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Summary

Join Natasha, a current F3 trainee, for an immersive and in-depth teaching session on DVTs and PEs. Participate in interactive case studies like that of Gregory House, a hypothetical patient presenting with an intriguing set of symptoms. Learn how to tease out differentials and develop acute and long-term management plans. Dive deep into the pathophysiology behind these conditions, understanding them from the formation of a clot to its journey to the lungs. Natasha will review a hallmark concept, Virchow’s Triad, and its role in a prothrombotic state. Also on the agenda: a deep dive into D Dimer assays. By the end of the session, you’ll have firm grasp on how to interpret and use D Dimer tests, and how to rule out DVTs. This is a must-attend course for all medical professionals who want a masterclass in managing DVTs and PEs.

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Description

This session will provide comprehensive knowledge on the A+E management of Pulmonary Embolism, aimed at medical students and junior doctors. The teaching will also cover the role of D Dimer in an investigation panel, including common differentials for a raised D Dimer, as well as its drawbacks as a diagnostic test. Our speakers will cover how patients may present, typical investigations and management plans specific to Pulmonary Embolism. As always this will be an interactive session involving case-based discussions and MCQs. Tune in at 6pm!

Learning objectives

  1. By the end of the teaching session, the medical audience will be able to recognize the clinical features and symptoms of DVTs and PS, increasing their understanding of these conditions for differential diagnosis.

  2. The learners will understand the pathophysiology of DVTs and PS, including the role of venous stasis, hypercoagulability, and endothelial injury in their formation and progression.

  3. Participants will be able to identify risk factors and use risk stratification scoring tools effectively in the diagnosis and initial management of patients with suspected DVTs and PS.

  4. The medical audience will learn about the acute and long-term management plans for DVT and PS, thereby enhancing their practical skills and patient care techniques.

  5. The attendees will gain expertise in the appropriate use of D-Dimer in the diagnosis of DVT and PS, including when to use this test, interpreting the results correctly, and understanding its sensitivity and specificity.

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Computer generated transcript

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

My Rainbow Wheel has decided to stop. Ok. Hi, everyone. I'm Natasha. Um currently in F three and we're just continuing on with our, a survival series. We're gonna be talking about D Diers, DVTs and PS. Um As always, I've just got my ipad beside me. So if I'm doing the polls or if you have any questions just popping through and we'll try and get through as many of them as we can. All right. So learning outcomes wise, what we're gonna gain from today's session, we want to appreciate what the clinical features are of DVTs and PS. We want to understand the pathophysiology behind them and recognize any risk factors and the risk stratification, scoring tools for them. But after recognizing this, you obviously want to understand how to, you know, have uh appropriate acute management plan and a long term management plan. So, very similarly, what we always try to do is start this off with a case as how you would see anyone in A&E. So nursing trial just tells you that this gentleman is gonna come in with a swollen leg, that's all you know, and you start seeing this 45 year old gentleman. His name is Gregory House. Um, he's a bit of a character really. And he comes in complaining of a five day history of right leg pain and swelling. He's been managing with a walking stick, which he's found following a sports injury a long time ago and he denies any cough, hemoptysis, shortness of breath and no infective symptoms when you ask him. So the most important question, sometimes you need to ask people in A&E is why are you here today? What's changed that this is and what has brought you in? So he says that this is likely due to a sports injury, he's very opinionated and it's likely musculoskeletal. He would appreciate some analgesia and he can be well on his way home, he's got less bit of chronic pain. He takes a few pills, but he's also got CO PD and he is a smoker with no known allergies. So with all of that there, the first thing you want to do is obviously examine him and as A&E fashion, you want to do an E to e so you look at his observations all fairly stable in themselves right now and his airway is patent, his chest is nice and clear. His heart sounds are regular. His radial pulse is strong, his calf feels firm tender and definitely a bit swollen. Compared to the other side. It's G CS is 15 out of 15. Its tummy are all fine and this is what his right calf just generally can look like. I know that was quite an influx of information. But if we take it from there, what will be your differentials at this point in time? So, to make it easy on you as well, I'll give you a little poll. But if you think of anything else, I'd be more than happy to discuss with you if you think what it could be. So, yeah, you've got quick responses. Can we get anybody else as well? Come on. What do you think this could be? We've got a gentleman that's come in five day history of a right leg swelling. He's got no infective symptoms. It's a bit tender, it's a bit firm. It's a bit swollen. Yeah, I agree with some people. There's still a little bit of ambiguity going on before it. Um, and these differentials that I've listed down as options can all be quantified and like, um, can be taken in as a differential for a DVT. And this is not just because I'm doing a DVT lecture, but yes, we're going down the RO route of thinking that this is DVT. So, because we're gonna be talking about DVTs, let's take a minute, stop from thinking about the case and talk about VT ES and venous thromboembolism as an umbrella term. What exactly is this about? And this covers two things that we're gonna talk about in this presentation itself. One is DVTs. DVTs are basically either an acute or a chronic occlusion in your deep venous system most commonly found in your lower limbs. But you can find it in your upper limbs as well. And it's commonly affected by the formation of a clot known as your thrombus. And we also have pulmonary embolisms which are also either an acute or chronic occlusion in your pulmonary arteries. How do they come about? They come about from that thrombus that we talked about earlier. Fragments of that thrombus can actually break up and that can travel all the way up to your lungs becoming an emboli. So we kind of understand how this clock forms and how this clock travels and goes from said lower limbs to lung. But what exactly is your pathophysiology behind it? Anybody we've talked about it all about in med school, but there is this beautiful triad. If anybody remembers the name of it and we will talk about it. I just wants to show off, you can tell me what that name of that triad is, which is the basic pathophysiology of any VT E and understanding those three components will take us a long way. Yeah, try it. So, so Rudolph Vow basically stated that with these three components, so either a combination from all three of these components, basically leave us in a more prothrombotic state. So if I ask you to visualize in a line of equilibrium, let's say, and we've got a prothrombotic state and a fib fibrinolytic state. What veras triad basically tells us is that with these components of different factors, all working together, it tips this equilibrium and makes us a bit more into a pro thrombotic state and increases that risk of thrombosis. How because one it will result in local cytokine production. It will also cause more um leucocytes adhere to the endothelium, but it, these happen altogether. So if I were to ask you, which is the most important factor in the triad, which would you vote for or would you say they're all pretty much equal when it comes to how much each one of them would, you know, um take how much each one of them would affect A DVT or a VT E? Yeah. So realistically, all of them have an equal amount of importance. But at the end of the day, no one criteria in isolation can cause VT E. It is a combination of different aspects in all three of them working together. And what is really important at the end of this presentation is understanding that looking at s tribe really gives you an idea as to understand how they come about with the clot and also how to treat it because treatment is based on these components, which is number one, you are wanting to get over our um venous stasis. Basically, you want to try and prevent that. Number two is anticoagulation, which we will talk about later. And number three in combination of everything is reducing risk factors. But enough said about that, let's talk about venous stasis for now, first component. And if we think about different elements such as af ventricular dysfunction being immobile, basically, that's what stasis is, isn't it? And having high risk of venous stasis through venous insufficiency where you've got all this blood that's pooling down bottom of your legs, you've got venous obstructions either through tumors, obesity or even pregnancy. And our second state is being in a hypercoagulable state. And this can be seen in most commonly malignancy, pregnancy, estrogen use and any type of trauma or especially major abdominal surgery or lower limb surgery. And trom ofilia have got hematological conditions. And the third one, endothelial injuries, which is as simple as it is vessel wall injury. And if you think about it just externally, it could be things like trauma surgery, venipuncture or even internal to your endothelial wall lining. So this could be things like your atherosclerosis, your hypertension, any lines that you're putting in and it's these combinations in together which form the basis of your pathophysiology for both DVT and PE. So with that said, we've talked about the path of physiology. Let's talk about D diamonds and I feel like all of us will have a little bit of strong feelings about D Diers, especially when you're a junior doctor. Have you ever been in a clinical scenario or have you ever known a clinical scenario. Friends talk about it when working, where you're talking about AD dimer and you had to chase AD dimer and you just found everything a little bit pointless. A little bit, just overwhelming that this was even done. That's fine. Um, a lot of people do have these situations. I'm not saying every single situation is a bad situation, but you will tend to find that ddimer are often misused and we're trying to learn how to use it correctly and when to use it. Ok. So what exactly is a ddimer? What does it do? It is a blood tube. So it's a test that you take. Obviously after venipuncture, it is most commonly across the UK. It's through your blo your blue tube. Um and it detects fibrin fragments. So if you think about your clots and when the clot breaks down, it basically leaves all this fibrin split proteins in this fibrin mesh, what your D dimer does is, is it beautifully is very sensitive to this and it picks up all of this fibrin fag fragments that's in your body and it detects it and it collects it and that's your measurement. So that's all great and wonderful. But we need to know a few more facts about D dimer and you better pay attention because you've got a little pop quiz coming right after this as well. Number one, people have this huge thing where we talk about sensitivity and specificity. So let's talk about it. Now, like I said, has an extremely high sensitivity, 96% sensitive to pick up on clot degradation. So it is really good and sensitive to pick up on that. However, it has very poor specificity. The reason is because ad dimer will be raised in any clinical condition where your clot turnover is increased. And that just means where you have any amount of clot breakdown and clot reformation or like it forms itself and it degrades itself. Ad dimer will be increased. And this is any clinical con condition such as any infections like pneumonia, cellulitis, malignancy, hemorrhages, trauma, um high intensity workout. So what you tend to find is that in different clinical scenarios, a DDIMER would be raised and that's what means it's a poor specificity. However, it's use of the D dimer actually to rule out a DVT because when you do it and you're quite sure that this is not a DVT and you do ad dimer and it comes back negative. This is 96% sensitive to rule out A DVT and that's where people actually get quite mixed up about the use of the diers. Second fact is to just understand that a normal D dimer level will increase with age. So as people get older, a baseline D dimer level will slightly increase and that's why nice have suggested doing an age adjusted DDIMER. So this means either by timing by five or timing by 10 for your like ddimer essay and like measurements that you would use in your trust. So when do you use ad dimer? Well, there are a few things. Number one, you need to use it in the overall clinical picture. Number two, we we'll go through when and how you use it based on pretest probability, well, score and risk stratification. And that gives you a better idea as to when to actually use this test. Major exceptions for using ddimer are for pregnant women or postpartum women because they are physiologically in a hypocoagulable state and D diers will be naturally raised. So if you are a suspicion in a pregnant or a postpartum woman, most of the time our cog have even said that any suspicion or any worries, you would just immediately go to the investigation rather than doing a ddimer and another high um high risk population. Uh IVD use where they are extreme high risk and the as well. So you'd just be, you'd earn the side of caution for that population as well. So we're back at it, got a little game of either fact or fiction, which is basically like true or false if you think about it. So hope you're paying attention. So if I were to ask you, is the D dimer a hematological test in a blue test tube, do you think that's true or do you think that's false? Come on. I know we can get more people than that Come on. Beautiful. Yes, that is true. Next question is it used as a diagnostic tool due to its sensitivity. I've got quick answers today. So lot of splitting votes. It is used as a diagnostic tool to help you and help you for diagnostically because of its sensitivity because it has a high sensitivity. So yes, it is a diagnostic tool for sensitivity. Does it help you rule in a DVT or a PE? Perfect. Yes. So sorry for like the lack of communication while speaking about two, I didn't want to give away the answer for three. But yes, you're using AD dimer because of its high sensitivity to rule out a DVT and a PE. So next one does a positive D dimer help confirm a diagnosis of a DVT or a PE. So if you got a positive result, does that mean that a diagnosis of a DVT or a PE is confirmed? Just because you have a positivity dimer? That's right. Yep. It does not confirm a diagnosis of a DVT P. It is basically a tool to help you try and rule out that's the point and that's what we're trying to employ here. Next question. Does age affect the dima results? What do we think as you naturally age? Yeah, because as you're naturally aging, even your ve vessel wall would tend to break off as well and that degradation will increase as well. That injury will increase permeability will increase, which will then in fact, increase your D dier result, last one. Ddimer can be raised in athletes. Do we think that's true? Do we think that's false? So D diers can in fact be raised in athletes if you just think about how high intensity their workouts are and how the vessel wall itself can actually just be. Well, I wouldn't say injured but how it actually hypertrophies in itself causing that clot degrade, causing that degradation product to increase the diers will naturally increase in extremely fit athletes as well. So this exercise is just basically to instill in you why we use the Diamma and when it is appropriate. Ok. So house is a little bit lonely cos we've kind of taken a step away from him. So let's go back to our case and let's talk about his swollen leg. So first things first, let's examine his leg. Now it, it sounds, it sounds so silly to talk about exposure, but you would be surprised how many times people just doctors just ask them to just roll up their jeans up to their mid knee or just a little bit just over their calf. No, make sure that you indeed have proper exposure all the way to their mid thigh, especially inspection wise, I want you to understand that even in inspection, you can have a rough idea about risk factors. So this could be about someone's age. This could be if they are slightly overweight, if they're pregnant? Are they immobile? Um, any obvious trauma that you can see just on an inspection when you look at their legs, uh, any signs of erythema, any signs of edema, any distended collateral veins that there? And why are the collateral veins getting distended or engorged? Might it be? Just because the main veins are get, have a clot? So the collateral veins are basically trying to supply it. Are there any signs of chronic venous insufficiency such as varicose veins or ulcers? And when you palpate them, what are you palpating for? So, palpate the temperature have a squeeze of the calves. Are you trying to see whether it's tender, does it feel firm? Is extremely swollen? Uh Is there pitting edema? And you want to always, always, always compare with the other leg. You might tend to find that that pitting edema is bilaterally. You might tend to find that that deep tenderness along your um deep venous system is bilaterally as well or are there changes that are new or is it old on both sides of the legs or one leg? And most importantly, under this as well, you want to do measurements and that measurement is 10 centimeters below your tibial tuberosity and measure both calves. So I understand whether there's any difference or asymmetry in calf size. So clinical features wise is you're thinking about a painful unilateral. So definitely remember that unilateral leg swelling that is warm to touch and may come with a bit of erythema in itself. It's important to know sometimes in cases of DVT that it can be asymptomatic. And it's important at this point to just be an uh side of caution. Why are you so concerned about DVTs? You're concerned about it based on the complications. First complication is obviously what we talked about earlier is the complication of it becoming a pulmonary embolism. Another very common complication for patients that have had DVTs. And this can happen within the two years after DVT is something known as post thrombotic syndrome. And that's basically just because of that increased um chronic venous insufficiency that has led to venous hypertension there. And this can lead chronic swelling, skin changes, erythema and in the leg and causing even ulcers and even gangrene. And this is quite a significant complication. So when we want to approach DVD S, there are a few things that I want us to consider and keep in mind. Number one, it's good to have an idea where you think the location of this DVT is gonna be so it could be distal. So below your popular track to find is if it ever was below most of the patients, if it's come up actually are asymptomatic, and they actually tend to resolve spontaneously without any symptoms. If it's proximal and above the trifurcation, this may tend have a higher, greater chance of affecting your bigger veins such as your femoral vein, your iliac vein and your popal veins. Just percentage wise, about 50% of patients with proximal DVTs go on to have peas within three months to six months. So it is extremely high and obviously others, you can have it in your upper limbs as well. But it's always having a good idea about what the vessel is or the location of the thrombus. Now, when we talk about etiology, it's basically a pathophysiology that we've already discussed. So it's good to have a try at the back of your head. But apart from beha triad and it's related, you want to know whether this is a provoked, are there risk factors that have likely caused this to have tipped that equilibrium into that state or is it unprovoked where you actually have no identifiable risk factors at all? And it remains a bit of a mystery that will require further investigation. So this beautiful diagram over here just shows you stages of chronic venous insufficiency. It basically just describes the fact that your venous return is so poor, increasing your venous hypertension, increasing all that blood flow down, gravitating towards the bottom of your leg, not allowing that supply to come all the way back to your heart. And it can go from normal veins to spider veins to varicose veins, causing swelling skin changes and even ulcers. Our third point is thinking about risk factors. So we've talked about this indirectly already. So I'm not going to just list them out for you, but it's good to have an idea about the risk factors that are likely tipping people into a pro thrombotic state. Um So slides will be available. You can definitely just go through this, but let's just get through the presentation if that's alright. The most important thing is risk stratification and you're gonna know the answer to this because I expect you to know the answer to this. What is the scoring tool that we use for DVTs? Any guesses? Yeah, 100%. We used the wells score for a DVT. Beautiful. Yes. Well score. So what is the well score as well as criteria for your DVT? But what is it actually there for us for? And it's actually used to assess the likelihood and the risk of DVT. But most importantly, it helps us guide further investigation as to what we want to do after we get this beautiful score. And it basically changes people into different risks. So you could be in low risk, moderate risk or high risk of developing a DVT. Something important to remember about DVTs wells criteria for a DVT. Is that the point to remember is a wells of two, if it breaks the wells of more than two or wells of under one, and we'll go through why? So coming back to house, if I were to ask you to do a well score for him, so he's fit and well no signs of cancer, you know, that he has been mobile. It's not been bedridden. He's not had any major surgery. His calf swelling is more than three centimeters. He's got no collateral veins present. His entire leg is swollen. His, he has some tenderness. He has no tenderness, sorry along his deep venous system, but he's got pitting edema confined to his symptomatic leg, no paralysis, paresis and no previous DVT. And you're fairly confident this is a DVT cos this is simple. This is bread and butter for you. What do you think his well score would be? So if we just go through it where he would score points, his calf swelling is more than three centimeters. That's one point over there. His entire leg is swollen. That's one point over here and he's got pitting edema confined to the symptomatic leg. So that is three points. So he's got a wells of three. So how do we diagnose and manage this? Bear in mind. He's got wells of three. So let's go through it. Number one. Well, score is so important. It helps you identify what you need to do. Next. Diagnosis for a DVT is by ultrasound or ultrasound Doppler and having this the back of your mind, it looks more complicated than it is and we'll go through it and then we end up with the management of anticoagulation or do we think it's something else? It's not a DVT? So let's look at this table. We've already technically talked about it. We suspect a DVT and we've done a wells score and it's a two level score. And what that means is that it gives us a little breakdown about the points that we need to think about. So we'll go through as though this is house and we think his well score is three at the minute. We think A DVT is likely. So he's gone for an ultrasound scan as soon as possible. So an ultrascan at least within the next four hours, if it's positive, it's starting on anticoagulation. If you can't get him to an ultrasound scan immediately. Let's say this is three in the morning on A&E. What we tend to do is we are quite sure that this could be a DVT. Highly likely we treat them with treatment dose and Oxin that one dose. We ask them to come back the next morning for the ultrasound scan to confirm. No, if the ultrasound scan came back, negative considerations can this can differ slightly according to hospital policy. So you can do ad dimer to definitively rule out a pe and think about your differential diagnosis or you can also just repeat an ultrasound in 6 to 8 days later. Because this is because sometimes when you've got those distal, based on the locations I was talking about below your popliteal traffic application. If you want distal clots, these can then tend to travel up and spread. So it depends on limitations of your ultrasound scan. It just depends about whether it was. So that was just a reason for it. That's why they have made this measure to repeat an ultrasound scan. Now, if a DVT is unlikely and you've got a wells less than one, that's when you do ad dimer. Because if it is negative, you can consider other diagnosis, you've ruled out a DVT. But if it has come back as positive, then you go down this route of needing to confirm it. So hopefully, that makes sense and we'll talk about anticoagulation. So treatment dose of Lola Heparin, this is an oxy barin. And then now it's when and if you want to start people on DUA, I don't wanna expect you to do this on A&E, this is something that the clinics will help you with or your GP will help you with, but it's good to know. So if they're stable, there's no renal impairment or Columba disease, you would offer Apixaban and Rivaroxaban. If it's not suitable for them, then you would do low molecular weight heparin for five days and then offer Adoxa or even Warfarin. If they have active cancer, it's doac Toxiban and in any renal impairment based on their creatinine clearance. So if it's between 15 to 50 you would offer Apixaban or Rivaroxaban. And if it's under 15, you would offer Enoxaparin or Warfarin. Now, these are nice guidance based on 2020. So you'd always ideally look at it but you wouldn't be starting anyone on it immediately in an A&E perspective. And this is just a note if you're starting someone on Warfarin, they need to have two consecutive I nr s that are able to, before stopping your bridging therapy. Long term management is something that will, it's like DVT clinics. So what you need to know is that if you're starting someone and you think that they've got, for example, a provoked or unprovoked pe they'll be started on anticoagulation, which is suitable for them for a minimum period of three months after this period, they need to be reviewed in a DVT clinic which is either run by specialist nurses or hematologists or even respiratory consultants. And they're reviewed in these clinics to talk about the risk and benefit of the anticoagulation treatment. Where do they go from here? Are they gonna stop it, continue it or change the treatment? And it's based on if it was a provoked DVT or an unprovoked DVT, if it was provoked, have we addressed their risk factors? Have we removed it? Have we eliminated them? And if it's unprovoked, is there a cause underlying this? Is there a hematological cause that we need omphalia testing or are you concerned about cancer? Are you concerned about Lupus sl E? So it takes a little bit of a while to get through it, but that's a clinic idea and an approach to a long term management patient. So hopefully that makes a lot of sense. No, we're gonna talk about a couple of months later. You're back on another A&E shift and you know that he was treated with a DOAC following a confirmed DVT on ultrasound scan. So that was great. You know, you got him started. You knew what to do. You've sent him off, haven't seen him for a while. So you're about to see a new patient and a tri nursing trial just told you that he's back two months later and he's a bit unwell and he's complaining of shortness of breath and he doesn't look very good at the minute and three days of dyspnea, pleuritic chest pain, got a bit of a productive cough. He says as well. It's a bit greenish, got a bit of tinge of red in it thinks he's coughing out a bit of blood and he tells you that, um, I don't really think I was taking that do II didn't really think you were right. So that's all fine and great. So you examine him and if you look at his observations compared to what it was for the first time you saw him two months ago, he's a bit tachycardic. His BP is a little bit lower than what it used to be. He's on uh 4 L on a nasal cannula. Um, and you do a general exam on him. He's got a bit of generalized wheeze. He's known CO PD. He's a bit tachycardic. His right calf feels firm and is still quite tender. His G CS is 15 out of 15 and his tummy is nice and soft. So you tend to tell me no poles for this one. What are differentials when you're thinking about a patient like this? Yeah, great. We're thinking about peas. That's, that's brilliant. I want you to be thinking about peas. But what could make you think, you know, this wasn't a pea in terms of other differential. So he's complaining of a little bit of chest pain, he's complaining about a productive cough. Anything else that you can think about? He's known co PD pneumonia. Yes. Burn it. Yeah, I want you to be thinking about other causes as well. Things that are very similar because exacerbation of CO PD. Yes, 100%. Yeah. The reason is, is because when it comes to DVTs and PS, what you tend to find in real clinical practice is that there is no just one fixed symptom, there is no just one sign to actually help you make a diagnosis. It's about the entire clinical picture and it's just about clinical picture, risk stratification and risk factors together to help you diagnose a pe. It's probably one of the most difficult diagnosis to do, which is a pulmonary embolism sometimes. So with that said, let's simplify a pe in the easiest way possible. And how do we do that? We talk about the symptoms so very commonly it is this new onset dyspnea with pleuritic chest pain, they can have a cough. Normally with OPS, they can be quite lightheaded. You can have some syncope and they have features of DVT signs. They are quite tachycardic. They can have a low grade fever and they've got this new onset um oxygen requirement. Now, it's really important to think about the complication of right heart failure and the signs associated with it. So this can be hypertension, elevated J BP and a tricuspid regurgitation. And the reason for that is because peas are so serious because of their hemodynamic compromise that it can cause. So if you just think about where this thrombus that has become an emboli has gone, so if you think from your lower limbs, it has basically gone all the way up through your vena cava into your right atrium and back out into your lungs. And what can happen in a massive pe when you have about more than 50% of obstruction in your pulmonary vasculature is a circular collapse can actually happen just like that because of the fall in cardiac output. And it's because that right side of your heart is failing, it's unable to pump an adequate amount of blood through your already reduced pulmonary volume, that's there to the left side of your heart. And with that said, there are a few things that we can do before that becomes so severe. And these are just common investigations So E CG, we can see sinus tachy, we can see the textbook ECG pattern. If anybody wants to, everybody will remember this. Um You can see some right heart strain as well and your ECG can actually just help you with differentials wanting to exclude. Sometimes it could come in with a CS, they could come in with an M I. So yes, the textbook pattern is definitely your S one Q three T three. There's no evidence to say that this definitely suggests pe but there was some correlation in terms of right heart strain. What you can find on ECG are things like your right bundle branch blocks. You can see some ST um ST depression or T wave inversion in both your anterior leads. So this is your V one to V four and your inferior leads your 23 and F. So it's good to keep that at the back of your head. And obviously for P ES, it's good to, if they're needing a bit of oxygen, you want to do an ABG, you want to differentiate and make sure especially with him with CO PD, you want to have an idea what his gas is like. You wanna make sure he's not acidotic. You want to make sure that it's not just type two respiratory failure with acidosis or is it just type one respiratory failure? So when it comes to bloods, what blood tests do you think from this option on the polls would help indicate a severity of a pe. Would it be a B NPA troponin? An apolipoprotein or a high sensitivity C RP? Yeah, 100%. So troponins are used as an indicator of how severe right heart strains are in severe P ES. Chest x rays, chest x rays are a beautiful tool which is right beside us that we can order just like anything to make sure that we don't have any major consolidations, any major trauma, pneumothorax to have caused these symptoms. CTPA is the gold standard for a pe and obviously, you've got other things that you can do if you're worried. So if you think that this person also has a DVT, you do an ultrasound Doppler person is pregnant that that quite happens of whether you should do ABQ scan or a C TPA scan. And you can also do an echo when you're query about this right heart, right ventricular strain or failure. So, we're back to what matters and a little approach to P ES in terms of a few things. So the first thing is timing. So it's good to just have a better understanding about when does it happen. So if it's an acute, it's at the onset of your occlusion. If it's subacute, this could be within days to weeks. And if it's chronic, they could present with complications of chronic emboli like, and you can even see signs of almost pulmonary hypertension a point in time Now, when we talk about severity, I know someone has beautifully pointed out pes earlier and um we're gonna talk about pesci as well. But first, when you talk about severity, I want you to ask two questions. Are they hemodynamically stable? And is there any evidence of any heart strain? Nonmassive means that they are stable? No evidence of heart strain submassive is they are stable, but there is some evidence of heart strain, either that you've picked up on your CT or your echo or biochemically by your troponin. And massive is when you are hemodynamically unstable, needing inotropic support. Now, pes pes E is a scoring tool which is a prognostic scoring system and you only use pesci after you have confirmed the pe imaging wise. The reason is you use PES E to determine severity for two things for one outpatient or inpatient treatment and two, it helps determine mortality. So it groups people into five different risk groups for a 30 day mortality. And that's when you use pesci location wise for ap it's just good to have an idea about these things. So it can be almost segmental or subsegmental. So these are your collateral or your lower order pulmonary vessels around the borders. Your lobar would be your right or your left main pulmonary arteries and your saddle would be basically an embolisms that's lodged in your bifurcation of your pulmonary arteries themselves. And when we talk about etiology, we've obviously talked about ow triad, which is beautifully done. We've talked about it in DVTs in the sense that are they provoked, are they unprovoked? And this is related to our risk factors. So huge risk factors that you will find are number one dvts and having previous CT es cancer and recent surgery, immobility and any lower limb trauma or fracture and pregnancy just being in its physiological state, high risk and you will tend to find that these major risk factors are already in our risk stratification tools. Other risk factors are things like your C OCP pills, long distance travel. Obviously, if they are thrombophilic and being overweight with that said, let's talk about our risk stratification tool. So we're gonna talk about similar things. We're gonna talk about wells again, but the wells obviously looks a bit different for a pe similar rules apply wells is used to assess the likelihood of the risk of your pe and it's to help you guide for further investigations, it divides patients into low, moderate or high risk of a pe. I didn't give you any examples of revised geneva or P but we'll just talk to you about it cos it's not commonly used revised Geneva. Similar principles apply for wells. It's most commonly used in Europe of very different trusts. It doesn't account for any clinical acumen. So it doesn't have the, do you think a pe is a number one diagnosis or equally likely component? Now, perk, perk is basically known as a pulmonary embolus rule out criteria. And it was basically an American thing which came up and designed this to make what is already a low risk population into an absolute no risk population. And they have about a set of questions, eight or nine questions and all of it have to be a no so that Puck can effectively rule out a pe and that's the criteria. And PSE we've obviously talked about the severity in that sense. So now coming back and talking a little bit more about wells in itself, we want to talk about houses, wells score. So does he have features of DVT? He does have features of DVT. You are fairly confident. This is a pea bread and butter for you. He is tachycardic. He has no immobilization, no surgery. He has had a previous DVT. You saw him on the first admission and he has some hemoptysis but no malignancy. What do you think his well score is going to be? So if we go up from the top, he has clinical signs and symptoms of a DVT. Currently, you are sure that this is ap he is tachycardic. That's 7.5 and he had a previously, sorry, he's had a directive diagnosed PV and DVT and he's got hemoptysis as well. So have I not calculated that right? So 367.5. Yep. So hopefully that gives us the answer that we need. So, coming back to management and this is how we do. It's based on that same step, two step or two. The two level model of a well score and this little criteria is four. So if we have under four, you do a ddimer. Sorry guys, if you do under four, you have ad dimer and this D dimer will definitely help you appreciate whether it rules out ap and then you can think about alternate diagnosis or if it comes back positive, you do a C TPA. And if it's over four, you just immediately do a C TPA. You don't have to use D dimer as a buffer. But coming back right to the top here, if you think about a suspected pe, you need to understand whether they're stable or are they hemodynamically unstable and will they require higher level support such as ITU or HD U and consideration of thrombolysis or inotropic support? So with that said, let's talk about acute management, which is basically anticoagulation questions that you need to ask yourself. Are they hemodynamically stable? Do they need itu or HD U support? And what is their petty score and severity appear, especially if they are stable in themselves. So if they are stable and you already know that they have a PE on their C TPA, and you've start them on anticoagulation if they are at high risk and this means that they've got high pity scores or features of heart, right? Heart strain you'd ideally want them to be on a high level of care to be monitored. However, if they are low risk with a low score and no features of right heart strain, you'd be more comfortable with considering discharge with anticoagulation, follow up troms. Now, this is a senior led decision and you wouldn't be have, you wouldn't have to make this decision as a junior, but it's always good to know that this is an option and when it is indicated. So with that said, our indications include them being hemodynamically unstable. And if you are obviously concerned or you're suspicious about pe and they are hemodynamically unstable with yourself, their BP is through their boots. They're hypoxic, they're tachycardic and the symptoms that they were coming in beforehand or in situation of a cardiac arrest with a confirmed or suspected pe. And also third indication is if you have a confirmed pa with deterioration despite any anticoagulation. So similar things worsening, right? Ventricular heart strain, increasing oxygen requirements. Now, this is similar to our previous anticoagulation slides, similar rules apply. So we don't have to go through it too much. Um And the similar rules apply for long term management and referring them to a pe clinic. So very quickly, we've just got a couple of cases left and then we can take it from there, talk about case one. We've got a 67 year old lady complaining of leg swelling. Now both her legs are swollen. She's got pitting edema. She's got a productive cough. She's got a little bit of arthro ea. And you've done a wells on her, her wells is two and her wells is two because she's had a previous DVT in the past and she does have some collateral veins that are quite distended and it's quite tender. She's complaining of obviously her right leg, her right calf being worse than her left. So, with the wells of two, in consideration of, you know, query this DVT, what would you do for them? Would you do a de dimeth first or would you do an ultrasound scan? Ok. So we've got things, things back a split in the middle. So let's refer. So we've got, we've done a well score on her and we think it is likely to. So yes, we immediately go and do an ultrasound as soon as possible and her ultrasound actually came back negative. So we did a ddimer and her D dimer came back positive. What do you do then? So my question is if her D dimer came back as positive, would you repeat an ultrasound scan or would you? Yeah, you would, you would repeat an ultrasound scan as well. Now, question for you guys is based on the symptoms that I was talking here, you know, bilateral swollen legs, pitting edema. She's got orthopnea. Is there anything at the back of your mind that you're thinking that this could likely be apart from a query DVT and this is just to keep differentials at the back of your mind. Yeah, we want to be thinking about heart failure as well. It's very, very, very unlikely two have, you know, a DVT when you have bilateral swollen legs. So someone's asked, would you have done a deer first? Mm. Well, no, realistically because in this scenario, that's one thing to do. Number one, you would just do a wells score and your wells score would immediately show you for a wells of two. You would do just do an ultrasound. And the reason is also because she's got high risk factors as well in the past to put her in a prothrombotic state. So you can still query a DVT but ad dimer might come back raised anyway, in this context because she has, she might have, you know, past medical history of heart failure, she might have loads of other things. So if we go very quickly to case two, just before we end 63 year old guy, he has central chest pain, he's complaining of shortness of breath. It's a little bit tacky. He's hypoxic. He's on 6 L of oxygen. You have a listen to his chest. He's got right basal crackles. His crp is 100 and 30. His troponin is 200. His chest X ray, he's got a right sided like uh lower lobe consolidation. His wells is three. His wells is three because his heart rate's over 100. He's had a previous DVT in the past. So his risk factors are, he's a smoker, long haul flights and he's a bit overweight. So, with that said, would you do a ddimer on him or would you C TPM? So, we've got a wells of three. Interesting. So I think about it. So we've got a wells of three. What does that mean? According to the well score, it means you do a ddimer. This is according to protocol and according on basis of what guidance is you do ad dimer. And let's say this is his ddimer result. His D dimer is 600. His nor normal range is 220 to 550. Sounds like a silly question. But do you C TPA him or do you think about an alternate diagnosis and we'll talk about it? Yeah, I think, I think the point of these cases are, it's not clear cut. These are real life cases by the way. And I want you to just start understanding that the well scoring system and the, the, the need for a well scoring system and how it just guides you. It is a guide. So in this case, it is told us for a well score of under four user D dimer. But we also know he's got a right sided consolidation. He's got ACR P of X much. It is likely to be raised. Unfortunately, more likely than not. It's not horrendously. Raised but it is because it is affected. So yes, you would go down the route of the C CPA. Now, a clinician or a slightly higher senior clinician can then make the decision to just say let's cancel out the D I mean, this is, I am concerned about a pe because of, I'm concerned about the risk factors that he's had. I'm concerned about the signs and symptoms that he has had and there is a high risk of him actually having a pe and that's still completely suitable in itself. And you would just opt for a C TPA first. So these things tend to be a little bit more gray, but it's really good to understand when to use a well score and how it guides you, how to use the ddimer appropriately and always speak to a senior in that sense. But using these three steps, I feel like it will encourage your weight and how to move forward in terms of D Diers VT ES and P ES. Hopefully that's all alright. I really appreciate if you guys could do the feedback form. Give me a second if you have any questions. Just let me know. Thank you very much. Don't forget to do the feedback form for us. Um We've got our next session next week which is Falls and Silver Trauma surveys. But yeah, thank you very much. You guys, you guys have a good weekend. Thank you for coming. Just don't forget to do the feedback form for us. We really appreciate it.