So they find the femoral artery and they put a catheter in. Ok. So they have access, they then with, um, they have live x ray that's going on and they inject dye so that they can see a lot a real time angiogram of where they're going with the, with the wire. Ok. They then feed the wire to the stenosis. OK? Or we can see this with the Embolectomy diagram. So the catheter would be just a wire that goes distal to the stenosis. You'd then blow up a balloon, which would then look like that. And then you just crawl back, you just pull back and that would pull back the, um, the embolus. And then you'd be able to like, just pull it all the way out of the o out of the leg. Essentially with thrombolysis, you do the same, you get a catheter, but then you just inject some thrombolytic agent which will dissolve the clot with angioplasty. You do the same, but it's a specific balloon which has a stent mounted on it. And a stent is basically just a, like a mesh tube that goes into the artery and you can inflate the balloon that it's sitting on and then it expands and it just basically keeps the, the actual artery patent. So you'd find the stenosis, you'd go through the stenosis and then you'd inflate your stent. And then the stent would now make the tube patent with an endarterectomy. You have the stenosis, you would cut into the artery. Ok. Open the artery up and this would require you to clamp proximal and distal. So it doesn't bleed everywhere. You'd then actually physically take the, the stuff out and then you'd patch sew a patch of the cut. So that then the um the artery is then sealed again and then a bypass is just, you just bypass it. So you just um have a vein or a graft and then stitch it before and after the stenosis. And then we've got a new root for the blood to go. That's literally all it is. And then finally, amputations. The indication for an amputation is if tissue is dead, deadly or dead useless. So if it's dead, it's non viable. There's literally nothing that can be done and we can't bring it back to life. We'll just hack it off if it's deadly. You know, they've got a septic, horrible foot. You know, there has to be a decision made about, you know, what to do. But most likely that foot is more deadly to the patient than it is useful. So, you'd, you'd cut it off so that to, to preserve the rest of the body and then if it's dead useless, if it's just, you know, yeah, for example, paralysis or, you know, major trauma where communes a fracture and they just can't repair it properly and it's just completely useless. You can just, um, uh, amputate for a better functional outcome if they have a prosthesis. Um, and the important concept to know is that, you know, there's different levels of the of the amputations. You can have digital amputations of the of the digits. You can do it at the midfoot, you can do it at the ankle, you can do it below knee amputation, you can do it above knee amputation, you can do it uh like a hip disarticulation, the more proximal the amputation, the worse functioning in it. Because you can imagine with the knee, if you amputate above the knee, they've now lost a joint. So that prosthesis will just have to be like a straight line. Whereas if they amputate below the knee, then you can have the prosthesis coming off under the knee and then they have a, a functional joint that's anatomical for them. OK? Um And it's just the same for if you go distal to that. So um you want to avoid doing a proximal amputation, but also um the more distal the amputation, the like harder it is for the wound to heal because the blood supply is worse. So if you amputate really close to the aorta, then your, your uh healing outcome will be good, but the functional outcome will be, will be bad. So every amputation is a decision about what level should be done. OK? And then that's the presentation over. Uh how long was that last? About just over an hour. So I hope um that wasn't too heavy. Uh If you, if you're watching live, like if you could do some feedback, that would be really appreciated. And if you're watching online as well, uh if you fill in the feedback form, that would also be very much appreciated. Um And if there's any questions from anybody, please fire away. Uh, if there's any questions about the foundation program as well, what to do if you get, get a place where you don't want to, you know, get me up and there we go.