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Ok. Yeah. All right. I think we'll just kick start and then people can just join in. Hi. Hello guys. Welcome to our third series. Um, third session on our series Concer finals. Today we're gonna cover vascular surgery by our two lovely F ones based at Conquest and Jack. Um So we do these sessions every day, Tuesday at um seven PMU K time on metal. Um So it'd be great if you guys could join us every Tuesday. We cover all specialties um gearing towards finals. Um But yeah, so I, I'll drop it to you guys, Jack and Ch Hi. Good evening everyone. So, Jack and I will be doing a tutorial on vascular surgery, uh trying to give you a holistic view of what to expect in your final year. Um And when you're on the wards when you're working, so we're gonna cover these topics. Um So we'll start with peripheral arterial disease. So you can define that as chronic insufficiency of the arterial blood supply of the limbs. It's most commonly in the legs due to stenosis or occlusion of the vessels. The primary primary pathological cause of this is usually atherosclerosis, less common causes. You have like, um, Buerger's disease or radiation induced vascular sur uh uh injury. So, some symptoms of P AD, you've got pall of the lower limb, reduced temperature, paresthesia. Often the patients will say they get pins and needles in their, in their lower limbs. Sometimes they can get cramp and there's something called intermittent claudication and then some risk factors, you've got non modifiable risk factors. So the age if they're above 55 if they're male, if you got any, if they've got any family history of vascular disease, such as DVT and the usual smoking, diabetes, hypertension and uh high cholesterol. So we use the RD Fontaine classification of P AD. Uh There's four classes, one being asymptomatic, two is intermittent claudication. Three is rest pain and four is tissue loss. So I'm gonna talk about um intermittent claudication, which is pain brought on by exercise and relieved by rest. Uh investigations for this is usually you wanna do your pedal pulses. So your dorsalis pedis, your uh uh your posterior tibialis. And um you can also do a dle duplex ultrasound scan. You can use the uh uh A BPI um and you can do a CT angiogram or an MR angiogram if you really want to. So your A BPI interpretation is your ankle brachial pressure index. Um 1.1 to 0.9 is the normal range. Then you've got 0.9 to 0.5 which classifies as intermittent claudication, less than 0.5 is rest pain, less than 0.3 is tissue loss and more than 1.1 is when your arteries are calcified. So how do we manage? Uh P AD? So we've got conservative management. So, smoking cessation is very important to, to guiding them towards recovering from P AD. Um exercising helps. Um And then you've got dietary modification, all of these help with like issues with hypertension. Um And then you've got medical management, you've got antiplatelets. So you can use clopidogrel, that's the first line. And then aspirin after uh statins are good to reduce your cholesterol. Uh Usually we use atorvastatin and you've got hypertension control. So you've got your hypertensive drugs, uh like your Arbs and your ace inhibitors and you wanna have tight glycemic control as well. You can also manage P AD surgically and broadly speaking, you can classify them as a endovascular or surgical. And then with endovascular, it's usually percutaneous transluminal angioplasty. Um And it's typically used for short segment stenosis, usually less than 10 centimeters. Um And then surgical management, you would, we, we would do bypass procedures using synthetic grafts or vein grafts. Um and then amputation for non viable limbs. Can anyone tell me what key features you like to find in a history of assessing someone with, with P ad just some questions you may want to ask, feel free to put it in the chart. You don't have to, if you don't want to, ok, duration of symptoms. Yeah. Anything else? Ok. That's fine. It's all on the next slide past medical history. Yeah. Worsening. Yeah. So that's all good questions. Um, so these are the questions you would want to ask? Essentially you wanna know. Where is the pain? When did it begin? Is it worse by walking? How far do you need to walk before you can stop? Um, does the pain go away when you stop? Pain ever occurred? Rest and night? Do you have to hang your legs off the edge of the bed and it gets better after that? Do you not notice that your legs are a bit colder? Any pins and needles, any change of color? Um And then obviously, yeah, like you said, past medical history is important. So if they're smoking, if they got hypertension and if you got family history of any vascular conditions, so just a quick question here. Uh A 56 year old gentleman presents to his GP complaining of buttock pain on further questioning, the pain occurs on exertion and is relieved by rest. The man informs his GP that he has a separate, more private issue regarding his performance in the bedroom. So which aspect of the, of this examination would likely lead you to the correct diagnosis? So I'll put a pole up here. Ok. So we're between C and D mostly D, right? I'll stop it there. So the answer is actually D femoral pulses. So it's very important to assess this, especially if someone's coming in acutely. Um If you, you wanna start down and move your way, move your way up um from your dorsalis pedis to, to your femoral pulses if you can as well. There's something also called um leriche syndrome. Now, um this is actually a symptom or it falls under a symptom really and it's um of P AD and it's essentially occlusion at the bifurcation of the aorta. And it's usually in uh this classic triad of erectile dysfunction, intermittent claudication of the buttock and your thigh or you've got absent a weak femoral pulse. Right. Next, we'll talk about acute lower limb er, ischemia. Er, so it's defined as the abrupt interruption and perfusion that threatens the viability of the lower limb. So you can remember the clinical features by remembering the six ps pain, pallor, pulselessness, perishing cold, paresthesia and paralysis. If acute limb ischemia is left untreated, you've got irreversible tissue damage within six hours which will lead to limb loss and possibly mortality as well. So, some causes of uh acute ischemia, you've got acute thrombus with preexisting atherosclerosis. Sometimes it's known as acute on chronic ischemia. You've got emboli and some other causes could be aortic dissection. A popliteal aneurysm. Uh you could have trauma, uh direct trauma. Oh, it could be iatrogenic as well. This is a very full slide. But essentially it talks about the investigations and uh management of uh acute limb ischemia. So, patients with acute limb ischemia usually has have sorry, significant comorbidities such as ischemic heart disease or renal disease. Um And when you're reperfus them, you wanna be aware of reperfusion injury, it's a complication of acute limb ischemia. It's due to the sudden increase in capillary permeability, um such as compartment syndrome. So, investigations, you wanna do your normal bloods, you wanna coag screen your FBC S and your UN es uh nice to have a tr in there as well. Uh You wanna repeat that after three hours if it's raised, uh you can have a Doppler ultrasound. Um And if it's positive, you can then have a CT angiogram. E CG is useful for looking for a cardiac cause uh of the ischemia. And how do we manage acute limb ischemia? Well, then you got conservative and you got surgical uh conservatives usually using IV Heparin. Uh and it's for classes Ruford one and two A and surgical. You can then further um split them into an embolic cause or a thrombotic cause for the emboli. You can, you can do an embolectomy. Um or you can also do a bypass surgery and thrombotic. You can do local intra arterial thrombolysis angioplasty and also bypass. You've got another question here. So a 71 year old gentleman presents the ed complaining of sudden onset back and left flank pain that radiates to his left groin. He has never experienced symptoms like this before started this morning, localized around the left side of his lumbar. He has tried paracetamol, failed to help past medical history. Is notable only for hypertensions, uh which is being treated with amLODIPine and he is apyrexic. So which of the diagnosis is most likely, I'm gonna put a pole out there. Give it a few more seconds, split between P and C. All right, I'll stop a bit. So the answer is actually a leaking abdominal aortic aneurysm. Um So AAA, it can present similarly to renal colic. So the answer between B and CI can understand why it's quite close. Um AAA usually presents in a triad of shock. You got sudden onset uh midabdomen of flank pain and you got a pulsatile abdominal mass. Um and renal colic is usually in, in patients that are younger than 50. So that moves us on to then AAA. So it's abdominal aortic aneurysm. It's an abnormal localized dilatation of the aorta exceeding the normal diameter by over 50% or the diameter by three centimeters. Um And it's a true aneurysm. It means it covers all three layers of the, of the vessel wall. So some clinical features of um AAA, you can have, well, most are asymptomatic actually, uh less than 50% of it is detected on exam by a pulsal TN and expand cell mass in the abdomen. Um And then 40% is detected uh on imaging uh incidentally. Um you've got the, the symptoms usually arise from the expansion of the aneurysm rupture or peripheral embolism. And they, they could present as abdominal back or flank pain, distal peripheral embolization or ischemia. Upper gi bleed from the aorta aortoenteric fistula or you can have syncope or shock as well with a large pulsal mass mass, sorry, uh, ultrasound in ct abdomen with contrast, uh, the usual investigations of choice and some differentials there, you can have ischemic bowel perforated peptic ulcer disease, pyelonephritis, um, acute pancreatitis as well. And, um, for surveillance in the UK, uh, it would be yearly ultrasound scan. If, uh, it's between three and 4.4 centimeters, di the diameter 4.5 and 5.4 you have it every three months and if it's above 5.5 in males, you would have a surgery and if it's above 5.2 you would, uh, in, in women, you would do a performed surgery as well. So, in terms of surgery, then you've got AAA repair, you can have open or endovascular repair. Um, there's a debate whether one is better than the other and some consultants prefer one over the other. There's no, there's no fixed, um, a choice. It's more of a preference really for open surgical repair. You can use synthetic grafts to repair the aneurysm and the aorta is usually clamped infrarenally so that you want to prevent renal ischemia and then endovascular what we call a, um, it basically has small groin incisions um and then it doesn't require cross clamping of the aorta and it's usually carried out under radiological guidance. And um there's a high early reintervention rate if an endoleak occurs. And just another question here. So a 59 year old lady presented to Ed with a central crushing chest pain radiating into the epigastrium on examination. The patient had an early diastolic murmur, auscultated in the third I CS left sternal border observations revealed heart rate of 92. A left arm blood pre BP, 1 63/73 and a difference in the right arm of 114, 60/68 resp rate of 19 saturating 96% on room air. And uh as a normal temperature, 36.7 12 lead E CG shows there's some ST segment elevation in leads 23 and A VF. So there's a lot of information to unpack, but which of all of these would be the most boring feature. I'll put another pole out, right. So most of you have answered E and that is the correct answer. It's well done. So that brings us on to aortic dissection. So, in dissection, it's a separation in the, the aortic wall intima causing blood to flow into a new F channel composed of the inner and outer layers of the media. These are just the types. So some clinical features then of a dissection, you've got a ripping or tearing substernally uh which is usually indicative of the ascending aorta. We've got interscapular pain, which is usually the descending aorta that's affected, it radiates to the back and down the arm. So it, it, it could very easily mistaken it for an M I dissection can affect aortic branches. Um And you usually have a wide pulse pressure and you can also hear an early diastolic murmur. So aortic regurge, uh and you've also got a loss of uh, the peripheral pulses, investigations you wanna do. So you wanna start with the bedside investigation. So you've got BP, ecg that you can do quickly send the bloods off. Um do a group and save and cross match just in case. Um urgent CT is usually required with contrast. And then for treatment, you wanna always start with the at E approach. Um and you wanna have the vascular team contacted as soon as possible. Uh You wanna control their BP so you don't wanna re aggressively provide them fluids. Um You wanna let you wanna allow for permissive hypotension. So you don't avoid the rupture from worsening and then you can do surgery as well. Uh That depends on the type. Well, you've got two types really, you can do open and you can do a ta which is thoracic endovascular aortic repair. And um it depends on the timing as well and you've got two types. Um So type A is uh immediate emergency surgical repair. Uh usually involves the ascending aorta can propagate to the aortic arch and the descending aorta. And the tear can essentially originate anywhere along this path. Type B. It doesn't involve the ascending aorta and it occurs in any part of the aortic arch and the descending aorta. And it's usually conservative for that first and then elective repair after six weeks, if uncomplicated. Next question here is. So, 72 year old gentleman presents to the ti a clinic following a recent visit to Ed due to left arm weakness. He has undergone carotid artery, Doppler, ultrasound scanning um for stenosis and is determined that the necessity for carotid endarterectomy. So what imaging finding would be the most compelling indication uh in this patient? So, if you've got a good split, um but majority have got the the closest to it. So it's actually 74%. So, uh stenosis of the right carotid artery. Uh And before we move on to carotid artery stenosis, I just wanna go back to the um endoleaks. So there's five types of endoleaks, right? So leak, uh type one would be a leak at the attachment sites of the graft. And then type two would be filling of the aneurysmal sac by your collateral vessels such as your lumbar vessels and your I MA vessels. Um Type three would be a leak through the a defect in the graft. Type four would be through the fabric of the graft uh due to its porosity. And then type five would be the expansion of the aneurysm sac without any evidence of leak on imaging. Um Just to let you know you'll have these slides um with you. So sorry if you've gone a bit too fast, I'll hand it over to, to Jack to continue on. Yeah. So, um the correct answer for that question was um d purely based on it is a bit confusing. Um But it's purely based on the side of, of, of the, the deficit. So the patient presented with a left sided deficit. So you're thinking there would be a lesion contralateral to that. So, affecting the right, the arteries supplying the right side of the brain. Um And therefore the correct answer was was d because that was the only option where there was more than 70% stenosis in the right uh carotid artery. So this is uh uh technically a vascular condition. Uh but it's, it's investigated a lot in patients with tia or stroke. So you hear a lot about it when you're revising neuro potentially. But it's important to just to be aware of that vascular surgeons perform a carotid and arterectomy uh and knowing the indication for it. So it's usually uh patients with a ta get an ultrasound scan of their carotids. And if there's more than 70% stenosis um on the side, contralateral to their symptoms, then then you'll consider surgery they can have by uh bystander lesions on the opposite side as well and they might be operated on it at the same time. Uh But this question was being a bit specific and nitpicky in terms of which side uh is the indication for. Um So I've got a few pictures on some of my slides. So this is a spot diagnosis. Um This is, so if I give you a clue, the abnormal side is the patient's left side, which is our right. Um Can anyone you can, you can type in the chat box if you, if you can guess the diagnosis. So, compartment syndromes, a good differential. Uh DVT is more what I was looking for. So, compartment syndrome is a good differential for this though. Er but we're gonna talk about DVT, this is a particular type of DVT. So it's got a specific name. It's essentially a severe, very severe DVT, affecting the whole limb. So it's, it's got this strange name FGS Cerula Dolans, but it's, it's one to know about, not often asked specifically, but um could come up. So um so DVT is a blood clot that usually develops in the deep veins of the body. So often we talk about it in the leg. Um and it's just important to note that it's normally the deep veins rather than the superficial veins. The superficial venous pathology is more varicose veins and superficial thrombophlebitis. So DV DVT as in the name is, is, is affecting the deep veins in the leg. Uh So the classic presentation patients normally have calf pain. Uh and on examination, they've got lower leg swelling, redness and warmth. And this is important to know this is normally unilateral. So, if you've got a patient with bilateral leg edema, you're thinking less of a DVT and more of a systemic issue. So, heart failure or hypoalbuminemia in, in liver failure, that type of thing. Uh There's a, there's a classic sign called Homans sign. It's not very specific. It's essentially when you dorsiflex the foot, they get some calf pain. So you can get that in other musculoskeletal disorders as well. So it's not the most specific sign but want to know about. And then obviously, you've got this severe form of DVT which affects the whole leg. Um You can also, in terms of investigating for a DVT, we will know about the well score. So this incorporates sort of risk factors and, and clinical signs and examination. And then depending on the well score, uh you might jump straight to Doppler ultrasound scan to identify the DVT. Uh or you might wait to see the D dier result. Um And basically, in all patients where you're suspecting a DVT, you do a well score on a DDIMER. Um It's important to know as you probably most of you already know DDIMER um very sensitive but not very specific. So that's, that means essentially the D DA is negative, you can be fairly confident that the patient doesn't have a DVT. But if the DDM is positive, there's still a chance that they might not have a DVT because you can get raised DD in other conditions. So fo different forms of information cause D dama to be raised, it can be raised in pregnancy. I, those are other things. So it's not very specific to DVD and uh it's usually above 500 nanograms per meals. Um So the aim of treatment is essentially preventing a pe. Um So first line is, is a direct oral anticoagulant. So a Duac normally Apixaban or Rivaroxaban are the first line choice just to remember the mechanism of action and factor to a inhibitor. They both have X in the name. So it's a helpful reminder. Um an alternative is low electro heparin for five days and then you go for a doxy or a bigger channel which are other DAC. Then the old school method was low electro heparin bridging to Warfarin that's very rarely used. Now, um So the key thing to know about treating DVT is how long, how long should we anticoagulate for? Now, if it's, if it's provoked and there's a clear risk factor which you can then remove, for example, a recent surgery or a long haul flight is classically talked about. Um So if it's a reversible risk factor, uh then we can treat for three months and then stop, consider stopping the anticoagulation. It is an unprovoked cause. Uh So we can't identify a clear risk factor. We normally treat for at least six months and then in situations where maybe there is a risk factor, but we can't get rid of it. Um For example, like if someone has malignancy that we're treating, but it's still present, you might continue anticoagulation or if they get in recurrent DVT episodes, then we anticoagulate for life. So this could also, these two types of things can also occur in, in patients with, with clotting disorders or thrombophilias or that type of thing. So, you'd consider anticoagulation for longer periods just before we move on from, from DVT, just in, just in our experience. Um If a patient comes in and they've got like lower limb swelling, um yes, it's, it's, it's usually your first instinct is DVT, but sometimes they've got, you want to know about the history of surgeries that they have sometimes if they've had a knee surgery, uh or any osteoporotic changes that could sometimes cause the swelling as well as it presents the almost the same way. If you've got like pain in your lower limbs, you got swelling. Um of, of course, you've got your well score and D dier but just, you know, not to be tunnel visioned into, into DVT. Uh So this is just covering a sort of linking back to basic principles. So we've got works triad, er which talks about how clots are formed. Uh So hypercoagulable state is one component which is hard to control. This is, for example, with genetic conditions, you've got vessel wall injury. This is normally the triggering feature in arterial arterial clot formation. It's normally based on platelet activation. So it vessel wall injuries. In terms of arterial system is normally treated with an antiplatelet because it's platelets that are the, the the pathophysiologic cause. So that in m in peripheral arterial disease, which we talked about or in in stroke, it's antiplatelet agents are the ones we focus on. Uh whereas stasis is sort of the main culprit in venous venous clots. So af is po potentially sort of an outlier in terms of this, this idea with this pattern. But DVT and pe we treat with anticoagulants cos it's normally due to stasis and clotting factor activation. So that's why we go for anticoagulants here rather than antiplatelets. Um So this is the fifth question. So a 54 year old lady presents to the GP with uh distended, uh lengthened and tortuous leg veins. Uh her GP diagnoses her with the varicose veins. We just want to know what the underlying cause is of varicose veins. So it should be a relatively straightforward one. Yeah. So we, we've got a few responses most of you have gone for B. Um So that's the correct answer. Um So it's essentially incompetent valves of the venous system. Um uh So varicose veins, as we said in the question, are distended, tortious veins in the leg normally affecting the superficial leg veins. So the saha veins that can also affect veins that aren't in the legs. So, esophageal testicular veins, you can get varicose type veins there, but again, caused by valvular incompetence. So it's a mechanical problem with the valve itself. Uh So clinically, they present with again, distended, tortuous leg veins, which which you can obviously see in which the patients normally can present with due to cosmetic concerns. So it's actually more a more common condition in males, but you see more females presenting with it often due to cosmetic concerns, but it can be associated if it's severe with uh pain and heaviness of the limb or throbbing sensation and cramps. So alongside varicose veins, you also often see features of, of I've put CVI here, which is chronic venous insufficiency, which we'll discuss next. So this is sort of er incompetence of the valves causing venous hypertension and blood stasis and blood pooling in the legs. So, investigations you could consider for varicose veins or these types of symptoms that you could consider a BPI just to rule out arterial disease. There's a specific test called tourniquet test or tr and dieng test, which involves tying a tourniquet er at the upper region of the leg to try and block off the suing femoral junction and sort of helps you delineate the level of, of the vein o of the valve incompetence whether it's higher up or lower down. Uh But but the main investigation you'd also consider is a duplex ultrasound scan just to look at venous flow. And again, identify if there's any more sinister pathology, potentially DVT that kind of thing. The treatment for, for varicose veins is essentially the conservative treatment is graduated compression stockings. Uh So which applies pressure to try and help blood flow back up to the heart. Um because essentially in these patients, the valves aren't working properly. So you've got retrograde flow and their calf muscle pump is not efficient enough to overcome the flow. So it pools in the legs. So, so the compression stocking sort of acts in a similar to what your calf contraction does to push blood back up to the heart. Uh And then you can consider referral to vascular surgeons who can perform things that venous ablation, essentially killing off the distended superficial vein. Um And this can be extended to the patients symptomatic, for example, they've got pain or heaviness, which is, is from the varicus veins or they've got any skin changes or ulcers that might be related to an underlying chronic venous insufficiency. So, next question, um, a 67 year old man presents with a discontinuation of the skin on the top of his left hallux. Um It's causing him significant pain especially at night time, which has caused him to dangle his legs off the side of the bed to gain relief from the pain. So, what is the most likely diagnosis in this case. So a few people have put uh b as the answer which should be correct. Um So the answer is arterial ulcer. Um And there's some key aspects of this history which point to an arterial ulcer. Um So one is that it's at the tip of his, his hallux, which is the big toe, the anatomical word for big toe. Um So it's the fact that it's very distal uh and also the fact that the pain improves when he dangles his leg off the bed, suggesting that gravity improves blood flow to the area and relieves the pain suggests it's more of an arterial problem um rather than venous. Uh so, ulcers just to go back to the basic definition is essentially an abnormal disc discontinuation in the skin or mucous membrane. So obviously, you can get gastric and esophageal ulcers. But, but in vascular, we're talking specifically in relation to the skin. Um So arterial ulcers are essentially ulcers that are due to inadequate arterial blood supply. So it's often um closely associated with peripheral arterial disease, which we've already talked about and characteristic features of an arterial. So it is very distal because if you think about that, you've not got arterial supply, then the tissue furthest away is receiving the least amount of blood. So it's most likely to die off first. So it normally affects distal regions, tips of the toes, that kind of thing. Uh pain is worse when you elevate the limb because if you've got, if you're elevating the limb up and the artery drains back to the heart, you're getting reduced blood flow even further than you already have. Um And it's associated with other features of peripheral arterial disease. So, intermittent claudication, um and then signs of acute limb ischemia, potentially. Um Because if you think about the basics of the vessel, intermittent claudication is similar to, to stable angina in that you've got a narrowing. So when you've got activity dependent oxygen demand, you then get pain and then acute limb ischemia, you've got sudden onset pain like you get in an M I because there's a, there's a sudden obstruction. Um You can also get loss of hair due to poor blood flow. Um, investigations generally ultrasound scan just to, just to confirm blood flow through the arterial system. And the treatment would be um wound dressings and then treating the underlying peripheral arterial disease, which we've already talked about. Um, key thing to note is a, an aspect of peripheral arterial disease is critical limb ischemia. So it's, it's part of the classification that we've already discussed. But critical limb ischemia specifically is diagnosed when the patient has rest pain or neck pain or tissue loss, which we've seen in the patient in this question. So the next one, a 72 year old lady presents with a painful shallow break in her skin is located one centimeter superior to her right lateral malleolus. She explains that wearing white socks and keeping her legs elevated, improve the pain on examination you be. But you know that both her legs are edematous and have a brown pigmentation to them. What's the most likely diagnosis in this case? So, we've got um a bunch of responses already. I think all of you have put an A which is the correct answer says venous ulcer, um key features that point to this are the location. Um So it's essentially just above your, your lateral ankle. Um And the fact that when she elevates her leg, which which improves venous return back to the heart. And the fact that she's wearing tight compression socks help the pain also suggest it's venous rather than arterial. Um So venous ulcers are rather than being due to poor arterial blood flow. They're due to sort of chronic venous insufficiency often due to impairment of the valve. Uh So a similar cause to varicus veins. Um and they're associated with, with chronic venous insufficiency, which is impairment of of flow of the veins due to valvular reflux and results in venous hypertension. Um So you often get these ulcers in what's called the gator region. So this is from sort of the bottom half of the lower leg, the bottom half of the shin to just above the ankles. Um As we've seen pain is, is helped by elevating the limb and wearing something that compresses the, the venous system. So other signs of chronic venous insufficiency are often present. So the lower limbs can be edematous, patients can get venous eczema. Um So this is essentially eczema that's due to uh venous or, or blood being static in the venous system. Um you get hemocorin deposition, which is sort of um blood leaves the venous system and the iron breaks down and leaves iron deposits in the skin which causes pigmentation of the skin. Chroa phlebectatic is a specific sign which is sort of the small dilated veins around the ankles. Lipodermatosclerosis is like you get sort of an ups edema that's worse around the calf and, and, and less bad around the ankle and it's associated with pigmentation or erythema as well. Uh, due to scarring of the soft tissue again, due to venous stasis. And then you can get this white scarring from ulcers that have healed. Um So these are all signs of chronic venous insufficiency. We'll run through some pictures of those just to be aware of. Um, and then the treatment for venous ulcers is essentially compression managing. Um, so if you have this sort of picture on someone's legs and they've also got pruritus, so it's a bit itchy. Can anyone tell me what they think it might be? It's one of one of the things we've just discussed, that's a sign of chronic venous insufficiency. But if you, if you can type it in, in the chat, yes. So we've got hemocrine deposition and eczema. So it does look very similar to haemocin deposition in this picture. Uh Some of the pictures you may see it. Um And it's more than erythema. Um But this is given that you've got the clinical context of the patient itching as well and this sort of dry pattern, it's probably more likely venous eczema or it's also called stasis dermatitis. So this is venous eczema. Can anyone tell me what this one is? Pop it in the chart again, you can describe it too if you'd like. Yeah. Ok. So this one is um called lipodermatosclerosis. So the, the common description that you get is an upside down champagne bottle. So they've got sort of a thin ankle and the edema is more towards the calf. Uh It's essentially due to the venous stasis. You've got um sort of scarring of the soft tissue which causes earth human and pigmentation in this uh strange edema that pools in the upper calf rather than the lower calf. This one is someone's really popped this in the chat. But so this is the, I suppose a differential of your thinking about venous eczema. So this one's the haemocin deposition. So you get these dark pigmentations. Um Yeah. Yeah. Hemy in that position and it's due to sort of iron ii it is extravasation of blood and then the iron in the soft tissue breaks down and leaves this dark pigmentation. Uh You know what this might be a picture of, yeah, it's a very specific sign. So it might be hard to remember from the slide before. So this one is called uh Corona phlebectatic. There we go, someone you popped, it could make it easier to understand what I'm saying. Um So this is again, a very specific sign uh could be called spider veins. Yeah. Um But you see them around now called these small dilated superficial veins in people with chronic venous insufficiency. Um And then this is I'll just talk about this one. This one's essentially a white keloid type scarring after venous ulcers healed. So at atrophy blanche, it is called um so these are all specific sort of spot diagnosis signs, potentially unlikely to come up in a written exam that you might see it in a patient in an OSC or a clinical examination if you've got a vascular station. Um So not the nicest picture, but this moves us on to the next topic. Um So can anyone tell me what this might be? You can pop it in the chat if you know it, it's a, it's an eponymous eponymous type of um condition says named after somebody. Yeah. So someone's someone's got it, it says Fornes gangrene. So we're gonna move on to talk about gangrene. So for gangrene is just a specific one that's good to know as it can come up. Um And it's gangrene that essentially affects the genital region and perineal region. So it's good to look out for it. You've got someone that's got sort of rash or ehe uh down below, it's just to be aware of to rule out. Um So we're going to talk about gangrene. Um So gangrenes essentially tissue death due to poor blood flow or bacterial infection. Uh So it's always good to classify. So you classify gangrene most easily into dry and wet. Um and so dry, gangrene is essentially ischemic gangrene. So it's due to poor blood flow, often peripheral arterial disease, but severe peripheral arterial disease such that they have now got tissue damage. Um And now the tissue itself is dying. So the the symptoms often diminished peripheral pulses in the leg. Uh The the lesion itself is dry and black and cold. Um as opposed to wet gangrene, which is sort of patients normally warmer cos it's infectious, warmer. Um It's normally an accident, but essentially investigations are similar to those that you do. For peripheral arterial disease. You want an ABP to get an objective measure of of the restrict your blood flow. Uh can consider ultrasound Doppler scan. Uh MRI angiogram of of the arteries in the lower leg is probably probably better quality. Um And the treatment is similar again to peripheral arterial disease, which is the underlying cause. So we can treat with IV heparin with antiplatelets. Um and then surgical intervention and often we consider amputation because they've now got tissue loss and death which can propagate and often consider amputating this limb. Um And obviously, the, the point of amputation depends on the, the level where you've got blood flow because you still need blood flow to heal. So, if you've, for example, if you've got a necrotic big toe, but there's no blood flow below the knee, then you'd have to, even though only the toe is necrotic, you'd have to do the amputation at the knee. Cos that's where you've got blood flow for healing. Um But it's essentially again, similar to arterial ulcers. It's, it's treating the underlying cause, which is the peripheral arterial disease. Um So then the other form of gangrene is wet gangrene, which is sort of infectious. It's, it's, it's not cold or dry, like like dry gangrene is, but it's, you get more of a warmth, it's hot. Obvious. Obviously, one of the signs of infection normally is exudate. Um uh which is why it's known as wet gangrene. Specific types of wet gangrene to know about is necrotizing fasciitis, which is sort of subcutaneous infection often can be associated with sparing of the skin. So, but you've got a severe sub cutaneous infection, then you've got gas gangrene, which is normally caused by clostridium uh pergens. Uh And the common sign that you're seeing gas gangrene is sort of crepitus because these are bacteria that form form gas when they cause an infection. Hence the name uh and again associated with systemic signs of infection. So patients like afebrile has chills. Um And you would also see what, whichever region is affected. You'd see the four hallmarks of inflammation. Um Can anyone tell me you can put in the chat, the, the four hallmarks of inflammation going back to basics re it, um, hot red, swollen, painful. Yeah. Good. That's essentially the right answer we've got. So, Rubor is redness or erythema. These are all the Latin terms. Um Calo is essentially the hot feeling. Dolo is pain or, or suffering. And then you've got um the edema are the swollenness. Um So they are the four hallmarks of, of inflammation of any kind. So you'll see that in more in wet or infectious gangrene rather than dry gangrene where it's or it's cold and dry. Um So yeah, and then two more is, is, is the word for edema when you think about the before hallmarks. Um And then if you just go back a second jim and then investigations, you'd, you'd consider doing a wound swab to identify the specific bacteria that's causing it, do blood cultures in case there's systemic infection and the patient might have septicemia. Um And then treatment is I antibiotics, obviously en life trust dependent. So you look at your trust guidelines with antibiotics specific to the area, but I think empiric antibiotics might be like vancomycin and, and tizo kind of thing. But you'd chat with microbiology about that. Um And then consider surgical debridement and maybe amputation depending on the severity of the gangrene. So I think that's all the topics we were planning on talking about today. Um With some, with obviously the questions in between. If anyone's got any particular questions that they want to ask based on what we talked about, then you can pop it in the chat and we can try and answer if there's no questions as well. That's all good. Thank you for coming guys. So just don't forget to fill in the feedback form. It really helps us. Um And like I said, in the beginning, join us every Tuesday for a session that will where we'll cover different specialties, get to its finals. Um But yeah, thank you. Ok. Doesn't allow us any questions I think. Do we have access to slides? Uh Yes, we would um If everyone, if everyone's OK with it, we would publish the recorded session. Um And we'll also put the slides as well. So, yeah, so it's in the catch up session. Um With, with regards to the question about access to slides, it also the recordings. If you need it, we'll just stay on for a bit guys just to make sure everyone is filling the form and stuff if that's ok. Right. I think, I think we're gonna end the chat. I mean the call now. Um But good job guys. All right, I'll just end the call. Thanks, Doc. Thank you.