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VTE Prophylaxis Orthopaedic Exams
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VTE Prophylaxis Orthopaedic Exams
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Language: EN.
Segment:0 .
Now before we move on, we decided to do something slightly different this time. I've got one waiting for admission if we admit that so that I can launch something. Now we've decided that one way of testing you guys in.
Your understanding of the topic is we have decided to include questions that can come in part one of the exam and shortly you will see in front of you a poll with three questions. We will wait for you to answer these questions. And you go.
So as you can see, there are some questions in front of you, I would like each one, please, to try and answer these questions. We will give you a couple of minutes. Can you all see it, please, mentors? Can you see it? Yes, good. So please, candidates answer this if you can. And I can see that no one has voted, can you see it all, guys, please?
We can't see it, Abdullah, but not sure how we can choose the answer. So that's because we're co-hosts. We don't. OK, fine. Sorry the all participants please answer the questions because the quicker we answer those questions, Amjad I can I use you as a Guinea pig, please? Would you be kind enough to see whether you can answer any of these questions?
I can't. I cannot submit it. I can answer the question, but just answer. Let's see what happens. Click on something it doesn't allow me to submit and falling at the bottom. Mm-hmm Yeah OK, let's start again. So relaunch. Uh, continue, continue, let's see you again.
OK can you see it? Yeah, I can see it. I answer it, but. It, you know, there is a Submit icon there down at the bottom. Yes scroll down, answer all the questions and just answer all the questions. Yes Oh sorry, I have to answer. I thought that just one question. No, no.
OK, that's interesting. No one else is answering questions. Here you go. So people are answering now, I've got two people answering. OK, so guys, please answer it. I will wait for something like 80% of people answering Yes. And once we get that, we will stop it and then we will retest you guys at the end of it to see whether that presentation made any difference.
I will end the polling now. We've got 76% voted. I am not going to share the result. OK especially my. OK, now back to the topic. Well, I don't know which one is yours because it doesn't show me any names. It just shows the percentage. Let's move on. So since we back to the topic, let's start about how the clot forms.
The clot is a combination of two factors. The cell factors and the protein factors or the chemicals in this, both of them need a triad, which is called a virtuous triad, which I know all of. There are three important aspects. Number one is to increase coagulation of the blood, and this can be because of conditions like cancers from Ophelia, which is like a congenital conditions inflammatory disease.
The second factor is stasis of blood slowing of the flow of the blood, which make it more prone to clotting. And this happens with immobilization, varicose veins and obstruction localized or even because of a tumor. The third factor is a vessel wall injury that exposes the proteins, the collisions of the vessel wall to the blood flow, and that starts a cascade of events starting from the platelets being attracted to that collision to try and block that area, and that the releasing chemicals that would activate the coagulation cascade leading in a formation of a clot that the vessel or injury can be because of surgery, chemical irritation, inflammation or infection.
The importance of this triad this is what we actually screen for before the operation. Any operation you check for these? Next, again, this is an important slide. This is a busy, busy slide, and I'm not going to attempt to explain every bit of it. Unfortunately, it will be beyond any presentation to talk it. However, I am putting you a link to videos on YouTube in the next slide, which explain it in a very nice way.
Please spend some time. Each video takes something like four minutes, five minutes. Please spend some time reading it. In addition, it is explained well in the books like Ramachandran or van miscovich. What I will say, which is trying to brief that, is basically we have two pathways. We have the intrinsic pathway and the intrinsic pathway. One of them, which is the intrinsic you check with the aapt, the extrinsic you check with the PT and INR.
The chain of events starts with factor 12, which can be activated by the exposure to collision to 12 a. And that leads to factor 11 activation. And then factor IX activation. And then in the presence of factor VIII activation of factor 10, which is the important common factor the same. Well, similarly, in the intrinsic injury in the extrinsic pathway, a trauma leads to activation of factor seven, which activates factor X to 10.
A now 10 8 is an important factor. Once the activation happens, it activates prothrombin two to thrombin and then activates fibrinogen to the fibrin, which is the protein that mainly presents in the clot. Then this gets debrided in the presence of plasminogen, which again gets activated into plasmon, and then it degrades the clot. The degradation products of the fibrin is what we check through the d-dimer, so the d-dimer actually is the degradation of the fibrin.
As you can see here, there are important other factors we mentioned factor VIII. We mentioned the calcium. We if you look at the left hand side, you will see active protein c, which inhibits factor VIII and factor V a. So the presence of that protein stops the clotting and the lack of protein C allows the clotting to go slightly uncontrolled.
OK, now this I found useful tutorials on YouTube. I don't want to waste your time by launching these videos. Please look for handwritten tutorials about hemostasis in YouTube. It's really nice. And it is made in a way that allows you to practice drawing the cascade, which is a very important and very common question in the exam to draw the clotting cascade.
Please, please, please practice drawing it while talking and lining up or labeling will where each medication work? OK it is important for you to understand the medications you use and the common way of asking the question in the exam. I can't remember the last time they said, tell me about warfarin. They don't normally start it like this.
Usually what they do is they will ask you. I do, professor, and then you suggest the medication and then they ask you, how does that work and what is the dose, you know, the practicalities of it. And the reason is you are to be a consultant. You can choose whatever medication you want to choose, but you have to justify it. However, the common medications used are warfarin heparin factor Xa inhibitors target thrombin inhibitors and aspirin and clopidogrel.
If you look here on the right hand side, it is a simplified diagram and I have highlighted where the warfarin work. Basically, it works by stopping the vitamin K dependent anticoagulants, which are factors to seven, 9 and 10. Because it stops production of them in the liver. It takes three, two to three days to start working, and it needs to be built up as the body consumes or degrades the older factors that do exist and have been produced in the past.
Once it starts working, it has a long life and it takes five days, at least for the INR to come back to normal again. As you mentioned, as you noticed, we check it with INR levels. It can be reversed by 2 things, either as you know, give vitamin K or by reverse it acutely with fresh frozen plasma to replace all the clotting factors.
There is an important thing that not many orthopedic surgeons know, and it comes from the hematologist. If the patient is started on warfarin, they go through a phase of hyper coagulopathy, hypercoagulable for about a day or two, and they always recommend using low molecular weight heparin or heparin during that period to stop the patient getting a clot. So when you start warfarin during the first two days, there will be a risk of actually the patient getting a clot.
The next medication is heparin, and again, I have highlighted where it works. It basically works in two factors factors 10 and factor two. It forms a combination combined with anti thrombin three, which stops being thrombin. It is usually a molecule, a protein that is produced naturally and has high molecular weight of 5,000 to 15,000 tons.
The low molecular weight heparin are the ones that are less than 8,000 tons, and they work only on factor 10a and they are given subcutaneously. If a bleeding happens, then we could stop it by proton mean sulfate, which is the antidote. And again, you can give a fresh frozen plasma in acute phases. Other side effects for long term use is osteoporosis, allergic reaction and thrombocytopenia.
The DOACs are the oral medications, which are new medications, and they are divided into factor Xa inhibitors and anti thrombin inhibitors. The fact that any inhibitors are apixaban, edoxaban and rivaroxaban taken orally. And there is no need to monitor them. There is a remark whenever the patient is on apixaban, edoxaban or rivaroxaban, INR a or PT do not have a value in checking whether they are working or not.
And there is a paper written saying specifically, please do not be fooled by normal INR into thinking that the fact, the apixaban is not working. It could be working with normal measurements and the only way of knowing is time because they have a predictable elimination time, which is 36 to 48 hours. And please check the local guidelines because the hematologist would have produced that to tell you when it is safe to do elective procedures or acute procedures.
Similarly, the direct thrombin inhibitors like dabigatran, they are exactly the same. However, the long life, they have a longer half life. Aspirin is the oldest, well, one of the oldest anticoagulation, and it works by stopping from but saying a to working, and there they stop the aggregation of the platelets. It is effective in the prevention of DVT and PE and p.e., and now nice has recognized it again the importance of it.
Now people who work in Scotland know that sign, which is the equivalent of nice in Scotland, has long been advocating its use, even from I remember from the early 2000s. It is safe to operate even with the aspirin in pair however, it has to be discussed with the anesthetist. It is better if we wait for a day or two. Clopidogrel, however, irreversibly blocks the aggregation of the platelets and then hence we have to wait for a new cohort of platelets to be produced.
Hence, we have to wait for five days. We'll talk about non-pharmacological prophylaxis, and I will be talking about mobility, foot and calf pumps. Ted stockings and IVC filters the most important factor in stopping the clot forming is the natural way, which is mobility, and the mobility works by using the calf muscles as natural pumps to push the blood through the valves in the veins of the lower limbs, as demonstrated here.
And that's why it is very important to encourage the patient to start mobilizing as early as possible after the operation. And again, that's why nyce has recognized it as an important milestone in the patient journey, so a lot of the guidelines state. Once the patient starts mobilizing, we can reduce the prophylaxis of anticoagulation. Next is full of pumps, as demonstrated with that picture.
It tries to mimic the effect of the calf muscles, and it's more important when the patient is in bed for pain relief or because of the use of or, more importantly, when the patient is in the operation. In addition, they can. They have we have to exercise caution using them in if there is an already peripheral vascular disease, fragile skin or anything that would stop us putting it on the skin or the shape of the leg, for example, makes it awkward or applying pressure uneven on the whole leg.
Moving to the tight stockings, they have got a gradual compression along the way. There is evidence that the combination of both at the same time, which I have seen some hospital use where they put the Ted stocking and then they put the cuff pump on top is actually detrimental because it reduces the efficacy of the pump. Ivc filter is not something you would be expected to request, but if there is a frequent DVT and clotting and the patient is high risk, sometimes they can mention that it is already on there.
Or you can mention it as a suggestion and the way they work, they have different shapes. The way they work is they are inserted in the inferior vena cava, and they hopefully capture the big clots. They don't capture the small clots they have, they capture on the big clots. There is a debate about how effective they are, and whether they actually can cause clots themselves. Hence, don't suggest it.
But if it's been mentioned, just mention that this is how they work. There can be temporary sometimes for patient patients who have cancer and they are going through a big operation, they can be inserted and then removed after the operation. A lot of medications there there we should mention are tranexamic acid, and the way tranexamic acid works is by stabilizing the clot, by stopping the activation of plasminogen to plasmon.
Uh, it can be used in elective surgery, and there is more and more evidence coming that it is safe and very good actually for knee replacement, for example, where it reduces the need for a blood transfusion. And there is a crash trial which mentions its use in the trauma fresh frozen plasma replaces quickly. The consumed clotting factors and platelets can be given again to enhance the patient's ability to clot.
Let's talk about some common conditions that we may encounter, and again, the question comes in the exam that this patient has this condition. What do you think as part of the workup? So all these increases the chance of patients getting a clot. The first four conditions are congenital. They will just say this patient has a protein C deficiency or whatever.
And I've highlighted how it works in that diagram. All what you need to say is they've had they've got a high risk of infective DVT, and I will be discussing them with the hematology and reverse sorry discuss, according to the local hospital protocol. There is a acquired condition which is antiphospholipid syndrome, which is an autoimmune and acquired condition that again, can lead to coagulation.
Let's talk about DVT now. DVT, I mean, I'm going to talk briefly, you all know about this. It's a condition where a clot forms in the deep veins of the leg. The incidence in 1 and 1,000 increases by risk factors like congenital as virtual trials. If they ask you about the risk factors, it is virtual trials triad.
The presentation is after an incident of immobility on operation cancer. Any pressure and then patient comes with pain in the leg with swelling and edema. The investigation is by venous venous duplex and d-dimer, and the gold standard is the venous duplex scan. The treatment is assessment for prevention. And then you talk about anticoagulation and rarely IVC filter.
And, as I mentioned, don't suggest it. Just be aware of it. And if they say that everything fails, you say, I'm aware of it, that you don't. The complications the risk of DVT is not DVT itself, because most of these clots dissolve themselves. However, it can lead to peace, which I will be talking about in a second.
But they can lead to chronic venous insufficiency, leaving the patient with chronic, swollen pitying edema in the leg with skin changes and high pressure in the veins of the leg itself and can lead to a recurrence of the DVT itself. Thromboembolism is the traveling of the clot from the defense of the leg all the way to the arteries of the lung.
It leads to sudden shortness of breath with puretech pain and tachycardia. It can vary depending on the size of the clot from mild shortness of breath or even asymptomatic to death. The assessment again, the question in the exam comes a patient comes five days, six days, whatever after complaining of these symptoms and they want for you to say, I will go and see the patient, take a history, assess the patient and the tests I will be asking for would be an EKG, a big chest x-ray, and the gold standard is cetp.
And as you can see here, the eye will pay your attention to these marks. You can see the dark shadow representing the clots. These areas there and the treatment, I will be discussing him with the Chest Physicians. However, the treatment principles are coagulation from prophylaxis, and sometimes they will need HDU beds for oxygen support, and I will want that the patient has a high risk of recurrence.
But embolism is not part of the technical thromboembolism as such, but it is a condition that we have to differentiate between the two. The reason is it it can happen again after operation, but usually it happens in the early days rather than later days. Like a DVT pe, as you can see, it causes petechiae in the skin with hemorrhage to the brain. However, we might give a talk about this in more detail later.
Now, this is an important slide, because the exam. This is a typical answer about how you would. Assess the patient for DVT. The question can come like how would you prevent DVT from happening or how would you devise a hospital protocol for DVT prophylaxis or how would you screen for dvt? These are all common leading to the same answer, and the answer have to be divided into these headlines.
The first one is pre-op and post-op and pre-op. I've highlighted separately screening and stratifying. So which is exactly as NICE guidelines say, if screen patients and you stratify their risk factors and then preoperatively you, make sure that they are hydrated, they are aware, they are stratified and you discuss their intraoperative management, which can include mechanical prophylaxis and postoperative operatively.
You encourage early mobilization, mechanical and chemical prophylaxis and early assessment of patients presenting with worrying symptoms. And then you talk about chemical and non-pharmacological factors, and then you have to mention the local guidelines derived from the NICE guidelines. So this is again how you phrase your answer. Moving on to the next slide, which is nice guidelines, again, as I mentioned to you, this has been changed in March 2018.
And the important things that have been highlighted are the coming back of aspirin and the strengthening of the mobility. As a factor for prevention and brief, I will summarize that there is a small summary of it. You can download that from the internet, and I will put in the telegram group a small summary of all the NICE guidelines in a way that is practical.
However, it's the same as these slides. So for any immobilization, stratify the patient, you have to start low molecular weight heparin for if the out of the risk out out is higher than the risk of bleeding and keep that until the patients start mobilizing or up until '42 days. Similar thing for hip fractures pelvic fracture however, they say that pneumatic compression is reasonable if the oral prophylaxis is contraindicated.
Sorry if chemical prophylaxis is contraindicated. Elective total hip replacement, the new thing they have divided into three lines. So the first line is low molecular weight, followed by aspirin or mechanical. At 10 days or the second line, apixaban, dabigatran or stockings. So a total knee replacement, the new thing which is very important.
You have to be aware of is they have started to consider aspirin from day one and it's only for two weeks or you can use low molecular weight heparin. However, people continue to use apixaban and dabigatran. Knee operations that are short with no risk, then you don't need to do anything. Otherwise, you give low molecular weight until mobility or 14 or 20 days or 14 days or again, the same thing for foot and ankle surgery.
Again, if there is no risk factors and the operation is short. No need. Again, if there is, you give something for a short period of time. Spine surgery because of the risk of bleeding into the spine is important, so they advocate using only mechanical prophylaxis. However, if there is a high risk, you can use low molecular weight heparin.
But after you that after a reasonable time where a clot would have formed to stop the bleeding into the spine in major trauma, the importance of mechanical prophylaxis is very stressed again. And that's it. No, it's something I think for spinal surgery, you need to be careful. It's usually local guidelines. As Abdullah was saying, yes, we tend to use mechanical prophylaxis more than everything else, but you can use the usually in our local guidelines, we use enoxaparin, which is low molecular weight heparin, but you use it after to 24 hours after the operation in a small operation or in a big operation.
You can use it after 48 hours or if the drains is used, you can use it 24 hours after the drains is out. OK, so this is our local guidelines here in our. OK, thank you. I didn't know that. It's like that. You go to a screening number one when you go to screening. So every patient in the hospital has to be screened for risk of DVT.
This is the most important information. You need to make sure all patients, all patients coming to the hospital, they need to be assessed screened for risk of DVT and then it doesn't matter what guide, what protocol you are using. The majority of all the patients, they have to have a risk assessment for DVT fresh frozen plasma versus octopus.
Any thoughts you should say? We should say we should say I would give a vitamin K IV and our expertise stops here, and then I'll call the hematologist and ask for advice if they ask you what option. Or if you want to say the options are fresh, frozen plasma, or octuplets. And I wouldn't say anything more.
I'll stop there. Perfect thank you very much. Regarding the mode of mode of action of these drugs is extremely important like heparin and factor two factor two drugs like dabigatran. So dabigatran D4 they use I use the sintoma synonymous of die means like two so dabigatran for factor 2 and x for zeroual two.
Or what is rivaroxaban about? Seven anything has x is factor 10 activated factor 10. So that's the anonymous or sorry, the mnemonic I was using for these factors. So to remember that the mode of action. And I think it's really helpful to remember this in the example, it's helpful you.
Segment:0 .
Now before we move on, we decided to do something slightly different this time. I've got one waiting for admission if we admit that so that I can launch something. Now we've decided that one way of testing you guys in.
Your understanding of the topic is we have decided to include questions that can come in part one of the exam and shortly you will see in front of you a poll with three questions. We will wait for you to answer these questions. And you go.
So as you can see, there are some questions in front of you, I would like each one, please, to try and answer these questions. We will give you a couple of minutes. Can you all see it, please, mentors? Can you see it? Yes, good. So please, candidates answer this if you can. And I can see that no one has voted, can you see it all, guys, please?
We can't see it, Abdullah, but not sure how we can choose the answer. So that's because we're co-hosts. We don't. OK, fine. Sorry the all participants please answer the questions because the quicker we answer those questions, Amjad I can I use you as a Guinea pig, please? Would you be kind enough to see whether you can answer any of these questions?
I can't. I cannot submit it. I can answer the question, but just answer. Let's see what happens. Click on something it doesn't allow me to submit and falling at the bottom. Mm-hmm Yeah OK, let's start again. So relaunch. Uh, continue, continue, let's see you again.
OK can you see it? Yeah, I can see it. I answer it, but. It, you know, there is a Submit icon there down at the bottom. Yes scroll down, answer all the questions and just answer all the questions. Yes Oh sorry, I have to answer. I thought that just one question. No, no.
OK, that's interesting. No one else is answering questions. Here you go. So people are answering now, I've got two people answering. OK, so guys, please answer it. I will wait for something like 80% of people answering Yes. And once we get that, we will stop it and then we will retest you guys at the end of it to see whether that presentation made any difference.
I will end the polling now. We've got 76% voted. I am not going to share the result. OK especially my. OK, now back to the topic. Well, I don't know which one is yours because it doesn't show me any names. It just shows the percentage. Let's move on. So since we back to the topic, let's start about how the clot forms.
The clot is a combination of two factors. The cell factors and the protein factors or the chemicals in this, both of them need a triad, which is called a virtuous triad, which I know all of. There are three important aspects. Number one is to increase coagulation of the blood, and this can be because of conditions like cancers from Ophelia, which is like a congenital conditions inflammatory disease.
The second factor is stasis of blood slowing of the flow of the blood, which make it more prone to clotting. And this happens with immobilization, varicose veins and obstruction localized or even because of a tumor. The third factor is a vessel wall injury that exposes the proteins, the collisions of the vessel wall to the blood flow, and that starts a cascade of events starting from the platelets being attracted to that collision to try and block that area, and that the releasing chemicals that would activate the coagulation cascade leading in a formation of a clot that the vessel or injury can be because of surgery, chemical irritation, inflammation or infection.
The importance of this triad this is what we actually screen for before the operation. Any operation you check for these? Next, again, this is an important slide. This is a busy, busy slide, and I'm not going to attempt to explain every bit of it. Unfortunately, it will be beyond any presentation to talk it. However, I am putting you a link to videos on YouTube in the next slide, which explain it in a very nice way.
Please spend some time. Each video takes something like four minutes, five minutes. Please spend some time reading it. In addition, it is explained well in the books like Ramachandran or van miscovich. What I will say, which is trying to brief that, is basically we have two pathways. We have the intrinsic pathway and the intrinsic pathway. One of them, which is the intrinsic you check with the aapt, the extrinsic you check with the PT and INR.
The chain of events starts with factor 12, which can be activated by the exposure to collision to 12 a. And that leads to factor 11 activation. And then factor IX activation. And then in the presence of factor VIII activation of factor 10, which is the important common factor the same. Well, similarly, in the intrinsic injury in the extrinsic pathway, a trauma leads to activation of factor seven, which activates factor X to 10.
A now 10 8 is an important factor. Once the activation happens, it activates prothrombin two to thrombin and then activates fibrinogen to the fibrin, which is the protein that mainly presents in the clot. Then this gets debrided in the presence of plasminogen, which again gets activated into plasmon, and then it degrades the clot. The degradation products of the fibrin is what we check through the d-dimer, so the d-dimer actually is the degradation of the fibrin.
As you can see here, there are important other factors we mentioned factor VIII. We mentioned the calcium. We if you look at the left hand side, you will see active protein c, which inhibits factor VIII and factor V a. So the presence of that protein stops the clotting and the lack of protein C allows the clotting to go slightly uncontrolled.
OK, now this I found useful tutorials on YouTube. I don't want to waste your time by launching these videos. Please look for handwritten tutorials about hemostasis in YouTube. It's really nice. And it is made in a way that allows you to practice drawing the cascade, which is a very important and very common question in the exam to draw the clotting cascade.
Please, please, please practice drawing it while talking and lining up or labeling will where each medication work? OK it is important for you to understand the medications you use and the common way of asking the question in the exam. I can't remember the last time they said, tell me about warfarin. They don't normally start it like this.
Usually what they do is they will ask you. I do, professor, and then you suggest the medication and then they ask you, how does that work and what is the dose, you know, the practicalities of it. And the reason is you are to be a consultant. You can choose whatever medication you want to choose, but you have to justify it. However, the common medications used are warfarin heparin factor Xa inhibitors target thrombin inhibitors and aspirin and clopidogrel.
If you look here on the right hand side, it is a simplified diagram and I have highlighted where the warfarin work. Basically, it works by stopping the vitamin K dependent anticoagulants, which are factors to seven, 9 and 10. Because it stops production of them in the liver. It takes three, two to three days to start working, and it needs to be built up as the body consumes or degrades the older factors that do exist and have been produced in the past.
Once it starts working, it has a long life and it takes five days, at least for the INR to come back to normal again. As you mentioned, as you noticed, we check it with INR levels. It can be reversed by 2 things, either as you know, give vitamin K or by reverse it acutely with fresh frozen plasma to replace all the clotting factors.
There is an important thing that not many orthopedic surgeons know, and it comes from the hematologist. If the patient is started on warfarin, they go through a phase of hyper coagulopathy, hypercoagulable for about a day or two, and they always recommend using low molecular weight heparin or heparin during that period to stop the patient getting a clot. So when you start warfarin during the first two days, there will be a risk of actually the patient getting a clot.
The next medication is heparin, and again, I have highlighted where it works. It basically works in two factors factors 10 and factor two. It forms a combination combined with anti thrombin three, which stops being thrombin. It is usually a molecule, a protein that is produced naturally and has high molecular weight of 5,000 to 15,000 tons.
The low molecular weight heparin are the ones that are less than 8,000 tons, and they work only on factor 10a and they are given subcutaneously. If a bleeding happens, then we could stop it by proton mean sulfate, which is the antidote. And again, you can give a fresh frozen plasma in acute phases. Other side effects for long term use is osteoporosis, allergic reaction and thrombocytopenia.
The DOACs are the oral medications, which are new medications, and they are divided into factor Xa inhibitors and anti thrombin inhibitors. The fact that any inhibitors are apixaban, edoxaban and rivaroxaban taken orally. And there is no need to monitor them. There is a remark whenever the patient is on apixaban, edoxaban or rivaroxaban, INR a or PT do not have a value in checking whether they are working or not.
And there is a paper written saying specifically, please do not be fooled by normal INR into thinking that the fact, the apixaban is not working. It could be working with normal measurements and the only way of knowing is time because they have a predictable elimination time, which is 36 to 48 hours. And please check the local guidelines because the hematologist would have produced that to tell you when it is safe to do elective procedures or acute procedures.
Similarly, the direct thrombin inhibitors like dabigatran, they are exactly the same. However, the long life, they have a longer half life. Aspirin is the oldest, well, one of the oldest anticoagulation, and it works by stopping from but saying a to working, and there they stop the aggregation of the platelets. It is effective in the prevention of DVT and PE and p.e., and now nice has recognized it again the importance of it.
Now people who work in Scotland know that sign, which is the equivalent of nice in Scotland, has long been advocating its use, even from I remember from the early 2000s. It is safe to operate even with the aspirin in pair however, it has to be discussed with the anesthetist. It is better if we wait for a day or two. Clopidogrel, however, irreversibly blocks the aggregation of the platelets and then hence we have to wait for a new cohort of platelets to be produced.
Hence, we have to wait for five days. We'll talk about non-pharmacological prophylaxis, and I will be talking about mobility, foot and calf pumps. Ted stockings and IVC filters the most important factor in stopping the clot forming is the natural way, which is mobility, and the mobility works by using the calf muscles as natural pumps to push the blood through the valves in the veins of the lower limbs, as demonstrated here.
And that's why it is very important to encourage the patient to start mobilizing as early as possible after the operation. And again, that's why nyce has recognized it as an important milestone in the patient journey, so a lot of the guidelines state. Once the patient starts mobilizing, we can reduce the prophylaxis of anticoagulation. Next is full of pumps, as demonstrated with that picture.
It tries to mimic the effect of the calf muscles, and it's more important when the patient is in bed for pain relief or because of the use of or, more importantly, when the patient is in the operation. In addition, they can. They have we have to exercise caution using them in if there is an already peripheral vascular disease, fragile skin or anything that would stop us putting it on the skin or the shape of the leg, for example, makes it awkward or applying pressure uneven on the whole leg.
Moving to the tight stockings, they have got a gradual compression along the way. There is evidence that the combination of both at the same time, which I have seen some hospital use where they put the Ted stocking and then they put the cuff pump on top is actually detrimental because it reduces the efficacy of the pump. Ivc filter is not something you would be expected to request, but if there is a frequent DVT and clotting and the patient is high risk, sometimes they can mention that it is already on there.
Or you can mention it as a suggestion and the way they work, they have different shapes. The way they work is they are inserted in the inferior vena cava, and they hopefully capture the big clots. They don't capture the small clots they have, they capture on the big clots. There is a debate about how effective they are, and whether they actually can cause clots themselves. Hence, don't suggest it.
But if it's been mentioned, just mention that this is how they work. There can be temporary sometimes for patient patients who have cancer and they are going through a big operation, they can be inserted and then removed after the operation. A lot of medications there there we should mention are tranexamic acid, and the way tranexamic acid works is by stabilizing the clot, by stopping the activation of plasminogen to plasmon.
Uh, it can be used in elective surgery, and there is more and more evidence coming that it is safe and very good actually for knee replacement, for example, where it reduces the need for a blood transfusion. And there is a crash trial which mentions its use in the trauma fresh frozen plasma replaces quickly. The consumed clotting factors and platelets can be given again to enhance the patient's ability to clot.
Let's talk about some common conditions that we may encounter, and again, the question comes in the exam that this patient has this condition. What do you think as part of the workup? So all these increases the chance of patients getting a clot. The first four conditions are congenital. They will just say this patient has a protein C deficiency or whatever.
And I've highlighted how it works in that diagram. All what you need to say is they've had they've got a high risk of infective DVT, and I will be discussing them with the hematology and reverse sorry discuss, according to the local hospital protocol. There is a acquired condition which is antiphospholipid syndrome, which is an autoimmune and acquired condition that again, can lead to coagulation.
Let's talk about DVT now. DVT, I mean, I'm going to talk briefly, you all know about this. It's a condition where a clot forms in the deep veins of the leg. The incidence in 1 and 1,000 increases by risk factors like congenital as virtual trials. If they ask you about the risk factors, it is virtual trials triad.
The presentation is after an incident of immobility on operation cancer. Any pressure and then patient comes with pain in the leg with swelling and edema. The investigation is by venous venous duplex and d-dimer, and the gold standard is the venous duplex scan. The treatment is assessment for prevention. And then you talk about anticoagulation and rarely IVC filter.
And, as I mentioned, don't suggest it. Just be aware of it. And if they say that everything fails, you say, I'm aware of it, that you don't. The complications the risk of DVT is not DVT itself, because most of these clots dissolve themselves. However, it can lead to peace, which I will be talking about in a second.
But they can lead to chronic venous insufficiency, leaving the patient with chronic, swollen pitying edema in the leg with skin changes and high pressure in the veins of the leg itself and can lead to a recurrence of the DVT itself. Thromboembolism is the traveling of the clot from the defense of the leg all the way to the arteries of the lung.
It leads to sudden shortness of breath with puretech pain and tachycardia. It can vary depending on the size of the clot from mild shortness of breath or even asymptomatic to death. The assessment again, the question in the exam comes a patient comes five days, six days, whatever after complaining of these symptoms and they want for you to say, I will go and see the patient, take a history, assess the patient and the tests I will be asking for would be an EKG, a big chest x-ray, and the gold standard is cetp.
And as you can see here, the eye will pay your attention to these marks. You can see the dark shadow representing the clots. These areas there and the treatment, I will be discussing him with the Chest Physicians. However, the treatment principles are coagulation from prophylaxis, and sometimes they will need HDU beds for oxygen support, and I will want that the patient has a high risk of recurrence.
But embolism is not part of the technical thromboembolism as such, but it is a condition that we have to differentiate between the two. The reason is it it can happen again after operation, but usually it happens in the early days rather than later days. Like a DVT pe, as you can see, it causes petechiae in the skin with hemorrhage to the brain. However, we might give a talk about this in more detail later.
Now, this is an important slide, because the exam. This is a typical answer about how you would. Assess the patient for DVT. The question can come like how would you prevent DVT from happening or how would you devise a hospital protocol for DVT prophylaxis or how would you screen for dvt? These are all common leading to the same answer, and the answer have to be divided into these headlines.
The first one is pre-op and post-op and pre-op. I've highlighted separately screening and stratifying. So which is exactly as NICE guidelines say, if screen patients and you stratify their risk factors and then preoperatively you, make sure that they are hydrated, they are aware, they are stratified and you discuss their intraoperative management, which can include mechanical prophylaxis and postoperative operatively.
You encourage early mobilization, mechanical and chemical prophylaxis and early assessment of patients presenting with worrying symptoms. And then you talk about chemical and non-pharmacological factors, and then you have to mention the local guidelines derived from the NICE guidelines. So this is again how you phrase your answer. Moving on to the next slide, which is nice guidelines, again, as I mentioned to you, this has been changed in March 2018.
And the important things that have been highlighted are the coming back of aspirin and the strengthening of the mobility. As a factor for prevention and brief, I will summarize that there is a small summary of it. You can download that from the internet, and I will put in the telegram group a small summary of all the NICE guidelines in a way that is practical.
However, it's the same as these slides. So for any immobilization, stratify the patient, you have to start low molecular weight heparin for if the out of the risk out out is higher than the risk of bleeding and keep that until the patients start mobilizing or up until '42 days. Similar thing for hip fractures pelvic fracture however, they say that pneumatic compression is reasonable if the oral prophylaxis is contraindicated.
Sorry if chemical prophylaxis is contraindicated. Elective total hip replacement, the new thing they have divided into three lines. So the first line is low molecular weight, followed by aspirin or mechanical. At 10 days or the second line, apixaban, dabigatran or stockings. So a total knee replacement, the new thing which is very important.
You have to be aware of is they have started to consider aspirin from day one and it's only for two weeks or you can use low molecular weight heparin. However, people continue to use apixaban and dabigatran. Knee operations that are short with no risk, then you don't need to do anything. Otherwise, you give low molecular weight until mobility or 14 or 20 days or 14 days or again, the same thing for foot and ankle surgery.
Again, if there is no risk factors and the operation is short. No need. Again, if there is, you give something for a short period of time. Spine surgery because of the risk of bleeding into the spine is important, so they advocate using only mechanical prophylaxis. However, if there is a high risk, you can use low molecular weight heparin.
But after you that after a reasonable time where a clot would have formed to stop the bleeding into the spine in major trauma, the importance of mechanical prophylaxis is very stressed again. And that's it. No, it's something I think for spinal surgery, you need to be careful. It's usually local guidelines. As Abdullah was saying, yes, we tend to use mechanical prophylaxis more than everything else, but you can use the usually in our local guidelines, we use enoxaparin, which is low molecular weight heparin, but you use it after to 24 hours after the operation in a small operation or in a big operation.
You can use it after 48 hours or if the drains is used, you can use it 24 hours after the drains is out. OK, so this is our local guidelines here in our. OK, thank you. I didn't know that. It's like that. You go to a screening number one when you go to screening. So every patient in the hospital has to be screened for risk of DVT.
This is the most important information. You need to make sure all patients, all patients coming to the hospital, they need to be assessed screened for risk of DVT and then it doesn't matter what guide, what protocol you are using. The majority of all the patients, they have to have a risk assessment for DVT fresh frozen plasma versus octopus.
Any thoughts you should say? We should say we should say I would give a vitamin K IV and our expertise stops here, and then I'll call the hematologist and ask for advice if they ask you what option. Or if you want to say the options are fresh, frozen plasma, or octuplets. And I wouldn't say anything more.
I'll stop there. Perfect thank you very much. Regarding the mode of mode of action of these drugs is extremely important like heparin and factor two factor two drugs like dabigatran. So dabigatran D4 they use I use the sintoma synonymous of die means like two so dabigatran for factor 2 and x for zeroual two.
Or what is rivaroxaban about? Seven anything has x is factor 10 activated factor 10. So that's the anonymous or sorry, the mnemonic I was using for these factors. So to remember that the mode of action. And I think it's really helpful to remember this in the example, it's helpful you.
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