foreign what's up Ninja nerds in this video we're going to be talking a little bit about pad Peripheral arterial disease this is part of our clinical medicine lecture series if you guys like this video it helps you you it benefits you please support us on one of the ways that you can do that is by hitting that like button comment down in the comment section and please subscribe it goes a long way also really urge you guys go down the description box below we got a link to our website there we have amazing notes illustrations we have developing prep courses for those of you preparing for your step one your step two your pants Etc so please check that out also you can get yourself some merchandise we just have a lot of great things there that I really urge you guys to go and check out all right let's start talking a little bit about pad we talk about pad Peripheral arterial disease this is a pretty common disease now when we talk about this I really want you guys think about it as though there's three particular types I think it explains the pathophysiology and it cues you right up to understand the causes so there's thrombotic embolic and vasospastic this one isn't mentioned too much but it is very important in the critical care world when we talk about these we're talking about the peripheral arteries that are being affected these are usually of the actual distal extremities so for example upper arm lower arm but I'm sorry lower extremity but it is way more common to occur within lower extremity vessels than it is in the upper extremity vessels so usually what happens is you have some type of narrowing of the Lumen of these lower extremity vessels that reduces the oxygen supply to the tissues now the vessels that are most commonly affected are usually going to be for example here of the aorta and then it bifurcates into your common iliacs usually this is one particular bifurcation that I want you guys to remember this is where a lot of disease can actually occur so this is called the aorto iliac arteries you can get a lot of like plaques or emboli that can get stuck there another one is as we kind of go down your iliacs your common intellectual Branch into your external internal external eventually become femoral and popliteal so we'll say that this Branch from here to here is going to be What's called the femoral pop-libial arteries and these are also commonly affected by thrombotic and embolic complications the last one here is going to be your tibiofibular vessels so these are going to be also relatively affected they can be hit by some vasospastic disease as well because usually the vasospastic disease hits the farthest distal vessels so usually the ones going to like the foot and usually around the ankle region so again this one here and here would be your tibiofibular arteries now we know that these are the arteries that are most commonly affected in patients who have what's called Peripheral arterial disease or pad what is causing these vessels to become diseased well one is a thrombotic complication and naturally what can happen is you can have these plaques that occur within the vessel wall usually due to atherosclerosis what they do is they can narrow the actual Lumen and make it harder for blood to get through look there's a narrowing point there there's a narrowing Point here so very little blood flow is going to be getting through here and so this will lead to a decreased oxygen supply to the tissues and this is because of these plaques if you will same thing over here we can have a plaque it's really narrowing the actual amount of blood flow getting through here sometimes you can even form a thrombus on top of a plaque so you can have a thrombus that developed on the plaque and that can literally almost allow for no blood flow through here and that's pretty scary but either way let's say that in all of these scenarios what you're noticing is is that there is a massive reduction in O2 Supply to the tissues or maybe no O2 supply to the tissues if this happens the tissue starts to become very ticked off and you know whenever you don't Supply oxygen to the tissue it can actually start to develop something called ischemia and if that is not reversed in time ischemia can lead to infarction of the tissue now we'll talk about how these patients usually present but with ischemia it depends upon the actual degree of ischemia they may present what was called claudication they may present with critical limb ischemia and they may present with acute limb ischemia so that's usually the big things to think about is they usually can present with something called claudication which we'll talk about a little bit later what's called critical limb ischemia which will abbreviate CLI and then acute limb ischemia which is again abbreviated Ali these are going to be some of the potential findings that you can see and the scary complications associated with this now the question that arises is okay it's a plaque that's developing here and then sometimes you can have a plaque that actually develops a thrombus on top of it which really can be super super scary right so this right here I just want to abbreviate this you know highlight this this is a thrombus right so this thing right here which is this black stuff warming on top of that plaque that's a thrombus whereas these here there's no kind of like black plaque there there's no kind of cloth that's actually forming there this is a plaque if you will so atherosclerotic plaque so these are two different things plaques can really narrow it thrombus on top of the plaque can completely obliterate blood flow the question that comes here in both of these scenarios is what's causing the plaque to form well the plaque usually forms because of one particular etiology atherosclerosis so we have to ask ourselves the question is atherosclerosis is really the driving factor of these plaques being formed which is really kind of like making it very hard for blood flow to get through here what is the particular things that lead to atherosclerosin you guys can remember the mnemonic we're literally going to repeat it all the time anytime atheros comes up sad CHF smoking is a huge risk factor here Advanced aged is a huge risk factor here greater than 55 usually is going to be one for females greater than 45 for males diabetes mellitus is a huge risk factor having dyslipidemia or cholesterol so if you guys know Rob who's behind the camera he has cholesterol that's through the roof that would be one particular reason it's under control now the other potential risk factor here is going to be hypertension so having that high blood pressure and finally having a family history is a huge risk factor as well but all of these things are problematic issues and this can lead to the increased risk of atherosclerosis atherosclerosis can form these plaques but what's the scary complication that can result on a plaque sometimes you can rupture the plaque just a little bit and what can you form on top of this a thrombus and that could reduce the blood flow even more or completely cut it off we'll go into that more in the complication section all right so pad disease of the peripheral arteries usually the distal are the lower extremity vessels we talked about those we talked it's usually a plaque that forms because of atherosclerosis in scary scenarios which we'll talk about a little bit later you can form a thrombus on that plaque which obliterates blood flow significantly the other type of cause of pad is embolic so there's this clot that started off as a thrombus somewhere broke off and now it's freely circulating through the bloodstream and then what happens is it maybe goes and gets dislodged in one of these aorto iliac vessels or it goes and gets dislodged in a femoral popliteal vessel or it may even go and get dislodged into one of these tibio or fibular vessels and all of these scenarios guess what it is the exact same concept there is a reduction in the O2 Supply sometimes this reduction can be to the point where there is literally no to supply and we'll talk about that again a little bit later and because that gets into the degree of ischemia because now you're not getting these tissues muscle tissue skin tissue hair tissue all of these are not getting blood flow good enough and so they can start to become very very upset they can start screaming they develop ischemia and this can cause claudication it's going to become a recurring thing you'll never forget that's critical in ischemia depending upon the severity or acute lemoschemia depending upon the severity now other things that we will talk about a little bit more in the complication section is that ischemia we already said claudication is usually effective not getting blood flow to the muscles that they cramp up they get really really tight they cause a lot of pain but also think about this in patients who have this you're also not giving blood flow to the actual skin it can be cold they can have less hair the growth they can also have again a lot of power to their skin so those are other findings to think about not just pain with movement all right or pain at rest but this is the concept I want you to understand here now the question that comes is what did that emboli come from there had to be a thrombus that got situated somewhere that then popped off you're gonna pop off who almost dropped there um that then broke off into this systemic circulation and caused this problem one is an atrial thrombus usually atrial fibrillation so atrial fibrillation is a really big trigger another one you know this is a complication of postmi we call this after a patient has post MI they can develop something called a LV aneurysm we talked about this in the cad lecture or a pseudoaneurysm is another one when it's a little pocket where stasis of blood flow can occur and you can form a thrombus and the last one is a triple A so an abdominal aortic aneurysm this is a little pocket where it's very very dilated which you have stasis of blood flow and again a clock in form and all of these scenarios you break a little piece of the clot off break a little piece of the clot off here break a little piece of the clot off here and all of these now look boom I embolize that embolize that embolize this and then these can go and fly down into the aortic iliac vessel into the femoral popliteal vessel or into the tibial fibular vessel block it off lead to ischemia and lead to the complications which we'll describe later all right I think that makes sense right the last one I want to briefly talk about because it's not mentioned often but it is something I see a lot in the critical care world is vasospastic bad all right it's not a thrombus right or a plaque it's not an emboli it's where the vessels are clamped down intensely so look at this in this particular scenario you have what's called massive Vaso constriction so these are this vasoconstriction is intense you see how these vessels are super super constricted when you have this intense intense vasoconstriction this is usually of the distal vessels usually for the fingers and for the toes so when you have a patient who has very very decreased blood flow maybe diminished pulses they have discoloration of their skin and it's of the distal extremities and they don't have any plaques or they don't have any emboli risk factors you want to think about this because this can really really cause very very little O2 Supply and if the O2 supplies significantly reduced this can lead to some of the features that we'll describe a little bit later as the result of ischemia and this could be potentially one of the most common is this can lead to what's called digital necrosis where I'm not even kidding these patients fingertips start turning black and can fall off okay it's pretty terrifying so this is some of the things that you can see now the question is is what in the heck is causing the vasoconstrictive process here we know what caused the mli we know what caused the plaques and then the thrombus to form what's causing this massive vasoconstriction again usually you think about this in the critical care world so you're thinking about patients who are super super sick they are likely in some type of shock and this is usually shocks that cause reflexive systemic vascular resistance to increase so their cardiac outputs low so they reflexively constrict their vessels so in patients who have shock and they have a low cardiac output they'll increase their systemic vascular resistance so imagine here you have a patient who has a problem with their heart or maybe a problem with getting blood flow out of the heart right so maybe let's just say for example they're in cardiogenic shock and because of this it's hard to get blood out of their heart into the systemic circulation and because of that their cardiac output is very very poor so if they have a poor cardiac output one of the ways that your body will try to compensate to increase blood pressure is it'll literally try to clamp down on your vessels to increase the blood pressure and now what happens is it'll release things like norepinephrine and epinephrine and squeeze down on these vessels and that's one of the problems here is that it causes massive vasoconstriction so it's going to cause massive vasoconstriction and you're going to cause very little blood flow to get to the tissues here right so that's one potential mechanism here is it's going to really clamp on the vessels the other one is vasopressors so it's the same concept a patient is usually on vasopressors because they're in shock so you see how it kind of like goes together and they're getting drugs like norepinephrine or epinephrine or things to that effect that are super rich in alpha-1 receptor activity and what do they do they massively increase the systemic vascular resistance clamp down on the vessels and now look at the blood flow through this tiny little vessel massively reduced leaves the digital ischemia so these are the concepts that I want you guys to understand so when a patient has peripheral artery disease in other words they have disease of the lower extremity vessels think about plaques which can then become a thrombotic complication emboli and vasospastic things now let's talk about the complications of pad all right my friends we have a patient who has pad prefer arterial disease right and now they come to you with particular complications or things that may be concerning for PD and again we talked about how there's thrombotic pad there's embolic PD there's vasospastic PD when we talk about these Peripheral arterial disease oftentimes one of the most common causes of that chronic picture that these patients have is usually that that plaque cause that thrombotic pad where they don't necessarily have a thrombus that forms on their plaque to just have these plaques that are naturally within their vessels and so usually these plaques again we already talked about this a little bit but we'll quickly remind ourselves aorto iliac is going to be one of the vessels that's constantly plagued the other one is going to be the femoral poplidial and then after that we come to the last guy here which is going to be the tibiofibular and again what you're noticing here with these particular diseases with this this concept of what's called claudication it's pain so they have like literally like pain within their calf muscles or pain within their thighs pain within their hip and buttock Area Pain within their feet during some type of exertional activity so let me explain the concept behind this and claudication what happens is you have these vessels that have plaques they're not completely occluding the actual Lumen they're allowing for some blood supply to get through here but it's definitely reduced it's much more reduced in comparison to normal patients so there is a reduction in O2 Supply now what happens is when you have a reduction in O2 Supply this may cause the tissue to potentially develop ischemia but this is usually not too bad in patients who are at rest what happens and what really makes this worse is if these tissue cells decide to increase their oxygen demand so now what I'm going to do is I'm going to tell these tissues hey you're not getting a lot of oxygen but also just to mess you up even more I'm going to increase your O2 demand and so the way that I'm going to do that is I'm going to have you exert yourself so there's going to be some type of exertion on those muscles so for example let's say that you have a plaque with an aorto iliac vessel your hip and buttock area right are going to be depending upon that O2 Supply but it's not going to get a lot you start walking or doing some type of exercise that uses those muscles and causes them to have to consume more oxygen more ATP you're increasing their demand when you do that and you have a combination of a reduced O2 Supply and an increased oxygen demand this probably should sound familiar in the coronary artery disease lecture it's the same concept it's just different vessels this will produce ischemia because there is a mismatch between the two and so this is why we see the pain in the muscle which is the heart muscle and coronary artery disease it's the skeletal muscle and Peripheral arterial disease so that's really where this comes about is this oxygen supply demand mishap mismatch and this will precipitate things such as pain and usually this is because of the muscles not getting enough of that oxygen supply now the pain is very particular on your exams to correlate with so oftentimes aorto iliac this will cause whenever the patient exerts themselves the ischemia to the actual muscles is usually the hip and buttock muscles so this will cause hip embodic pain usually during exertion the femoral pop lidio supplies more of the calf area so this will precipitate more of the calf type of pain and the tibiofibular will cause more of the foot pain so this is what I want you guys to think about here is that in these patients they have plaques so again this is usually associated with the claudication is usually associated with what type of pad out of all those types the thrombotic type right but again what I really want you to think about with the thrombotic pad is they don't necessarily have a clot on top of the plaque they just have a plaque that's narrowing that vessel this isn't common and embolic and it's not really common in the vasospastic type either now one more thing that's really really interesting is if we do something where the supply is low we don't have an increase in O2 demand what this may do is you can potentially so this all these things will increase the ischemia right increase O2 demand and decrease O2 Supply but if I wanted to decrease the ischemia what could I do it's where I'm not causing as much pain so effectively hopefully my goal would be to reduce the pain and depending upon where that that plaque vessel is what I would do is is I would decrease the O2 demand and I would do that by resting and if I decrease my O2 demand what this will do is is this will help this process to decrease the excuse me so now it'll just be a reduced O2 Supply and no increase O2 demand that won't allow for that mismatch to occur as much there's one other thing though when you have less blood flow coming through here yes you're going to get less O2 Supply but less blood flow in general so here let's actually do this in two ways let's say here we have a reduced blood Supply and as a result this will knock down your O2 Supply but it also knocked down just in general the blood flow through that particular artery right so if you have reduced blood supply through these vessels it reduces the O2 Supply and it reduces the blood flowing through those vessels why is that important pulses if I check the pulses in these particular patients what do I expect to feel a good banging pulse or a very diminished pulse a diminished pulse because this is reducing the actual blood flow through there so look for decreased pulses in these patients all right so I think we have a pretty good idea now of claudication usually again in thrombotic PD not embolic not vasospastic and it's usually not a clot that forms on there it's stable plaques reducing the O2 Supply through these disease vessels reducing O2 Supply leads to ischemia especially if there's an increase in no due demand but if we reduce the O2 Demand by resting we'll decrease the ischemia and decrease the pain the next point is critical in ischemia so again it's important to understand that with claudication it's the same kind of concept you can develop pain it's just with this it's more intermittent this will talk a little bit more it's very very interesting when we get into the pathophysiology here so same concept critical in ischemia is usually seen in those patients with that thrombotic pad phenotype right so they don't necessarily have a clot that's formed on top of the plaque they just may have this stable plaque and it's really really bad like the plaque is nearly almost occluding most of the actual lumen and so because of that imagine here you have an aorto iliac vessel you have a femoral popliteal vessel and these poppies are just literally like look how much room I have here it's very little so now blood is going to be really really hurting and squealing as it's trying to squeeze through these like tiny little lumens now and so what I'm going to notice is the difference here between this and this is the blood type Supply was reduced here it is massively reduced okay so there's a massive reduction in blood supply now that does two things it reduces the O2 Supply and it also reduces the blood flow as we talked about before big differences is then this scenario it is massively reduced so a massive reduction in O2 Supply and a massive reduction of blood flow okay with that being said when you have a reduction in O2 supply to the tissue in this one it was very very low in this one it was just a little bit low this one you required increase in demand that's why you get intermittent claudication this one you don't need no dang demand for this one these patients can develop ischemia at any point it doesn't matter this is usually a rest that's how bad it is so these patients develop a very severe ischemia to the point where they can have pain and again this is usually affecting those muscles the skeletal muscles in this case at rest that is why this one is terrible now if the ischemia is super super severe that is what we're going to see is we're going to see pain at rest rather than pain with exertion improving with rest this occurs at rest one other big point is that this pain at rest it's chronic right it's chronic so critical Imaging is usually a chronic process so usually it's persisting for greater than two weeks I want you to remember two weeks that this pain will continue to persist now the muscles are not the only thing that's affected my friends when you don't get O2 supplied to the tissues this is not just the muscles we're talking about Hair Skin So the other things that you could potentially see is you can have ischemia not just the muscles but to other tissues like which one for example I could have ischemia to the hair so patients could have hair loss right that's one potential thing I could also have ischemia to the skin and they could have skin atrophy so these are other potential things that you want to look for it's like really really thin skin a lot of hair loss and con combination with a lot of pain here's where it gets really really bad if the ischemia really really continues it can actually cause the skin to become undergo necrosis so now the tissue starts undergoing necrosis and usually the areas that actually start to becoming necrotic are on the lateral malleolus and around the digits and they really form these like punched out circular super super painful ulcers and so you're going to get these things called arterial ulcers the reason why I'm saying arterial is because there is Venous ulcers and these poppies are painful and what happens that is really really bad with these ulcers is that these ulcers can become infected if bacteria jumps into the ulcer it can literally cause an infection that can cause the patient to progress into something called sepsis and so this is usually whenever these ulcers become infected so you really want to watch out for that too so if a patient starts having arterial ulcers you need to make sure that you tell them hey keep this area clean because it can become infected you can become bacteremic and septic same concept as you if you have a patient with pain at rest they're starting to have hair loss atrophy of the skin you notice some necrosis you may see ulcers the worst sign is when they're extremities their digits start literally becoming like black and it starts mummifying an appearance when this happens we call this gangrene this is literally necrosis but it's what's called coagulative necrosis of the skin this is called gangrene but there's two types one is you usually have what's called dry gangrene right which is that kind of like blacking black mummification of the digits or the in this case maybe the foot if it becomes infected and so now that black extremity becomes odorous it starts having drainage or discharge and it has a lot of like this kind of like nasty looking appearance then what can happen is it could mean that that dry gangrene has become infected and if it becomes infected this is called wet gangrene the scary thing is is that wet gangrene can cause bacteria to spread into the bloodstream and can precipitate sepsis so these patients are really at risk for some serious disease process and progression so so far we see a little bit of a difference here between claudication the other concept here is the blood flow this is also very helpful payment rest is key evidence of necrosis like arterial ulcers and gangrene is key but the other one is obviously here reduced blood flow same concept you will have diminished pulses they can be really really hard almost absent but here's the other thing you can develop this weird type of sign where they call it Burger sign I don't know how to spell so I'm not going to write it down but this concept here is where the the actual color of the limb is it's dependent upon positions so if I lift my leg up the leg will actually have to have they'll have to push blood flow Against Gravity and what that will do is that'll cause the limb to become whitish in appearance then when I bring the foot down I'm letting the arterial flow with gravity and it'll return back to its normal color and that's a what's called Burger sign and so this is usually where you can actually see positional changes so positional changes which alter pallor or rhubarb in other words whiteness or redness of the extremity there is positional changes in that extremity and that's super super helpful again it's called Burger sign okay so now with that being said we have a patient who has intermittent claudication critical imagechemia we should be able to differentiate these two now the last one is acute limit ischemia acute lymph ischemia usually for this one we can see this in two scenarios the most common is embolic pad the second one is going to be thrombotic PD and this is where I need to be very specific and what I mean is this is not a plaque this is not a stable plaque this is a plaque that ruptured and a clot formed on top of the plaque that's that example I gave in the first prior lecture to this one now when these happen now look at this you have an embley blocking all of these vessels here is any blood flow getting through here no so because of this you're literally having we're going to use this as the most severe example here little to no blood supply is going to be getting through here so we'll put blood supply because again we've been using that terminology a lot all right so there has been little to no blood supply getting through here in this example it was emboli afib left ventricular aneurysm posted my complications or aneurysms and this thrombotic complications so you have a plaque like atherosclerosis you rupture the plaque and then form a thrombus on top of that either way all of these things are reducing the blood supply are giving you almost no blood supply if that's the case you get almost no oxygen supply and you get almost no blood flow so now I have no oxygen supply no blood flow if I have no O2 Supply or almost very little of it what is going to start happening to my tissues they will become ischemic immediately and it is crazy how intense this can be so they will develop insane ischemia and does this have to have any exertional component to it no so this may start beginning to sound a little bit like critical limb ischemia right they kind of sound similar in the fact that very very little blood supply almost no blood supply quick ischemia with no exertion quick ischemia with no exertion usually at rest kind of sounds similar so what we know is this ischemia will cause an insane pain in the muscles all right so what we'll see is they will have pain that'll occur in the muscles and it'll be at rest but to really amplify this this is more chronic this is acute so you can also think about critical limb as chronicling ischemia Ali acute lymph ischemia this is greater than two weeks you would probably develop this pain in less than two weeks and that can help you in when they're presenting this in the vignette if they present this and the pain came on abruptly within the past couple hours it's not this it's likely this all right that's one thing the other thing is not only will you have intense pain sometimes this ischemia can literally progress to the point where the patient starts to experience destruction of particular tissue this can really hit the muscle so bad where it causes paralysis of the muscles so if you really destroy the muscles you can cause paralysis of them where it's almost impossible to move the extremity you can start destroying the nerve endings within the skin and lead to paresthesias so I could have pain I could have paralysis I could have paresthesias what's another thing that can happen again if this ischemia is bad enough yes it can potentially start causing things like in severe cases it can start causing necrosis of the tissue so you may see if it is not treated and not reversed you may start seeing some discoloration such as you know gangrene that's beginning to start to form a necrotic digit so you may see that but I want you to really kind of associate this more in your brain with the critical limb ischemia but you can see this if we come over here we had no O2 Supply which would give us pain out of proportion paralysis if it really started destroying the muscle tissue paresthesia if you start destroying the actual nerve tissue and then we get almost no blood flow are you going to have any pulse if I'm getting almost no blood flow through no so these patients usually are pulseless and if I got no blood flow coming through there am I going to have any color to my actual skin no so power is another potential finding and so with this being said there is one other finding which is it can cause the skin to have difficulty if you start causing destruction of it it can have difficulty regulating temperature and it's called poiculotherma but oftentimes some textbooks won't add it but what this leads to is the common presentation of acute lymoschemia which is what we call the five peas and this is severe pain paralysis which is destruction of the muscle tissue paresthesias which is the destruction of the nerve endings pulselessness which is due to the lack of blood flow Impala which is due to the lack of blood giving color to the actual skin this is the classic presentation of acute ischemia in severe cases yes you can develop necrosis but this is usually at the point to where the patient is gone with a very little blood flow for a long period of time and they can't start developing gangrene Etc but this is the concept that I want you guys to get across here with pad so understanding this now we now have intermittent claudication critical limb ischemia and acute limb ischemia the one thing that you're probably like Zach what about that vasospastic type of pad vasospastic pad can cause acute lymph ischemia but usually it's of the distal like extremities and so they can start developing very very decreased pulses they can't start developing cyanosis or necrosis of the digits so also think about that one but this gives you the biggest thing that you guys need to know for PD with respect to complications now let's take and tackle the diagnostic approach now with that being said we have a patient comes in with maybe intermittent claudication that's their primary Chief complaint so pain when walking improves when they rest they have some of the risk factors they're smokers their Advanced age they have diabetes they have high cholesterol hypertension family history all of these things are super suggestive of pad one of the first tests is to get an ankle brachial index and what it's looking at is it's looking at the blood pressure and the ankle and the blood pressure in the brachial artery and you're comparing the difference here here in the lower extremities there's these nasty plaques which are reducing blood flow here in the brachial it's a healthy vessel so therefore this pressure is going to be a lot lower so if you look at this what will happen is the top number of the ankle brachial index the ankle pressure will be low the brachial will be normal and so what happens is the overall number should get smaller and smaller and smaller so the smaller the ankles the solid blood pressure is the more severe the pad where's the cut off though so normal is 1 to 1.4 borderline 0.9 to not 0.99 once you get less than 0.9 you have Pad but as you get worse so generally as we get to like 0.6 to 0.9 we're in kind of like that really nasty kind of moderate pad and if we start getting really low to where it's kind of like less than 0.4 then we're getting into the Super severe pad and so that's really important but this is going to be your first line test to obtain anything less than or equal to 0.9 is Pad but the lower and lower you go the more severe the pad is once you've done this and it shows that they have an ABI that's suggestive of pad if you really need to you should assess these patients for revascularization indications would be that they're refractory to medical management they have critical limb ischemia or acute limb ischemia they need to be revascularized ways that we do this is we can do two tests and it depends upon their contrast risk all right so they have a risk of contrast induced nephropathy they have terrible kidneys if they do do a duplex arterial ultrasound and they'll kind of give you the different velocities of the blood flow and tell you where this actual disease process is occurring how severe it is if they don't have a contrast induced kind of nephropathy or any risk of that then I would go to the better test which is an angiography you can do this via CT you can do this via MRI or you can even do this potentially via digital subtraction angiogram which will probably be one of the best ways because it'll show you oh here's some occlusive material here oh here's some kind of plaques here oh there's an emboli that's a completely cutting off the blood flow of the left iliac so you're able to tell the actual disease process where the occlusion is where the disease is and where you have to attack now once we have done this and we've determined hey they have pad using the ABI I can even determine the severity of it I need to assess the risk for revas their knee for revascularization duplex ultrasound or angiography I've determined the disease I've determine the severity of it then I need to treat it for gangrenous limbs so those who have critical limb ischemia or maybe acute limb ischemia where the tissue is starting to die and it is no longer viable you got to amputate so it's either above the knee amputation AKA or below the knee amputation bka okay and these are the indications again as to why is they have wet gangrene acute lymoschemia or critical imagechemia that is no longer a viable limb now critical limb ischemia again if the patient is beginning to show needs for revascularization so they have again pain with rest they have arterial ulcers they begin to have potential signs of like some beginning gangrene you can consider them to potentially get revascularized but I would say it's more of the pain with rest non-refractory I mean refractory to Medical therapy if they are revascularization such as using a stent to place in that area or doing a graft or an endardectomy where you cut out the plaque would be the best thing so either stent the opening provide a graft which is going to be again an alternative route or cut the plaque out so here's the stent if you do the stent what happens is when you place the stent the stent is at risk for thrombosing so you should put them on Dual antipolios for at least a year and then after that the stent thrombosis risk goes down so then continue them on aspirin again here's an example of a graph kind of bypassing that potential like plaqued up area and or you can cut out that plaque and just get rid of it with acute limit ischemia the best thing to do here is actually skid them on Heparin to kind of prevent the clot from actually propagating and getting bigger and then you need to send them to get that actual that actual vessel potentially whether it's surgically or Interventional Radiology wise they go in and suck that clot out sometimes if they can find the area they can actually inject some TPA into the area as well but generally thromboemboleectomy where you go in Via catheter or you open up the vessel and pull that clawed out it's the best therapy they need for non-critical ischemia which is again any patient with intermittent claudication and these patients it's best to treat the underlying cause and one of the best ways by doing that is to reverse any of the reversible or modifiable risk factors can you stop smoking yes can you change your age no can you change your diabetes yes so change your diet change some exercise can you change some of the other Concepts like and these patients usually their cholesterol is really high yeah I can put them on Statin therapy can I change their hypertension put them on blood pressure medications and can I change their family history no okay so those are the things that I can potentially do is change their diabetes their blood pressure and I can also help with their diet and also help with taking them to stop smoking other things that are helpful is potentially reducing the risk of thrombosis of a plaque and that is where anti-platelets come into play anti-platelets something like aspirin would be super beneficial for these patients to prevent if this plaque ruptures they get a clot on top of that that'll lead them to go into a critical or acute limb ischemia so putting them on antiplatelets is super super important claudication otherwise is best and I am going to say this again it is best treated with exercise exercise has been been shown to be one of the most beneficial therapies for patients to develop intermittent claudication other things that you can consider is if they're on an anti-platelet prevention there is solostice silosol is interesting because it's an anti-platelet and a vasodilator so it'll dilate the vessels and it'll have an anti-platelet function which will be both beneficial in improving blood flow past that occlusion occlusive area so this is the things that I want you to remember for treating Peripheral arterial disease all right my friends that covers it I hope it made sense I hope that you guys enjoyed it and as always until next time [Music] [Music] thank you